Episodes

  • 01:48:03

    The Dark Triad (Psychopathy, Narcissism, Machiavellianism), sexually violent predators, Ted Bundy, and porn.

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    On this week’s episode of the podcast, I interview...quite a few people! We are covering Ted Bundy, America’s most infamous serial killer, and since the world has been fascinated by him lately, I figured I’d get a group of mental health professionals in a room to talk about him. His horrific acts made the news and have scared people for decades now, and rightfully so. Did media and pornography cause this? What was his diagnosis and was it correct? We have so many questions...


    As my special guests and panel of experts, I invited Dr. Tony Angelo, who is head of services for a local prison and in charge of prisoners transitioning into normal life. I also invited Dr. Randy Stinnett, a clinical psychologist who co-manages an outpatient behavioral health department in a local community health clinic. Also with me is Nathan Hoyt and Adam Borecky, 4th year medical students who will be going into psychiatry.


    Traits of psychopathic antisocial behavior


    Criminals like Ted Bundy are skilled manipulators. They often scope their environment to see who will be the easiest to manipulate. They will treat you like you are their long, lost friend, but everything they do is an attempt to pull you in. They “hook” you so that they can get you to do something for them.

    Ted Bundy came off as friendly and charming, described as “one of us.”  A friend of his from Washington State even said, “He’s the kind of person you’d want your sister to marry.” As disturbing as this is, it is a common trait of psychopathic antisocial behavior.

    Ted Bundy displayed many traits of psychopathic antisocial behavior. Some of the most recognizable traits were:

    Viewing others as a pawn in his chess game

    Master manipulator

    Desire control/power

    Sexual gratification in his choices

    Enjoyed having an audience

    Calculated predatory aggression

    Strategic planning

    Feeling that some other entity is operating inside of him

    Empathy qualities:

    Normal cognitive empathy

    Very low affective empathy


    Someone with low affective empathy will not feel your emotions or know your emotions from a mirror neuron experience. Rather he can only read facial expressions and body language without allowing cognitive but not affective empathy.  


    In episode 2 of the Ted Bundy documentary on Netflix, Confessions with a Serial Killer, in his first arrest Ted Bundy said, “A funny thing happened to me on the way to labor law class. I got two weeks on the spa on the labor floor here. And, a yes, I intend to complete my legal education to become a lawyer, and be a damn good lawyer. Uh, I think things are going to work out, thats about all I can say.”


    When he said this, he had a right sided smile and outwardly looked fairly happy and calm. According to studies done about microexpressions, the right sided smile is usually demonstrating contempt, but for him does not look as negative, and because in so many of his videos he has it on his face, he likely thought highly of himself and looked down on others.

    I have noted that very good liars look positive, but often still leak microexpressions of very subtle negative emotion. Bundy seems to have expressed anger when he felt thwarted. In his statement, he makes a joke, yet showed a flash of fear or sadness while doing so. Bundy’s emotions of fear, anger, sadness, and pain leaked out through the microexpressions on his face, which are always a truth-telling mechanism.

    Below is the quote with my inserted microexpressions in it:

    “[contempt] A funny [anger] thing happened to me on the way to labor law class. I got two weeks on the spa on the labor floor here [fear or sadness]. And, a yes [contempt, sadness or fear], I intend to complete my legal education to become a lawyer, and [contempt] be a damn good lawyer [anger]. Uh [pain], I think things are going to work out [fear], thats about all I can say.”

    *Note it is hard to determine exact expressions from the poor quality of this video- but my microexpression research team discussed the above and this was our consensus.  The fear or sadness comment comes from the eyebrows going up in the middle, but it is hard to determine if there is fear or sadness due to the poor quality of film.


    It is believed psychopaths feel little or no fear. Did Ted Bundy feel afraid?

    Most of the video of Ted Bundy did not show a physiological reaction to stress. But it is likely to some degree (although much less than others) that he experienced fear.  It is thought that those with primary psychopathy have dysfunctional emotional processing due to issues in their amygdala. Studies show they have less fear then control groups and secondary psychopaths (more the sociopath or baked ones) which have more trait anxiety or fear (Skeem, 2007).    

    What was Ted Bundy’s possible diagnosis?

    Primary psychopathy: These typically have low affective empathy and low fear, however not all that are primary psychopaths become criminals. They are sometimes able to still follow the rules while not having any fear or empathy and can even be prosocial.

    Sociopath (or secondary psychopathy): These are typically “baked” into being anti-social. Sociopaths are typically “made” to be the way they are, often resulting from a traumatic childhood. Abuse and trauma may influence their later life ability to attach to others.  They have higher trait fear, more borderline traits and more mental disorders.

    Antisocial Personality Disorder:  This is how the DSM classifies people who have a history of illegal behaviors, deceit, impulsivity, failure to plan ahead, aggressiveness, reckless disregard for safety, irresponsibility and lack of remorse.  This is usually a criminal psychopath or sociopath with repetitive crimes. They display low empathy and low connection with others. Their behavior usually results in crimes against others.  

    Ted Bundy’s bipolar diagnosis:

    When Ted Bundy was assessed while awaiting his death sentence, he was given a diagnosis of bipolar disorder. However, most depressed people become less violent and don’t have much of a desire to have sex. It is also interesting to note that out of all of the violent events that happen in the US, only 5% of them are due to mental illness (Stuart, 2003). Therefore, we can conclude that most violent acts are not done by people with mental illness.

    Could he have been in a manic state?

    Most manic states end in death, jail or psychiatric hospitalization. Ted Bundy had no record of being hospitalized in a psychiatric hospital and was only put in jail after he was caught. Bundy was also capable of living a “normal” life. He was an active citizen, joined a church, was married and involved in politics. He played these roles for years.


    With mania, this would not have been possible. Those who are manic cannot stop their mania. Also, Ted Bundy displayed reason in the midst of his crimes. He covered his tracks and could pretend to be something he wasn’t. Those who are manic do not have the ability to pretend to be something they are not, nor have the ability to plan and cover up.

    DSM 5 antisocial disorder:

    Ted Bundy would fall more in line with a DSM 5 antisocial disorder leaning more towards primary psychopathy. With this disorder, you must be 18 years or older and have commited conduct disorder before age 15. Also prevalent is a pervasive pattern of disregard for the rights of others since the age of 15 and psychopathic manifestations. Additionally, they must meet 3 or more of the following behaviors:

    Fail to conform to lawful behaviors

    Deceitfulness

    Impulsivity

    Irritability

    Aggressiveness

    Reckless disregard for the safety of others

    Irresponsibility

    Lack of remorse

    Nearly all of these traits were displayed in Ted Bundy’s pattern of behavior. Even when he was young he showed predatory aggression (which I discuss in a prior episode) when he set up tiger traps at camp and injured a young girl. Although he prayed with people before his death, Ted Bundy’s memorable quote, “I am in the enviable position of not having to feel any guilt,” showed he was wired with some primary psychopathy.

    Low IQ

    Although Ted Bundy has been referred to as a criminal “mastermind,” he may have had a average or only slightly above average IQ. The article by Ceci, 1996, found that cognitive ability tends to be a good predictor of academic performance; measures of academic achievement (LSAT, GRE, SAT) correlate very highly with measures of cognitive ability.

    Although we do not know Bundy’s actual LSAT score, only that he believed it was “mediocre,” there is certainly no evidence that states he was a genius.  Rather than a genius, I would say he was not impulsive, very calculated, and often planned and put a lot of energy into his criminal actions.

    Hearing voices

    Ted Bundy often referenced hearing voices that told him to do bad things. However, it is not believed he had schizophrenia. Occasionally antisocials will use this as a way to avoid responsibility for their behaviors.

    We call it MBD: minimize, blame and deny

    Was pornography to blame?

    Ted Bundy blamed his behaviors on pornography. However, pornography is not viewed as a cause of sexual violence. In persons who have preexisting conditions for sexual violence, it is a viewed as a contributing factor.

    In Episode 4 of the documentary, he is quoted as saying, “I never said (pornography) made me do it. I said that to get them to help me. I did (murder) because I wanted to do it.”

    The research confluence theory states men with hyper masculinity that also involves psychopathic tendencies have low agreeableness, abuse, hostility towards women, impersonal sexuality combined with sexual permissiveness. When you have a confluence of those two things and violent pornography it may be a contributing factor to Ted Bundy’s violent, abhorrent behavior.

    It is important to note that pornography has not been present in our society for very long. Yet, crimes against women have been happening since the beginning of time. It is because of this fact that many doubt that pornography is to blame for crimes of this nature.

    Hald, 2010,  found that the correlation between violent pornography and attitudes supporting violence against women (r=0.24) was significantly higher (P< 0.001) than the correlation between nonviolent pornography and attitudes supporting violence against women (r=0.13): however these are still low correlations.  

    Antisocial personality disorder and psychopathy as a mental illness:  

    Just because antisocial personality disorder is in the DSM, it doesn’t mean it should be viewed the same way we view schizophrenia, bipolar, major depressive disorder, etc. Largely, antisocial personality disorder is not something that is treated by psychiatrists. There is no medication for it and most with this disorder are not interested in help. If they come to see a psychiatrist, it is typically because they want something from you.

    Narcissism diagnosis:

    Ted Bundy had traits of narcissism as displayed in the DSM 5 criteria: a pervasive pattern of grandiosity, lack of empathy and a need for admiration which begins by early adulthood. To meet the criteria, 5 or more of the following behavioral features must be met:

    grandiose sense of self-importance

    preoccupied with fantasies of unlimited success and power

    special or unique and can only associate with high status entities

    requiring excessive admiration

    sense of entitlement

    exploitative

    lack of empathy

    often envious of others and believes others envy him or her

    arrogance and haughtiness

    I would add that some narcissists are low-self esteem, but I believe he was a high self-esteem psychopathic narcissist.  

    Machiavellianism

    Machiavellianism overlaps with narcissism and antisocial disorders. They are more likely to deceive and manipulate others for their own personal gain. They see people as objects for use and manipulation. They will have normal amounts of empathy unless they have traits of psychopathy.

    The opposite of machiavellianism are people who display honesty and altruism.

    In viewing Ted Bundy, it is highly probable that he displayed high Machiavellianism with traits of psychopathy and narcissism—thus having all the dark triad.

    How did Ted Bundy come to be this way?

    Home-grown sociopaths don’t necessarily have a need to be seen and appreciated by others. They often have been made the way they are due to horrific abuse, and usually prefer to be left alone. But, psychopaths who are born with low physiological arousal, have more of the predatory aggression which we see in Ted Bundy.

    A person with primary psychopathy can either choose to live in society and do things to help, although without empathy and with difficulty attaching to others. Or they can choose to do illegal things to get their drives met. Whichever one they choose will write their brain and pattern of behavior that they will follow. These people can be incredibly helpful to society or incredibly harmful.

    Determinism versus free will

    It often comes down to determinism versus free will. In other words, did he make the choices or did his mental illness cause them? Ted Bundy went to prison for the choices he made, not the psychological predisposition that he had. However, when one goes into determinism, they will blame others for the choices that they made.

    It is important to remember these people do have a choice. Because, ultimately, there is another dimension here, which is the moral dimension. We all have the responsibility to others and to society.

    However, there are people who have less choice than others. For example, a person with a frontal lobe injury will have less “choice” than someone who does not. Ultimately, choice must be in line with responsibility. But I have known people to “check themselves in” for desires to do bad things, and get help. Sometimes we only have a small choice to change our environment.

    Treatment

    With the Ted Bundy type of psychopath, therapy will most likely not benefit them. This type of person should be put in prison for life.

    Therapists must be especially on guard with someone like this, which can be uncomfortable for therapists and clinicians. You must view your interactions with them like a chess match. Because, everything about your interactions is a game to them.

    Towards their therapists, they may exhibit these types of behaviors:

    Play into your desire to “make a difference,” which is fertile ground for them to manipulate you.

    Express prosocial behaviors.

    Trap you by making you believe you have reached them in a way no one else has.


    However, the “baked” sociopaths, or those with features of antisocial behaviors, can benefit from therapy. Clients will very rarely be as healthy and whole as you want them to when they leave therapy.


    However, the goal is for them to leave with better connection to people, not use sex as a coping strategy, be more intimate (non-sexually) with humans, and relate better to authority. This will lower their risk of sexual violence, and help them on a track to be able to fit into society.

    Approaching therapy

    You can give all the tests you want, but one of the most valid tests of psychopathy is the “hair on the back of your neck” test. You just know it when you’re in the presence of psychopathy. It will alarm your body’s natural detection mechanisms. You can just “feel” it. I know that isn’t technical jargon, but it’s so true.

    The goal in therapy should be to change their mindset away from objectifying people. It is suggested that you get access to their large criminal history in order to learn what they have done and use that strategically in their treatment. This will arm you with the knowledge of what they have done and what they are capable of.

    Approaching them with the idea that they are likely to continue their cycle of behavior unless they do something to change it is an ideal approach. Discussing the importance of change itself and how change occurs can be helpful.

    Focus primarily on the dynamic risk factors or “stable factors”:

    Issues with authority

    Intimacy

    Hostility and attitudes towards women

    Targeting those aspects one by one and digging into each one is a strategic approach. Improvement in each of these areas will lessen their risk of continuing their behaviors significantly.

    Final Thoughts

    There will always be that one in a million person who will use their predisposition to harm others and create a life of criminal behavior.

    However, the glamorization of criminals like Ted Bundy from the media tend to breed a culture focused on the fear of these one in a million criminals.

    It is important to remember that the media carries a bi-directional quality. Where the consumer drives what the media will pay attention to. Limiting the attention we give these types of criminals will lessen their need to be publicized and noticed.

    For Nate Hoyt’s extensive notes on this episode - go here




  • 01:03:30

    How to treat violent and aggressive patients

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    On this week’s episode of the podcast, I interview Dr. Michael Cummings. Dr. Cummings works at a state psychiatric hospital for the criminally insane, so he has extensive experience in treating patients for aggression and violence.

    The different types of aggression

    The words “aggression” and “violence” are sometimes used synonymously, but in reality, aggression can be physical or non-physical, and directed either against others or oneself. Violence is more of a use of force with an intent to inflict damage.

    One study looked at the principle types of aggression and violence that occur in psychiatric patients, and broke it down into three categories:

    Impulsive violence (the most common category)

    Predatory violence (purposeful and planned violence)

    Psychotically-driven violence (least common)

    Within 5 state hospitals, 88 chronically or persistently violent patients with 839 assaults, the rate of impulsive violence was 54%, and predatory violence was 29%. Psychotically driven patients logged 17% of total violence (Meyers, M. Cummings et al., 2013). Studies show psychotically driven violence decreases the longer the patients are in care and medicated.

    Predatory Violence

    Predatory violence is what people typically think of when they think of psychopathy, or someone with antisocial personality disorder. It is violence with a purpose, and that purpose is usually to gain something. They typically show a lack of fear and very little autonomic arousal even when they are being violent.  The amygdala and the temporal lobe is underactive and the communication between them has a weak signal. People with predatory violence also have lower affective empathy.

    Some of the early research done by Adrian Reign measured blood pressure, galvanic skin response and heart rate when showing neutral, frightening or peaceful pictures to children. Of those who lacked effective response or autonomic response to those pictures, 75% percent of those individuals became violent criminals by age 18. Interestingly, 25% of them became prosocial and entered jobs as police officers, bomb disposal experts, and so forth.

    True psychopaths are a very tiny part of the population. About 2% of women score significantly on the psychopathy checklist. About 2-4% of men have elevated scores on the psychopathy checklist. Not all of those individuals, however, are violent, and many persons who are psychopathic are more interested in profit. Some become the crime bosses (not actually doing the violence themselves) and others end up in politics.

    Impulsive violence

    Impulsive violence or aggression is actually the most common, and in many ways the most complex, form of violence that occurs in a variety of mental illnesses, including:

    psychosis

    mood disorders

    personality disorders

    anxiety disorders

    PTSD

    It is essentially an imbalance in impulse generation and a failure of the prefrontal cortex to evaluate the impulse and weigh the consequences. All of us generate a variety of impulses, some good and some bad, including impulses driven by our irritability and anger.

    In predatory aggression there is increased medial prefrontal cortex activity whereas in reactive aggression there is decreased activity.

    What can cause impulsive violence to be an issue:

    Traumatic brain injury

    Some of the dementias including frontotemporal dementias

    Anoxic brain injury

    Intellectual disability

    Personality disorders

    Drugs

    Drug detox

    Psychotic aggression

    Psychotically driven aggression is most often a result of delusional ideation or the belief the person holds that they are in some way being persecuted and being taken advantage of. Psychotic or mentally ill people do have an increased rate of violence compared to the general population. The mentally ill are responsible for around 5% violent crimes, meaning non mentally ill people are responsible for 95%.

    Psychotic Delusions leading to violence

    Ones study looking specifically at the first episodes of psychosis found that in about 458 patients, anger was associated with certain types of delusions that led to the violence (Coid, 2013).

    The underpinnings of delusion-driven violence usually stems from when people have delusional beliefs that are persecutory in nature. When they believe that someone is out to get them, it removes inhibitions against acting out violently, because that person’s view is they are protecting themselves. Typically, this violence comes from the belief they are being spied on or persecuted.

    Persecutory delusions associated with a command hallucination is a particularly potent precursor to violent behavior. If your delusion tells you your neighbor is the devil, and your command auditory hallucination is that God is telling you to “kill him and save the world from destruction”  it can lead to a very bad outcome.

    IQ and aggression

    There is also an association between the IQ and aggression (Huesmann, 1987).

    A recent study in state hospitals looked at what correlated with persisting violence, and across all of the types of violent behavior, cognitive deficits (particularly impairments and executive functioning) were associated with elevated rates of violence.

    Men are more violent than women

    Men are likely more violent than women because they have historically been the hunters, which involves violence. Women were gatherers more often than not, and consequently, men have a standing evolutionary tendency toward more frequent use of violence. Women can be violent, but if you look at the rates of violence between men and women, men are clearly more violent.

    The purpose of aggression  

    You could say the healthiest outcome for our aggressive and violent impulses is when we use our innate ability to be aggressive to engage in things like a healthy competition. Or even to provide motivation and drive to achieve.

    In the beginning, humanity formed tribes, and aggression allowed someone to climb up the dominance hierarchy within the tribe. It also allowed them to protect themselves from other tribes. It was basic for survival.

    If we look at animal psychology, there is a lot we can learn about the aggression and dominance hierarchy, like how apes interact with each other, or form alliances. As a way of creating alliances, often an alpha ape will groom other males.  The violence comes out when the clans come against each other. When one ape is wandering from its clan, two apes from another clan may attack one single ape viciously.

    In other circumstances, if a dominant ape is taken away from his clan for a couple of days and brought back into the clan, a couple of other apes may have formed a new alliance against the prior leader and attack him.

    As human beings, we are also like this. Many of our social interactions and group structures have the same kinds of alliances and effects of absence can play out similarly. Of course as humans, we do have higher verbal centers, and philosophy or spirituality, that allows an individual to be less violent and to transcend their base instincts.

    Aggression and autism

    People with intellectual challenges most often exhibit impulsive violence, particularly those on the autistic spectrum. The person may have a greater difficulty processing or understanding their own emotions if there are significant intellectual deficits. They may also have elements of not being able to judge a response or to moderate a response. The general pathophysiology of the autistic spectrum disorder suggests that the connections between neurons and the autistic brain is not what it should be, and they are not differentiated so that information processing can be fragmented.

    Treatment of aggression Psychotic aggression treatment

    Treating with an antipsychotic medication is helpful and decreases violent episodes. In one study, clozapine helped psychotic aggressive patients with executive dysfunction more, compared to using haldol or olanzapine (Krakowski, 2011).   

    Psychopathic aggression treatment

    A predatory-violent individual needs to be contained in prison if there is a demonstrated past of persistent violence.

    There is evidence that by enhancing intellectual empathy, psychopaths will be less violent. There is also interesting research that by giving oxytocin, the hormone that increases affiliation and collaboration, may have a moderating effect on some psychopathic individuals.

    However, in terms of psychopharmacology, we don’t have any specific medications to control that behavior. Some medications, such as clozapine, can affect the underlying issues behind psychotic behavior and thereby reduce it, but there is no direct treatment for psychopathic violence pharmacologically.   

    Impulsive aggression treatment

    Dr. Cummings discussed the use of Mood stabilizers helping in persons with borderline personality disorder, SSRIs and trazodone helping in dementing illness in the elderly and alpha 2 agonists in people with things like autism or TBI. Alpha 2 agonists (clonidine) can fool the brain stem into thinking enough norepinephrine has been released, then less norepinephrine is secreted, making the brain stem calm down.

    Essentially, in an emotional disorder, if you change the affective (limbic) tone, you can decrease the likelihood of emotionally reactive aggression, for example, by using mood stabilizers lithium and divalproex.  

    Using an antipsychotic, and not just a mood stabilizer, doesn’t show any benefit for traumatic brain injury patients. Antipsychotics have been used for people with autism spectrum disorder, and some evidence shows that drugs like risperidone can be helpful to control outburst issues. If there is evidence of sexual aggression (or aggression occurring at women after puberty), using an GnRH agonist—antiandrogen treatment—can sometimes be necessary).

    Psychotherapy for aggression

    There have been a number of anger management therapies that have been used over time. Therapists can help people be aware of their anger and manage their impulses, or push their anger and aggression toward a more prosocial response.

    For people with borderline personality disorder, dialectical behavioral therapy, mentalization based therapy or transference therapy are important. For schizophrenic patients, a good therapeutic alliance is important to create medication compliance. I have touched on how to process anger in my microexpression series and will have future episodes focusing more on the psychotherapy approaches to anger.  

    Overall in therapy, we must assume that our patients will lie to us sometimes because they are afraid, and double check to insure they are following our prescribed protocol. We must also work hard to build trust and a therapeutic alliance.

    Final Thoughts

    Violence and aggression deserve much more attention as a specialty than we have given it in the past. It is a major burden for family members and friends.

    Please submit any questions you have and we will submit them to Dr. Cummings and to answer.

    (In the podcast details about specific medications are discussed for psychiatrists who are interested in advanced psychopharmacology.)

    Further reading:

    Link to Ideal blood levels are found in Resource Library

    “California State Hospital Violence Assessment and Treatment (Cal-VAT) guidelines”




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  • 01:05:11

    How Empathy Works And How To Improve It

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    What is empathy?

    Empathy is the ability to understand another’s state of mind or emotions. It is also is being able to feel, understand and share with someone else in what they are saying, their meaning of life, their motivations and values.

    In research there are 3 types of empathy that are commonly described: cognitive, affective, and compassionate.

    Cognitive empathy

    Cognitive empathy is also known as perspective taking, and it can help someone understand another’s personal experience. It also tends to reduce interpersonal aggression. Cognitive empathy is exactly what it sounds like—cognitively understanding someone’s situation, emotions, and motivations. When we understand someone else, we are more likely to view their behavior as similar to our own.

    One study of Asperger syndrome showed they had lower cognitive empathy but NOT affective empathy. (Dziobek, 2008)

    Affective empathy

    Affective empathy is about a shared emotional experience, one of feeling together. It uses the mirror neuron system, which I will discuss later on in the article. Affective empathy forms powerful emotional relationships.

    Boys with higher aggression had ½ the affective empathy, but the same level of cognitive empathy, as the non aggressive control group (Schechtman, 2002)

    Compassionate empathy

    The third form of empathy is compassionate empathy, which is also called empathic motivation, prosocial concern, or sympathy. This is when you feel moved to help another from how to experience their reality.  

    The science of empathyMirror Neurons are sharing neurons

    Our brain has neurons solely designed to mirror other people. From birth, when we focus on another's movements, emotions and intentions, our brain lights up automatically, and largely unconsciously, around 10% the same way. Our own body-state can be derived from someone else outside of us. We can therefore understand and map out the mind of others by placing ourselves in a comparable body state. This process is important for empathy, intuition, transference, countertransference, enactment, projection, internalization and intersubjectivity.    

    The discovery of mirror neurons:

    In 1992, while studying a monkey's brain with electrodes attached to the motor area (the area that lights up when movements by the body are made), researchers accidentally discovered that not only would the neurons become activated by the monkey reaching out to pick up a piece of food, but also when the researchers made a similar movement. Later, the same team published a paper that showed that there were mirror neurons responding to mouth actions and facial expressions. Further studies confirmed that around 10% of neurons in certain areas of a monkey's brain had mirror abilities. Later, these studies were expanded to humans.  

    Current research:

    A recent study summarizing the data of 125 fMRI studies of humans (brain imaging that shows what is active), found that there were many areas of the brain with this capacity. (Molenberghs, 2012) Beyond seeing actions performed by others and having them represented in our brain, there are 3 other areas of the brain that are activated in a similar fashion:

    Ever wonder why watching people embrace enthusiastically at an airport is fun? When you observe someone being touched, a similar area in your brain (the secondary somatosensory cortex) activates in a similar way as the person being touched.  (Keysers, 2004)

    When you only hear something, like someone cracking open a peanut, how do you know what is occurring? Another study showed that there was a similar brain circuit firing in both doing the action and hearing it, and just hearing it. This study also showed that those with higher scores on perspective taking (ability to slip into another's shoes) had stronger activation of mirror areas! (Gazzola, 2006)   

    When we watch someone grieve at a funeral, ever wonder why we feel their sadness?  When you feel emotion, you experience the emotion in your brain, like they are to a lesser extent.  (Gaag, 2007)

    When normal college students looked at photographs depicting emotions, out of their awareness their own face muscles depicted the same emotion on an EMG.  

    “We are hard-wired to feel what other experience as if it were happening to us.” (Marco Lacoboni)

    We used to say, metaphorically, that ‘I can feel another’s pain.’ But now we know that my mirror neurons can literally feel your pain.

    “Mirror neurons dissolve the barrier between you and someone else.” (Vilayanur Ramachandran)

    Now researchers are saying that the mirror neuron system is involved with:

    Understanding another's actions and intentions

    Neural basis for the human capacity of empathy

    Learning new skills by imitation and rehearsing

    Non-empathic types—the Dark Triad

    The “Dark Triad” refers to three types of disorders that cause people to have low empathy for others. The big common denominator for these people is a deficit in affective empathy, but after matching for primary psychopathy, the others are no longer predictors of low affective empathy (Wai 2012). The Dark Triad consists of: narcissists, Machiavellians and psychopaths. People who have narcissistic traits and machiavellian traits often have some primary psychopathy traits as well.  

    Individuals high in narcissism had positive feelings when looking at sad faces and were accurate at recognizing anger (higher cognitive empathy may be bias at grandiose self reporting). Individuals higher in primary psychopathy (they can usually maintain cool composure and carefully execute planned behaviors with a lack of morality, whereas those with secondary psychopathy respond to their negative emotion when they harm others) felt positive when looking at sad, angry or fearful images and more negative when looking at happy images, and were rather inaccurate at identifying all emotions.

    Machiavellians felt negatively with happy images and positively with sad images, while they tended to inaccurately identify happy or sad emotions.

    Empathy and the medical field

    Studies show that empathy declines in third year of medical school (both for men and women, but women are higher in empathy in general)  (Hojat, 2009) but that doctors can also increase their empathy through certain practices. (Riess, 2012)

    In a study of 20,961 patients, primary care providers with high empathy have been shown to have lower rates of metabolic complications compared to moderate to low scores (4.0 per 1,000 patients vs 7.1 and 6.5 respectively) (Canale, 2012).  

    There have been many studies that show both cognitive and affective empathies ability to change patient care when high and low empathy are demonstrated. For example, there is a correlation to a doctor’s ability to more accurately diagnose depression and anxiety, understanding interactions, more positive patient outcomes, increased therapeutic alliance, more patient satisfaction, and fewer malpractice claims. Doctors who showed higher empathy were more likely to have their HIV patients take their medications (Flichinger 2015).

    Research on “Therapist Effect”

    Some doctors or therapists have better outcomes. Empathy seems to be important in therapist effectiveness and can be increased.  

    Different studies show outcomes vary between patients, of which 5-12% can be attributed to a particular therapist.   

    One study of 91 therapists over 2.5 years: the best therapist showed a change of 10 times the average mean, the worst showed the an average increase in symptoms.  (Okiishi, 2003)

    Higher interpersonal skills has been linked to better outcomes when studying therapist effect. (Anderson, 2009)

    Higher-empathy therapists have higher success regardless of theoretical orientation. Lower-empathy therapists linked to higher dropout rates, relapse rates, and weaker therapeutic alliance. Empathy was shown to have an effect size of 1.22-1.43 when independent observers rated empathy for substance use outcomes. (Moyers, 2013)

    In a big study on therapist effect (69 therapists, 4,580 patients), they found that years of experience, gender, age, profession, highest qualifications, caseload, degree of theoretical integration did not predict outcome. The amount of time spent targeting improving specific skills and reviewing therapy recordings predicted client outcome.  

    Can we improve our empathy? Studies show that we can. Here are some things that can improve your ability to empathize:

    Optimize your sensorium—keep yourself healthy. When you are tired, hungry, chronically stressed and with poor focus, it will be harder to enter into the experience of another.

    Try to understand the person’s emotions that you are with.

    A study showed by trying to pay attention to emotion mimicry was increased (linked to affective empathy)

    Read fiction (Bal, 2013) allow yourself to be transported into the book.

    Do not play violent video games (Anderson, 2010)

    Work through our “countertransference”

    Talk through difficult situations

    Patients have different ways of relating—learning to understand others, to see their way of being as “adaptive,” can be empathy promoting.

    Learning to read emotions and body language more accurately  

    Learning to accept feedback

    Calming your own hyperarousal through practices like mindfulness

    Tuning your mirror neurons

    Noticing when connection or disconnection is occurring

    Practice empathy towards viewpoints that are not your own

    Becoming mindful of the emotion, the distress, the meaning behind the distress

    Can therapists lose our empathy?

    Studies show we can experience empathic strain and rupture. Empathic failure may lead to aggression. It is hard to empathize when we feel subjected to powerful influences from patients: complaints, requests, accusations, subtle seductions, bits of blackmail, challenges.  Throughout history, rulers have decreased empathy in their warriors and people by stirring up disgust towards those they seek to kill.

    We are more likely to empathize with those we interact with frequently, find similar to us, or find thoughtful and kind.  We need to humanize people’s actions and see them like us, to not lose the part of us that could consider that we too could be in their situation.

    Consider the stages of empathy:

    I think of empathy in terms of 3 categories: the moment to moment emotional experience, the meaning and context of the emotion in their life, and the subjective experience evoked and created by the unique connection I am having in the here and now with the person.  

    Level 1: There are moment to moment flashes of emotion on someone’s face, changes in body language, and current distress. Empathy can be experienced by just witnessing a flash of emotion and allowing the person to know you see it and that you hear them. During this, we can try to understand the person’s emotions, and ask them to verify what they are feeling, if we are correct in our questions, such as if they are feeling sad or angry about something.

    Tuning into their experiential state and then asking if you are on the right track: (note if the patient gives a different word then do not contradict) can be helpful.

    Ask them a few questions to clarify:

    Perhaps you feel happy?

    Perhaps you feel frustrated?

    Perhaps you feel sadness?

    Perhaps you feel disgusted?

    Perhaps you feel concern or fear?

    Perhaps you feel a sense of pride?

    Perhaps you feel disconnected or numb?

    Perhaps you feel a sense of embarrassment or shame?

    Use their own words and repeat what you hear from them:

    Patient: “I just feel so tired and sad all the time.”

    Doctor: “It makes sense you feel tired because you have been so busy with your new jobs. In light of your recent losses your sadness also makes sense.”

    Matching rhythm of voice, tonality, emotionality.

    Matching an infant's cry rhythm (but not intensity) calms and regulates the infant

    Imitation

    Recognition of what the patient hopes for:

    I hear you have hopes for… desires for… dreams for… aspirations for...

    Level 2: This is where we try to know the context of the flash of emotion, the distress either in the distant past (how early relationships informed it) or recent life situations. Sometimes the quantity of distress is only as high as it is because it is linked to prior loss or prior trauma. We can find the context of the emotion by matching their emotionality, their demonstration of emotions on a level that we feel is appropriate. We can look at the meaning of the emotion and the context of the meaning of that emotion in their lives. We can also empathize with the meaning of the emotion once they’ve identified its context.

    Even if they flash anger towards themselves, but maybe they in doing that are not accomplishing the energy of the emotion, and they are missing how the anger can help them accomplish their goals. Thus when the anger is pointed at themselves, we can explain that the anger should be pointed outward, and give energy to action.

    Example: anger towards self looks like, “I am worthless” instead of anger towards abuser: “he should not treat me like that, I will set up a boundary.” The empathic statement can be “it must be hard to feel the anger pointed at yourself, telling you that you are worthless, and perhaps although it was adaptive to do this growing up, makes it hard to set boundaries now.”

    Level 3: This level is when the person is having emotion that occurs because of their relationship with you. It is the interpersonal, and commenting and empathizing with any distress (or positive emotion) that your relationship is creating is a level 3 empathic statement. When a patient demonstrates anger towards their therapist, it’s helpful to ask if they are feeling anger towards you and if they feel comfortable talking about that emotion.

    We can create psychological safety for a patient to give feedback to us by telling them we like to hear what they are feeling towards us. For example, my mentor, Dr. Tarr, tells his patients:  

    “I very much want to hear your positive and negative feelings, particularly about me, and particularly negative ones. It will be helpful for you to share any feelings of disappointment, feelings of not being understood, feelings of not being responded to or criticized, or mannerisms or things I say that affect you undesirably. I hope you can understand that this is not a usual social situation, where you don’t tell people negative thoughts, here I hope you have the courage to say them out loud. It will be very helpful to say it has it is happening; we can learn much more than if it comes out later; we know it’ll be hard—but this kind of a laboratory where we discover what goes on between us.”



  • 00:56:39

    ADHD: Diagnosis, Symptoms & Treatment

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    In this week’s episode of the podcast, I interview Dr. Michael Cummings about psychopharmacology for Attention Deficit/Hyperactivity Disorder (ADHD). We talk about the symptoms, the treatments, and the typical myths about the disorder.

    What is ADHD?

    ADHD is a brain neurotransmitter disorder that affects a person’s ability to concentrate, their social interactivity, and their impulsivity.

    Diagnosing ADHD

    People who truly have ADHD typically experience inattentive and hyper symptoms across all areas of their life. For example, if they are in a job that requires periods of attention to complete or organize a project, it will be inherently more difficult for people with ADHD.

    One of the things that’s important in diagnosing people (particularly younger people) is their collateral history. People around the person with suspected ADHD are often more aware of the person’s deficits than the person themselves. When they reach adulthood, the problems might be made more obvious when they integrate into normal society and notice they struggle with symptoms of ADHD (compared to other people).

    Although not required for diagnosis, PhD level psychologists can do psychological testing, along with ADD/ADHD testing and IQ testing, to get a full idea of the patient’s symptoms. It helps confirm the diagnosis because these tests are widely used among the entire population, which provides a large sample mean to compare with. It’s also helpful to get a benchmark of performance before beginning treatment and then follow it up with later testing to see how effective the treatment has been.

    Myths about ADHDIf a child is hyper, he or she has ADHD.

    ADHD diagnosis has, at times, been a fad in the public, leading to many misdiagnoses and overmedicating, especially in children. Children are inherently hyperactive and less attentive than adults are. Doctors who are performing diagnostic tests must really pay attention to the criteria in children to make sure that the magnitude of the problems truly cause stress and social dysfunction before they try to diagnose or medicate a child.

    For example, the LA times published an article that ⅓ of the children in Orange County suffered from ADHD. Real studies show that prevalence in children is around 6-8%, in adolescence about 2.8%, and in adults about 2.5% of the population.

    ADHD disappears with the onset of puberty.

    Attentional deficits sometimes remains into adulthood, while hyperactivity may disappear as a child matures.

    We are giving people methamphetamines as medication.

    Methamphetamines and amphetamines are completely different drugs on a molecular level. The methyl group paired with amphetamines increases its absorption and effect on the brain. The amphetamines that are used to treat ADHD are essentially variants of dextroamphetamines.

    There are even versions that are difficult to abuse, such as with vyvanse, where lysine (the amino acid) is bound to the amphetamine. The lysine make the amphetamines unabsorbable unless it’s in the GI tract. It cannot be inhaled or injected and still be effective. Similarly, some of the slow-release versions are encapsulated in pills that won’t release the drug easily, except very slowly in the GI tract, making it difficult to divert or abuse those formulations.

    Dopamine stimulants are the only treatments for ADHD.

    There are other drugs that are useful for ADHD symptoms. They are (for the most part) drugs that increase brain norepinephrine. They can be used for people who don’t tolerate increases in dopamine, or for other reasons cannot be treated with dopaminergic agents.

    The most common side effect from amphetamines are increased anxiety, insomnia, increased sweating, hypertension, heart rate and blood pressure. These are things that can be overcome by titrating the drug more gradually, or being very attentive to the overall dosing of the drug.

    Amphetamines are likely the first line of treatment, unless a person has anorexia, is still growing, or still has strong family genetics with a history of addictions.

    What are true warning signs of child ADHD?

    When the child is struggling socially, has attention deficit, is struggling academically, and the problems are noted by the educators and parents alike, it may be time to seek out a diagnosis. Most teachers get pretty good at recognizing the one or two children in the class that are most impulsive, most hyperactive, and less attentive, so it can be helpful to ask them first if they’ve noticed something disruptive about the child.

    Often, boys with ADHD are easier to spot, because they tend to act out more. Girls tend to more often fall into the inattentive subtype, but may not be hyperactive or disruptive. They may not do as well academically, though intelligent, and that is a cue that they should be tested for the inattentive subtype. The problem is that unlike many disorders that have clear markers, attention—and the ability to modulate attention—always varies.

    One of the characteristics of people with ADHD is that they tend to be impulsive, often acting without thinking through the consequences of their behavior, which can lead them in some cases to do things that will get them in trouble in school or in their social group. It can become a self-reinforcing phenomenon. If a child is often in trouble and begins to take on the “troublemaker” attitude, the behavior can continue as part of their identity. There is even an association between ADHD and the development of conduct disorder and/or antisocial personality disorder.

    ADHD in adults

    Sometimes I treat young adults who were high functioning enough in high school to be able to get by academically, but they noticed a major difference in college when the coursework became more difficult. They’d procrastinate as long as they could, and only get things finished at the last minute when adrenaline kicked in and stimulated their brain to do the work.

    ADHD has been recognized as a failure of the reticular activating system to adequately stimulate the portions of the brain stem (the cortex and basal ganglia) in a way that it works for non-ADHD people. It can feel a little like the brain is drowsy all of the time.

    Another characteristic of ADHD is that patients tend to be more able to concentrate on subjects they are interested in. For example, medical students who prefer higher-risk, fast paced environments tend to not need their medication when they are in emergency room rotations. When they are in a subject matter that is not as interesting to them, they might need to take their medication to function at a higher level and retain the information. I try to help my ADHD patients increase the meaning in what they are doing on a daily basis as a form of treatment.

    People with ADHD have a higher rate of injury than the general population. There are many circumstances in which not paying attention to your environment is dangerous.

    One study shows that there is even a correlation between car accidents and ADHD. Driving requires attention and responses, and if people are prone to do impulsive things, but are not prone to pay attention, it can increase their rate of accidents.

    There is a noted decrease in risk of drug abuse when someone is treated appropriately with dopaminergic drugs, than there is if someone with ADHD is untreated. One of the things that occurs in people who don’t receive appropriate treatment and education (but they have ADHD) is that the first time a person takes a stimulant medication, maybe experimenting in college, illegally borrowing some for a test from a friend, they will report it as being the “first time they ever felt normal.” It can be a powerful lure to revisit the experience of feeling more normal, and being able to pay attention (I am in saying this, not recommending you ever share your ADHD medications, but nevertheless it is commonly reported to me on history as how they found out they might need treatment.)

    Without guidance and education, it can be a pathway to drug abuse rather than an appropriate treatment. Proper treatment can greatly enhance quality of life.

    Treating ADHD

    I once had a patient in the emergency room that told me she put a little bit of methamphetamines in her coffee every morning. She wasn’t getting high off of it, but I did wonder if she was self-treating something she had naturally noticed was a problem for her—inattention.

    People with ADHD should also be receiving a broad spectrum of psychosocial treatment and therapy, not just medication. If a child is under the age of 6, he or she should be given behavioral therapy as a first line treatment. The initial approach of diagnosis should be made carefully. If the person does have ADHD, the first treatment should be psychosocial interventions, afterwards, if that does not work, they can try medication.

    The main category for pharmacological treatment of ADHD are dopaminergic stimulants. These drugs essentially serve to stimulate the production of dopamine (amphetamines) or to block its reuptake (with drugs like methylphenidate). Amphetamines increase and release proper neurotransmitters and block reuptake, while methylphenidate is more purely just a reuptake inhibitor for dopamine.

    Medications that contain amphetamines will stimulate motor activity in healthy people, while it will actually return a hyperactive person to a calmer state as the dopamine regulates in their brain.

    For those who don't respond to dopamine increasing drugs, the other approach has been to increase norepinephrine with drugs like atomoxetine or some of the noradrenergic antidepressants, thereby increasing the person’s alertness. About 70% of people respond to dopaminergic agents, and 30% don’t respond, or can’t tolerate the increase in dopamine because of either insomnia or increased restlessness.

    Sometimes people with ADHD can also have comorbid anxiety. One professor explained that there is a survival advantage of both having ADHD and being willing to do high-fear tasks, but they also can have comorbidity with anxiety that keeps them from taking too high of risks and killing themselves.

    Often, when a patient comes to see Dr. Cummings that has both ADHD and anxiety, his first line of defense is to try and increase serotonin through SSRIs, along with the drug they are taking for ADHD. Some could take an antidepressant as well. Most children and adolescents with ADHD do best with a dopaminergic agent, although those are also problematic in some people.

    Exercise also has a positive effect on ADHD, specifically anaerobic exercise. It can aid several neurotransmitters, including norepinephrine and dopamine.

    Issues with ADHD medication

    Sometimes children who are on ADHD medication can experience a loss of proper growth hormone, causing different issues. If someone chronically takes a stimulant, they will be about an inch or an inch and a half shorter than if they did not take a dopamine stimulant. If that’s a problem for them will depend on the inherent genetic makeup of the person. If the child comes from a family of very tall people, it might not be a problem to lose an inch or two. If the family is short, losing an inch or two might be more of an issue socially and culturally.

    Also, anorexia can be an issue, because dopaminergic medications can decrease appetite. It occurs to some extent in everyone who takes a dopaminergic drug, definitely enough to cause widespread clinical concern. However, there are approaches, such as taking drug holidays from the medication, that can help regulate the decreased appetite. Whether someone should take a drug holiday, or break from taking their medication, will depend on how disruptive the person will become when they are not on a stimulant. If it will cost the person social interactions and friendships, it is usually better to keep them on the medication.

    Other abuses of ADHD drugs are very similar to the abuse or appropriate use of any molecule. The person who is using a stimulant appropriately is using it to improve their functionality—they are using it to pay attention and have a normal life. The person who is abusing a stimulant is taking it for the purpose of getting high. They are seeking the euphoric effects of the stimulants rather than positive life change. Someone who is trying to get a “speed run” will take a gram of medication, while someone who is trying to medicate for ADHD will take 20,30, or 50mg of methylphenidate in order to maintain their ability to concentrate.  

    The true identification of abuse of amphetamine medication is a person’s deterioration in their ability to function in a balanced manor. Not sleeping for days because of stimulants, even if someone is able to get A’s on tests, is not improving their functionality and may hurt them long term.

    In conclusion

    As a whole, doctors need to be more careful when diagnosing ADHD. There is a tendency to over-diagnose, leading to over-medicating. Even if you receive a diagnosis, there are also several cognitive behavioral therapies that have been developed to help people deal with the psychosocial components of having ADHD. These can be self-administered through computers. There are also mindfulness practices to help the person monitor themselves so they are better at social interactions. Exercise should also be optimized. Repeat psychological tests can help guide effective treatment. Patients who have had ADHD untreated for years might have subsequent low self esteem. Approaching the uniqueness of the patient and their presentation will help the patient thrive!



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  • 01:01:12

    Understanding Placebo

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    On this week’s episode of the Psychiatry and Psychotherapy podcast, I interview Mark Ard, M.D., a third year psychiatry resident at Loma Linda University. On the state level, he works towards developing means of access to care, in-patient psychiatric care, affordability of care, and further access to mental health.

    Mark is also the person who encouraged me to start pursuing weight training through Starting Strength, which we will link in this article.

    Link to show on: iTunes, Google Play, Stitcher, Overcast, PlayerFM, PodBean, TuneIn, Podtail, Blubrry, Podfanatic
    Understanding Placebo

    David Puder, M.D., Mikyla Cho, Mark Ard, M.D.

    What is placebo?

    The original meaning of the word placebo is, “I will please.” That statement comes from a time when doctors didn’t have our modern code of ethics, and they would prescribe whatever would make the person feel better. They probably had the best intentions, but they also would have known that whatever they were prescribing might not have been a real medication for the symptoms the patient was experiencing.

    Doctors, even then, knew that suggestion was powerful, sometimes more powerful than the medicine they were prescribing.

    Laypeople who hear the word “placebo” automatically think of sugar pills. They may think only that it’s something a doctor gives to placate and make people feel better when they aren’t getting the active medication. Placebos have long been used as a comparison arm for clinical trials. Usually it is in the form of an inert sugar pill or sham-procedure. Researchers can observe a psychobiological response known as the placebo effect.

    But when thinking about the word “placebo,” we must think of the entire effect of it, and it is perhaps better termed “the meaning effect.” As I discussed in last week’s episode of the podcast, the meaning we give something creates belief, and belief is a potent change mechanism, even when it comes to our physical health. It is especially potent when it comes to mental health.

    The placebo effect encompasses the therapeutic alliance, expectations, natural healing of the body and mind, and the environment of therapy. It involves the power of suggestion, mood, and the beliefs behind even one positive or negative interaction with a doctor. It also, as we will see, involves studies involving heavy-hitting medication.

    When there is an increased ritual, there is an increased placebo effect. During a hospital stay, the surgery preparation, meetings with doctors, nurses and therapists can have an incredibly therapeutic effect on a patient. It is possible to see biological mechanisms triggered by psychosocial context and attribute it to a placebo effect.

    What is the power of suggestion, the meaning effect, placebo effect, and how do we use it or avoid it in our practices and when testing new medical treatments?

    Why do we study placebo?

    We study placebos because we need to understand how meaning works, how belief works, and on the other side, if a medicine actually works.

    As doctors, we need to be able to read studies critically, with an eye for placebo. We need to see what actually works and what the study was controlling the treatment group to. We also need to know if there parts of the treatment that are working only because of the placebo effect, and if so, how do we use that to heal people.

    How does the placebo effect work?

    The efficacy of the placebo goes up because of the expectation and meaning we give to placebo.

    In one study, half of the patients got the actual medication, half got the placebo. In the same study, in another group, 25% of the patients got the placebo, and 75% of them got the actual medication. In both of these studies, the participants were told the percentage chance they would get the real medication. In the study where only 25% of patients received the placebo, more people experienced positive changes from the treatment, whether they received the placebo or not. Most people believed, because of hearing the percentages, that they would probably get the medicine. That belief increased the placebo effect.

    In groups with lower percentages receiving the actual medication, the response is lower, even with real medication.

    Researchers think placebo effect works because of expectation and classical conditioning mechanisms. Such understanding may be an oversimplification of a very complex phenomenon but it provides a useful framework. Expectation is how much the patient believes in the therapy. Higher expectation leads to hope and positive outlook, which results in better outcomes. Exactly how this works is still under investigation. There are multiple theories as to the underlying mechanism, but overall, we can say that there is a bidirectional interaction between expectations and emotions, and we respond better when expectations are high and our mood is good.

    Classical conditioning contributes to the placebo effect by modulating conscious expectation and non-conscious learning. The white coat effect is a classic example of how our body responds to a conditioned stimulus. Also, when a patient feels better after taking a pill, it becomes a conditioned stimulus, and the body may respond positively even after taking a placebo medication because of its conditioned response.

    Expectation can be shaped by many factors. Broadly, these factors can be grouped into patient effect, clinician effect and study design effect. Patient effect refers to patient characteristics such as beliefs, values, cultures, and the meanings associated with the illness and the treatment.

    In a study of IBS patients, Vase et al found that expected pain levels and desire for pain relief accounted for up to 81% in the variance in visceral pain intensity. There is also a greater dopamine release in patients who had higher expectation. (De la Fuente-Fernández). Conversely, pessimists were more likely to have negative side effects (when compared to optimists’ responses) when told a placebo would make them feel bad.(Geers)

    How a patient interprets and generates meaning in a given treatment condition is widely variable and difficult to control for. A similarity in demographic characteristics would not account for all of them. Direct-to-consumer (DTC) advertising of antidepressants is an example of how a society can shape one’s view and expectation of the illness and the treatment. The promotion of antidepressants inherently depends on the biological model of depression. By simplifying depression as serotonin deficiency, antidepressants were promoted as a simple solution to a complicated problem. These advertisements are designed to convey that “psychopharmaceuticals have an obvious, objective, and scientific relationship to the symptoms they are supposed to treat”(Greenslit, 2012). The reality is more complex and difficult to understand than the advertising, but the narrative is believed and shapes decision making.   

    An interaction with a clinician can shape the expectation of outcomes as well, especially if there is a strong alliance. Warmth, empathy, duration of interaction, and communication of positive expectation may significantly affect clinical outcome (Kaptchuk).  

    One article (Verhulst et al., 2013) deconstructed the correlation between the medical alliance and placebo. The placebo effect encompasses the beliefs, values, and expectations that patients have about a treatment. We can help shape a patient’s belief and expectations by giving realistic illustrations of the treatment, which are more valuable than false hopes; this is the medical alliance that we as healthcare providers can utilize. Part of the medical alliance is the idea of concordance between the physician and patient. There is both narrative concordance, the shared understanding of the patient’s condition, and the relational concordance, the shared relationship structured based on scripts, boundaries, and interactional rules. Ultimately, by utilizing the idea of concordance and a strong alliance with the patient we can influence how they view a treatment and better the outcomes via the placebo effect.

    Study design can also change expectation. Having a higher chance of being assigned to the treatment group and having a choice (Rose 2012) increases the expectation. The degree to which placebo resembles the treatment is another important consideration, because unblinding can lead to decreased expectation. (Some studies utilize active placebo to make unblinding more difficult.) In pharmacological studies, active placebo usually contains some real medication that contains some of the expected side effects to imitate the expected treatment.  

    The mechanisms that control placebo effect:

    Opioid system

    This system bolsters a lot of the evidence for pain relievers—you have more of a placebo effect on the patient if they know they're getting the medication than if it’s snuck into an IV. The opioid system in the brain begins to work as a pain reliever before any actual medication sets in, if it’s even administered.

    Dopamine system

    Dopamine signaling is involved in expectation and response. Our brains will respond as if something is happening if it believes it will happen. This pathway is also involved in habit formation and novelty seeking. The brain lights up in the same way to a placebo as it does to an active intervention. There is a fascinating link between dopamine deficiency and Parkinson’s disease; placebos can induce dopamine release, leading to improvement in Parkinson’s disease motor dysfunction.

    In another study, people were told they were getting either a cheap medication or an expensive medication. Even though they both received placebos, the group who was told they were getting the more expensive medication experienced a greater placebo effect.

    Even the color of medication can affect a person’s response. Brand names can affect a person’s response. A person who is told they are receiving an anti anxiety medication will calm down, even if it’s a placebo.

    Prefrontal cortex

    The third “system” is prefrontal cortex, which is involved in associations and meaning. This is also one of the main areas involved in improvement of depression (Murray, 2013).


    What is the effect of placebos on the medical profession?Is placebo testing accurate?

    Some industries fail to examine things with an accurate and rigorous placebo. For example, in a recent study on Botox used for depression, ¾ of the subjects knew if they had received the placebo or not (Finzi & Rosenthal, 2014). Some studies also neglected that placebos can actually change brain chemistry, and activate or deactivate different areas of the brain.

    We often think that the patient who is administered a placebo, in taking the medication, thinks it is real and thus the whole placebo response is merely from taking the pill. But in those results we neglect the human factors that come into play when a person meets with a psychiatrist that is doing the patient interview, and how it could be the therapeutic alliance and feeling cared for that influences outcomes and spontaneous remission of symptoms.

    For the medical field to determine that it’s not only the placebo effect taking place, that the medicine or treatment actually works, many factors come into play.


    Discussing negative side effects with patients

    How do you talk about medication as a doctor without scaring the patients with a side effect list? Studies show that by listing side effects, people are more likely to experience the side effects.

    I usually discuss the side effects with patients if they occur in more than 1% of patients or if the side effect is life threatening. Also, if the patient feels like they need to stop the medication, I tell them to call or email me. Even knowing they can reach out of they are experiencing problems gives patients a sense of peace, and could decrease negative placebo effects of the medicine, and increase positive effects of it.

    In medical education at large, there seems to be a loss of the science of connection and a focus on medicine rather than being able to emotionally connect to people, and mental health is part of the human experience.


    Therapy and the placebo effect

    Placebo and psychiatry have an interesting and complicated relationship—both are concerned with the mind-body connection. Using placebo in psychiatriatric research is, therefore, more challenging. It is more difficult to tease out the true effect of a treatment since mental illnesses have significant psychosocial components.

    Higher therapeutic alliance, higher empathy, and higher interpersonal skills all have better outcomes. Beyond the model of therapy, each therapist’s kind of connection to their patients deeply affects a patient's’ response.

    The value of the therapeutic alliance can be as powerful as medication, and also bolster the effectiveness as the medication itself.

    In their paper Wampold, Frost, and Yulish (2016) reviewed the history of how placebo was used in randomized control trials for testing the efficacy of psychotherapies. They found that when poorly designed placebo therapies were used as controls, the psychotherapy treatment group had superior results. It is difficult to have a truly controlled placebo. For example, it can be obvious whether a therapy is a placebo or a true psychotherapy and the providers administering the treatments would also know which was the true treatment. People have advocated that different psychotherapies are beneficial because of their common factors such as the therapeutic alliance, discussing expectations, and instilling hope. These and other factors common to the variety of psychotherapies can also be found in the placebo effect, which facilitates the argument that placebo psychotherapies are not inert. Therefore when we look at studies that compare psychotherapies to a placebo therapy, we must be aware that the comparisons may not be completely accurate.

    In therapy practice there are no effective placebos to be given to compare, so effect size with therapy is very different than effect size with medication vs placebo. A broader and more nuanced understanding of the placebo effect is important in two ways. First, it allows a clinician to critically evaluate studies that compare the treatment with placebo. Placebo should be evaluated within the framework of mental illnesses. Secondly, understanding placebo allows a clinician to maximize the clinical outcome by focusing on factors such as alliance. Placebo teaches us about the complexity of the mind body connection, and calls for a more integrated approach in treating mental illnesses.

    The effect size in double blind studies, however, does not tell the whole story of the effectiveness of the psychiatric relationship, because it does not take into account the part of the placebo response that actually came from a psychiatrist’s relationship with the patient.

    Even since the beginning of psychopharmacology, in the 1940’s, placebo effect has increased. In part, I believe that’s because we’ve reduced mental illness to a few symptoms and then say those can be helped or fixed by a pill. For example, there is commonly believed language around depression that says it’s a serotonin deficiency. So, patients take medicines to boost their serotonin (SSRI medication). That is not the only thing going on in depression, and it’s not necessarily true. So SSRI medications have a large placebo effect.

    Further, different psychiatrists will have different effectiveness with patients (McKay, 2006). The authors analyzed data from the Treatment of Depression Collaborative Research Program (TDCRP) that compared imipramine hydrochloride with clinical management vs. placebo with clinical management and found that 7% to 9% of outcome variabilities depended on the psychiatrist providing the treatment. When using BDI, the results were statistically significant (p < 0.05) and when using the HAM-D the results were marginally significant (p = 0.053). Therefore the authors concluded that the psychiatrist effect was at least equal to or greater than the treatment effects. The effectiveness of a psychiatrist is also critical in proving optimal treatment.  


    Non-therapeutic medical fields and doctor-patient relationships

    Even the awareness that the placebo effect exists should make medical workers understand that we need to consider people’s outside lives, not just the psychopharmacological effects of the medication. If little things have a placebo effect, and that is directly related to meaning and belief, what are the patients experiencing outside of the medical office that is influencing them?

    Conclusion

    Our brains were made to create meaning out of things, and this meaning can change the very nature of the brain. When we understand placebo we become better guides to our patients, steering them away from things that don’t do anything, and towards things like having a connected relationship with a caring person, which can be the treatment itself. We also look not only at how powerful a medication was compared to the placebo, but also if the patients thought they were taking the real medication or not. We also learn that belief is powerful and can understand how people get swayed into cults and taking things which have been proven to only be harmful.  

  • 00:57:48

    Perinatal Mood and Anxiety Disorders

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    In this podcast and article Dr. Kelly Rivinius, a licensed clinical psychologist who helps women suffering from PMAD, gives her insights about PMAD, its risk factors, prevention, and her own experience with perinatal OCD and anxiety.

    David Puder, M.D. and Kelly Rivinius, Psy.D. have no conflicts of interest to report.  


    Article the accompanies this episode go: here

  • 00:47:19

    Therapeutic Alliance Part 2: Meaning and Viktor Frankl’s Logotherapy

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    In this week’s episode of the podcast, I’m going to be emphasizing the meaning that I, as a therapist, can help draw out of other people’s experience through a therapeutic alliance.

    David Puder, M.D., Kristen Bishop, Brooke Haubenstricker, Mikyla Cho

    In the celebrated book Man’s Search for Meaning, author Viktor Frankl wrote about his intimate and horrific Holocaust experience. He found that meaning often came from the prisoners’ small choices—to maintain belief in human dignity in the midst of being tortured and starved and bravely face these hardships together.

    “The way in which a man accepts his fate and all the suffering it entails, the way in which he takes up his cross, gives him ample opportunity—even under the most difficult circumstances—to add a deeper meaning to his life. It may remain brave, dignified and unselfish. Or in the bitter fight for self-preservation he may forget his human dignity and become no more than an animal.” - Viktor Frankl

    “We who lived in concentration camps can remember the men who walked through the huts comforting others, giving away their last piece of bread. They may have been few in number, but they offer sufficient proof that everything can be taken from a man but one thing: the last of the human freedoms—to choose one’s attitude in any given set of circumstances, to choose one’s own way.” - Viktor Frankl

    Frankl argued that the ultimate human drive is the “will to meaning,” which could be described as the meaning to be found in the present and in the future. For example, I have had patients who are suicidal, yet they would not kill themselves, despite part of them desiring death, because they would not get to see their grandkids grow up. The meaning of the future moments and being able to help their grandkids in some small way empowers them to keep going to treatment.

    People’s meaning keeps them going, even when other drives, like sex or desire for power, are completely gone. In this way, Frankl noted, “Focus on the future, that is on the meaning to be fulfilled by the patient in his future…I speak of a will to meaning in contrast to the pleasure principle (or, as we could speak also term it, the will to pleasure) on which Freudian psychoanalysis is centered, as well as in contrast to the will to power on which Adlerian psychology, using the term ‘striving for superiority,’ is focused.”

    This idea led to the beginning of a new type of therapy—logotherapy.

    Helping a patient find meaning

    Being unable to find personal meaning in our lives can lead to depression, hopelessness, anxiety, and suicidality. As a physician, I see this often, and I try to help my patients find meaning in their lives. However, the approach I have learned from Dr. Tarr (my mentor), and from my studies, is different than the normal approach of just asking people, “What is your purpose?” or, “What is your vision for the future?” The technique I use is based on another principle called “psychic determinism,” which means that everything has meaning. There is nothing that a person says, no flash of emotion, no change in body posture that is meaningless.

    When you believe this, you view the patients’ words differently. The meaning may not be readily apparent; it may be expressed in primary process mentations and have an unconscious-type meaning like dreams, which may be difficult to understand. Suffice to know at this point that the mindset we have when we approach people is that everything they say has meaning; every sequence of thoughts that they say is deep and valuable.

    We start from small moments of meaning that are coming from their words, their body language, their microexpressions, your experience of them in the moment, and we take those small moments of meaningfulness and start to verbalize what we find meaningful. Listening to our patients and helping them to understand the hidden meaning in their lives, even in the midst of work or difficult times, can help them withstand trauma, stress, and hardships.

    No rambling is random

    Sometimes patients will talk for awhile, changing subjects rapidly, and we may think it is random, but it isn’t. Even when schizophrenic patients talk, there is meaning behind what they’re saying. When we allow for free association, we can derive a sense of meaning from the commonalities in topics that come up.

    For example, a patient might be talking about how they are angry at their significant other, then immediately report that when they were young their mother would often yell at their father, and their father would cower in his room in silence. How is their current anger related to how they felt as a child watching this drama? How might the two be linked? What about the microexpression of disgust that flashed as they reported both topics.  

    As you look deeper, the meaning becomes more evident. In this particular situation, the disgust or revulsion they experience recollecting their father’s cowardice magnified the disgust they felt toward their significant other. Understanding the link and the uncovered meaning helped them tolerate the intensity of that negative feeling, and helped them develop new meanings about their current and past experiences.

    Even hallucinations and delusions generated by some mental illnesses have meaning. When I’ve given patients antipsychotics and they’ve adapted to the medicine, we explored their hallucinations and they were able to see why they wanted to believe in an alternate reality—it gave them a sense of power or control, or related to a deep underlying fear in some way. As we developed meaning in their real lives, they felt more comfortable in their actual reality.

    When we sincerely believe that everything the patients say has meaning, the patients themselves feel meaningful. Ascribing meaning enhances the patient’s esteem tremendously and makes them feel safe enough to continue to freely associate. Incredible progress can be made with patients in this way.

    To get people to free associate, you need to reduce the shame enough to get people to feel safe enough to be able to share their uncensored thoughts and feelings.

    Empathize with the meaning

    “Men are not moved by events but by their interpretations.” - Stoic Epictetus

    Relationships can allow for deeper understanding and meaning to develop in life. To strengthen our relationship with our patients, we must understand what they’re saying and then empathize with that meaning.

    We often think in the context of our own lives, and as therapists or physicians we need to allow people to be the experts of their own lives. A word or phrase may mean something completely different to our patients than it does to us, so we must ask the patients to help us understand their interpretations and the meanings they assign to the events they’ve experienced. It is important that the patient communicates their meanings and that assumptions aren’t made. Misunderstandings can cause feelings of isolation, leading to strains or ruptures in the relationship. If this happens, try to reconnect, as this conveys respect.

    Try to deeply connect with the patient emotionally through empathy and listening. Listen to what is said, what is not said, and what makes the patient defensive. We can listen to the rhythm, the sound, their vocal cadence, and watch their face for emotional cues.

    Even if we believe the patient isn’t entitled to the emotions they are experiencing, we have to search for the meaning they’ve assigned to their pain. That meaning is what we can empathize with, no matter the circumstance. When we empathize, we can join them in their distress or enjoyment, and we can develop a deeper therapeutic alliance that is patient-centered and emotion-centered.  

    “To feel with a patient and share distress and hopelessness and mistrust of the future, is therapy. You are an observer in taking history, but you’re a participant as a therapist. To share together, is therapy.” - Dr. Tarr

    Meaning develops emotional endurance

    People who have chronic pain who believe they are enduring it for a deeper meaning report feeling far less physical pain compared to those who do not report a deeper meaning. Even in birthing units, women report the highest amount of pain, but also often the highest amount of satisfaction. The child being born gives meaning to the pain, and this meaning is so powerful that some women choose to endure the pain instead of accepting medication.

    Help patients find meaning in their symptoms. Most symptoms are adaptive, even eating disorders, cutting, and other harmful behaviors. These things have helped people cope with the realities of their lives in some way. We don’t want them to judge their symptoms, but we want them to identify what the meaning behind them.

    To really connect with a patient, we must convey to them through our words and actions that they mean something to us, and that we empathize with the meanings they’ve assigned to their lives.

    Here are a few phrases I like to use that convey to the patient that I want to connect with them:

    “What we are talking about together is meaningful.”

    “We want to make sure we are understanding each other.”

    “I think I know what you mean. Please tell me if ______ is what you meant. I want to make sure I am understanding you and that we are in tune with each other.”

    “If you feel I misunderstood you, please tell me right away so we can clear it up as soon as possible.”

    “We will know together, find out together…”

    “Could you give an example, elaborate on that, I want to be sure I understand what you are sharing with me.”

    “I can understand in part how that interaction would make you feel that way.”

    Logotherapy, created by Viktor Frankl, helps patients understand and develop meaning in their lives.

    Viktor Frankl’s book not only chronicles how the principles of logotherapy helped Frankl survive the Holocaust, it also recounts his observations of how others used meaning to retain their human dignity during times of great suffering. So what is this “logotherapy” that helped people survive?

    Essentially, logotherapy is a meaning-centered approach to psychotherapy. Frankl first published his ideas on logotherapy in 1938, and it is now known as the “Third Viennese School of Psychotherapy.”

    The Viktor Frankl Institute lists the three principles that are the basis for logotherapy:

    Freedom of will

    Will to meaning

    Meaning in life

    The core tenants can also be elaborated in another way, as done by the Viktor Frankl Institute of Logotherapy in Texas:

    Life has meaning in all circumstances, even the most miserable ones.

    Our main motivation for living is our will to find meaning in life.

    We have freedom to find meaning in what we do, and what we experience, or at least in the stand we take when faced with a situation of unchangeable suffering.

    Frankl noted that there are a variety of ways in which we can find meaning, such as by our actions, our experiences, our relationships, and our attitude toward suffering. Indeed, logotherapy has been utilized to help treat a variety of psychiatric illnesses, such as anxiety, depression, obsessive-compulsive disorder, and even schizophrenia. Currently, there are several logotherapy institutes around the world in Africa, Asia, Europe, and North America that focus on educating the public about logotherapy and applying it to find meaning in people’s lives.

    Here are some studies about logotherapy:

    One study (May, 2010) found psychological safety and psychological meaningfulness was significantly related to engagement in work. 73% of the variance in engagement in work was able to be explained, with 62% coming from meaningfulness and 42% coming from psychological safety.

    One study (Mahdizadeh, 2016) of patients after heart surgery found that those receiving logotherapy had improvement in mood. Additionally, this study found that logotherapy did not change the physical capabilities of the patient post surgery. However in the patients who had little to no symptom relief and continued limitation of functions post-op, it still showed an improvement in mood 6 months after the study was completed.

    Another study (Robatmili, 2014) had the logotherapy group work on describing what was meaningful, setting goals, and then had the group facilitate each other moving towards their goals. In this treatment group, the “meaning of life” scores increased and depression scores decreased. Discovering and pursuing meaning is facilitated by helping through the following steps: (a) establishing the therapeutic relationship; (b) increasing insight regarding identity, values, and goals; (c) reframing meaninglessness and depression; (d) discovering meaning within the meaninglessness and depression; and (e) pursuing the fulfillment of meaning.

    Once you have some positive attributes, you find other positive attributes—like a snowball effect of developing positive meaning in life. One study (Zhang, 2018) showed this after surveying 1,000 elderly people in Hong Kong. There was a higher level of meaning associated with happiness, health status, and decreased healthcare utilization.

    Another study (Mahdizadeh, 2016) showed that when educational interventions based on the main concepts of logothearpy were made, it lead to an improvement of the patient’s quality of life after CABG surgery in persons over the age of 35 (specifically, scores in QOL were improved psychologically).

    In one study (Mosalanejad, 2013), an infertile experimental group that used logotherapy showed significant decreased psychological stress scores.

    One case review (Southwick, 2006) looked at adding a meaning-based intervention into the treatment of chronic combat-related PTSD showed positive enhancement of outcome when combine with traditional therapies and medications.

    A study of women with breast cancer (Mohabbat-Bahar, 2014) showed logotherapy to be helpful at reducing anxiety.  

    I also discussed a study (Thomas, 2014) regarding how structured sessions helped cancer patients improve their sense of meaning in life.  

    A qualitative interview study on nursing home residents (Drageset, 2017) found that meaning could be found in physical and mental well-being, belonging and recognition, personally treasured activities, and spiritual closeness and connectedness.  This present study also showed a link between well-being of patients’ hope for an improved state of health and are in accordance with previous studies showing significant associations between meaning, hope and well-being among older people in nursing homes.

    Finally, a study (Leveen, 2017) explored how poetry can be used to increase a sense of meaning in physicians caring for patients.    

    Conclusion:

    By focusing on what is said by our patients and those we care about and by believing that everything that is said has meaning, we can increase our connectedness with them.  We can also slowly find the deeper sources of meaning and purpose which can help make sense of suffering and physical and emotional pain.






  • 00:49:34

    Psychiatric Approach to Delirium with Dr. Timothy Lee

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    This week on the podcast, I am joined by Dr. Timothy Lee, the Loma Linda residency program director and the head of medical consult and liaison services. One of his specialities is delirium, so this week we will be discussing both hypoactive and hyperactive delirium.  

    What is delirium?

    Delirium is an acute change in a person’s sensorium (the perception of one’s environment or understanding of one’s situation). It can include confusion about their orientation, cognition or mental thinking.

    With hyperactive delirium, a patient can become aggressive, violent and agitated with those around them. A patient experiencing delirium can have hallucinations and hear things, they can become paranoid, and they are overall confused. A family, or non-psychiatric medical staff, might be concerned that the patient is experiencing something like schizophrenia.

    Hyperactive delirium symptoms in patients:

    Waxing and waning—it comes and goes

    Issues with concentration

    Pulling out medical lines

    Yelling profanities

    Throwing things

    Agitated

    Responding to things in the room that aren’t there

    Not acting like themselves

    Hypoactive delirium is much more common than hyperactive delirium (based on research studies), but it is often missed because the presentation is much less dramatic. People with hypoactive delirium are confused and disoriented, but they do not express their confusion verbally or physically.

    Hypoactive delirium symptoms:

    Slower movement

    Softer speech

    Slower responses

    Withdrawn

    Not eating as much

    Often, nurses and physicians can miss the fact that the patient has the typical confusion that denotes delirium because the patient is quieter, so it doesn’t come to the attention of the medical team or psychiatrist consult service.

    Delirium can even be confused for depression. One Mayo Clinic study showed that when consulting a doctor about their depression, 67% of the time, the patient ended up having delirium.

    Why does delirium happen?

    Often we see it happen, even to relatively healthy people, in physically stressful situations—post surgery, during an acute illness, or even just being stuck in the hospital for a few days. This does not mean it is indicative of a sudden onset of a long term mental illness, such as schizophrenia.

    To consider what can cause delirium, I like to think systematically from the top of the body and work my way down. This is by no means exhaustive, but it can be helpful.

    Many things can cause delirium. I like to think about starting at the top of the body and going down, as a way to not miss the cause. Here are a few we would consider as we go down the body:

    Stroke—check strength in both arms and legs, have the patient smile

    Hypertensive emergency

    Infection or meningitis

    Physical trauma—concussion, head injury with initial loss of consciousness, then after regaining consciousness they can have delirium

    Brain bleeding

    Medications that affect the brain, such as ones that produce anticholinergic side effects. (They suppress acetylcholine, causing brain imbalances and confusion. Anti-allergy medicines, pain medications, and some psychiatric medications are anticholinergic.)

    Circulatory issues

    Thyroid imbalances or parathyroid hormones

    Cancer

    Heart attack

    Traumatic injury to the heart

    Aspiration pneumonia

    Lung infection

    Lung cancer

    Viral pneumonia

    Pancreatic inflammation

    Urinary tract infections in women

    Liver cirrhosis

    Hepatitis

    Gallbladder inflammation

    Low bilirubin

    Hepatic encephalopathy

    How do we identify delirium in a patient?

    Asking certain questions to the patient and/or medical team and family can help us understand if the patient is experiencing delirium. Often, a patient experiencing delirium will still know where they are, what they are doing, and who they are. The main test to really determine if it’s delirium is the “clock drawing” where we ask the patient to draw a clock with the hands showing 11:10.

    Here are some questions and tasks we ask the patient to answer and perform to test for delirium:

    Does the person know who they are?

    Does the person know where they are?

    In what detail does the person understand where they are?

    Does the person know the date?

    Can they orient to the situation? Do they know why they are there and the circumstances that led to them being in the hospital?

    We might ask the patient to repeat back a few words for us.

    We will ask them later if they remember the three words we asked previously.

    We test for concentration, like asking the days of the week in reverse order.

    We try to assess their visual and spatial ability.

    We might ask them to draw a clock to look for spacing, impairments, or difficulties.  

    Some tests that are common to determine delirium are:

    The Mini Mental Status Exam (MMSE)

    The Montreal Cognitive Assessment

    How to help

    It is important, if the patient has loved ones with them, to educate the family about delirium, because both hypoactive and hyperactive delirium can be terrifying to watch.

    When it comes to giving medications, it’s important to follow a few rules, Dr. Lee says. Giving medications with anticholinergic side effects can make the patient more agitated. When prescribing meds, be careful not to switch from a hyperactive delirium presentation to a hypoactive delirium presentation by just sedating the patient but maintaining confusion. Medications like benzodiazepine, barbiturates, sedatives and pain medications (beyond what is needed for pain) can all cause worsening of delirium.

    If the confusion is from an infection, an antibiotic should eventually help the cause of the delirium, however it may take a few days for the confusion to improve after the cause is eliminated.  At times antipsychotic medications are used to help the delirium and reduce the time needed to stay in the hospital.

    Even after the cause of the delirium is gone, and the delirium seems to have improved very quickly, a person may still have lingering cognitive issues. It’s important to be conservative in terms of how quickly you taper them off of the antipsychotic medication used to treat the delirium.





  • 00:37:34

    Ketamine and Psychedelics with Dr. Michael Cummings

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    Blog by David Puder, M.D., Mark Ard, M.D., Mikyla Cho,

    On this week’s episode of the podcast, I interview Dr. Cummings, a reputable psychopharmacologist, about ketamine. We talk about psychedelics, the research behind it, both the positives and the negatives. We will look at how it is or is not helpful in psychiatric treatments.

    (Disclaimer: There are no conflicts of interest to report. Neither Dr. Puder or Cummings is affiliated with any companies in favor of ketamine and other drug companies.)

    Ketamine

    Although ketamine has recently become a medication of great interest in psychiatry, it actually is a fairly old medication. It was first synthesized in 1962 and began human trials for anesthesia in 1964. It was finally approved by the FDA as a dissociative anesthetic in 1970.

    What has piqued interest in psychiatry is that infusion of a smaller dose of ketamine produces a rapid response in terms of reversal of depressed mood, suicidality, and some treatment-resistant depressed patients.

    The literature is rich (in one sense) as the most recent consensus statement (Sanacora, 2017) looked at seven randomized controlled trials, all of which support a robust antidepressant response and anti-suicide response. The difficulty with those trials is the majority of them lasted only one week. A few of the later trials lasted two to three weeks with two to three infusions per week. So, what’s lacking at this point is adequate data regarding long term treatment response and data about transitions to more traditional antidepressant treatments.

    This area is of great interest, largely because of the limitations of our current antidepressants. In the STAR D antidepressant trials, 48.6% of people got a 50% reduction in depressive signs and symptoms with the first antidepressant, whereas only 37% of depressed patients achieved remission with the first medication.

    Limitations of ketamine in Psychiatry

    People receive low-dose infusions of ketamine for depression and suicidality, and there seems to be short term response to this, though the long term effects have not been measured.

    The decrease in depression and suicidality is typically robust, but short lived. There is a fairly rapid decay of the antidepressant response following infusion. The infusions are done over 40 minutes. About thirty percent of the patients will become fairly unresponsive to light verbal stimulation. They then recover, but within a few days their mood will begin to deteriorate.

    The study comparing 2 days/week to 3 days/week showed fairly equivalent effectiveness of ketamine for the several weeks it was studied. The other limitation of ketamine in terms of an ongoing treatment for depression is like all NMDA antagonists, these drugs are psychotomimetic and cause dissociation. They can induce psychotic signs and symptoms, and those do begin to become more prevalent with repeated infusions.

    Currently adverse effects are known for chronic abusers, and can include cognition problems and bladder issues and we don’t have adequate data telling us how long it would be safe to continue ketamine infusions and how to make a transition from ketamine to a more stable, longer lasting treatment.

    Ketamine and Dissociative States

    Those who described their experiences during the ketamine infusion note a loss of sense of personal boundaries and a sense of union with the universe. There are fairly dramatic changes in their thinking.

    Ketamine inhibits the brain’s primary activating receptor, the N-methyl-D-aspartatic receptor, blocking the effects of glutamate, which transiently enhances plasticity.  Ketamine blocks presymptic inhibitor interneurons, blocking glutamate, leading to more glutamate overall in the brain. This “glutamate surge” leads is what is thought to lead to a rapid release of BDNF which is a growth factor for the brain.  This may be responsible for the short term improvement in depressive symptoms.

    People also use ketamine as a recreational drug because of its ability to induce a dissociative state. It has been a drug of abuse for a number of years since its introduction in the 1970s. It goes by “Special K,” and a number of other names. Many people abuse it after drinking and at raves. If they take a high enough dose, they can lose their ability to hear and see and become stuck in a “frozen state.”

    It can produce delirium, which can be either stuporous or agitated. The related drug, phencyclidine (PCP, aka angel dust), causes more severe dissociation and psychosis. However, the effect of ketamine and phencyclidine are in the same direction and by the same mechanism.

    People refer to Ketamine’s dissociative state as the “K Hole,” when one can’t move and experiences this depersonalization. Ketamine is sometimes used as a “date rape drug” because the person can be in a very vulnerable state.

    Ketamine dosage

    Ketamine dosage given for depression is at 0.5 mg/kg, which results in a plasma concentration of approximately 70-200 ng/mL.

    Ketamine dosage given for anesthesia results in plasma concentrations of 2000-3000 ng/mL.

    Doses people use at raves or for anesthesia are about an order of magnitude higher than those used for infusion for treatment of depression.

    Peak plasma concentration with antidepressant infusions of ketamine are about 200 ng/mL. For recreational or ICU anesthesia purposes, it is closer to 2000 ng/mL.

    Side effects/risks of ketamine infusion

    When people are recovering from the antidepressant infusion, there is still a risk. They may become agitated, confused, or hallucinate, which is why one of the recommendations for treatment centers using ketamine is that they have adequate expertise in controlling psychomotor agitation and confusion if those things occur.

    During ketamine infusion, about one-third of patients also exhibit a fairly pronounced sympathetic arousal during the initial portion of the infusion.

    About 30% of patients achieve a heart rate of 110 and a blood pressure of approximately 180/100. (Sanacora, 2017)

    One of the recommendations for ketamine infusion centers is that they take a good cardiac history and be sure that the person can tolerate exercise. Additionally, the drug should be administered by someone who is ACLS certified and has access to a crash cart.

    For cats recovering from surgery (Jasani, 2015) on ketamine use for animals), it is helpful and ideal to put them in a quiet environment. The same is true for humans. Patients should be put in a quiet, safe environment so that one does not induce an agitated delirium because the patient is responsive to the environment, but their interpretation of that environment may not be based on reality and can produce an agitated response.

    Mechanism of action

    In many cases of treatment-resistant depression, it is necessary to alter the plasticity of the brain to get a response. Ketamine, perhaps via the blockade of glutamate at NMDA receptors, and perhaps via downstream mechanisms from that, seems to do this.

    This correlates to some extent with how we know antidepressants and electroconvulsive therapy works. They have looked at CT scans for what is important in gaining a response, and for decades, it was thought that it was the seizure. Now, it may actually be the postictal neuronal suppression period that accounts for the therapeutic benefit because that is associated with turning on rapid response genes.

    One small study looked at simply exposing people repeatedly to isoflurane, an anesthetic agent, causing repeated neuronal suppression. They also received an antidepressant response from that. So it may be that turning neurons off transiently can be beneficial in terms of resetting them at the DNA level and making them more plastic. Ketamine may not be the only anesthetic agent that alters longer term functioning of neural circuits.

    Ketamine Clinics

    Although ketamine has become popular, the major risk is not that the drug may not have psychiatric utility, but that we are still fairly early on in using it. The risk is that the use will outrun the data we have available to guide us. This may already be happening, as evidenced by the surge of new ketamine clinics.

    Often, the clinics are started by anesthesiologists, and there is no clear psychiatric evaluation that may precede patients starting ketamine.

    Currently, the data we have now essentially points to ketamine as treatment for major depression, refractory to other treatments. In many ketamine clinics, they’re using it to treat all complaints, but the data on this ranges from slim to none at all.

    There may be a lucrative pull toward these clinics as they are usually cash pay since insurances don’t currently cover this.

    Advice to Those Considering Ketamine Clinics

    One should first get a very careful psychiatric evaluation, including a diagnosis of their mental disorder and a careful review of their treatment history to be sure that they have received optimal treatment in terms of established long term treatment options.

    If one does decide to pursue ketamine treatment, then they should work with a psychiatrist who is well-versed in not only using ketamine, but is also knowledgeable in using other means to address depression, such as more traditional antidepressant medications and psychotherapies (especially day treatment programs).

    Other Concerns with Ketamine

    According to existing literature, ketamine is not a cure all for major depression. It may help “jolt” a brain that has become resistant to treatment into being more plastic and transiently being less depressed, but it is not a cure for the underlying condition.

    Another concern is that we don’t know what the patient will be like after long-term treatment with ketamine. Will they have had a full recovery? Experience persistent issues or treatment complications?  Cognitive issues? Bladder issues?

    Ketamine may be most helpful for patients who have failed multiple treatment modalities, such as full doses of antidepressants or even ECT. It may provide a means to enhance treatment response to get the person out of the immediate danger of severe depression and suicidality. However, at this point it is not a standalone treatment.


    Ketamine and Psychotherapy

    If ketamine is a dissociative drug, it might be best to have the person off of ketamine before starting psychotherapy so that their brain is fully functional. The psychotherapy would need to follow after the person’s dissociation has dissipated.  The half life of the parent compound of ketamine is about 2.5 to 3 hours. The active metabolite (norketamine or N-desmethylketamine) is up to 12 hours.

    By the time the person is 60 hours post-infusion, the ketamine is gone. It is unlikely that there are prolonged dissociative effects, at least not with one, two, or three exposures. However, there is no data stating just exactly how many exposures to ketamine is considered safe in terms of avoiding a more protracted delirium.  

    Final Thoughts on Ketamine

    This is still a new frontier that will most likely be revisited as newer and larger studies are done. Ketamine is promising in that it does suggest that if we can discover more useful and somewhat more gentle NMDA antagonists, we may discover a new avenue into treating more resistant depressive illnesses.

    PsychedelicsHistory of Psychedelics

    Psychedelics are illegal is most areas of the world. Because of a few studies and their ability to alter mental states, they are a gaining interest in some areas of psychiatry.

    They have been used for millennia in some Native American and other indigenous populations. Historically, they have been used primarily in terms of religious rituals, often under the guidance of a shaman or medicine man helping to guide an individual in respect to life issues. Traditionally, they were often used only once or very sparingly as a support to what were ritual-based psychotherapies. The interest in psychiatry is if these would facilitate some form of psychotherapy while using the psychedelics.  

    All of these drugs, such as psilocybin, LSD, and ayahuasca, are all essentially very potent 5-HT2A serotonin agonists, with many of them also being agonists at other serotonin receptors.  

    They produce a state similar to ketamine.

    The person has an alteration of their sense of self, a loss of boundaries.

    They have a sense of being in touch with the universe.

    They become much more influenceable under those circumstances.

    Of course, like ketamine, psychedelics have also been prone to being drugs of abuse like the psychedelic area of the late 1960s. Studies (Kalasinsky, 2014; Palamar, 2016) of people who have used street ecstasy have found that the drug was often mixed with other chemicals, such as methamphetamines and bath salts, making it very different than what could potentially be given at a pharmaceutical grade.

    Psychedelics dosagePsychedelics in high doses

    Much has to do with the dosing and concentration that is present when abused, which are often both very high. These drugs can cause permanent changes. For example, LSD can induce a persistent hallucinosis that’s essentially the result of a permanent change in receptor status that usually occurred with repeated, very high dose exposures.

    Psychedelics in modest doses

    Frankly at this point, we don’t know very easily how to separate the benefits and risks of these drugs. Although used as they were traditionally, there were often very limited exposures and very controlled environments. This suggests that these drugs should perhaps be used with caution for therapeutic benefits.

    Studies about Psychedelics (Rafael, 2018 for most recent review)

    Psychedelics have shown benefits in a variety of open label, small studies, and lack adequate control group of mostly short duration for everything from depression, to anxiety, and to even inhibiting the use of substances like alcohol.

    Psilocybin has been studied in decreasing depression in cancer patients

    Patients will take the medication or placebo, wear an eye covering, and listen to some light music while lying down on the hospital bed. If patients do undergo an experience of some sort, there is a person in the room they can talk to.

    Most studies typically report a positive primary result, but are limited by their very small samples and lack an adequate control group. Therefore, much of our data is still very early on with respect to the hallucinogens and their possible benefits.

    In contrast, the wealth of data from traditional cultures that have used these substances for millennia shows that when these drugs are used in a very controlled, limited manner, they do not seem to induce ongoing mental disorders.

    Research is still at an early stage and may open new routes for treatment by modulation of serotonin receptors in ways that we haven’t approached before. It may turn out that hallucinogens themselves may or may not be the right agents to use in the long run. But, this may point to a new approach to altering brain plasticity to enhancing treatment.

    Study designs and placebos affect study results.

    Some studies use saline or sugar pills as placebo, and patients are likely to know they have not received the treatment in those cases. A good placebo produces some degree of change and level of consciousness. For example, an infused benzodiazepine might be a possibility.

    A normal saline infusion or an oral sugar pill would not produce an adequately blinded study since both hallucinogens and ketamine produce a fairly rapid effect that anyone being exposed to the drug would be aware of.

    Another example is a study that used botox for depression (Finzi, 2014). 75% of the Patients knew if they have actually received the botox or just an injection of normal saline since the effects on the muscle were so different. These studies would then become suspect because particularly in treating mood disorders, the placebo response rate is typically fairly high, often around 30-40%. Therefore, studies really do need to blind both the participants and the researchers by giving an active comparative placebo.

    The Hawthorne effect can bias the study because if you expect something to happen, you tend to see it, whether it actually exists or not. However, the results of a study can change once it becomes a multi-site study.

    Open label studies have a higher rate of positive findings than those of randomized controlled trials.

    In an open label trial, the patient and the prescriber of the treatment both know what the patient is receiving and consequently, they can be biased by their beliefs.

    If you compare open label studies to studies in which neither the patient or the prescriber knows what the patient got, the rate of positive results is about twice in the open trials than what it is in the controlled trial.

    We can fool ourselves into seeing something that wasn’t actually there about half the time.

    Final Thoughts

    Longer trials of up to six months should be done for ketamine research to address several questions.

    How often can a patient receive treatment?

    What are the long-term effects?

    What is the point at which one should stop because of any long-term effects on a person’s brain?

    How do we transition from ketamine infusion to alternative treatments?

    Does ketamine ultimately make the person more responsive to other pharmacologic interventions or psychotherapeutic interventions?

    Psychedelics also still need to be studied more extensively.

    We need to understand more fully what is happening in the brain as a result of very potent stimulation of 5-HT receptors.

    Perhaps we can use that as a jumping off point to look for other means to modulate or encourage treatment response using those receptor systems.

    We do not know enough about ketamine and psychedelics to be able to tell if they will have positive long term effects on mental health and be useful to psychiatry. These topics will need to be revisited as more research is done.

    dos Santos, R. G., Bouso, J. C., Alcázar-Córcoles, M. Á., & Hallak, J. E. (2018). Efficacy, tolerability, and safety of serotonergic psychedelics for the management of mood, anxiety and substance use disorders: a systematic review of systematic reviews. Expert review of clinical pharmacology, (just-accepted).

    Finzi, E., Kels, L., Axelowitz, J., Shaver, B., Eberlein, C., Krueger, T. H., & Wollmer, M. A. (2018). Botulinum toxin therapy of bipolar depression: A case series. Journal of psychiatric research, 104, 55-57.

    Kalasinsky, Kathryn S., John Hugel, and Stephen J. Kish. "Use of MDA (the" love drug") and methamphetamine in Toronto by unsuspecting users of ecstasy (MDMA)." Journal of Forensic Science 49.5 (2004): JFS2003401-7.

    Palamar, Joseph J., et al. "Detection of “bath salts” and other novel psychoactive substances in hair samples of ecstasy/MDMA/“Molly” users." Drug and alcohol dependence 161 (2016): 200-205.

    Sanacora, G., Frye, M. A., McDonald, W., Mathew, S. J., Turner, M. S., Schatzberg, A. F., ... & Nemeroff, C. B. (2017). A consensus statement on the use of ketamine in the treatment of mood disorders. JAMA psychiatry, 74(4), 399-405.



  • 00:50:04

    What is psychodynamic theory?

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    On this week’s episode of the podcast, I interviewed Allison Maxwell-Johnson, a social worker and PhD student of clinical social work. I refer patients to her regularly for psychoanalysis, and she has had a wonderful impact on their mental health journey.

    Link to show on: iTunes, Google Play, Stitcher, Overcast, PlayerFM, PodBean, TuneIn, Podtail, Blubrry, Podfanatic

    Psychodynamic therapy is a form of talk therapy where the practitioner work focuses on the patient’s emotion, fantasies, dreams, unconscious drives and wishes, early and current life relationships, and the relationship that is forming between the patient and therapist.  

    The history of psychodynamic therapy

    Sigmund Freud is known as the father of psychodynamic therapy. He practiced in the late 1800’s and early 1900’s. Some psychiatrists and therapists think that Freud has been debunked because he is a controversial figure. But my colleague, Allison Maxwell, and I, think his impact on furthering the mental health field has been positive.

    Historically, people with borderline personality disorder, somatic disorder and post traumatic stress disorder (PTSD) were all grouped under the title of “hysteria.” A few hundred years ago, these people would have been killed as witches, put in asylums, and there wasn’t much ability to, or interest in, digging into their psyche. There was certainly no warmth or empathy given to them.

    Freud began to grapple with those deeper, tougher issues, claiming it wasn’t just a medical disorder. He gave empathy, and a level of connectedness to his patients that hadn’t been done before. As the first psychoanalyst, he was a pioneer in his field, and he figured out that having an emotionally connected relationship with his patients (he would even have is patients over for dinner and go for walks with them) could actually heal the patient.

    Affect

    Affect is something therapists need to pay attention to when it comes to each individual patient. It’s about noting the facial and emotional state of the person. Is the patient emotionally flat or expressive? Are they depressed or happy? Are they peaceful or agitated?

    We focus on their emotional state and try to lean in to understand what a patient is feeling during a session. As the doctor or therapist, what is the emotional reaction you're having to the patient, in the moment? Analyze the situation—both your feelings and theirs. Ask them for clarification on their feelings, then ask yourself how you can use that information to understand and connect with the patient emotionally.

    There are multiple emotions going on which can be conflicting. We need to ask ourselves if we can empathize with the distress that is in the room.  

    It’s not only about intellectually understanding what’s happening with a patient, or diagnosis. It’s about understanding how to create an emotional connection and help someone.

    Transference

    A therapist applies the principle of transference when we pay attention to the emotional state the patient has towards them. If the therapist reminds them of their abusive father, and they react emotionally, it’s a classic transference situation.

    Understanding transference can help a therapist remain empathic and curious, even when a patient is angry at them. Transference can be seen in their complete reaction towards you, both from their past, and how you are interacting with them.  

    Countertransference

    As therapists, we are also humans. We will have reactions to the patients we work with.  Countertransference is the complete reaction we have towards our patients, both coming from how the patient reminds us of people from our past, and our reaction towards the things that the patient is uniquely doing.

    The unconscious exists both in our patients and in us. If we can keep countertransference in our awareness as therapists, we can try to understand what is happening interpersonally—why we do or don’t like our patient, and why we feel angry or upset with our patients.

    As therapists, we should not react to our patients out of direct emotion, but understand that countertransference is happening, and be curious about the meanings behind our feelings, and their feelings towards us.

    Studies that show psychodynamic theory works:

    For the curious, read this article by Jonathan Shedler, “The Efficacy of Psychodynamic Psychotherapy” PDF

    Mentalization-based therapy

    Mentalization therapy is an emotion-focused therapy for people with borderline personality disorder. It helps them question whether they are accurately mentalizing, or understanding, their own experiences and their therapists emotional experiences. The positive effect of mentalization-based therapy is measurable. It has a mean effect size of 1-2, meaning it is 1-2 standard deviations from the control group—it works.

    People who were in and out of psychiatric hospitals with suicide attempts, after mentalization therapy, can have great success in achieving a normal life.

    Study on Mentalization based therapy with 8 year follow up: PDF

    Transference Based Therapy:

    Article on transference focus therapy increasing a patient’s narrative coherence and reflective function: PDF

    In conclusion

    As therapists, including psychodynamic principles can help us connect with our patients. It will protect us from burnout, and give our patients the chance to feel emotionally connected with someone, in a corrective and healing way. It can be incredibly rewarding, rather than draining, when we feel connected, and our patients usually express gratitude as they heal.



  • 00:11:28

    Advice for medical students applying to psychiatric residency

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    Timothy Lee has talked to thousands of medical students about how to applying for residency programs, and here, he gives us a few tips on how to make it through the gauntlet, and how to have your best chance at landing the program you want.


    Here is what Timothy Lee says:

    Stay calm

    Many students have been fine tuning their personal statements, and trying to get their resume just right, or hurrying to press the faculty to write letters of recommendation. It can be very stressful.


    It’s okay to turn in information a little bit later, in order to have all of the paperwork you need. It’s even okay to review your statement after you’ve already turned it in. No one will lower their opinion based on that. You will need to have applied for the majority of the programs you are interested in by early or mid-October, otherwise the program director might wonder if you’re applying to them later as a backup plan.

    What matters in a personal statement?

    Every program director will have different opinions on what you write, and every program director will be looking for different things from your personal statement. For some people, it’s a chance to get to know the applicant a little bit. For others, it doesn’t really matter that much.


    As long as your grammar and syntax are competent, you should be fine. Some people don’t worry about the format, and others are more particular. To be on the safe side, if you have access to a good mentor, run it by them. Also, don’t be too wordy—stick to a page and a half.

    Do step scores matter?

    Step scores are a very convenient screening tool for what matters, but there are studies that show that step scores are not directly correlated to success in residency performance. They are helpful, but are not the end-all-be-all. It’s only one part of the picture of an applicant. However, if you are going for a highly-competitive school, you might need to worry about step scores a bit more.

    Apply to the right number of programs

    The number of programs is not the only way to increase your chance of success of getting in. Pay attention to the types of programs you are applying to as well. If you are applying for a good number of programs, make sure at least half of them are are ones you are a solid and potentially attractive candidate for.

    Keep a good perspective

    Ultimately, you are more than your CV, step score, or personal statement. If patients like you, that’s going to go a long ways. Your patients won’t know your scores, or where you graduated from medical school. They will know if you were competent, caring and connected. That is ultimately what matters.


  • 00:45:50

    Therapeutic Alliance Part 1

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    What is a therapeutic alliance?

    The therapeutic alliance is a collaborative relationship between the physician and the patient. Together, you jointly establish goals, desires, and expectations of your working partnership.

    Every interview with a patient, whether it’s for diagnostic, intake, evaluative, or psychopharmacology purposes, has therapeutic potential. The treatment starts from your first greeting—how you listen, empathize, and even how you say goodbye.  

    It’s built from a partnership and dialogue, like any other relationship. It’s not built from medical interrogation. It’s not about pulling medical information to be able to make a diagnosis. We have to make it a positive experience for patient, so they can begin to talk about what's negative in their lives.

    The therapeutic alliance is full of meaning, and it uses every emotional transaction therapeutically. If they get angry, sad, or have fear you will abandon them, as a therapist, it’s our job to figure out how to help them through that feeling within the relationship. The doctor can express desire for the patient to share, in real time, how the patient is feeling, even about his or her relationship with the doctor.

    Why do we care?

    We all know that some talk therapists have better outcomes than other talk therapists. What’s interesting though, is that some some psychiatrists’ placebos worked better than other psychiatrists’ active drugs. One study of NIMH data of 112 depressed patients treated by 9 psychiatrists with placebo or imipramine, found that variance in BDI score (a score that measures depression) due to medication, was 3.4% and variance due to psychiatrist was 9.1%. One-third of psychiatrists had better outcomes with the placebo than one-third had with imipramine.  

    Another book argues that the therapist is more important to outcome than theory or technique. Many other studies have shown that therapeutic alliance directly correlates to success rates.

    What builds a therapeutic alliance?

    Research shows there are a few things that grow therapeutic alliance:

    Expertness

    Facilitating a greater level of understanding

    When residents are worried they are an imposter, I tell them that humility is good, but realize that you have experience that most will never have, medical school, being highly educated, being around vast different ways of thinking and reflecting on the world...

    Consistency

    Structuring your office to run on time.

    Being consistent to respond to refill request, lab results, or patient’s questions.

    Non-verbal gestures

    Eye contact

    Leaning forward

    Mirroring of emotion occurs naturally when people pay attention to emotion

    Maintenance of the therapeutic frame

    A dual relationship (eg, dating) breaks down therapeutic alliance. Patients will test the frame. It can be helpful to say, "There will be positive and negative feelings between us and what will be safe is to talk about them."

    Empathy, attunement, positive regard

    Patient: “Therapist is both understanding and affirming."

    Patient: “Therapist adopts supportive stance.”

    Patient: “Therapist is sensitive to patient’s feelings, attuned to patient, empathic.”

    Research has found that for beginning therapists, setting and maintaining treatment goals is harder

    Research has shown that strength of therapeutic bond is not associated with level of training

    Therapist should appear alert, relaxed and confident rather than bored, distracted and tired

    Foundational concepts of the therapeutic alliance

    Our profession gives us a privileged glimpse into the human heart and mind. Each patient is idiosyncratic, unique, precious. Each patient has unique strengths which we should place focus on.  Some therapists can be in a hurry to find out what's wrong, but we should also want to find out what's right with our patients.

    Our own feelings, as therapists, about the session are not intrusions but clues. If you are experiencing boredom, perhaps you are not understanding the main point the patient is trying to explain. Be curious for what you are missing. If you start feeling something different than you did at the beginning of the encounter, notice it. Try to empathize for the patient with what changed.

    Our goal is for the patient to feel understood, heard, accepted, felt. To be understood is to be accepted.

    A strong alliance will provide a "Corrective Emotional Experience"  (Franz Alexander), which means past relational pain and difficulties are worked out in a new relationship. When your subjectivity (your feelings, thoughts, goals) come into contact with the patient's subjectivity, a unique "intersubjective relationship" is formed from your mutual influencing of each other. A new dyad (2 coming together) is formed by looking at new meanings, understandings and connectedness. As a therapist, you are a “participant observer” as you observe the patient’s behavior and also become a “significant other” in their life through your interactions (Harry Stack Sullivan).

    Here are some things to consider on a first encounter with a patient:

    The patient will feel: examined, fear being seen as crazy, fear of not being liked, discouraged, hopeless, helplessness, needy, fear you are a mind reader, or even fear that you sleep with your patients.

    In developing this relationship, it’s important to understand they can formulate defenses that are adaptive. Try to empathize with that underlying emotion. Starting with what's an adaptive response and solves something, looking for what’s maladaptive does not.

    The patient may question your competence. They might say you look very young to be a doctor. The appropriate response would be to dig down and see why they are feeling what they are feeling. Say something like,"Perhaps you were looking for someone who looks older; of course you’re entitled to worry about how competent I am and how much I may be able to help you."

    Therapists are always worried about being ineffectual. It's very natural to feel like an impostor in our position. It’s also normal to feel—when someone's angry at us, our mirror neurons lead us to be angry back.

    Always face the patient, without desks between you, lean slightly forward, give appropriate eye contact, and do not do excessive note taking (you should be observing at least 90% of the time). Ideally, a clock is positioned behind the patient which can easily be seen by you without making obvious movements.

    On Listening: An Active Process

    Connection is non-verbal, and is equally as important as verbal communication, sometimes more so.

    Omissions (what is not said) in the patient's stories and memories are important.

    Point out common patterns you hear.

    If every time you say something to the patient he says "no, that's not it" then point out that to the patient.  

    Be aware when asking "why" questions, you are likely going to arouse the same defensive emotional reactions that occurred when the patient as a child was asked "why did you do that?" by the parent.  At times, "why" can communicate disapproval. For example you ask, "Why do you feel that?" And they say, "I DON'T KNOW! Are not you the doctor!"

    Dr. Tarr has some good advice on nonverbal communication: "I participate. I respond. I react to my patient and to his verbal and nonverbal communications.  At the same time I observe what's going on, what the patient is saying and what he is not saying. I am particularly attuned to evidences of anxiety, to what I am feeling and thinking, and where, if anywhere, the interchanges are going. I am wondering how best to formulate for this particular patient what I observe that may help him feel understood and responded to."

    Observe that defenses (sublimation, reaction formation, intellectualization), although they reduce anxiety, may misrepresent reality.  

    Assume an attitude of "reverie," like a good maternal object, receiving toxic stuff from patients and then giving it back to them in a detoxified form (Wilfred Bion).

    Create a "holding" place for patients in which patients have a transitional or play space (Donald Winnicott).

    Listen in a way that notes what the patient is trying to say about your relationship.

    Patient: "I feel lonely even when I am with people."  Doctor: "Do you feel lonely here with me now?" Patient: "No, I feel you understand me somewhat."  Doctor: "I want to know if there are any times where you feel more lonely in our sessions, it will help me to understand what is going on between us."

    Listen to their moment to moment change in emotions.

    Try to enter a bit into their feeling, be present with them, mirror the emotion/feeling, use their own words, ask them to find their own words.

    If you don’t get why they are sad, then stay with it, ask them more questions, have them deepen your understanding of it.

    Once they feel you truly understand the effect will change. When people feel heard, deeply understood, it is pleasurable.  

    Shame- patient looks down

    “I can understand why talking about this must be difficult.”

    “Perhaps as you talk about this you feel…”

    Try to find the adaptive function: “I hear switching to a new doctor is hard, I think that is a common experience, I think it is adaptive to be hesitant at first in what you share, we are just meeting."

    Anger/Frustration:

    “Would you say that as you mentioned this you feel frustrated.”

    Find the adaptive function: “your anger here seemed to have the goal to protect you and your family”  “your anger likely kept you alive!"

    Sadness

    “Perhaps you are feeling sad as you say this?”

    Find the adaptive function: “it makes sense that you feel sad here, I think crying and feeling sad shows how much you valued your dad and therefore the loss hurts that much more."

    Disgust

    “I am wondering if you feel disgusted by this?”

    “I hear you feel disgusted…” (ask with a questioning tone).

    Find the adaptive function: “Feeling disgusted by how your sisters turned on you and cast you out of the family makes sense, it sickens you to see the level of their resentment and bitterness."

    Fear

    “I hear a deep concern or perhaps fear regarding this.”

    “Might there be a deep concern or perhaps fear regarding this?”

    Find the adaptive function: “After your traumatic event, it makes sense that you would no longer want to put yourself in that situation, it sounds like you are trying to protect yourself."

    Listen to the patient’s goals, purposes, aspirations, fears, hopes, values, meanings.

    How do you create and maintain a working alliance:

    Be sensitive to empathic strains and prevent them from developing into empathic ruptures.  

    Ask for feedback. Reflect on the "we" aspect of the encounter. If the intervention/participation failed to have the desired result then look at what went wrong with the communication.  

    “As we were talking together when did you really feel we were on the same page?”

    “When did you feel we were understanding each other?”

    “When did you feel we were communicating meaningfully?”  

    “When were you feeling disappointed?”

    “When did you fell I was not responding enough?”  

    “When did you feel frustrated, misunderstood, or impatient?”

    Be able to define and predict interpersonal conflicts that may cause a disruption of the shared empathic relationship. Set the groundwork for openness.

    For example:  

    Doctor: "Tell me about your past psychiatrist?  “What worked and what were your disappointments with your past psychiatrist?"

    Patient: "He was kind of a jerk."  

    Doctor: "Can you tell me more about that?"  

    Patient: "He always would just stare at this computer, and often answered his pager during sessions."  

    Doctor: "Thank you for sharing that, I will stop typing and finish this later, I hope that if you ever have any feedback for me you will know that I will want to hear it, even if it is negative, and will appreciate knowing your experience of things."

    Patient: “Ooo I was not talking about you.”

    Doctor: “Ok, nevertheless it is a good reminder to not be focused on the computer, but if you are bothered by things or frustrated it will be helpful to know.”

    The therapeutic alliance is an incredibly powerful relationship, and if it is managed with care, it can affect positive change in a patient’s life.

    In future episodes on therapeutic alliance I will dig deeper into specifics of it, and pull upon the depth of my mentorship from Dr. John Tarr.

  • 01:10:20

    How to Treat Emotional Trauma

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    This week on the podcast I spoke with fellow therapist, Randy Stinnett Psy. D, about how trauma works, and how we can help our patients overcome it.  

    What is trauma?

    Emotional trauma comes from stress that is overwhelms a person’s neurological system. Some stress can be good and formative, or it can be bad and get stuck in the brain, causing someone deep emotional pain.

    Think of climbing Mount Everest. Some people choose to do that, and it’s easily one of the most stressful situations you can put yourself in on purpose. That’s good stress if you have trained for years and are ready for it. If someone forced you to climb Mount Everest, it would register in the brain as a trauma.

    Trauma is too big for the mind, brain, and nervous system to assimilate. It’s a memory, or experience, that gets stuck because the person believed it would result in their death, or at least serious injury.

    The brain has several mechanisms to keep something stuck so that the person will remember it, and try to avoid getting hurt in the same way in the future. It is a survival instinct.

    People commonly demonstrate symptoms of trauma when they’ve:

     

    Experienced a sexual violation

    Seen violence

    Experienced violence or abuse

    Been neglected—experienced the absence of something that they should have had.

    Been in near death experiences like car accidents or war

    People who have PTSD, or post traumatic stress disorder, have experienced a soul-level of brokenness, and even talking about the event, or having a memory of it, can bring it back with the same force that occured in the actual accident. They often have recurring nightmares, or repetitive symptoms that continue long after the event.

    Typical PTSD symptoms alternate between chronic shut down and fight and flight

    Fight and flight symptoms are:

    Sweating, nightmares, flashbacks, anger, rage, panic, hypervigilance, tense muscles, painful knotted gut

    Shut down symptoms are:

    Dissociation, freezing, emotional detachment, voice trembling, difficulty getting words out, numbness, apathy, fear, helplessness, dizzy, empty, nausea

    Moments in connection mode look like:

    curiosity, exploration, relaxed and full breathing, feeling grounded, true smiles

     

    Body movement and trauma

    We’ve all heard the reference to Pavlov’s dogs—the bell rings and the dogs salivate because they know it is dinnertime. Pavlov discovered many more things than that dogs drool. Once, his lab was flooded with freezing water that nearly filled the cages of the dogs. When they were finally able to get the dogs free, the dogs interacted differently with the world around them. They seemed hopeless.

    Humans work the same way.

    PTSD rates were 16% for survivors of 911, and 33% for survivors of Hurricane Katrina. Why? Traumatologists speculate it was because during 911, survivors were running away from the catastrophe to save their lives. In Katrina, the victims were airlifted out and placed in gyms, for sometimes months at a time. Those in lower socioeconomic levels had no money, no home, and nowhere to go—they were trapped.

    The body is designed to move away from danger, but if the body can’t move, trauma can set in.

     

    Attachment based trauma

    Having a negative attachment with parents often sets people up for later traumas in life to be a bigger assault on the nervous system and psychological functioning, than it would have been as a standalone event.

    Patients who experience unhealthy attachments often struggle with emotional regulation and boundaries.  

    Many people, as children, were not heard and mirrored in their emotions and experiences. When they discussed their problems with their parent, and it was met with disdain or shut down, the patient has most likely developed the idea that they have no voice. The stress was not contained and thus all the raw emotion is still there and unprocessed. This leads something to continue to be traumatic in the brain.  

    This follows the same pattern as polyvagal theory. When we are in connection mode, we are open hearted and happy. When we feel stress, or lack of connection, our sympathetic nervous system kicks in and we switch into fight or flight mode. If that disconnection continues, our parathetic nervous system takes over and we go into full-on shutdown. When children are repeatedly ignored or abused, they switch in and out of shutdown mode, causing trauma.

    Polyvagal theory and attachment theory, and how they affect children (and adults too), are demonstrated best in the Still Face Experiment video (link to prior article I wrote on that experiment).

    Attachment trauma is repeated trauma. It can occur in childhood, or any other time throughout our lives within relationships.

     

    Notes to therapists on dealing with PTSD

    Studies show that having an emotionally connected therapist, while someone is reprocessing their traumatic memories, can help heal the emotional damage of those memories.

    Displaying emotional stability

    Patients often superimpose all of their abusers onto their therapists. As therapists, we need to realize this, and stay steady during the entire course of therapy. Remaining calm, safe and empathic is one of the most healing things we can do for them.

    It is a way of being, not just an action, or a reaction, towards our patients.

    Receiving feedback

    As therapists, it’s important to be able to receive feedback from our patients about what is working for them without it being an adversarial situation.

    We must respond in a way that allows the patient to have their own voice. First, validate their emotional experience of the patient. Next, thank them for being honest with you. Ask for the whole story behind their feedback.

    I am not saying this as some sort of technique, but rather this should come out of the belief that 1) their emotional experience is valid and needs a voice 2) it takes courage to voice any feedback and this is important for their growth and success.

    When these things are truly believed, we are empathizing and thanking them, out of the core of our being, and not just as a technique.  

    Where they were expecting rejection, you end up validating their experience. Finally, ask them how it feels, in the moment, to be heard and to be able to safely express their opinion. Allow them to experience a felt difference between you and their abusers. This provides a corrective emotional experience!

    Know when to limit the stress

    Understanding the different nervous system’s functions will help you know when enough is enough for your patient.

    Study the symptoms of the activation of the somatic, autonomic, sympathetic, and parasympathetic nervous systems. This is imperative, and if you cannot slowly uncover the stressful situations in a way that the patient can manage it without engaging shutdown mode, you will end up doing more damage than good.

    Emotional connection

    One psychiatry resident asked my mentor, Dr. John D Tarr, if it was better to keep inpatient people at an emotional distance, so the patient would not get attached and want to continue to stay in the hospital. My mentor responded that we always want to be connected to our patients, to be empathic. When we feel they are getting attached and don’t want to leave, we need to open up that dialogue to how we can help them experience connection outside of the hospital.

    Studies show that patients who feel connected to their doctor are more engaged in treatment—they go to therapy, take their medications, and continue their mental health journey.

    Trauma-based memories are different from normal memories, like knowing what you ate for breakfast this morning. Trauma-based memory has a sensory aspect to it. They are stored in a different part of the brain than where we function for our daily, normal connection mode.

    As therapists, when we access those memories with patients, the patient begins to switch to a different part of their mind, and demonstrate symptoms of trauma physically. They may tremble, sweat, and sometimes even their voice changes—it can be hard to get the words out, they whisper, they sound child-like.

    To understand how people respond to trauma, we have to know that emotions have primacy, or first dibs, on our reactions. Our brain deems them more important than our executive functioning—our ability to reason and plan our lives’ daily tasks.  

    If the patient is open to it and we have established a good, trusted attachment and connection, we will talk about their traumatic memories. If we do not have a connection in that way, I will not explore deep traumatic memories with them. It is more important to build a safe, secure relationship first.

    Trauma gets stuck in the non-analytical parts of the brain—our emotions, creativity, experiences, art. It’s image-based, somatic (physical body), it’s non-verbal. Parts of the left hemisphere of the brain deals with logic, reasoning and language. To integrate this part of the brain, the patient will have to access the emotional parts and then put words to their experiences.   

    In that conversation, these are some of the questions I will ask:

    What did you see?

    What did you feel emotionally?

    What did your body experience?

    What do you believe about yourself as a result?

    Allow for freedom

    Also, when we require our patients to do anything, even to stay for the whole hour of therapy if they do not want to, we are reinforcing the trapped feeling. Keep an open dialogue about what your patient is feeling throughout the therapy session.

    If the patient is suicidal with a plan and intent, they likely need a safe place to get through the intense time. I will tell them, “My goal is to not keep you here indefinitely. We will come up with a plan to get you out of here, and for you to be healthy.”

    In general, try to give your patients, especially the PTSD ones, choices. Create boundaries and give guidance, but allow them to have freedom in their choices.

    Summary  

    In this first discussion with Dr. Stinnett, I wanted to highlight some introductory understanding on trauma.  We discussed how trauma is stored differently in the brain and how the polyvagal theory is connected with this journey.  We highlighted the importance of emotion, connection and feedback. Please leave comments below on your thoughts regarding this blog and podcast!  

     

  • 00:51:32

    Setting Boundaries in Relationships

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    What are boundaries?

    When we refer to boundaries, we are talking about emotional walls that are healthy. Boundaries are meant to keep us in relationship with the people that we love.

    Think of them as your property lines around your house. You know where your lines are, where your property ends and your neighbors begins. Therefore you know what you are supposed to take care of and what your neighbor is supposed to take care of.

    A boundary defines our self. Within ourselves, our “property” consists of our physical body, our desires, our intellect, and our ability to make decisions. It gives us a sense of defining what is “me” and what is “not me.”

    We are not supposed to take on too much of other people’s emotional experiences. When I was a newly practicing psychiatrist, I didn’t know that, and I felt depressed after meeting with a depressed patient. It is possible to have an understanding of what is happening in someone’s emotional world, but not take it on yourself.

    There is a psychological principle that is common among people who struggle with having good boundaries with others. It’s called “siding with the aggressor.” For example, if someone grows up in a home where the father is constantly displaying angry behavior, a child might learn to develop a sense of humor if he or she learns that will diffuse the situation. Rather than running away from, or fighting back, these people joined with the aggressors, paying attention to them, calming them, helping them.

    Early on in childhood, people who side with the aggressor understand how to make others happy. This continues into adulthood and is formative in new relationships in how the person would choose to interact with others.

    I don’t think of it as a weakness, I think of it almost as a superpower—these people are incredibly skilled interpersonally when they get older. They know how to react to others, how to make others happy, and how to make angry people calm down. They are great peacemakers, therapists, and psychiatrists. It was an adaptive feature for them in childhood.

    But as they grow into adulthood, they need to learn to choose when to use this superpower, or when to have a boundary.

    My wife, Lindsay, first began learning about boundaries when she was experiencing burnout as a young, working woman. She never said no, always went above and beyond the requirements of her job. And at the end of the night, she was exhausted. After awhile, she started to become upset—upset at herself, and even a her situation.

    Within the Big 5 personality types test, Lindsay scores high in Trait Agreeableness. People who are high in that trait value relationships, are empathic and helpful. They will do things they don’t want to, merely to maintain their relationships. Women typically test higher in the trait than men.

    I see many women come into my practice who have high markers of agreeableness—they haven’t found (or been able to express) their boundaries. They have issues with chronic pain, problems with expressing anger, either within themselves, or towards others.  

    It’s also common that these people have no idea that their “helpfulness” is causing them huge amounts of physical pain. People who are caretakers, who feel looped in to being someone’s source for happiness, life, wellbeing, often get looped into these types of situations if they don’t have a strong sense of self. Obviously, many people are caretakers for their relatives. I’m not talking about being a nice person versus being selfish, or being a caretaker versus letting someone you love be alone.

    I’m talking about the emotional position of your heart during those situations. Are you able to say no when you need to? Are you asking for help when you need to? Are you taking time for yourself? Are you in pain? What is your emotional state when someone calls and asks for help? Do you check in with yourself before you say yes?

    How do you know when you need to start establishing boundaries?

    Typically, with people who have no boundaries, the resentment will build and build, and they will do something drastic to relieve their pain—cut off the relationship, quit caretaking altogether, stop being friends with the person, get a divorce. Or the resentment will build up in their body, causing either depression (as the anger is turned inward) or body pain (as the body carries the burden).

    The truth is though, that when someone with no boundaries says yes, it might be ingenuine. They are saying yes out of guilt and obligation, not out of a true desire to say yes.

    When we do things out of obligation or compulsion, we lose passion for that task, and begin to build resentment. If we aren’t making the choice to say yes, we are thus protecting our ability to say yes to our passions, joys and desires.

    Good fences make good neighbors

    As you’re setting up your “fence,” you want to keep the bad out, but it will also keep the good in.

    When we talk to people about boundaries, they are often scared of beginning to say no.

    When you learn to say no, and you begin to make new friendships with people, you will tend to set higher standards for how you want to be treated during those relationships.

    How to set up healthy boundaries

    Look at the people you have a hard time saying “no” to. Is it your boss? Someone in authority? Someone who is a family member?

    What do you fear losing from them if you say no? Is it love? Respect? Provision? For a boundary-less person, being a pacifier has some advantage. Maybe you were the peacekeeper in your house growing up. Maybe you weren’t allowed to say no. Maybe abuse was involved. Or maybe you were simply a sensitive, sweet child who heard repetitively that it was a good thing to be kind and helpful. Whatever the case, there is some sort of relational reward to say yes, and to keep the peace. Pay attention to what you’re getting out of saying yes to that person.

    Become aware of body sensations you're having when you think of setting boundaries, of saying no to someone. Do you feel tightness in your chest? Numbness in your hands? Is your heart racing? Do you have anxiety?

    Have a pre-programmed response for when someone asks you for something. Lindsay likes to say, “Can I get back to you later with an answer?” It allows her to take off the social pressure of saying yes immediately, and be able to respond with a truthful answer later on.

    Before you say yes to anything, think about your ultimate goals and boundaries. We all have a purpose, we are all unique. If we spend all of our time doing only what other people want us to do, we won’t accomplish our goals. When we start to focus on ourselves more, we can see where the opportunities to say yes, or no, will take us, and we can see if they line up with our ultimate goals.

    Have safe people in your life, so that when you don’t have the strength to say no or speak up, you can talk to them. You can ask for help. It could be a therapist or just someone you can feel safe with. Lindsay has a group of women she has talked to once a week for 12 years. On that phone call, they discuss what they are dealing with and how they are growing.

    Have conversations with your current friends where you set boundaries. I go on walks with people all of the time. I often ask if we can switch topics on the way back. Normally I would be the listener the whole walk, but with my new boundary, it lets me also talk about something that’s going on in my life. People are always responsive when I ask for this, and it’s always positive. People who are higher empathy have a harder time asking for what they need.

    Throughout our lives, we have new possibilities for relationships every day. We can take care with adding those who are good, positive, safe people, who will understand our “no” and will allow us to uphold our new boundaries. When you’re looking for new, good friends, look for people who are full of grace. They are also full of truth—they are kind and open, but also honest.

    Parenting and boundaries

    Children are difficult to have boundaries with. It can be because we love them and want to give them the world, because we know they aren’t fully emotionally developed, or because we want to ease some of our own exhaustion by giving in!

    One key to holding our boundaries when our kids throw temper tantrums is to respond to tears with empathy, not just say “yes” to ease our discomfort. If we resonate with them, it will help both us and them. For example, if your child is screaming and crying about leaving the park early, try saying, “I know it must feel hard for you to leave something that is so fun. We will come back again. Nevertheless right now, it’s time to go. At home, you have toys too and can play with them.” This offers empathy, hope and it keeps a boundary.

    If we give in and let them stay, we are teaching them a bad habit. We should never set a boundary that we aren’t willing to follow through on. It helped Lindsay and I to remember the statistic that even giving in to 1 out of every 8 tantrums taught the child that tantrums worked, and they would win. It reinforced their negative behavior.

    If we make them leave and don’t care that they are upset, we aren’t recognizing their emotions and are being unempathic.

    Letting children feel stress, and being empathic and reassuring when they’ve completed the task, is more helpful for them as they grow. If you step in every time and relieve the stress (such as not making them go to school when they don’t want to), you’re not preparing them for adulthood.

    Keep your boundaries, and express empathy.

    Boundaries in romantic relationships

    Dating is hard work. There are several boundaries to navigate during dating. When you have talks about boundaries in dating, if they don’t respond appropriately, you definitely need to evaluate whether you want to continue dating them or not.

    Be honest and open right from the start.

    Physical boundaries

    This is a hot topic in society today—consent, verbal consent, being able to talk and have conversations. Many of my patients do not want to follow through with physical relationships with people, but they have a hard time saying the actual word “no” when they are in the moment. Define what you want and don’t want, long before you get into another relationship. If someone does not respect your “no” that should be a deal breaker.

    Spiritual boundaries

    Define what you want and don’t want, what you believe spiritually. What are your worldview deal breakers? Defining your deal breakers and writing them down, and asking your friends to help keep you accountable, is important.

    If you are Muslim, Jewish, or Christian, make sure that you know what you want in a partner, and that you aren’t letting go of boundaries that will one day matter to you again, just so you can date someone.

    Conversational boundaries

    Part of dating now is “ghosting,” or shutting down communications when you don’t want to have real conversations about how you’re experiencing someone. I believe this has developed unhealthy communication patterns in society.

    When Lindsay and I were dating, she almost broke up with me because I demonstrated some anxious behaviors during our dinners together. I would shake my leg, or eat three loaves of bread in ten minutes! She nearly ended it without telling me why—she just thought I was odd.

    But when she talked to her friends, they urged her to communicate how she was experiencing me. When she told me what she was feeling, and I told her I was behaving that way becuase I was nervous—I was so into her! She was pleasantly surprised and we continued dating. Now, we have been married for 6 years and have two children together.

    When you’re dating, make it a point to not shut down just because you’re having a negative experience of someone (if that experience isn’t too bad, of course). Try communicating to the person what you’re feeling. This will go a long way in setting up the relationship (and changing your personal habits) to developing positive communication patterns.

    Dealing with relationships and change

    People view consistency as a positive. That means that as humans, we are wired to strive for create an equilibrium in our relationships. And agreeable, boundary-less people strive for consistency in behavior more than others.

    When someone that didn’t have boundaries starts saying “no,” the people in their lives start to sit up and notice what they would deem “inconsistency.” The first time you say you cannot help with that thing you’ve helped with every week, they may be nice about it. But the second and third time, they’ll start to say that sentence we all fear…”you’ve changed…”

    When you grow in your boundaries, there will be people who don’t like them. They will shame you, yell at you, push every button that they can to get you to comply in the way that you used to.

    Understand that by saying no, you may not be as helpful in relationships, volunteer organizations, or work situations as you used to be.

    But, by saying no, you will also free up your time to be able to accomplish what only you can accomplish in your life. Saying no to trivial things that are daily time-vampires will free you up to do the things you are passionate about. That passion will grow, your freedom will grow, and you’ll be able to really start to feel in control of your own life and schedule again. People will respect you.

     

  • 00:52:13

    The History and Nuances of Bipolar Illness

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    Below is a detailed review of the podcast episode, with most of the content that Dr. Michael Cummings and I (Dr. Puder) discussed.  Special thanks to Arvy Wuysang (MS4) for his work in the initial transcription and organization.

    The history & nuances of bipolar illness

    Bipolar Illness was first discovered by Emil Kraepelin, who was also the first to describe schizophrenia in the 19th century.

    Kraepelin noticed another major mental illness in which people had episodic disturbances of mood. He saw either elevation of mood and increased energy, along with a decreased need for sleep, and often impulsive or psychotically related behaviors.

    Then, the same patient would experience the opposite, sleeping through the day, demonstrating lowered energy and depression.  These patients were noted to have normal function in-between these episodes. 

    Nuances of the bipolar illness diagnosis

    The Diagnostic Statistical Manual of Mental Disorders (DSM) identifies bipolar illness primarily by the presence of at least one episode of mood elevation to help distinguish it from unipolar or major depressive disorder.

    Here are some defining symptoms:

    Patients are fairly normal between episodes.

    When they’re manic, their mood elevates their lack of sleep. They will sleep four to five hours at first, later progresses to no sleep at all on a nightly basis.

    Every true manic episode will end in three places: hospitalization of some type, jail, or death.

    Initial peak is in the 20s and 30s. Although, people suspect that many individuals who become bipolar don’t initially declare themselves.

    They often present with a series of recurrent depressive episodes and then, at some point, they exhibit a period of mood elevation meeting the criteria for either hypomania or mania, which earns them the diagnostic label of bipolar mood disorder.  

    There are two types. Type I, in which the person has fully evolved to mania or mood elevation and fully evolved episodes of depression. Type II, in which the person may have a milder form of mood elevation but still has fully evolved periods of depression.

    Grandiosity is a major part of mania. Although historically some people with bipolar illness have often been incredibly productive during episodes of mood elevation, before they become disorganized or psychotic.

    There is often impaired judgment during manic episodes. For example, someone who is manic will propose to 5 different girls, max out multiple credit cards, buy extra houses/cars/boats, etc.

    Bipolar and the limbic system

    Underlying pathophysiology is centered around the limbic system. Involves the temporal lobes and and structures which swings upward into the mamillary bodies into the anterior cingulate gyrus, which then projects forward into the frontal lobe. That circuit goes through periods of hypo-activity or depression in people who are bipolar. They have depressed metabolic rates of the system upto 30 to 40 % below normal. During periods of mood elevation, there is an increase in metabolic activity and instability in that limbic circuit. The mood is an element of that, but the person’s overall activity, sleep-wake cycle, circadian rhythms, along with all the things related to the functioning of the limbic system are disturbed in bipolar illness.

     Bipolar illness and sleep patterns

    There are some models of the illness that suggest that perhaps the core of the pathophysiology of bipolar illness is an abnormally regulated biological clock.

    In most of us, the nerve cells, the neurons that make up the biological clock, are very tightly linked to each other in terms of their operation. They literally form two pacemakers or oscillators in a very small structure that sits right on top of the optic chiasm called the supraoptic nucleus.

    Normally all of our circadian rhythms are regulated by this master clock. In healthy people, it’s very difficult to get the two oscillators to separate from each other. In bipolar people, those oscillators drift apart relatively easily. Something as simple as loss of sleep during the latter half of the night will cause them to diverge from each other.

    When that begins to happen, the overall functioning of the limbic system begins to oscillate in an unstable manner.

    People have looked at things like disturbed sleep as being a very common precipitous of a mood episode. If somebody has a difficult day or disturbing event, and they’re genetically vulnerable to being bipolar, they may not sleep well at night, and the next night they may not need to sleep as much. The night after that, they really don’t sleep, and then their mood begins to elevate and another episode is initiated.

    Genetic markers of bipolar illness.

    Bipolar is typically passed on genetically, and can be linked with other similar markers of illness. Around 100 genetic markers have been linked to bipolar illness.

    They overlap with schizophrenia in part, but not entirely. People with bipolar illness have a much more normal brain in terms of development then do people with schizophrenia. But, there appears to be an inherent defect in the operation of the limbic system elements with these periodic repeating of overactivity and underactivity, plausibly related to the core biological clock.

    Mood stabilizers have an effect in terms of decreasing and stabilizing the activity of the limbic system. They tend to push that clock back toward being phase-linked or operating together as a single oscillator, rather than as divergent oscillators.  

    Mood StabilizersHistory of Lithium

    The very first mood stabilizer discovered was lithium. It was very popular in the 19th century for the treatment of gout because it decreases uric acid crystals.

    In the 1940s, a psychiatrist named John Cade (1912-1980) served in World War II and was a prisoner of war for three years. After the war, he worked in a repatriation hospital in Australia and became fascinated with bipolar illness. At the time, he looked at the earlier history and thought that uric acid somehow caused bipolar illness. That turned out to be a wrong hypothesis. But, it led him to use lithium urate, a soluble form of uric acid, in hamsters, to see what would happen. The hamsters got lethargic and sleepy upon administration.

    He decided to give his lithium compound to ten patients—six of them were bipolar, four of them were schizophrenic. They all became less agitated, though the schizophrenics didn’t change all that much. However, all of the bipolar patients’ moods stabilized.  

    It’s amazing how he didn’t kill any of these patients in spite of giving them gigantic doses of lithium. His initial dose was 1300 mg, three times a day. Most of the patients got ill with that. If you give somebody too much lithium, they develop nausea, tremor, and diarrhea. You can make them very seriously ill with lithium because it has a very narrow therapeutic index. The distance between therapeutic and toxic is not very far. Optimal dose for most patients 0.6 - 1.0 mmol/L. Toxicity usually begins at about 1.5 mmol/L, serious toxicity begins at about 2.0 mmol/L.

    At Loma Linda and at patton State Hospital, most patients start at 900 mg at night, obtain a plasma concentration five to seven days later, and then adjust the dose.

    Dosing lithium

    Lithium should never be given in divided doses.

    The kidneys is spared by having a long trough period between lithium doses, so it is best to give it at bedtime.

    Lithium tends to decrease urine concentrating capacity. Almost everyone who takes lithium, their urine output will increase by about 20%, and their water intake will correspondingly increase by about 20% to compensate. There are a few people who get much more severe diabetes insipidus, an insensitivity to anti-diuretic hormone in the kidney.

    Over the course of many years, about 5% of people who take lithium will develop mild to moderate degrees of renal failure or insufficiency. That risk is minimized by keeping the lithium level < 1.0 meq/L and also by giving Lithium only once a day.  

    Lithium and suicidality

    It’s clear that lithium reduces suicidality, which may be a product of its ability to inhibit impulsivity. Suicide rates are substantially lower when people take lithium.

    In the healthy population, when they’ve done studies in areas with very low concentrations of lithium in the groundwater, rates of suicide and rates of homicide are lower in areas with lithium in the groundwater compared to areas that don’t have lithium in the groundwater.

    The amount of lithium that people are getting from the groundwater would be roughly the equivalent of taking 3 milligrams of lithium a day. This means that in the healthy non-bipolar non-mood disordered brain, it doesn’t take very much lithium to make people somewhat less violent.

    When would you take someone off Lithium?

    The best measure for lithium is to measure the eGFR (estimated glomerular filtration rate). If the eGFR declines to 50 or less, the person should not take lithium.

    The other common adverse effect that lithium has is to make the person hypothyroid.

    Lithium tends to decrease the synthesis and secretion of thyroid hormone. The good news is that if it makes somebody hypothyroid, we can easily replace the thyroid hormone with Levothyroxine, a synthetic analogue of the hormone. Frankly, your body doesn’t care whether you get your thyroid hormone from your thyroid gland or from a tablet.

    Dermatologic side effects

    Psoriasis is a contraindication to lithium use. It will greatly worsen psoriasis.

    If the person is prone to cystic acne, lithium will typically cause a worsening of cystic acne.

    One of the effects of lithium is to increase oil secretion in the skin. That can lead to both increased psoriatic plaques and cystic acne.

    History of other mood stabilizers

    The reason we have other treatments for bipolar illness, is largely the result of the work of Robert Post.

    Post was a psychiatrist who worked at NIMH and was doing an unrelated experiment. He was looking at kindling, or increased sensitivity of the limbic system, by putting electrodes into mouse temporal lobes and giving them a one second electrical stimulus once a day.

    Initially, when you do that, nothing happens.

    But about day two or three, the mouse will have a complex partial seizure, a temporal lobe seizure. If you keep doing it pretty soon the mouse will start having spontaneous seizures. Robert Post looked at that and thought that the nerve cells of the limbic system can become more and more sensitive, more and more hyperactive, less and less well-controlled. He thought that he could block that effect, in terms of seizures, with anticonvulsants. He then, made a leap in logic, thought that perhaps mood episodes are acting like electrical stimulus causing kindling in the limbic system for people with recurrent mood episodes, like in bipolar patients.

    He decided to treat some bipolar patients with an anti-epileptic.

    The first medicine he used was Carbamazepine (Tegretol). Tegretol is a very difficult drug to use because it induces its own metabolism, so the level keeps falling. It also is fairly toxic with respect to the bone marrow. So, you have to watch out for loss of white cells, red cells, platelets.

    He fairly soon turned to another anti-epileptic, valproic acid, which is a branched-chain fatty acid. He found that it was also effective in treating bipolar illness. Turned out that compared to lithium, valproic acid was more effective if the person was a rapid-cycling bipolar patient having more than four episodes a year. (Although lithium remain superior if the person is a classic type I bipolar patient.)

    In young women in general, valproic acid it can be problematic because it can cause Polycystic Ovary Disease.

    In pregnancy, it causes not only a risk of neural tube defects such as spina bifida, it also decreases the intellectual capacity of the offspring by about 10 IQ points, and roughly doubles the risk of autism in the offspring. It also causes hirsutism and weight gain.

    Psychiatry has pretty much examined every anti-epileptic introduced since to see if it had mood stabilizing properties.

    Lamotrigine (Lamictal) for example, does treat bipolar depression and does stabilize mood cycling, but has almost no benefit with respect to mood elevation. In fact, Lamotrigine as a monotherapy may actually cause switches into mania in some patients.

    People have looked at Topiramate and found that it may have some prophylactic capability but doesn’t seem very effective at all if the person is already manic or depressed. If their mood is already stable, and you’re just trying to decrease the cycling, it may have some benefit.

    Lamictal, used as a mood stabilizer, may have gotten more use than it should because although it does have antidepressant properties in bipolar illness, it is certainly not a benign drug.

    People were initially attracted to it because there’s not a lot of laboratory monitoring involved. The plasma concentrations of lamotrigine don’t correlate very well with its efficacy because it is very rapidly cleared from the blood compartment and taken into tissue. It’s easy to administer and when you’re not using it for seizures, usually can be dosed all at bedtime.

    It does carry a risk of Stevens-Johnson Syndrome, which is severe malignant rash, and which the person winds up looking like a burn victim because their skin literally dies and falls off.

    It also can cause lymphohistiocytosis, which is a similar autoimmune process, but involving the blood vessels and internal organs. Luckily, that is rare, but it's also typically a life threatening response to the drug

    The risk of the side effects above are increased by titrating the drug to rapidly. They discovered the side effects when they were using the drug initially for seizures. They were often increasing the dose by a hundred milligrams a day starting at 100 mg, and by day four, the person was on 400 milligrams. They found a 9% increased rate of malignant rash. If you slow down and don’t go faster than around 25 to 50 milligrams a week in the titration, the risk is reduced, but it’s still not zero. It’s probably less than one half of 1%, but it is a caution.

    The other caution with the drug of course in bipolar patients is it sometimes is not a very good monotherapy because it doesn’t provide any protection against mood elevation. It seems to be effective in treating the depressed phase of the illness, but not the manic or hypomanic phase.

    Oxcarbazepine has flunked multiple trials as a mood stabilizer. Oxcarbazepine differs from Carbamazepine in only one bond. In carbamazepine the bond between carbons 10 and 11 is an epoxide bond, while in oxcarbazepine that same bond is an ester bond.

    It appears, however, that the mood stabilizing properties of carbamazepine result from the epoxide metabolite, and of course oxcarbamazepine does not produce that metabolite.

    Oxcarbazepine can, in some individuals, reduce impulsivity, which seems to be a truism across the anti-epileptic drugs, but it’s not an effective bipolar treatment.

    There was only one study looking at it in forensic settings for impulsive or violent patients. It was a self-funded single investigator study and it’s been the only study that was ever produced, never replicated. It was suspicious in that the patients were all outpatients, self-recruited via newspaper ad. It’s database even for impulsivity and so forth is pretty limited. It does have some application in that regard, but it is not as good as people hoped.

    People became enamored with it simply because it was easier to use than carbamazepine, which isn’t to say that it’s benign. It induces hepatic enzymes, it causes dangerous hyponatremia in about 2.5% of the people who take it.

    There haven’t been any really good studies identifying it as an anxiolytic. Like most anti-epileptics, it can be sedating and somewhat calming, but you could get the same effect from literally any of the anti-epileptic drugs, probably safer would be gabapentin.  

    Antipsychotic use as mood stabilizer

    Some of the second generation antipsychotics have also shown mood stabilizing properties, albeit as an addon to a primary or classic mood stabilizer. This include drugs like Aripiprazole, Brexpiprazole, Cariprazine, Olanzapine, and Quetiapine. Quetiapine in particular is effective in treating bipolar depression, as is Lurasidone.

    Antidepressants as mood stabilizers

    Do not give an antidepressant to a bipolar depressed patient!

    There are now a host of studies suggesting that antidepressants offer little or no benefit with respect to depression in bipolar illness. It serves only to increase the rate of mood cycling and to risk a switch into mania.

    Cognitive side effects of mood stabilizers

    Lithium typically causes cognitive impairment only if the plasma concentration is too high, in which case it can cause decreased brain function all the way up to coma if the concentration is high enough. However, lithium used at therapeutic concentrations actually is neurotrophic.

    It’s been used now in some demented patients with modest results. MRI scans will show a thickening of the cortex if you put somebody on lithium.

    In contrast to lithium, antiepileptic drugs almost universally tend to dull cognitive performance. For example, one of the tip-offs that you’re giving the person too much topiramate is they start to lose the ability to find nouns, they become anomic.

    Barbiturate and Benzodiazepine use in bipolar illness

    Barbiturates were introduced in 1903. At that time, they were essentially the only psychiatric medication available. They treated literally everything that involved mood elevation or agitation with a barbiturate.

    In the middle ages, individuals that seemed to have manic episodes as we understand it today, were considered witches. They were given doses of sedation that would bring a normal person down. These manic individuals, however, would not be sedated with those doses.

    This is described in the book The Witches’ Hammer. Most of these tests were designed so that if you were the accused, you most likely won’t pass them. For example, one of the tests was being tied up and thrown into a mill pond. If you drowned, you were concluded not to be a witch, but of course you were dead. If you manage to float and you survived, you were concluded to have done so via witchcraft, in which case they retrieved you from the water and subsequently burned you.

    Frankly, psychiatry has come a long way!

    Importance of sleep hygiene in bipolar illness

    One of the most important things to teach bipolar patients is to emphasize the importance of sleep hygiene.  They should go to bed at the same time every night. It’s dangerous for them to casually stay up to watch tv or a movie etc. That may be a setup for them to have the next episode of mood disturbance.

    If they’re having difficulty sleeping, this is a group in which long term use of one of the Z drugs may be appropriate.

    Dr. Cummings’ personal favorite in that group is Eszopiclone (Lunesta), because it has a longer half-life. It’s half-life is around 4-6 hours, so it’s long enough that the person will actually stay asleep. It also has a broad dose range, 1 mg - 8 mg at night.

    It’s been used to treat primary insomnia in some individuals for up to decades without development of complete tolerance, or resulting in any withdrawal syndrome if the medication is stopped.

    Education for bipolar patients

    Patients and families need to realize that the more episodes of illness they have, the more resistant to treatment the illness will become, and the less responsive the illness will become to medications. This idea goes back to Robert Post’s study on kindling.

    Additionally, when people have more episodes, the cycle tends to become progressively shorter. If they were initially having an episode every two or three years, it may suddenly occur every year, to having multiple episodes for a year.

    One of the major costs for both families and individuals who are bipolar is that severe depression or severe mania is incredibly disruptive to the individual’s life. It can destroy their marriage, their job, and cause large setbacks.

    I (Dr. Puder) will bring patient's families in, get them on board with a plan to identify early symptoms such as decreased sleep, increased energy, and change in physical activity.  I want the family to keep in close contact with me if these things are developing, and I will alway get them in within the week.  

    Role of psychotherapy in bipolar illness

    For many bipolar patients, the common pathway into a mood episode is an environmental stressor that causes sleep disturbance, which then sets off the instability that they have innately in their internal clock, and then they’re off into a mood episode. Teaching the person good sleep hygiene, teaching them to be better able to cope with stressors is crucial.

    Psychotherapy can also train them to become more self aware, so that they may be able to spot earlier changes in their mood and recognize an impending episode sooner. This allows them to seek for intervention before things get out of hand.

    Focus on developing healthy habits like exercise and healthy diet.  

  • 00:59:11

    The History, Mechanism and Use of Antidepressants

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    In this week’s episode of the podcast, Dr. Michael Cummings and I talk about the history of antidepressants, and their use in overcoming depression and anxiety disorders.  Below is a short blog on the topic to complement the podcast and subsequently I you can find detailed notes on the topic further below.

    Link to show on: iTunes, Google Play, Stitcher, Overcast, PlayerFM, PodBean, TuneIn, Podtail, Blubrry, Podfanatic

     

    What is depression?

    The overarching term “depression” is characterized by feelings of sadness and hopelessness, anxiety, and loss of pleasure.  

    But there are many different types of depression and depressive disorders:

    Psychotic depression

    Bipolar disorder with depression

    Seasonal affective disorder

    Major depression

    Chronic depression (dysthymia)

    Postpartum depression

    Premenstrual dysphoric disorder

    Atypical depression

    Melancholic depression

    Depression due to a medical illness or medication

    Some symptoms of depression are:

    Weight gain or loss

    Sadness

    Anxiety

    Agitation

    Social isolation

    Sleep problems

    Guilt

    Loss of pleasure

    Loss of interest in activities

    Mood swings

    Major depression

    Major depression is characterized by a continuous feeling of sadness—it does not lift for long periods of time. The average length of an episode of major depression, if not treated, last around 11 months. People with major depressive disorder often had an average of four to eight episodes during their lifetime.

    Each episode of major depression usually makes the next episode more likely.

    The annual prevalence rate for major depression estimated in the US and in Europe ranges from 2-7%. But, if somebody has an episode of major depression, the odds that they have a second episode at some point in their life rises to almost 50%. Then, for each episode they have after that, the probability of the next one becomes more likely.

    For people who had recurrent episodes of major depression, by the time they were in their 50s, 60s, or 70s, they had often become chronically depressed or apathetic; their life had deteriorated significantly.

    Melancholic depression

    Melancholic depression is at the severe end of the depressive spectrum.

    These people have a severe loss of enjoyment, and they usually lack energy. They often develop mood congruent psychotic symptoms, such as delusions that they are guilty for everything in the world.

    This tends to be the most resistant form of depression. When severe. people who suffer with melancholic depression sometimes require electroconvulsive therapy to snap them out of a depressive state.

    Is depression a chemical imbalance?  

    People with recurring bouts of major depression can actually experience anatomical damage to the cortex and the spine, because depression is caused by, and can also cause further, chemical changes in the brain. How does this work?

    One main marker for major depressive occurence is a rise in the release of corticotropin from the pituitary, which eventually stimulates our adrenal glands to produce more cortisol.

    There is a 30-40% decline in the rate of metabolic activity among neurons. Lowered metabolic activity among neurons.

    There is a steep decline in the production of neurotrophic factors, proteins that promote neuron activity and cell growth in the brain. As a consequence, there is a thinning of the cortex, a loss of the dendritic spines on neurons.

    The history of antidepressants

    Doctors used to believe depression was norepinephrine or serotonin deficiency. We now view depression as the inability of the limbic system to be modulated by the neurotransmitters.

    Antidepressant medications target this problem by increasing the ability of these molecules that deal with our emotions, motivations and memory to do what they need to do.

    Before antidepressants

    Prior to the discovery of antipsychotics and and antidepressants, depressed and anxious patients were sent to restful places, or asylums. In the late 19th century, the number of asylums surged.

    They used psychoanalysis and psychotherapy to treat patients, but there was no medicinal treatment for psychiatric issues. They sometimes used chemically induced convulsive therapy to induce a grand mal seizure two to three times a week, and it was quite a brutal treatment.  

    Electrical induction of convulsive therapy came about in the 1940s. It was widely used in both mood disorders and psychosis.

    As a result of these two treatments, people had broken bones and muscle damage. Because of that, electroconvulsive therapy developed a horrible reputation.

    The treatment was later reformed in terms of paralyzing people and using anesthesia prior to treatment. These steps made electroconvulsive therapy much more humane than it originally was. Now people don’t experience the side effects they would have back then. It still remains the most effective treatment there is for severe melancholic or catatonic depression.

    As I discussed in a previous blog on psychopharmacology, in 1940 the original antipsychotic was originally an antihistamine. When doctors noticed the sedative effect it had, they started prescribing it for pre-surgery anxiety. It was the first time doctors prescribed a medication to treat mood.

    In 1951, Dr. Roland Kuhn discovered that imipramine, a drug originally tried for psychosis, was not in fact effective in treating psychosis. He did found that imipramine was effective in improving mood and anxiety symptoms.

    This led to to the discovery of other tricyclic antidepressants, such as amitriptyline, nortriptyline, and desipramine.

    First generation antidepressants

    After World War II, there was a surplus of hydrazine missile fuel leftover. People began experimenting with hydrazine as a base compound for development of drugs.

    One of the first drugs that came out of that endeavor was Isocarboxazid, which was initially used to treat tuberculosis.

    It turned out that a few people who were being treated for tuberculosis happened to be bipolar and became manic while taking isocarboxazid, which led to the discovery of monoamine oxidase inhibitors (MAOIs).

    MAOIs stop the breakdown of serotonin, dopamine and norepinephrine in the brain. MAOIs stop that enzyme from removing those chemicals from the brain. The result is more balanced neurotransmitters—and a lack of depression.

    Still, the possible side effects including incredibly high blood pressure when eating certain foods made scientists keep searching for better alternatives.

    SSRI antidepressants

    Selective serotonin reuptake inhibitors were introduced to the market in 1987, with the introduction of Fluoxetine. The SSRIs were almost instantly popular because they were much safer.

    These drugs increase the amount of serotonin available in the brain.

    The SSRI became very widely used very quickly for treatment of depression.

    They have even been found useful because the increased serotonin input to the limbic system they create (the part of our brain that deals with motivation, learning, emotions and memory) decreases the amount of anxiety and vigilance that the person has.

    SSRI was also found to be effective for:

    Post traumatic stress disorder (PTSD)

    Obsessive compulsive disorder (OCD)

    Generalized anxiety disorder (GAD)

    Social phobias

    Impulse based disorders (like binge eating)

    If someone was still resistant to SSRI medication and is still depressed, electroconvulsive therapy is still the best option available.

    When do you prescribe antidepressants?

    If the initial episode of depression is not severe to the point that it’s inducing suicidal ideation or impairing their ability to engage in activities of daily living, then psychotherapy and exercise should be the first treatment.

    If the following statements are true, antidepressants could be prescribed:

    The person doesn’t respond to exercise positively with fewer depressive symptoms

    Psychotherapy does not seem to be helping

    The depression is becoming severe

    Their family is genetically tended towards depression

    Overall, about 40% of the probability of becoming depressed is genetically determined, the other 60% arising from the environment.

    There are also important gender differences, women during their reproductive years have about twice the rate of major depression compared to men.

    If somebody has recurrent episodes of depression, an antidepressant should be considered, and possibly continued indefinitely.  However I often recommend for these patients a combination of treatments including exercise, diet, effective therapy, and over time can get them on lower doses or less medications.

    Below is a detailed review of the episode, with most of the content.  Thanks Arvy Wuysang (MS4) for your help with this!

    History of Antidepressants

    The investigation of antihistamines leading to the discovery of promethazine, chlorpromazine brought on a decade of intensive discovery and investigation of different antipsychotic compounds.

    Swiss Psychiatrist, Dr. Roland Kuhn (1912 - 2005) discovered the Tricyclic Antidepressant, Imipramine.

    His experiments with Imipramine led him to the discovery that it was not effective in treating psychosis. However, he found that Imipramine was effective in improving mood and anxiety symptoms.

    This led to to the discovery of other Tricyclic Antidepressants, both tertiary and secondary amines, such as amitriptyline, nortriptyline, and desipramine.

    As an after effect of World War II, there was a great amount of hydrazine missile fuel leftover. People began experimenting with hydrazine as a base compound for development of drugs.

    One of the first drugs that came out of that endeavor was Isocarboxazid, which was initially used to treat Tuberculosis.

    It turned out that a few people who were being treated for TB happened to be Bipolar and became manic while taking Isocarboxazid, which led to the discovery of Monoamine Oxidase Inhibitors (MAOIs).

    How were people treated for depression before the discovery of MAOIs?

    Sent to restful places in the country, the asylum movement of the late 19th century.

    Psychotherapy, psychoanalysis

    Convulsive therapy, discovered by the psychiatrist Von Meduna in Hungary.

    Was not originally electrically induced, was chemically induced convulsive therapy instead, quite a brutal treatment.

    Electrical induction of convulsive therapy came about in the 1940s. It became widely used in both mood disorders and psychosis.

    The treatment was later reformed in terms of paralyzing people and using anesthesia prior to treatment. These steps made Electroconvulsive therapy a much more humane treatment. It still remains the most effective treatment there is for severe melancholic depression.

    There were no effective pharmacological treatments for depression before the MAOIs.

    Winston Churchill, was thought to have depression and was treated with Amphetamines, which was later known to be ineffective as an antidepressant.

    Amphetamines or Methylphenidate are still occasionally used in anergic depressions, such as in HIV, or in the elderly depressed person who has a severe lack of energy as part of their depressive illness, but in combination with antidepressants.

    If someone with melancholic depression does not get treatment, how does the progression of their disease look like?

    A fairly negative development. The average length of an episode of major depression, if not treated, last around 11 months. People often had an average of four to eight episodes during their lifetime.

    Each episode of major depression makes the next episode more likely. The annual prevalence rate for major depression estimated in the US and in Europe ranges from 2-7%. But, if somebody has an episode of major depression, the odds that they have a second episode at some point in their life rises to almost 50%. Then, for each episode they have after that, the probability of the next one becomes more likely. For people who had recurrent episodes of major depression, by the time they were in their 50s, 60s, or 70s, they had often become chronically depressed, apathetic; their life had deteriorated significantly.

    What physiological effects within the brain contributes to the greater likelihood of a subsequent episode of depression?

    Major depression, aside from changing neurotransmitter signaling, reduces the metabolic rate of neurons in the brain. There is a 30-40% decline in the rate of metabolic activity among neurons. There is a steep decline in the production of neurotrophic factors, proteins that promote neuron activity and cell growth in the brain. As a consequence, there is a thinning of the cortex, a loss of the dendritic spines on neurons. There was evidence that although recovery after major depression is nearly back to original baseline, particularly in recurrent depression, or in people who alternate between major depression and a more minor form of depression called dysthymia, their brain may undergo gradually increasing anatomical damage (cortex and dendritic spines). The accumulating pathology appears to set them up for the next episode, to be more vulnerable to stress diathesis and the occurrence of the next episode of depression.

    One of the key chief characteristics of major depression is a rise in the release of Corticotropin Releasing Hormones (CRH), which in turn produces an increase in the release of Adrenocorticotropic hormone from the pituitary that stimulates the adrenal glands to produce more cortisol.

    Cortisol functions as a stress hormone. The intent is to help counterbalance stress and return us to a baseline state. However, in major depression that positive benefit fails, and essentially the person’s brain winds up being exposed to chronically elevated levels of cortisol, which has an involutional effect on DNA transcription in cells in the brain, particularly in the limbic system. This have been suggested as the source of treatment resistance as people develop more episodes of depression.

    How does melancholic depression differ from other types of depression?

    Melancholic depression is at the severe end of the depressive spectrum. These people have a severe loss of enjoyment, they’re anhedonic, they lack energy. They often develop mood congruent psychotic symptoms, such as delusions that they are guilty for everything in the world. They have very pronounced negative rumination. They lose interest in food. In fact, if they’re not treated, they just sort of curl up and die.

    Tends to be the most resistant form of depression. These people often wind up requiring electroconvulsive therapy to them out of that depressive state.

    Depression comes in a range of severity. Dysthymic disorder, is the chronic milder form of depression. Major depression, starts just above dysthymia, and progresses to Melancholic depression.

    How severe of a depression warrants a treatment with antidepressants?

    If the initial episode of depression is not severe to the point that it’s inducing suicidal ideation or impairing their ability to engage in activities of daily living, then psychotherapy should be the first treatment. Psychotherapies such as cognitive behavioral therapy, interpersonal therapy, and brief analytic psychotherapy have been demonstrated to be effective in treating depression. Exercise also can be a benefit in mild to moderate depressions.

    If, however, the person doesn’t respond to those treatments, or the depression is becoming severe, or in particular, if this is somebody whose family is somewhat genetically loaded for depression, then treatment with antidepressants becomes a larger consideration. Overall, it’s thought that about 40% of the probability of becoming depressed is genetically determined, the other 60% arising from the environment. There are also important gender differences, women during their reproductive years have about twice the rate of major depression compared to men. Premenarche and postmenopausal women have the same rate of depression as men, suggesting that hormonal cycling during the reproductive years may add an additional burden in terms of vulnerability to depression in women.

    If somebody has recurrent episodes of depression, the thinking is very much along the lines of they should be on an antidepressant and it should be continued indefinitely. It used to be that if somebody recovered from depression, then after a year, everyone would be tapered off and discontinued. That changed when people began to recognize the progressive nature of major depression. Each episode makes the next one more likely, and the more episodes people have, the more resistant it is to treatment. We should be working to avoid the circumstance in which we now have an elderly depressed person who has lost the capacity to respond to most of the tools we have to work with. That’s a very difficult position to be. These are cases where we find ECT to be the only treatment that works.

    The advent of SSRIs

    The first antidepressants, the TCAs, were never a comfortable medication class in usage. This is largely because these drugs are cardiotoxic at relatively low concentrations. Six to eight times the therapeutic concentration is a potentially lethal concentration. So, taking a week’s worth at one time stood a pretty good chance of killing somebody. In a population prone to suicidal thoughts, that’s not a very comfortable position to be in. In the case of MAOIs, if the person is exposed to tyramine from food, or to sympathomimetic agents, cold medications in many cases, can produce hypertensive crisis with blood pressures that can cause vascular damage or death.

    The SSRIs were almost instantly popular after the introduction of Fluoxetine, in large part not because they were more effective than the older antidepressants, but because they were much safer. These drugs selectively inhibit the reuptake transporter for serotonin, thereby increasing the amount of serotonin available in the brain. But by and large, they don’t do a great deal else that is toxic or likely to produce problems. So that if somebody overdoses on an SSRI antidepressant alone, it’s almost impossible to kill the person. If you mix it with an agent that has other means for increasing serotonin, it can produce serotonin syndrome, which can cause death, but that’s a relatively rare negative outcome.

    The SSRI became very widely used very quickly for treatment of both major depression and dysthymia. For a host of anxiety disorders they have been found useful because increased serotonin input to the limbic system, particularly the anterior temporal lobe and the amygdala, decreases the amount of anxiety and vigilance that the person has. SSRI was also found to be effective for PTSD, OCD, GAD, social phobias, and even in impulse based disorders like binge eating.

    The SSRI antidepressants account for about 70% of the antidepressant prescriptions in the United States each year. They are as effective as the mix serotonin norepinephrine antidepressants, in mild to moderate levels of depression. They tend to become less effective than mixed mechanism agents in severe and melancholic depressions.

    The current model for depression have moved away from the basic idea of norepinephrine or serotonin deficiency. We now view depression as the inability of the limbic system to be modulated by the neurotransmitters. Antidepressants target this dysfunction by increasing the modulatory range of these molecules. It may be that in more severe depression, using a single lever to try to push the limbic system back into operating normally just isn’t as effective as using more than one lever.

    What are our treatment options for patients with melancholic depression that are resistant to antidepressants?

    ECT would be the best option in severe melancholic depression. There are other adjuncts available that have been looked at that show promise. Transcranial magnetic stimulation has shown positive benefit in terms of augmenting antidepressants, as has vagus nerve stimulation in some chronic recurrent depressions. Combining the antidepressant with an effective psychotherapy has been shown to have additive benefits. In many cases of depression, it calls for a multimodal intervention.

    One of the caveats with the antidepressants is that their efficacy is more limited than we would like it to be. If you look at most antidepressant studies, they report effectiveness in around 60 to 65 percent of samples based on the definition of response as a 50 percent reduction in depressive symptoms. If you’re severely depressed, it’s great to have a 50% reduction, but that doesn’t mean that you’re well. If you look at how many people go into remission in those studies, you’re now talking about numbers down in the range of about a third. That’s not a very satisfactory outcome if you’re the depressed patient. So, our antidepressant treatments indeed do have limits.

    We’ve looked at ways of augmenting antidepressants. Combining antidepressants with different mechanisms. Augmentation with mood stabilizers like lithium. In women in particular, supplementation with thyroid hormone is effective in some patients. One of the caveats in this as well, is that many people who are depressed and receive treatment don’t really receive adequate treatment. A number of years ago, the American Psychiatric Association (APA) did a survey in both primary care and psychiatric offices looking at dose and duration of treatment for major depression. They found that depressed people in primary care offices got what they judged to be adequate treatment about 41% of the time, and in psychiatric offices about 61% of the time. As psychiatrists, one of the things we can do is to be sure that our patients receive an adequate dose of antidepressants for an adequate duration. Duration in this case means at least six to eight weeks to see if the person will respond, while pushing the dose to the upper therapeutic range.

    The black box warning of SSRIs in increasing suicidality for younger patients.

    When you start treating somebody with an antidepressant, their energy level and their neurovegetative signs often respond before their mood does. This means that you have a more energetic depressed person. Studies going back decades suggests that that exposes the person to a period of vulnerability to suicidal ideation and impulse. The warning that the FDA issued was correct, that in giving somebody an SSRI will increase their risk of suicidal ideation early in the course of treatment. Their intent in issuing the warning was to try to clinicians to follow the patients closely during the first few weeks of starting the SSRI. Unfortunately, what happened because of the warning was that many prescribers stopped prescribing SSRIs for children, adolescents, and young adults. As a result, the actual rates of suicide went up, because young people were suffering from depression and were not receiving appropriate treatment. It was a great example of unintended consequences.

    Studies that looked at this concluded that the group receiving SSRIs had more suicidal thoughts, but their rate of completed suicide did not differ from the placebo group. And overtime, as their depression improved, their risk of suicide declined.

    Increased anxiety in the early stages of SSRI usage.

    Serotonin decreases dopamine release and that may cause akathisia in some patients, particularly elderly patients who may not have a lot of dopamine reserve to begin with. Increased anxiety initially is possible. When these drugs are used to treat anxiety disorders, it’s very important to educate the patient that initially their intensity of anxiety is likely to increase before it decreases because these drugs increase the amount of serotonin available within a few hours. In contrast, the improvement of symptoms is dependent on more downstream processes, such as downregulation of postsynaptic receptors and changes in second messenger populations inside the neurons, those processes take weeks. In many cases, you may need to use an anxiolytic to transiently dampen the effect of the antidepressant.

    Panic Disorders

    Initial panic attacks can be severe. Individuals with these conditions literally feel as if they are dying. This is a result of a false triggering of our fight or flight response. Essentially, having a panic attack would be a normal response to a life-threatening event of some kind. That system is largely located in the non-dominant temporal lobe, and involves the amygdala, the anterior temporal lobe, and the parahippocampal complex. That part of the brain is there to chronically monitor the environment for threats and allow you to either fight or run away before something bad happens to you. In some people, though, it appears that that system is triggered way too easily, it goes off when there is no threat. This becomes a horrible experience. People develop all sorts of anticipatory anxieties depending on what their environment is at the time the panic happens.

    These people often need help with behavioral exposure therapies to make them less sensitive to those environments. In fact, that’s thought to be how people with panic disorder, if it goes untreated, eventually become agoraphobic. They can’t go out of their own house, or in some cases their own room, because they’ve become phobic to the entire world.

    Use of Chlomipramine in OCD

    A number of studies have demonstrated that Chlomipramine are more effective for OCD than SSRI. SSRI can be highly effective for OCD if dosing is increased beyond what is required for depression, in the range of 300 mg a day or more. And instead of taking four to six weeks to get a response, it may take eight to twelve weeks. Chlomipramine, on the other hand is more effective because the effect is felt sooner. It is a very robust increaser of serotonin and may have some affinity for norepinephrine as well. It’s antihistaminic, tends to be anxiolytic. The combination of these effects may be why it is overall more effective. It’s a somewhat difficult drug to tolerate because it’s also a good alpha-adrenergic blocker, so it lowers blood pressure. People can get dizzy or can faint if they are taking too much. It’s very anticholinergic, which gives people blurry vision, dry mouth, constipation, and urinary retention.

    Decreased libido and difficulty of ejaculation as a side effect of SSRI use.

    Increasing serotonin tends to dramatically impair sexual function. In males it can result in erectile dysfunction, delayed orgasm, or anorgasmia. In females, it can result in vaginal dryness or anorgasmia as well.

    Arousal is based on activity by the parasympathetic nervous system using acetylcholine. Orgasm is based on the triggering by the sympathetic system using norepinephrine, increasing serotonin. The spinal cord can interfere with both of those processes.

    In most of the original package inserts for SSRI, they quoted dysfunction figures of 5-7%. Those were falsely low because they only reported those cases where people stated this spontaneously. When you actually ask people, how many were having difficulties, it’s more like 50-70% have some degree of sexual dysfunction. The dysfunction can be mild or it can be severe, with loss of functioning all together.

    Moving to a mixed mechanism agent will help fix that. Use of Buproprion, which is mostly noradrenergic, can sometimes reverse that effect of the SSRI. More recently, there is now a SSRI (vilazodone) that also is a partial agonists for the 5HT-1a receptors. Their rate of sexual side effects is much lower. But because they are proprietary drugs, they are much more expensive than generic SSRI antidepressants.

    Buproprion and Mirtazapine use for males with previous sexual dysfunction due to SSRI

    Buproprion is almost purely noradrenergic, consequently does not interfere with sexual functioning. In fact, it may actually improve the libido much more than the SSRIs.

    Mirtazapine is a unique drug that in that at higher doses it increases norepinephrine release by inhibiting auto-receptors for norepinephrine, alpha-2 receptors in the locus ceruleus. So you get more norepinephrine output. It also blocks 5-HT2a receptors, so it acts as a serotonin antagonist which may also provide some benefit with respect to sexual functioning.

    Benefits of optimizing testosterone levels in relation to depression.

    Unlike women, men don’t go through a tightly defined menopause with a sharp drop off in testosterone production. The peak of testosterone production in most men, however, is around 18 or 19 years of age. And then there’s a gradual steady decline thereafter. So that by the time somebody is in their fifth or sixth decade, erectile dysfunction becomes fairly common. It’s estimated that about 40% of males over 50 have some degree of erectile dysfunction. Checking their testosterone is worthwhile, because you may find out that they’re in a subpopulation that have had a more rapid decline than other people.

    Sildenafil, the PDE5 inhibitor can be highly effective in treating erectile dysfunction as a side effect of antidepressants. Cialis daily can be more effective if taken daily due to the long half life and build up.  

    Trazodone is less often effective than the PDE5 inhibitors. Because it’s an alpha antagonist it can work. The adverse effect, commonly known, is to cause priapism, a prolonged and painful erection. The other caveat is that it is a very potent antihistaminic drug. So you can wind up with the unfortunate situation of somebody who now is sexually functional but is too sleepy to be interested.

    We further talked about psychosocial details in the podcast.

    Concluding thoughts

    If we learn how to better modulate cortisol, that may help us a lot with treating refractory depression. There also are continuing developments going on in terms of learning more about direct electrical stimulation of the brain, which may be helpful in treating depressive and anxiety disorders. Once we evolve to the point where we have medications that can directly help increase some of the neurotrophic factors in the brain, that also may go a long way toward altering the long term course of depressive illness. With the medications we have now, we currently have to work with ⅔ response rate and ⅓ remission rate, which is just not adequate by anyone’s standards.

  • 01:38:11

    Emotional Shutdown—Understanding Polyvagal Theory

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    “Polyvagal Theory Simplified”

    By David Puder, M.D.

    Polyvagal theory explains three different parts of our nervous system and their responses to stressful situations. Once we understand those three parts, we can see why and how we react to high amounts of stress.

    If polyvagal theory sounds as exciting as watching paint dry, stick around, trust me. It’s a fascinating explanation of how our body handles emotional stress, and how we can use different therapies it to rewrite the effect of trauma. 

    Why is polyvagal theory important?

    For therapists, and pop-psychology enthusiast alike, understanding polyvagal theory can help with:

    Understanding trauma and PTSD

    Understanding the dance of attack and withdrawal in relationships

    Understanding how extreme stress leads to dissociation or shutting down

    Understanding how to read body language

    We like to think of our emotions as ethereal, complex, and difficult to categorize and identify.

    The truth is that emotions are responses to a stimulus (internal or external). Often they happen out of our awareness, especially if we are out of touch, or incongruent, with our inner emotional life.

    Our primal desire to stay alive is more important to our body than even our ability to think about staying alive. That’s where polyvagal theory comes in to play.

    The nervous system is always running in the background, controlling our body functions so we can think about other things—like what kind of ice cream we’d like to order, or how to get that A in med school. The entire nervous system works in tandem with the brain, and can take over our emotional experience, even if we don’t want it to.

    A story about a gazelle...

    Animals are a great example of how we handle stress, because they react primally, without awareness. They do what we would, if we weren't so well tamed.

    If you have ever watched a National Geographic Africa special, you’ve seen a lioness chase a gazelle. A group of gazelles is grazing, and suddenly one looks up, hyper aware of what is happening around him. The whole group notices and pays attention.

    After a moment, the lioness starts her chase. The gazelle she’s singled out runs as fast as he can (sympathetic nervous system), until he is caught. When he is caught, he instantly goes limp (parasympathetic nervous system).

    The lioness drags the gazelle back to her cubs, where they begin to play with it before they go in for the kill. If the lioness gets distracted, and the gazelle sees a moment of opportunity, he’s up and sprinting off again, looking like he suddenly came back to life (back into sympathetic nervous system response).

    When the gazelle was caught, with fangs around his neck, his shutdown response kicked in—he froze. When he saw the opportunity to run, his fight or flight kicked in, and he ran.

    Poyvagal theory covers those three states—connection, fight or flight, or shutdown. 

    Here's how they work...

    Connection Mode

    or...rest and relaxation...or myelinated vagus nerve of the parasympathetic nervous system coming from the nucleus ambiguus response

    During non-stressful situations, if we are emotionally healthy, our bodies stay in a social engagement state, or a happy, normal, non-freak-out state.

    I like to call it “connection.” By connection, I mean that we are capable of a “connected” interaction with another human being. We are walking around, unafraid, enjoying our day, eating with friends and family and our body and emotions feel normal.  

    It’s also called ventral vagal response, because that’s the part of the brain that is activated during connection mode. It’s like a green light for normal life.

    How does this look and feel?

    Our immune system is healthy.

    We feel normal happiness, openness, peace, and curiosity about life.

    We are sleeping well and eating normally.

    Our face is expressive.

    We emotionally relate to others.

    We more easily understand and listen to others.

    Our body feels calm and grounded.

     

    Freeze, Flight, Fight, or Puff Up

    ...or the sympathetic nervous system response

    The sympathetic nervous system is our immediate reaction to stress that affects nearly every organ in the body.

    The sympathetic nervous system causes that “fight or flight” state we have all heard of. It gives us those cues so that it can keep us alive.

    How does this happen? How does this look and feel?

    We sense a threat and freeze to scan the surroundings for real danger.

    We release cortisol, epinephrine and norepinephrine to help us accomplish what we need to—get away, or fight our enemy.

    Our heartbeat spikes, we sweat, and we feel more mobilized.

    We feel anxious, afraid, or angry.

    There may be flashes of facial expressions of fear and anger, with the background of more of a still face.  If positive emotions are present, they usually look forced.

    Our digestion slows down as blood rushes to the muscles.

    Our blood vessels constrict to the intestines and dilate to the muscles needed to run or fight.

    We may want to run away, or punch someone, or react physically in some way, or just puff-up and look scary.

    Our muscles may feel tense, electric, tight, vibrating, aching, trembling, and hard.

    Our hands may be clammy.  

    Our stomach may be painfully knotted.

    All our senses focus.   

    Our gestures may show guarding of our vital organs, fists clenched, or puffing ourselves up to look bigger or stronger.

    In fight or flight, at some level we believe we can still survive whatever threat we think is dangerous.

    Shut Down

    ...or the Unmyelinated Vagus of the Parasympathetic Nervous System coming from the Dorsal Motor Nucleus

    What’s interesting about this part of the parasympathetic nervous system? Its function is to keep us frozen as an adaptive mechanism to help us survive to either fight or flight again.

    When David Livingston was attacked by a lion, he later reported, “it caused a sort of dreaminess in which there was no sense of pain nor feeling of terror, though quite conscious of all that was happening.”

    When our sympathetic nervous system has kicked into overdrive, and we still can’t escape and feel impending death the dorsal vagal parasympathetic nervous system takes control.

    It causes freezing or shutdown, as a form self preservation. (Think of someone who passes out under extreme stress.)

    How does this look and feel?

    Emotionally, it feels like dissociation, numbness, dizzy, hopelessness, shame, a sense of feeling trapped, out of body, disconnected from the world

    Our eyes may look fixed and spaced out

    The dorsal motor nucleus through the unmyelinated vagus nerve decreases our heart rate, blood pressure, facial expressions, sexual and immune response systems

    We may be triggered to feel nauseated, throw up, defecate, spontaneously urinate

    We may feel low or no pain

    Our lungs (bronchi) constrict and we breathe slower

    We may have difficulty getting words out or feel constriction around our throat

    Our brain has decreased metabolism and this causes a loss of body awareness, limp limbs, decreased ability to think clearly, and decreased ability to lay down narrative memories

    Our body posture may collapse or curl up in a ball

    In shutdown mode, at some level our nervous system believes we are in a life-threatening situation, and it tries to keep us alive through keeping our body still.

    Some people who have had both attachment trauma and subsequent trauma can have chronic suicidality, and dissociation episodes that last days to months. Research shows that long term solutions include:

    Dialectical behavioral therapy

    Mentalization based therapy

    Transference focused therapy

    How trauma affects the nervous system

    As humans, we do the same thing as that gazelle when we perceive emotional or physical danger. We alternate between peaceful grazing (parasympathetic - connection mode), fight or flight (sympathetic system- fight and flight) or shutdown (parasympathetic- shut down mode).

    Our response is all in our perception of the event. Maybe someone was just playing a game when they jumped out to scare us, but we fainted. Whatever the reason, whether the incident was intentional or not, our body shifted into shutdown mode, we registered it as a trauma. our body shifted into shutdown mode.

    Or maybe the trauma event was really, life threatening, and our nervous system responded appropriately to the stimuli.

    No matter what the cause was, our brain believed what was happening was life threatening enough that it caused our body to go into flight, flight, or shutdown mode.

    If someone has been through such a traumatic event that their body tips into shutdown response, any event that reminds the person of that life-threatening occurrence can trigger them into disconnection or dissociation again.

    People can even live in a state of disconnection or shutdown for days or months at a time.

    Veterans often experience this during loud, sudden noises such as fireworks or thunderstorms. A woman who was raped might quickly switch into hypervigilant or dissociated response if she feels someone is following her. Someone who was abused might be triggered when even another person starts yelling.

    The problem occurs when we haven’t processed the original trauma in such a way that the original trauma is resolved.

    That’s what PTSD (post-traumatic stress disorder) is—our body’s overreaction to a small response, and either stuck in fight and flight or shut down. 

    People who experience trauma and the shutdown response usually feel shame around their inability to act, when their body did not move. They often wish they would have fought more during those moments.  

    A Vietnam vet may feel they failed their companions who died around them while they stood, frozen in fear. A rape victim may feel he or she didn’t fight off their rapist because they froze. A victim of abuse may feel they quit trying to escape their abuser, and that they are weak or failed.

    Much of “stress” training, which trains people to continue to remain in fight and flight mode, aims to keep people out of dissociation during real life or death situations. Unfortunately, these practices aren’t common beyond elite sports teams or special forces.  The right amount of stress, with good recovery, can lead our nervous systems into higher levels of adaptation.  

    Coming out of shutdown mode

    So how do we climb back out of shutdown mode?

    The opposite of the dorsal vagal system is the social engagement system.

    So, in short, what fixes shutdown mode is bringing someone into healthy social engagement, or proper attachment.

    Getting down into the nuts and bolts of how this works in our body can help us understand why we feel the way we do physically when your body is in fight, flight, or shut down mode.

    When we understand why our body reacts the way it does, like a string of clues and some basic science about the brain, we can understand how to switch states. We can begin to move out of the fight or flight state, out of the shutdown mode, and back into the social engagement state.

    As therapists, whether we are just establishing a connection with a new, anxious patient, or helping them deal with their deepest traumatic memories, knowing how to navigate the polyvagal states is important.

    It can also be helpful if you have just identified yourself in some of these symptoms. Such as, “When I’m with my parents, even as an adult, and they start fighting, I feel lightheaded and disconnected.”

    If you’ve seen some of these things in yourself, hopefully through therapy, and even understanding how this works, you can pull yourself out of a disconnected state.

    Studies show that some parts of the brain shut down during the recall of traumatic events, including the verbal centers and the reasoning centers of the brain (Van Der Kolk, 2006).

    This is why it’s important to conduct therapy, or coming out of shutdown mode, in a safe, healthy way, in a safe, healthy environment. This is why positive attachment is imperative. Otherwise, you run the risk of retraumatizing the patient.

    Because I am a psychiatrist, I am going to write this to demonstrate how to help a patient switch out of shutdown mode.

    However, these tips still apply to those who are just understanding how shutdown mode works. And it can even help those who feel shut down to begin to know how to try and attain a healthy social engagement mode again.

    Have a trust-based relationship. Because of the potential to re-traumatize, don’t even address intensely traumatic events—especially ones where you think shutdown mode kicked in, until the therapeutic relationship feels deeply connected.

    It’s important as the therapist to allow the patient to express things they couldn’t express to other people—shameful feelings, anger, sexual response, anything that feels frightening to share with others.

    Find your own calm center. If you can empathize with their distress, stay in the moment with them, and help them feel connected during their shutdown, you are throwing them a lifeline. You’re helping them come out of shutdown, into social engagement.

    It’s important to fight against the urge to dissociate, no matter how gruesome the subject matter is. As therapists, we could dissociate because of the mirror neuron response—to mirror our patient’s brain, and because when hearing horrific trauma, it’s easy to imagine it happening to us.

    The human experience is so powerful that when we re-engage the trauma, with someone else to support us, it rewrites that event in our brain, adding in the feeling of being supported within the trauma memory. We create new neural pathways around the trauma, and we can change our body’s response to it.
     

    Let the patient lead. Don’t go on a witch hunt. If the patient brings it up, lean into the subject. But it is harmful to prompt the patient into something that isn’t there by asking leading questions and trying to get them to confess. Don’t let your own experience lead you to imagine they have also experienced something.  

    Normalize their response. The entire polyvagal theory should make us say “thank you!” to our bodies. Even if that systems is overactive at times—unwarranted panic or anxiety—that our body is watching out for us, trying to keep us alive.

    Our body reacting in that way is the same thing as the gazelle either running away or going limp. And gazelles have no idea what emotions are in the first place.

    Now that the patient understands that their emotional response was adaptive, primal, and appropriate, we can get rid of the shame that their non-reaction caused.

    Help them find their anger. Anger is an incredibly adaptive emotion, and it’s one we don’t allow ourselves to have. We think anger is bad. But really, anger shows us where our healthy boundaries were crossed.

    Anger gives us energy to overcome the obstacle. We can help the patient see they had the emotional energy to overcome, but the energy wasn’t able to be manifested at the time they wanted it.

    If, in a session, we can get a patient to identify their anger, they will see that they were not completely unresponsive to the traumatic event. If we can help them feel even the tiniest movement of a microexpression of anger on their face—the slight downturn of the inner eyebrows—we can show them their body didn’t totally betray them in that moment.

    We can reconnect their body and their feelings to their emotions. This helps develop a state of congruence—where their inside feelings match their outer demonstrations of those feelings.

    Further, as a dissociative memory is explored, finding anger and reducing shame allows for the memory to fundamentally change. Anger brings them out of dissociation, even if it is anger at you, the therapist!
     

    Introduce body movement. Because shutdown causes us to freeze, reactivating body movements while talking about the trauma is a great way to reconnect the body and mind, to bring them out of shutdown.

    For example, one of my patients was in an accident. When the EMS showed up, they strapped her to a gurney to load her into the back of an ambulance. More than the actual accident, being trapped on that gurney was traumatic for her. For the entire ride to the hospital, she was terrified that she’d hurt her neck, and all of the anxiety that surrounds a neck injury caused her to be frozen in fear.

    Even in talking about the trauma in the therapy session, her body was stiff, frozen, and she was dissociating.

    I asked her, “In what way would you have wanted to move during that moment?” She said she would have wanted her arms to be able to move. I asked her to slowly, mindfully, move her arms in the way she would have wanted to.

    It’s important to do the movement mindfully and slowly, focusing on the sensation of the movement. That patient felt a huge release of energy. In the following sessions, she was able to tell the memory as a narrative, instead of dissociating.

    Having the patient move—slow punching, kicking, twisting, running slowly in place—flips the person from shutdown into the fight or flight mode, with the goal being to move into connection, or social engagement, mode.

    Body movement exercises, in conjunction with talking to a therapist, can fundamentally change the memory.
     

    Practicing assertiveness. Emotional shutdown can occur within relationships where one person feels they cannot communicate with the other person well.

    One therapist, John Gottman, describes this practice as stonewalling. Practicing assertiveness can help the patient feel more in control of their emotional state, and feel safe to move into healthy relationship patterns.

    Breath work, mindfulness, and yoga all have a role in becoming more connected to your here and now body. I will discuss this subject at length in a future podcast.  
     

    Become a Judo Master and practice strength training. Teaching yourself how to better protect yourself in the future can be powerful and also resets the stress system over time. I talked about strength training in a prior episode, and in the future will talk about learning to fight as an active way to not remain passive or a victim both in mindset and capability.  Further doing something hard, on an ongoing basis, allows for building inner strength which can keep you in fight and flight longer before going into shut down.

    Van der Kolk, B. A. (2006). Clinical implications of neuroscience research in PTSD. Annals of the New York Academy of Sciences, 1071(1), 277-293.

     

  • The Psychology of Procrastination

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    My podcast guest this week, Dr. Jackson Brammer, says he used to be an expert procrastinator.

    But after some research into why people procrastinate, he found a few tricks and tips to help him on his journey to live a more balanced life.

    Dr. Brammer started this path by investigating Impostor Syndrome. Impostor Syndrome involves feeling like you're not the person people think you are—as if you’re deceiving everyone. People with Imposter Syndrome believe if someone knew the real them, they would never receive the same level of trust or responsibility.

    People who deal with Impostor Syndrome take negative statements and magnify them, adding them to the pile of proof that they aren’t as capable as people believe them to be.

    For Dr. Brammer, Imposter Syndrome came from his ability to excel in school, despite consistently cramming for assignments and tests. He felt that someday he would be “caught” and everyone would know that he had “faked” competence.

    Recognizing this link led to the revelation that fighting procrastination might help him stop feeling like he didn’t deserve to be in his position.

    Link to show on: iTunes, Google Play, Stitcher, Overcast, PlayerFM, PodBean, TuneIn, Podtail, Blubrry, Podfanatic

    The Psychology of Procrastination

    Jackson Brammer, M.D., David Puder, M.D.

    What is procrastination?

    Procrastination is the act of avoiding something through delay or postponement.

    You might be procrastinating when:

    There is a gap between your intention and action

    You feel like avoiding something

    You find yourself  easily distracted

    You feel overwhelmed by tasks at the last minute

    You always feel rushed to complete a project

    You’re hesitant to truthfully update someone on your progress

    It usually brings about feelings of:

    Shame

    Guilt

    Anxiety

    Regret

    Anger

    Inauthenticity

    Why do we procrastinate?

    We procrastinate because our brains receive a reward for avoidance. Avoidance brings immediate relief from the distress associated with the task. Although we may experience discomfort in the final moments before a task is due, we rarely think about the past or future when procrastinating.

    This creates a problematic cycle, one that erodes at our self-confidence. It also causes us to keep up a steady stream of “I should be…” in our subconscious minds.

    The ingredients for procrastination
    Personal Factors of Procrastination

    There are fixed factors related to procrastination, things that are innate to each of our different psychological experiences. For example, someone with ADHD is more likely to procrastinate.

    The fixed personal factors are:

    Higher Impulsivity

    Lower conscientiousness—lower drive to be organized and accomplish.

    Limited attention-span

    Boredom / Low Interest - Interest can be considered an emotion with motivational properties related to approach

    There are also variable factors—things like our environment, our health that day, and other things that might affect our tendency to procrastinate.

    The variable personal factors are:

    Willpower

    Willpower is like a muscle. It can become tired, temporarily, after extensive use. However, we can strengthen our willpower through routine exercise. Try to place your willpower-hungry tasks at the beginning of the day. Also, take up some form of regular willpower exercise.

    Distress tolerance

    Willingness to ask for help

    Being unwilling to ask for help can relate to Impostor Syndrome, and can fuel procrastination. It is often based in the lie that we “should” be able to complete something without assistance.

    Task-focused vs value-focused

    Self-consciousness & anxiety

    A common but counter-intuitive driver of procrastination is fear of failure. We protect the self temporarily by avoiding the task that threatens it.

    The variable task or system-based factors are:

    Unclear goals & expectations

    This can become paralyzing, especially when we are unwilling to ask for help. Procrastinators may find themselves unable to start something because they don’t know how to start, but they don’t want to show “weakness” by needing to ask for clarification.

    Unrealistic goals & expectations

    Can lead to thoughts such as "I might as well not even try."

    Distractions

    Distractions from electronic notifications and office visitors can contribute significantly to our tendency to avoid.

    Lack of accountability or mentors

    Procrastination thrives in secrecy and isolation.

    How do we procrastinate?

    As we build a habit of procrastinating, we develop false beliefs that worsen the habit.

    “I work better under pressure.”

    This is simply not true. It would be more accurate to say, "I work under pressure." The adrenaline spike and stress of the situation make us think we are better off waiting, but in reality it’s unlikely that our delay will make the final product any better.

    “I’ll feel more like it later.”
    We deceive ourselves into thinking that we'll feel like completing the task later. We think we’ll drink caffeine, get a mental boost, or find the “perfect time” to do the task, but it never comes.

    “I did pretty well, considering I waited until the last minute.”
    This is a self-protective belief. If we don’t try and we fail, there is less reflection on the self than if we try our hardest and fail. We won’t discover our true potential if we don’t give ourselves ample time.

    “I have plenty of time, I'll do it later.”
    We are undervaluing the future self when we think this way. Humans are terrible at predicting the future. We often don’t start the project early enough to know how much time we’ll actually need.

    “I’ve planned and organized how I will complete the task, it’s time for a break!”

    Planning more than only the first step can be its own form of procrastination. Sometimes doing “good” for awhile gives us permission to do “bad.”

    “This is stupid, I don't even care about it.”
    Our fear and insecurities can lead to us devalue the entire project altogether. If you talk yourself into believing you don’t care about it, it won’t hurt as much if you fail. This is another self-protective belief.

    “There must be some way I can just not do this.”
    There isn't an easy fix for procrastination—we usually still have to complete the task.

    How do we stop procrastinating?Admit it

    To even begin to change, we have to become aware of the problem, then accept it. Once we accept it, we can often find the courage to change our patterns.

    Catch the cognitive distortions

    If you want to pursue therapy for your procrastination, cognitive behavioral therapy can help. More specifically, cognitive behavioral therapy will help you identify your cognitive distortions. The second episode of the Psychiatry and Psychotherapy podcast deals with cognitive distortions.

    Go through the list of false beliefs we listed and journal your common cognitive distortions.

    Here’s the quick breakdown of how you can look at your thinking patterns when you decide to procrastinate:

    Recognize when you have the emotion about the task you want to delay. Sometimes the emotion will disguise itself as a physical sensation, such as anxiousness, nausea, or a rapid heartbeat.

    Look at the thoughts that come with that emotion. Such as, “This is stupid, I don’t even care about it.”

    Look at the cognitive distortions that came with the thought. Is the task actually “stupid,” or is it something you should do, you’re just afraid to do it, so you’re demeaning it in case you fail? Be honest with yourself in your answer.

    Repeat. This can help you rebuild a habit of identifying the things we tell ourselves and have always accepted as truth.  

    Build your willpower

    Tackle the high-willpower tasks earlier in the day. Earlier in the morning, when your cortisol is high, when your brain is fresh, you’ll be able to take on the tasks you’ll need to be highly motivated for.

    Start strength training, or another disciplined physical task. I’ve found that with strength training, even if I don’t want to begin, and even if the whole workout is miserable, it teaches me that I can will my body to do what the program requires.  This is good for willpower training.  Another will power builder is to choose a difficult book, decide to read it in let us say 60 days, and then divide the book up into 60 parts to read every day.  I often recommend this to psychiatry residents and NPs I train, challenging them to read 3 books in 60 days using this method.

    Forgive yourself

    Practice self-forgiveness when you identify the pattern. We are both aware that we feel frustrated with ourselves when we know we’ve been procrastinating. That frustration is a sign we are trying to change, but it isn’t helpful in the actual change. It can lead to sadness and a lack of self confidence, which can worsen the pattern of procrastination because negative emotions lead to avoidance.

    Self-forgiveness reduces the negative emotions we associate with a task, thus reducing future avoidance and offering ourselves an encouraging approach instead.

    How can you practice self-forgiveness?

    Identify the emotions you feel that are associated with past tasks you haven’t completed.

    Identify the emotions behind tasks you felt you didn’t excel in, or that didn’t turn out the way you wanted them to when you did complete them.  

    Accept the emotion that is there, have self compassion and forgiveness for the emotional experience you had.

    Practice Mindfulness

    Mindfulness is another way to help fix procrastination. Mindfulness will help you be able to identify mental patterns, such as cognitive distortions. When we pay attention to ourselves through the gentle observation of mindfulness, we aren’t striving to “fix” or self-judge. Since becoming aware of the problem is one of the first ways we are able to change, mindfulness helps us be more aware of our actions in general. It can also serve as a form of willpower training.

    Download a good meditation, or use the app Headspace, and practice it daily to develop a habit of mindfulness.

    Define and focus on your values

    One of the most important things you can do is align your tasks and goals to your values. This automatically undercuts any excuses you’ll have because ultimately, the task, if you’ve signed up for it, aligns with your values.

    For example, if there’s a task associated with your job that you don’t want to do, you can still link it with something you believe in. Bottom line is that we value patient care, so even we don’t necessarily feel like doing small tasks throughout the day, we still do them because we link them to our deeper values.

    Define your goals

    It will also help to be able to clarify your goals—daily, weekly, monthly. Make those goals realistic so you don’t talk yourself out of them. Then, merely focus on starting the tasks, not completing them.

    Make the goals small and manageable, and focus only on what the very next step should be. In this way, you’re setting yourself up for positive reinforcement, instead of the negative thoughts that usually accompany procrastination. Avoid over-planning as a form of procrastination.

    Psych yourself up for the task

    Sometimes we need more encouragement to complete a task we are dreading. It’s why people have workout playlists. You can use the same psychology behind that to prepare for even daily tasks. Get a pour-over, trendy coffee, plan a reward for when you complete the task, figure out what makes you want to follow through, and do it.

    Since using all of these tools to beat his habit of procrastination, Dr. Brammer has been able to add more things to his life, and is still able to accomplish it all and feel confident. He’s happily married, a father of two, involved in his church, in a band, and is a practicing psychiatrist.

    Have you ever dealt with procrastination? What do you find your cognitive distortions are—what are the things you tell yourself to make yourself feel better about putting things off?

    For further reading on procrastination, check out some of Timothy Pychyl’s research.

     

  • 01:01:56

    How to Fix Emotional Detachment

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    This week on the podcast, Ginger Simonton, PhD candidate, and I (Dr. David Puder) talk about about how to deal with emotional detachment. In the psychiatry world, we call the state of emotional detachment, congruence. 

    What is congruence?

    Psychological congruence is someone’s ability to feel and express their inner emotions in a consistent manner with their outer world—their speech and body language.

    As an example, have you ever smiled when you’re talking about something sad? Or felt very emotional, yet had a flat face and still posture? Have you ever felt angry, but pushed it down and developed a headache? These are incongruent speech and behavior patterns.  

    Incongruence happens when we’ve lost touch with our inner world, our emotions that are represented with bodily sensations. Many of my patients experience emotions, but have a hard time expressing them with words, so they shove them out of their experience.

    Emotions are unavoidable.

    We experience them all the time, whether we know it or not. Common terms for pushing them out of our awareness are suppression, denial, repression, and other defense mechanisms. We may think we can suppress our emotions, but they will come out in one way or another—sometimes through physical pain and illness.

    There is extensive research on how the body processes emotion, and how that affects us physically. One of my favorite books on this subject is The Body Keeps the Score, by Bessel van der Kolk and The Feeling of What Happens by Antonio Damasio. I have spoken about the science of emotion in part 1, part 2, part 3 on microexpression and a popular episode on the polyvagal theory which give the science and application of understanding emotion.

    As psychotherapists, our job is to help people reconnect to those emotions, and be able to experience them in healthy ways. People bury so many of our psychological problems in our bodies that we don’t even feel comfortable in our bodies anymore, and we prefer to be numb.

    People further push unwanted emotions out of their experience through use of drugs, alcohol, and other addictions like porn, gambling, movie binging, or mindlessly scrolling forever on social media.

     

    How do we develop incongruence?

    But we don’t start out as emotionally disconnected, or incongruent. As children, we express our emotions as we feel them. If we are happy, we giggle, smile, or stick out our tongue as we work on a project. If we are sad, we cry. If we are angry, we bite, yell, spit or claw. If we have disgust we spit things out, push things away and protest against putting things in our mouth!  

    If our emotions are mirrored back, and our caretaker acknowledges them verbally, them we optimally will be connected to our bodily responses from a young age. This is why I always recommend starting any discipline or high emotional moment with kids by empathically mirroring their emotions in words, and adding meaning to why they might feel such a way.

    To get along with others, most kids, over time, develop a normal adaptive way to conceal emotions, which helps function in family and friendships. We learn that there is a context for truly sharing what is going on, and this is a good thing. Sometimes suppressing strong emotion until later is helpful!

    Stronger issues develop when repeated messages invalidate or shame our experience, or trauma moves us away from being congruent with our inner experience. It is also possible that there is no one who an individual connects with enough to be congruent around.

    For example, if everyone you know would shame or attack you, it might not be a good idea to bring out your deepest thoughts and emotions. These kinds of households often have heavy drugs or alcohol, severe mental illness, or predators.

    We are meaning-making creatures. We assign meaning to events in our lives, and that meaning becomes our guiding belief and principle, especially in key developmental periods in childhood.

    These meanings shape how we are going to interact with the world. Although unconscious and out of our awareness most of the time, when we live out of congruence without ourselves, it leads us to form these earlier, shaping meanings.  (click here for more on the science of meaning)

    How incongruence develops:

    A trauma occurs. A child hears his parents fighting. The child, when in the midst of it, seems to be physically sick, and this distracts the parents from their fighting and thus decreases the fighting.

    We assign meaning to it. The child, as always, relates everything back to him or herself. They think, “If there is yelling, if I become ill, the yelling will stop.”

    We structure habits and actions around that belief. The person continues to use being ill as an adaptive response to calm the parent’s hostility. Any emotional pain and discomfort is thus learned to be responded to when in the midst of only physical pain.

    We see patterns in our lives that reflect that belief. We react repeatedly in a way that demonstrates our belief. We notice it affects our relationships, and that further cements the belief in our lives. New connections are found with caring physicians, maybe specialists who have concern for the medical issues, which further reinforces illness being a way to both calm disagreements and get connection needs met.

    We have to either live with it, or deal with it. Until we revisit that moment and that decision, we cannot sift through that core belief. There is incredible hope for people with incongruence.

    The response to a healthy therapeutic relationship and subsequent changes in behavior can be astounding. To deal with it, it is necessary to both find new ways of connecting with others but also not be able to use the incongruent way of being for an adaptive means.

     

    How do we fix incongruence?

    Our goal as we progress in life is to connect our physical body, emotional experience and verbal communication. The best public speakers seem to speak from the core of their being. The most powerful messages come from getting in touch with ourselves and integrating it.  

    We can introduce the concept of reconnecting with the self in several ways:

    Art

    Art helps people bypass the logical areas of the brain and produce something raw and congruent to their inner experience. Painting, drawing, working with clay, or other forms of art help us connect with things deep down in our inner experience. Sometimes we ask people to make a self portrait or a picture of their home to discover new things and access something true.

    Then we ask for people to describe their pictures and link the congruent space of the art with what they share.  

     True Self 

    Ginger often uses the phrase “inner child” but I like to describe it as the “true self,” or the core of our being. Living congruently out of the “true self” is when how you imagine yourself lines up with what you do and how you articulate yourself. This is not a new idea, Karen Horney’s Neurosis and Human Growth is my favorite author on this topic.

    Learning that we sometimes have hidden this part of ourselves, and then gaining access to it and learning to live by it can be powerful. When we are around people who can give us grace and truth as we progress, we can find this more and more.  

     Bodyscan (or interception)

    Patients who have dealt with trauma often dissociate from their bodies. Even in this era of technology, it’s easy to forget we have bodies. People spend most of their time disconnected, scrolling the internet.

    When we experience our body and work through emotions at the same time, it brings us into ourselves and develops congruence.

    Ginger likes to ask the following questions when her patient is experiencing a triggering event, to be able to dig down to the root cause of incongruence:

    What is your body feeling as you talk about that?

    What emotion would you name that feeling you’re having?

    When is the last time that you remember your body feeling that way? The patient’s answer to this must be close to the original time of trauma, something usually in their childhood.  

    I like to ask as well:

    As you say that what are you feeling in your body?

    If your body could say something what would it say?

    I want to access their bodily memories and the source of their pain.  

     Taper off of harmful and unhelpful drugs.

    It’s easier to medicate incongruence, rather than actually deal with the root of it. It’s quicker. Substances like alcohol and drugs deeply affect people’s emotions. When patients are self medicating, they are usually trying to rid themselves of a symptom of emotional pain.

    I like to ask them, “What are you getting out of the substances? Sleep? Peace?” Once we can answer that question, we can get to the bottom of where the anxiety and fear or anger comes from. We can begin to develop congruence, which will in turn, bring peace.

    People medicate with illegal, and prescribed, legal drugs, as a way of dealing with emotional pain.

    Some doctors and therapists can be symptom based, rather than focused on what is underneath the symptoms. When they see a patient, they can be on a hunt, trying to identify what’s wrong, the bottom line, and then find a medication that will relieve symptoms.

    When we do that as therapists, we connect with the patient’s illness narrative, rather than who their core is, before they developed these problems.

    Some patients who come to see us are taking 20-33 pills a day for all their different illnesses. If there is so much medication involved, it can become difficult to do psychotherapy as likely the sensorium or total brain function is impaired.

    We have found when we establish a secure emotional connection with them, we can get some of these medications off the table, and then our patients can start to develop a range of emotions.

    Through an attachment with a a therapist, that is trusting and meaningful, people can start to feel what before they either consciously or unconsciously suppressed.  I have spoken about the worst medications here.

     

    How to stay congruent during tough circumstances.

    It is tough to apply all that patients have learned through therapy in their everyday lives. Our families and friends love homeostasis—usually, the people around us want us to stay the same. They say, “you’ve changed,” as if that’s a bad thing.

    When we’ve been healed, when we are congruent with ourselves, it can be difficult for our friends and family to accept the “new us.” They connect more easily with the old us.

    We have noticed that if the patient begins to grow, the whole family system needs to change as well.

    To maintain newfound congruence and healthy mental states, patients work to find healthy relationships they can be congruent within.  In the future I will talk about how to identify safe people and how to have healthy boundaries that keep us in relationships.

    sign up for an annual subscription to receive CME credit for this activity and more! Learn more Here.

    Special thanks to the MEND team for allowing me to collaborate with them!  Here is a link to the long version of how the MEND program works.  Here is a link to the program.    

  • 00:45:29

    The History and Use of Antipsychotics

    Psychiatry & Psychotherapy Podcast starstarstarstarstar
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    In my last post, Dr. Cummings and I talked about what psychopharmacology is, how medicine works in our body, and what factors affect medicine absorption rates.

    In the latest podcast, Dr. Cummings and I talked about antipsychotics, the particular branch of psychopharmacology that deals with medicines that treat psychotic experiences and other mental disorders, such as:

    Schizophrenia

    Severe depression

    Severe anxiety

    Bipolar disorder

    Psychosis exhibiting hallucinations and delusions

    The history of first generation antipsychotics

    The use of antipsychotics as medication began in 1933 in France. The research around developing antihistamines evolved into the introduction of promethazine. This drug produced sedative side effects, so doctors started prescribing it before surgeries as a calming agent.

    Eventually, a doctor studied the derivatives of promethazine, altered it, and developed chlorpromazine. It was mostly used as a pre-surgery anti-anxiety pill, until psychiatrists took note of the calming effect of the drug and began prescribing it to their patients.

    Prior to chlorpromazine, the options for treating psychotic patients were electroconvulsive therapy, hydrotherapy, and putting patients in an insulin coma. None of those are antipsychotic in nature.

    When two psychiatrists, Dr. Delay and Dr. Deniker, gave 38 psychotic patients a test round of chlorpromazine, they noticed the patients were calmer, and also less psychotic—they had less delusional thinking, fewer hallucinations, and fewer psychomotor-agitation symptoms. Deniker and Delay began giving talks on the benefits of the drug, and in 1955, chlorpromazine became available in the United States. Chlorpromazine is still used today as a treatment for different mental illnesses and mood disorders.

    Once the government saw the positive effects of chlorpromazine, it began to shut down mental health facilities. There was no longer as large of a need to house psychotic patients, and they saw an opportunity to cut costs. However, they did not create adequate sources in the community for ongoing care. California alone is estimated to have 40-60% of homeless people that have a mental disorder.

    Once chlorpromazine became a success, pharmaceutical companies rushed to create their own version of an antipsychotic drug. Because chlorpromazine was the grandfather of the first generation of antipsychotic drugs, the rest of that generation can be categorized by their ability to merely block dopamine D2 receptors in the brain.

    In repeated studies, dopamine antagonism is responsible for 92% of their effectiveness. It also led to the thought that people were psychotic because they had too much dopamine. Since then we have found that their are much more complex psychopharmacological dynamics going on in psychosis.   

    Second generation antipsychotics

    The next set of antipsychotics that came on the market were clozapineolanzapine, risperidone, and other related drugs. Those medications had less effects on motor movement than the first generation drugs.

    Clozapine is a poor antagonist of dopamine- blocking 30-40% of dopamine receptors but also promotes the activation of glutamate through activation of NMDA receptor, which increases activity in the frontal lobe (which helps with schizophrenia’s negative symptoms).  

    Clozapine had more system-wide changes than just dopamine suppression, and it had more positive response from patients. It was more effective—40-60% of people who won’t respond to a first generation antipsychotic, do respond to clozapine.

    However, in Finland in 1975, 6 people taking clozapine died due to agranulocytosis (lowered white blood cell count, leading to a severe lack of immunity). A lowered neutrophil count (called agranulocytosis) can show potential problems with fighting off normal bacteria we live with all the time.  When patients are on clozapine, initially they need weekly blood checks for this reason.

    Despite the risks, clozapine can be an incredible drug—I have one patient who was schizophrenic and homeless, and she is now back in school and recently graduated with a perfect GPA! People who had been dysfunctional for decades, who are given clozapine, can become extremely high functioning.  Key to success here was her willingness to work with me, despite having to try different things before something worked. 

    A trial run on a antipsychotic should be done at a minimum of 6 weeks, and blood tests must be conducted to make sure that the concentration of the medicine is at good therapeutic-dose levels. Dosage alone is sometimes not enough because we all metabolise drugs so differently.  I have uploaded recommended levels in my resource page.

    Third generation antipsychotics

    What is deemed the third generation of antipsychotics, aripiprazole and brexpiprazole are partial dopamine receptor agonists.  They keep dopamine at a max of 25% in the brain which due to the high affinity to the receptor it does not vary much based on dose.  

    The good thing about this generation of drugs is that they don’t lower blood pressure, cause insulin resistance, and are not sedating in nature.

    It works for some people, it doesn’t for others. But when it does work, it works really well.

    Side effects of psychiatric medicines

    Akathisia is the inability to stay still, characterized by a feeling of inner busyness. It is a miserable side effect, exhausting to the patient.

    If someone is experiencing this, they should immediately call their psychiatrist or go to an emergency room.

    One of Dr. Cumming’s patients described it as “ants running up and down the bones of his legs.” It usually involves an anxious feeling, and a desire to move the lower extremities of the legs. Akathisia can be caused by any drug that lowers dopamine (including SSRIs).

    This syndrome is so complex because it involves several compounds, including dopamine, norepinephrine, acetylcholine, and serotonin inputs. Options for treatment include: choosing a lower dosage, picking another dopamine antagonist that is less strong (quetiapine or clozaril), or prescribing a drug like amantadine, propranolol, mirtazapine or clonazepam (more nuance in the podcast on this).

    It is a harmful disorder, and one to watch out for in patients. If a patient is sent home from the hospital experiencing these symptoms, but is not properly vetted for akathisia, a doctor could be subject to serious legal repercussions.

    The questions to test a patient for akathisia are:

    Is the person moving? Can they not sit still?

    What is their internal sense of restlessness and anxiety?

    How much are they distressed by these feelings?

    Acute dystonia involves muscle spasms and it affects movement, causing the posture to twist abnormally. It can be painful for patients to experience. This occurs because of too little dopamine in the basal ganglia part of the brain.

    Parkinsonism involves muscle stiffness and slower movements. It’s usually uncomfortable, but not a miserable side effect. This also occurs because of too little dopamine in the basal ganglia part of the brain.

    The future of antipsychotics

    With each generation of new medicines, we’ve gotten closer to being able to help people stabilize their psychosis. We haven’t been able to achieve complete wellness.

    Dr. Cummings says he has hope that with further advances in the medical field, we will be able to identify who is at risk. There is hopeful data that we may be able to one day prevent the development of schizophrenia.

    History of Antipsychotics (notes by Arvy Tj Wuysang).

    1933, France

    Initiative to develop antihistamine as treatment began

    1947

    Promethazine

    Produced sedation and calmness in animal models

    Not highly effective in humans, but found to provide calmness in preoperative settings

    1950

    Discovery of Promethazine Derivatives, especially Chlorpromazine

    Initially tried in a surgical military hospital in France by Dr. Henri Laborit (1914-1995)

    Successful in making people calm and indifferent to impending surgery

    The medication was tried it in a volunteer

    The individual reported favorable effects, until he stood up and promptly fainted

    Determined as not safe in pre-operative setting because it was too effective as alpha-adrenergic antagonist in lowering blood pressure

    1952

    Dr. Pierre Deniker (1917-1998), psychiatrist, with Dr. Jean Delay (1907-1987), his superintendent in Sainte-Anne’s Hospital in Paris, led the Chlorpromazine introduction as a psychopharmacologic agent

    They were interested in the calming effect of the drug

    Tried the drug in psychotic agitated patients

    Treatment options in those days were limited to:

    Electroconvulsive Therapy

    Hydrotherapy

    Insulin coma

    None of which were antipsychotic in nature

    Tried it in 38 patients, made patients calmer, and less psychotic!

    Especially effective for positive psychotic symptoms like hallucinations, delusional thinking, psychomotor agitation

    Findings were impressive enough that Deniker began giving talks about the drug, including a conference in Montreal, that led to its introduction in North America

    1955

    Chlorpromazine was approved for usage as antipsychotic in the US

    Subsequently used worldwide

    Led to the deinstitutionalization of a lot of psychotic patients

    Created a problem of lack of follow up of psychotic patients

    I.e. California has around 357,000 homeless individuals, estimated 40-60% suffer from mental disorder with schizophrenia spectrum highly represented in that percentage

    State spends about $200,000 per year per person to care for people committed to state hospitals. Funds committed to patients that are discharged from state hospitals are very minimal.

    Led to development of a whole host of antipsychotic agents

    1960s

    There was an explosion in the invention of antipsychotic drugs

    US FDA took a stance, did not allow approval of antipsychotic drugs that are not clearly better than chlorpromazine or haloperidol

    1st generation antipsychotics all work by blocking Dopamine D2 receptors in the brain, counts for 92-23% of variance in mechanism

    Led to the simplistic dopamine hypothesis of psychosis

    1958

    2nd generation antipsychotic discovered by Eichenberger and Schmutz from the Swiss pharmaceutical company Wander AG, Clozapine

    Created because 2 other -antadine antipsychotics have been successful, Loxitane (Loxapine) and Perlapine

    Clozapine was initially thought of as a failure because it did not produce dystonia in white lab mice, as expected in 1st generation antipsychotics where it blocks dopamine effects in the brain

    Clozapine found to be a poor antagonist to dopamine, only blocks 30-40% of dopamine receptors. Although, it promotes release of glutamate, by binding to an allosteric site for glycine in the NMDA receptor, which in turn increases activity in the frontal lobe and suppresses dopamine release in the mesolimbic system.

    A number of small studies in the 1960s found that patients that don’t respond to 1st generation antipsychotics responded well to Clozapine treatment by showing better response of both positive and negative symptoms of schizophrenia.

    1970s

    1972, Clozapine usage was introduced in Austria

    1974, Clozapine usage was introduced in Germany

    40-60% of people that did not respond well to 1st generation antipsychotics, responded well to Clozapine

    1975, 5 people in Finland died after Clozapine treatment due to agranulocytosis

    Clozapine found to trigger formation of antibodies targeting bone marrow cells that make neutrophils and essentially shut down a person’s immune system

    Must monitor Absolute Neutrophil Count closely when prescribing Clozapine

    Monitor weekly for 6 months, then every 2 weeks for another 6 months, and monthly for another year (in the USA)

    Risk for agranulocytosis decreases with time: peaks at 4 months of exposure at about 1.3%, .38% after 1 year of exposure, .06% after 2 years of exposure

    Clozapine usage in the US today

    Siskind, D., McCartney, L., Goldschlager, R., & Kisely, S. (2016). Clozapine v. first-and second-generation antipsychotics in treatment-refractory schizophrenia: systematic review and meta-analysis. The British Journal of Psychiatry, 209(5), 385-392.

    15-20% of patients in California State Hospitals are on Clozapine, 53% in New York State

    Response rates to drugs other than Clozapine is pretty miserable in State Hospitals

    Olanzapine response rate even at high plasma concentrations is only 9%, compared to 40-60% for Clozapine. Every other antipsychotics’ response rate is between 0-5% for the severely psychotic, mentally ill patients.

    If patients meet Kane criteria (after John M. Kane)---treatment failure after two clearly adequate trials of antipsychotic treatment with minimum of 6 weeks duration with therapeutic plasma concentration---odds that they will respond to anything other than Clozapine is fairly low.

    Common mistake that clinicians make is to go by dosage as a measure of whether a person is receiving adequate medication

    Dosages only weakly correlates with plasma concentration since the metabolism of antipsychotic drugs is so variable

    Measuring plasma concentration to reach therapeutic levels is crucial in antipsychotic drugs administration, especially in patients who are seemingly refractory to treatment, to ensure adequate treatment

    Akathisia as side effect of antipsychotics

    Very rarely happens with Clozapine use

    Akathisia is a very miserable side effect of antipsychotics, described as “ants crawling up and down the bone of your legs” by a particular patient

    Characterized both by internal sense of anxiety and a near irresistible urge to move

    Barnes Akathisia Rating Scale, most commonly used to measure akathisia symptoms. Based on three main factors:

    Objective movement

    Internal sense of restlessness and anxiety

    How much are they distressed by these feelings

    Akathisia is a concerning and common reason for malpractice

    Underlying pathophysiology of akathisia is distinct compared to other extrapyramidal symptoms, involves not only dopamine and acetylcholine. It also involves norepinephrine and serotonin inputs to basal ganglia, makes it a difficult syndrome to treat successfully.

    Treatment options for akathisia:

    Use a less robust dopamine antagonist, such as Quetiapine or Clozapine

    Use lower dose of the antipsychotic

    Use Amantadine, increases dopamine release in the basal ganglia

    Was originally devised to treat influenza A

    Discovered to be effective in treating extrapyramidal symptoms, also effective for tardive dyskinesias (15% respond to amantadine)

    However, it is not as effective as B-blockers or Mirtazapine

    Amantadine is not anticholinergic (no memory problems, no GI side effects, no blurred vision, no urinary retention)

    Head-to-head trial between Propranolol versus Mirtazapine versus placebo, shows mirtazapine as more effective in treating akathisia

    Poyurovsky, M., Pashinian, A., Weizman, R., Fuchs, C., & Weizman, A. (2006). Low-dose mirtazapine: a new option in the treatment of antipsychotic-induced akathisia. A randomized, double-blind, placebo-and propranolol-controlled trial. Biological psychiatry, 59(11), 1071-1077.

    Mirtazapine at 15 mg at bedtime was effective in 43% of patients

    Placebo was effective in 7% of patients

    Akathisia may present as side effect in SSRIs and antiemetics (compazine)

    Expected or Therapeutic plasma concentration ranges for antipsychotics and mood stabilizers

    DSH Psychotropic Medication Policy (see resource page)

    Aripiprazole (Abilify)

    3rd generation antipsychotics, partial dopamine agonist

    Has high affinity for dopamine receptors, higher than 1st and 2nd generation antipsychotics. If Aripiprazole is present at therapeutic concentrations, 1st and 2nd generation will have very little interaction with dopamine receptors.

    Keeps dopamine signaling at about 25% of dopamine’s maximum signal transduction, tends to produce all or nothing response in terms of treating psychotics. Not much ability to vary where dopamine is blocked because of it’s high affinity.

    Side effect profile is very favorable. Largely metabolically neutral, tend not to cause weight gain, glucose intolerance, and lipid abnormalities. Low affinity for alpha receptors or histamine receptors, is not very sedating and does not lower blood pressure.

    Use outside of schizophrenia

    I.e. risperidone and olanzapine also exhibit utility as mood stabilizer and antidepressant.

    3rd generation antipsychotics also tend to improve mood, driven by quality of the molecules and in part by the desire of pharmaceutical companies to broaden their market

    Use in dissociative state, such as Borderline Personality Disorder

    Antipsychotics can help bring patients out of dissociative state in short period of time

    Borderline patients was found to have a significant limbic dysfunction, hence antipsychotics may be helpful

    Future of Schizophrenia Spectrum Treatment

    There is great need to identify individuals at risk for the disease and treat them with lower dose of antipsychotics. Hopeful data is currently present in support of this approach to lower the incidence and prevalence of schizophrenia.