I started thinking about this topic back in 2006. after a brief and intense love affair that ended in a breakup. The result of this process was the collection and reading of professional literature. When my future wife first entered my apartment, she came across scattered books and magazines with titles that spoke of love. She had been trained in couples therapy, so the topic was familiar to her. She later told me that she was pleasantly surprised because I was the only man in her life who was interested in this area. This interest led to many lectures, that were well received and appreciated. Colleagues from work jokingly called me Dr. Love. Reading of professional literature and many years of working with patients have convinced me of the importance of love in our lives. For many, although they came for treatment because of symptoms of anxiety, depression, stress, insomnia, etc., problems in intimate relationships lurked in the background. I am not talking about sex, because as we know, no one died from lack of sex, but from lack of love. Further research introduced me to John Bowlby and his theory of attachment, which I will briefly describe before returning to the topic of love.

Did you know that emotional attachment (intimacy) is an instinct (drive) that is crucial for survival? The human baby / child is the most powerless being in the first 7 years of life, and if it does not have a high-quality emotional connection with the parent (mother or surrogate), regardless of the physical conditions (food, warmth, care), the child is unlikely to survive or at best will have serious developmental problems. This innate need is based on specific brain cells that are active only for this purpose (the so-called “mirror neurons”) and, with the help of the hormone oxytocin, strengthen the bond between the child and the mother. The experience with mother is deeply and subconsciously remembered and is a model for all other close relationships in childhood and adulthood. In this sense, Freud was right to emphasize the importance of the first five years of life.

If a child’s emotional attachment is positive (secure), it leads to the ability to regulate stress, satisfaction in relationships with others, self-esteem, and mental health. Mental health depends on the system of integration, regulation, and balance of the so-called social brain in processing negative emotions such as anger and anxiety. These systems are optimally integrated, balanced, and regulated in the first 2-3 years of life based on a secure emotional attachment to the mother, so that from the age of 5 the child is able to self-soothe, because the “good mother” has become part of his internal landscape.

On the contrary, if this attachment is negative, the child cannot “count” on the mother to be available and able to calm him, understand and establish the feeling that he is loved. This insecure attachment takes several forms: an avoidant, anxious, and chaotic style. All styles are a risk factor for mental disorders and unsatisfactory relationships.

Traces of the first intimate relationship from childhood are evident in romantic love. The two stages that we all go through when we love are the phase of falling in love and the phase of devoted love. During falling in love, we are somehow lost to realistic judgment. Then we are in a state of intense longing for a loved one, and everything else does not matter, regardless of life circumstances and needs. We act irrationally and unpredictably. This condition, fortunately, is usually short-lived. Some even compare it to addiction, because of activation of the brain center and chemical (dopamine) as in people with cocaine addiction, which is manifested in bliss in the presence of a loved one.

When this stage is successfully completed, and we enter the phase of devoted love, we not only want to be in close contact with the person we love, but also perceive this person as a best friend, whom we look for support and safety. We completely relax and turn to other interests and desires. If we had a positive attachment to our mother as children, devoted love is characterized by longevity and stability, confidence and friendship, support when we are stressed, flexibility in response to conflict, and mutual respect.

If the attachment to the mother was insecure, and depending on the dominant style, the problems at this stage of love are numerous. For example, in the avoidant style, there is a disinterest in intimacy, frequent breakups and divorces, withdrawal under stress, lack of resolution of conflicts, unwillingness in meeting the needs of the partner, even a tendency for harassment. This over-reliance on independence and the apparent devaluation of intimacy, deepens the feeling of loneliness.

The anxious style is dominated by jealousy, frequent separations and reconciliations, concern about rejection, a tendency to control, and self-obsession.  There is a dependence on a partner to soothe the fear of loss and the need for attachment. These characteristics are not conducive to a long-lasting relationship, leading to even greater feelings of loss and anxiety.

In the chaotic style, problems are often extreme with a tendency to self-harm, the development of physical ailments, fluctuations between attachment and distancing from the partner, the manifestation of strong negative feelings of anger, anxiety, depression, and aggressive behavior. None of the strategies succeed in eliminating problems with traumatic fear, born under the influence of a frightened or frightening parent.

How can we help people with the love related suffering and accumulated problems described above? It is not easy, but it is not impossible. First, there must be a desire and insight in the attachment related difficulties. In addition, therapy is needed (formal or informal), which will correct the past and create a new template for a healthy relationship. As I said at the beginning, the desire to have a secure emotional attachment is inborn drive that exists in all of us throughout our lives. During therapy, we work on developing empathy, understanding, adaptive strategies for regulating emotions, developing flexibility in dealing with conflict, coping with traumatic events and losses, and most importantly, using ordinary situations (problems) and breaks in therapy to develop adaptive ways in overcoming attachment related distress. Therapy can be individual or together with a partner who is motivated for this kind of demanding therapy. In essence, for successful therapy of this kind, the most important is sensitivity for verbal and nonverbal communication and cooperation between the patient and the therapist.

I hope that through this blog, I was able to expand your interest in love in a different way, as an area that requires serious study, rather than how it is portrayed in heartbreaking movies and romantic novels. If you have encountered some of the issues identified here, or you disagree with the way I have explained them, and even if you 100% agree, it would be helpful for all the readers, including me, to comment and give your opinion on the matter.


I decided to write about yoga. Some of you might know that I have been seriously practicing yoga for 8 years, but the details of my turn to yoga are probably unknown. Since I am a doctor and a psychiatrist, I have known about the health benefits of yoga for a long time. For the interested, I would recommend a link from a doctor who systematically collects scientific studies that confirm this. (http://www.drmccall.com/117-health-conditions-helped-by-yoga.html).

My approach to yoga was gradual and began about twenty years ago when my older daughter was studying in New York. Within her collage, there was a yoga studio that she used regularly. She had experienced remarkable results in reducing stress and regulating mood. She talked about it with enthusiasm. Sometime later, my colleague from work discovered yoga as an antidote to the immense grief over the loss of his brother in a terrorist attack during on the World Trade Center in New York in 2001. The third early influence came from Andjela Cupic. I met Andjela at the celebration of the arrival of the millennium, organized by our mutual friend from Serbia in his home, in a romantic city, celebrated by the actress Julia Roberts with the film Mystic Pizza. She was a yoga teacher from whom I learned firsthand about yoga philosophy, spirituality, and yogic lifestyle.

The word yoga is of Sanskrit origin and means unification, uniting the body and mind with the higher self (soul, universal consciousness). I will not go into details here, but I will note that the principles of yoga are related to breathing exercises, poses, relaxation, meditation, positivity in thoughts and deeds, concentration, and visualization.

Equipped with this knowledge and encouraged by my future wife Tina Johnson, who was already practicing yoga, I also implemented it, at first very gradually and occasionally, and then more and more often. But the real turnaround happened in 2013 when the two of us participated in a yoga therapy program focused on mental disorders. This program took place in the Bahamas, in a Hindu temple, founded by yoga master Swami Sivananda. In this unusual environment, we were completely dedicated to learning, practicing, meditating, and lecturing, surrounded by people committed to the life of a yogi. Even though the program lasted only a week, I felt deeply transformed, which my body manifested (reacted) with fever, stuffy ears, eye inflammation, insomnia, and the inability to return to a regular life. I sent an email to a teacher from the Bahamas asking for advice regarding this physical condition. I wrote that I tried to help myself with breathing exercises, yoga poses and relaxation. She replied: “The connection between mind and body is deep, isn’t it? I have also discovered that if I do not process an important emotional state, my immunity drops, or I feel depressed. One of the assumptions of your illness may be that we spent 5 days doing practices that agitated old wounds and physically hit you where you are most vulnerable, so the body / mind needs more time to process these experiences. The time of illness and partial sensory deprivation gave legitimacy to stay at home and devotion to oneself. I believe that this opportunity arose because of your readiness to face the losses and traumas of early childhood. “

So it was. A profound inner transformation led to changes in my life that were fruitful and creative. The commitment to yoga was 100 times more intense than before training in the Bahamas. I practiced yoga mostly in a group and under the supervision of a teacher, which helped me avoid injuries and learn to align my body movements with proper breathing. I recently participated as a discussant with a psychiatry resident who gave a lecture on yoga therapy, an accredited yoga program that follows protocols in treating illness and improving health. Her lecture confirmed the further development of yoga in America as a legitimate way of healing that is studied in academic centers as a combination of the best that the West and the East can provide for our benefit.

I will end this review of yoga with a quote from Vanda Scaravelli’s book, Awakening of the Spine: “Yoga is a way of life, it changes you, and thus the way you treat other people and affects your environment. As the sun delicately opens the flowers, little by little, so yoga and breathing exercises open the body during slow and careful training. When the body is open, the heart is open. There is a transformation in the cells of the body. They work in a different way and new growth is possible. To re-establish contact with the body, you must be in contact with Nature, you must be in contact with the Cosmos. The balance is restored, and a huge amount of energy is released in accordance with these universal forces. ”

I hope that this short blog will encourage some of you to start practicing yoga and experience the transformation of body, mind, and spirit with all the benefits for you and your environment. If you are already yoga practitioner, write in the comments about your journey and experiences.



This lecture was inspired by three books written by three great scientists and clinicians. Rick Hanson and his book Buddha’s brain, Daniel Siegel with the book Pocket guide to interpersonal neurobiology and Louis Cozolino with the book The Neuroscience of psychotherapy.

I will present this lecture using questions and answers format.

 Question #1: How would you define what the brain is?

Answer: The brain is the body’s information processor that regulates the internal environment (body) and determines the response to the external environment (behavior)

 Question #2: Why do we say the brain is a complex system?

Answer: The brain has 1.1 trillion cells and 100 billion “gray matter “neurons. The brain is always on 24/7/365. Typical neuron makes more than 5000 connections with other neurons so there are approximately 500 trillion synapsis. The brain has potential for 10 to the millionth power brain states.

 Question #3: How does the brain develop?

Answer: The brain develops through synaptogenesis and apoptosis. We are born with many more neurons than we will ever need. Genes, environment, and experience affect the density of the neural networks.  As we develop and grow some networks are pruned.

 Question #4: What is the “experience “for the brain?

Answer: The “experience “involves activation of neural firing in response to a stimulus.

 Question #5: What is neural plasticity?

Answer: Neuroplasticity relates to changes in brain connections in response to experience. Structural change leads to change in brain function, mental experience, and bodily states. The sculpting of the brain by experience is also called memory. Memory is divided into explicit which relates to personal recollections and semantic memory, or implicit when it relates to bodily states, emotional residues, expectations, object relations, perspectives. Implicit memory also relates to behavior repertoire and inclinations, what it feels like to be “me”.

 Question #6: How are neural connections organized on a macro level?

Answer: Neural connections are organized into structural and functional brain networks.

Question #7:  Have you heard of the term Triune brain (or three brains in one)?

Answer: Triune brain theory was developed by Paul McLean, who was a senior research scientist and the National Institute of Mental Health. He claimed that our brain is designed by the evolution into three structurally and functionally distinct parts. The first one is reptilian, the second mammalian, and the third human.

 Question #8:  Our three brains do not necessarily work well together. Do you know why?

Answer: Each of these brains process information in a distinctive manner and has a separate agenda.

 Question #9:  What is the main agenda of the reptilian brain?

Answer: Reptilian brain is a so-called selfish brain because it helps us to survive individually. It is responsible for arousal, homeostasis, safety, and reproduction. The primary behaviors are: freeze, fight, flight, eat, and mate.

 Question #10:  What is the agenda of the mammalian brain?

Answer: Mammalian brain is social brain, and it helps community to survive. This brain is involved with learning, memory, and emotion.

 Question #11: What is the main agenda of the human brain?

Answer: Human brain is a self-aware brain, and it helps communities thrive. It is responsible for conscious thought, planning, problem-solving, refined analysis of information, inhibition of lower parts of the brain.

In summary Triune brain theory indicates that the reptilian brain is made of brainstem and cerebellum. It is an instinctive part of the brain that is on autopilot in its function. The mammalian brain occupies limbic system. It is a reactive part of the brain and makes fast decisions with survival value. The human brain is neocortex.  It is a reflective part of the brain because it reasons and rationalizes.

 Question #12: Do you know how are three brains influencing goal-oriented behavior?

Answer: The reptilian brain avoids hazards (“sticks “, threats, penalties, and pain). The mammalian brain approaches rewards (“carrots”, opportunities, pleasure). The human brain attaches to others and seeks proximity and form bonds.

 Question #13:  What is considered to be “normal “state of our brains?

Answer: Homebase of the human brain is the state when we are not threatened, ill, in pain, hungry, upset, or chemically disturbed. At that time, our brain is calm, and we experience strength, safety, and peace.  We are contented and experience gratefulness, fulfillment, and satisfaction. We are caring and experience love, closeness, bonding, friendship and belonging.

 Question #14:  What happens under stress?

The urgency of survival switches the brain into the reactive mode, powerful in the rapidity, intensity, and inflexibility of its activations. Fear (avoid system) gets activated and our perception is concerned about harms being present or lurking. Our primary action is flight, fight or freeze.  We consciously experience fear, anger, or weakness.

 Question #15:  Which brain structure is involved?

The amygdala is our inner eye (homeland security) that gets activated as an alarm system for threat appraisal and triggers the stress response system in our body which involves HPA axis with the release of adrenaline and cortisol.  In addition, the sympathetic branch of autonomic nervous system prepares the body for flight or fight.  Evolutionary bias is toward activation of the avoid system. Negative stimuli command more attention. If the stress is prolonged it has potential to cause dysfunction of the avoid system that leads to disorders such as:

  • Anxiety disorders characterized by excessive fear, anxiety, or avoidance.
  • Posttraumatic stress disorder related to life-threatening trauma, reexperiencing and excessive arousal.
  • Impulsive violence with excessive fight behavior, and
  • Depression with learned helplessness.

 Question #16:  Is there activation of the approach system when under stress?

Answer: When we cannot attain important goals that could lead to the activation of the approach system. We perceive scarcity, loss, unreliability, and do not expect any rewards. Our action is to grasp and acquire and consciously we experience greed, longing, frustration, disappointment.

 Question #17:  Which brain systems are involved?

Answer: Reward circuit with its mesolimbic dopamine pathway that leads to focused attention, intense motivation, goal directedness, craving, and persistence. Dopamine is responsible for life’s pleasures through movement, food, sex, and achievement. These are natural rewards, but if we use drugs of abuse the same mesolimbic dopamine circuit is activated, but much stronger to the point of dopamine flooding the whole brain. As a result dysfunction of the approach system could lead to addiction, compulsion, and hoarding. Apart from dopamine there is a significant release of other neurotransmitters such as opioid peptides, serotonin, and GABA.

 Question #18:  Is their activation of any other systems under stress?

Answer: When we feel isolated, disconnected, unseen, unappreciated and unloved attachment system gets activated and we perceive separation and neglect.  The main action behavior is clinging, seeking approval, and reproaching. Our conscious experience is loneliness, heartbreak, envy, jealousy, and shame.

 Question #19:  How is this knowledge relevant for psychotherapy?

Answer: Psychotherapy relies upon the power of relationships to trigger the neuroplastic process necessary for learning and growth. Identifying inherent problems in how the brain processes information and developing methods to circumvent or correct them is a solid foundation upon which to base a therapeutic alliance. An unmet need for safety, which is indicated by anxiety, anger, or helplessness is best addressed by activation of the parasympathetic nervous system and calming of the sympathetic nervous system through mindfulness and relaxation. An unmet need for satisfaction is indicated by frustration, disappointment, loss, failure, or the dreariness of life and could be addressed through activating and installing rewarding experiences of goal attainment, accomplishment, gladness, gratitude, pleasure, and success through behavioral activation. The role of experience both positive and negative and choices such as lifestyle, brain hygiene activities in shaping and reshaping of the brain provides a neuroscientific explanation for both psychopathology and treatment recommendation.


The word psychopathology has a Greek origin: ‘psyche’ means “soul”, ‘pathos’ is defined as “suffering”, and ‘logos’ is “the study of”.  These origins of the word are incorporated in many definitions of psychopathology.  For example: “Psychopathology is the systematic study of abnormalities in mental states and is one of the core sciences in clinical psychiatry”.

Descriptive psychopathology is one method for describing the subjective experience and behavior of patients and is the basis for our current clinical description of mental disorders.  In addition to this method, psychopathology may consider the theoretical constructs (for example cognitive, behavioral, psychodynamic, neurobiological, evolutionary, etc.) as a presumed explanation for abnormal mental phenomena. This method is called explanatory psychopathology.

In descriptive psychopathology, empathy is used as a clinical tool to understand and describe another person’s internal subjective state using precise and knowledgeable questioning.  Apart from empathy, additional skills needed by descriptive psychopathologist are accurate observation of behavior and attentive and focused listening. The goal is to help clinician in identification of symptoms, signs and syndromes for arriving to accurate diagnosis of mental disorder.

Ideally, a diagnosis of mental disorder should be based on knowledge of etiology or pathophysiology because this increases the likelihood of improving treatment and prevention efforts.  Unfortunately, for most mental disorders there are no biological markers that allow identifying or separating them, hence most of them are still defined and classified based on their clinical syndromes.

 Definition of mental disorder according to DSM-5:

“A syndrome of clinically significant disturbance in cognition, emotional regulation or behavior which reflects a dysfunction in the psychological, biological or developmental processes underlying mental functioning and leading to significant distress (mental pain) and/or impairment in social, occupational and other activities.”

The main descriptors of mental disorder definition are:

  1. A syndrome comprises a characteristic set of signs and symptoms that occur together, run a course together, and respond to treatment as a group. It is important to remember that a syndrome can result from different disease processes.
  2. Cognition is defined as a set of all mental abilities and processes related to knowledge: attention, judgment and evaluation, reasoning, problem solving and decision making, comprehension and production of language, etc.
  3. Emotional regulation is the ability to respond to the ongoing demands of experience with the range of emotions in a manner that is socially tolerable and sufficiently flexible to permit spontaneous reactions as well as the ability to delay spontaneous reactions as needed.
  4. Behavior is physical action and observable emotion associated with individual.
  5. Sensation, perception, learning, memory, thinking, motivation and emotion are considered as key psychological processes.
  6. Biological processes are the processes vital for a living organism to live.
  7. Developmental process pertains to the normal and atypical patterns of human development across the lifespan.

It is emphasized that:

  1. An expectable or culturally approved response to a common stressor or loss, such as the death of a loved one, is not a mental disorder.
  2. Socially deviant behavior (e.g., political, religious, or sexual) and conflicts that are primarily between the individual and society are not mental disorders unless the deviance or conflict results from a dysfunction in the individual.

This definition still does not provide operational guidance on specifying a threshold for diagnosis (when a dysfunction has produced a change from normal variation to pathology), hence reliance on “significant distress or impairment”.

Arriving to correct diagnosis of mental disorder is not an easy and straightforward process, as proponents of diagnostic checklists and time constraints of current clinical practice would like to impart on us.  It is important to underscore that diagnosis should be made in the context of an overall case formulation that includes:

–A biopsychosocial assessment

–A thorough history

–Multiple forms of assessment

–Periodic reassessment to check accuracy

According to Allen Frances, the biggest single cause of inaccurate diagnosis is jumping too quickly to conclusion.  He recommends method named “stepped diagnosis” to enhance the accuracy in the diagnosing especially for patients who present with milder or ambiguous symptoms or with a short a history of symptoms.

Here are recommended steps of this approach:


Step 1: Engage in Watchful Waiting

The first visit may not be the best sample of reality for the patient.  He or she may look quite different on repeat visits.  Except in the clear-cut cases, it is recommended to underdiagnose (or tentatively diagnose) during early visits.


Step 2: Make Sure the Symptoms Are Severe and Persistent Enough to Count

Only count psychiatric symptoms if they are grouped together in a recognized pattern, persist over time, and cause clinically significant distress or impairment.


Step 3: Educate, Normalize, Reassure

This step can help in depathologizing symptoms that might be normal, expectable, and transient reactions to life’s stresses and disappointments.  On the other hand, it is also important to avoid minimizing the significance of real problems.


Step 4: Rule Out the Role of Substances

Always consider whether substance use or a medication side effect is the possible cause of the patient’s presentation.  Careful non-judgmental questioning and laboratory testing may be helpful.  It is known that many medications cause psychiatric side effects— particularly in the elderly, patients on many different medicines and in persons who are taking one or more medications in high doses.


Step 5: Rule Out the Role of Medical Illness

Especially in the elderly, always rule out neurological or other medical illness as a possible cause of the psychiatric problems.


Step 6: Rule Out Bipolar and Depressive Disorders

Bipolar and Depressive Disorders are common, heterogeneous, and can include a wide variety of symptoms seen in many other conditions, therefore it is recommended to first consider Bipolar and Depressive Disorders before making another diagnosis.


Classification of Mental Disorders has multiple objectives:

  1. Communication: among clinicians, between science and practice
  2. Clinical: facilitate identification of treatment, and prevention of mental disorders
  3. Research: test treatment efficacy and understand etiology
  4. Education: teach psychopathology
  5. Information Management: measure and pay for care

State of classification of mental disorders is still not based on etiology or pathophysiology. Mental disorders are unique in contemporary medicine because most of them are still defined and classified based on their clinical syndromes; therefore, study of descriptive psychopathology is crucial both clinically and for the purpose of classification.

Good classification is based on:

  1. Reliability– degree of precision, i.e. agreement among clinicians (which is improved by operational diagnostic criteria and use of structured interviews)
  2. Validity-accuracy of diagnosis
  3. Utility (in three domains: use, decision making process and clinical outcome)
  4. Ease of use
  5. Applicability across settings and cultures
  6. How well it meets needs of various users (clinicians, researchers and users of mental health services)

The two most Common Classification Systems are:

  1. International Classification of Diseases and Health Related Problems (In 1948 the World Health Organization added a section on classification of mental disorders). Currently the 11th revision was released in 2018.
  2. In 1952 the American Psychiatric Association developed and published its own Diagnostic and Statistical Manual. The newest revision DSM-5 was published in 2013.

The DSM is used in the United States and to various degrees around the world.  With successive editions over the past 60 years, DSM has become a standard reference for clinical practice in the mental health field. The criteria and corresponding text serve as a textbook for psychiatry residents early in their profession who need a structured way to understand and diagnose mental disorders, especially since the publication of DSM-III in 1980 which introduced multiple innovations such as:

  1. Provided a definition of the term “mental disorder”
  2. Presented diagnostic criteria for each disorder
  3. Introduced the multiaxial diagnostic format
  4. Redefined a number of major disorders
  5. Added new diagnostic categories (e.g., personality disorders)
  6. Presented a systematic description of each disorder
  7. Published reliability data from field trials
  8. Utilized a descriptive, atheoretical approach


Current revision (DSM-5) also has multiple modifications:

  1. Incorporation of a developmental approach to psychiatric disorders.
  2. Recognition of the influence of culture and gender on how psychiatric illness presents in individual patients.
  3. A move toward the use of dimensional measures to rate severity and disaggregate symptoms that tend to occur across multiple disorders.
  4. Harmonization of the text with ICD.
  5. Integration of genetic and neurobiological findings by grouping clusters of disorders that share genetic or neurobiological substrates.
  6. The multiaxial system is eliminated.
  7. Reorganization of chapters.


Organization of DSM-5 Manual:

  • Section I: DSM-5 Basics


–Use of Manual

–Cautionary Statement for Forensic Use of DSM-5

  • Section II: Diagnostic Criteria and Codes

–Present the categorical diagnoses according to a revised 20-chapter organization that eliminates the multiaxial system

  • Section III: Emerging Measures and Models

–Assessment Measures

–Cultural Formulation

–Alternative DSM-5 Model for Personality Disorders

–Conditions for Further Study

  • Appendix

–Highlights of Changes From DSM-IV to DSM-5

–Glossary of Technical Terms

–Glossary of Cultural Concepts of Distress

–DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM)


The organization of this manual will follow lecture plan designed for the first-year psychiatry residents’ course.  Selected common mental disorders according to DSM-5 Section II categorical diagnoses will be presented, primarily from the descriptive psychopathology perspective.  In majority of mental disorders core symptoms will be identified and discussed in greater details.  Clinical tools such as structured questionnaire or rating scales will be included for assisting in correct diagnosing.




Major depressive disorder represents the classic condition in this group of disorders. It is characterized by discrete episodes of at least 2 weeks’ duration involving clear-cut changes in affect, cognition, and neurovegetative functions and inter-episode remissions. A diagnosis based on a single episode is possible, although the disorder is a recurrent in most of cases.



Major depressive disorder is episodic and frequently recurrent mental disorder manifested by the profound & sustained sadness &/or absence of joy and rewards accompanied with the clinically significant change in psychological and biological functions related to zest for life, motivation, cognitions, vitality, appetite, sleep & other important areas leading to suffering and/or impairment.


Diagnostic prototype

The person feels deeply down in the dumps and apathetic. Lacking energy or resolve, she may lie listless and motionless throughout the day. Loss of the ability to think clearly, to concentrate, and to make even the simplest decisions is prevalent. Life seems cardboard and tasteless, drained of pleasure, interest, and excitement. She eats and sleeps too little or too much. Thoughts are slow, heavy, and black, dominated by profound hopelessness, worthlessness, and the weight of unremitting guilt.


Video link: https://www.youtube.com/watch?v=_qTSjTRuzvk (video illustration)


Core Symptoms

Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation).
Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad, empty, hopeless) or observation made by others (e.g., appears tearful). (Note: In children and adolescents, can be irritable mood.)


Depressed mood may be experienced as feelings of sadness and gloom, despondency, despair or hopelessness. Often, the actual experience is indescribable but recognized as different in character from normal sadness akin to physical pain.  William James characterized it as a positive and active anguish, a sort of psychic neuralgia unknown to normal life.  Many argue that word depression is inadequate and propose to designate word melancholia for this pathological intensification of sadness.

Anhedonia refers to a loss of the capacity to experience joy and pleasure. It is a subset of the diminution of the intensity of emotions. In anhedonia, there is a total inability to enjoy anything in life or even get the accustomed satisfaction from everyday events or objects.  This deficit in the capacity to experience pleasure is now thought to include impairments in the processes of reward valuation, decision making, anticipation and motivation.


Additional Symptoms Necessary for the Diagnosis  

  • Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a month) or decrease or increase in appetite nearly every day. (Note: In children, consider failure to make expected weight gain.)
  • Insomnia or hypersomnia nearly every day.
  • Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down).
  • Fatigue or loss of energy nearly every day.
  • Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick).
  • Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others).
  • Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.


Conditions that need to be ruled out

  • The occurrence of the major depressive episode is not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or other specified and unspecified schizophrenia spectrum and other psychotic disorders.
  • There has never been a manic episode or a hypomanic episode.
  • The episode is not attributable to the physiological effects of a substance or another medical condition.


Additional Validated Rating Scales

Patient Health Questionairre-9 (PHQ-9)

Hamilton Depression Rating Scale (HDRS)

Beck Depression Inventory (BDI)

Major Depression Inventory (MDI)

Center for Epidemiologic Studies Depression Scale (CES-D)

Zung Self-Rating Depression Scale (SDS)

Geriatric Depression Scale (GDS)

Cornell Scale for Depression in Dementia (CSDD)


Heterogeneity of Major Depressive Disorder

  1. Course Specifiers: Single episode, Recurrent episode
  2. Severity Specifiers: Mild, moderate, severe, with psychotic features, in partial remission, in full remission.
  3. Additional Specifiers: With anxious distress; With mixed features; With melancholic features; With atypical features; With mood-congruent psychotic features; With mood-incongruent psychotic features; With catatonia; With peripartum onset; With seasonal pattern (recurrent episode only)


Epidemiological factors

Incidence: 6.6% in USA

Prevalence: 16.2% lifetime

Predominant age: low risk before early teens, but highest prevalence in teens and young adults

Predominant gender: females > males (2:1)

Course of illness: recurrent versus single episode

The illness begins with a single episode. In most of cases, the episodes are destined to become recurrent (estimates of recurrence range from ~ 50% within the first year to up to 85% during a lifetime). The length of a depressive episode is in the range of 5–6 months. 40% of individuals recover within 3 months of onset, and 80% recover within 1 year.  Approximately 20% of episodes becoming chronic (i.e., lasting beyond 2 years).  Lower recovery rates are associated with: longer duration, psychotic features, prominent anxiety, personality disorders, and symptom severity.


Suicide: 10-15%

Poor performance at work or school

Relational/marital problems

Self-medication with alcohol or drugs



Prognosis is depended upon

Response to treatment (remission is the goal)

Number of previous episodes

Severity of episodes

Acceptance of illness and required treatment and life modification.

The prognosis is positively influenced by a long-term strategy that maximizes the protective factors and minimizes the vulnerabilities.



Genetic and environmental factors create epigenetic change that leads to vulnerability of specific brain circuits.  At a later time period, precipitating risk factors can trigger onset of the episode.  The most important predisposing factors are:

Family history of MDD/ Mood disorders

Severe traumatic events

Cumulative adverse events or changes

Separation or loss of a parent before age 17

Lack of parental warmth during childhood

Severe, chronic, or disabling medical or mental disorders

Lack of social support

Dysfunctional beliefs about personal adequacy

Social skill deficits

Maladaptive coping

Unresolved developmental tasks


Frequent Comorbid Mental Disorders

Panic, PTSD and other Anxiety Disorders

Substance Use Disorders

Schizophrenia & other Psychotic disorders

Eating Disorders


Differential Diagnosis

  • Psychiatric: Depressed phase of bipolar disorder, adjustment disorder, dysthymic disorder, bereavement
  • Neurologic or degenerative CNS diseases, dementias
  • Medical comorbidity: Adrenal disease, thyroid disorders, diabetes, metabolic abnormalities (hypercalcemia), liver/renal failure, malignancy, chronic fatigue syndrome, fibromyalgia, lupus
  • Nutritional: Pernicious anemia, pellagra
  • Medications/substances: Abuse, side effects, overdose, intoxication, dependence, withdrawal


Tests and Other Evaluations

Laboratory Tests (Metabolic panel, CBC, UDS, TFT)

EKG, EEG (for selected patients)

(Neuro) psychological Testing (for selected patients)

CT / MRI (for selected patients)

Collateral information

Medical Records


General plan for assessment and treatment

  • Assessment of Symptoms, signs and Dysfunctions (Impairments)
  • Diagnosing Major Depressive Disorder
  • Evaluation of Suicidal Risk
  • Identification of Risk Factors for MDD
  • Diagnosing Comorbid psychiatric and medical conditions
  • Tests and other evaluations
  • Establishing goals of treatment
  • Choosing the best treatment intervention
  • Monitoring response to treatment


Treatment Goals

  • Reduction / Elimination of Symptoms of MDD
  • Improvement / Restoration of Functioning
  • Treatment of Comorbid Disorders
  • Reduction / Elimination of Risk Factors
  • Enhancement / Establishment of Protective Factors
  • Relapse / Recurrence Prevention


Biopsychosocial Treatment Model

SOCIAL-Relationship Based Treatments

Watchful waiting (prospective monitoring for four to eight weeks)

Interpersonal psychotherapy

Problem solving psychotherapy

Short-term psychodynamic psychotherapy

PSYCHOLOGICAL-Mind Based Treatments

Bibliotherapy (Psychoeducation, Guided Self-Help)

Pleasurable Activities –Behavioral activation

Cognitive Behavioral Therapy

Acceptance and Commitment Therapy

BIOLOGICAL-Brain/Body Based Treatments

Nutrition (anti-inflammatory diet, vitamin B12, Folate, D3, omega-3 fatty acids, SAMe)


Elimination of alcohol, tobacco, and others toxic substances

Implementation of sleep hygiene activities

Herbal products (St. John’s Wort)

Pharmacotherapy (SSRI, SNRI, DRI, TCA, MAOI, others)

Neurostimulation therapies (ECT, VNR, TMS, BLT)


Duration of treatment

All patients need to remain in effective treatment for at least 6 to 9 months
(Acute and Continuation Phase of Treatment) due to high risk of relapse.  Selected patients might require long term (maintenance) treatment.  Frequently, principles of chronic disease treatment model need to be applied including: healthy life style, education of patients and families and aggressive treatment of early signs of relapse/recurrence. If the patient doesn’t respond to usual treatment strategies, reevaluation of diagnosis, adherence to treatment plan, adequacy of previous trials, and treatment of comorbid conditions are recommended first steps before resorting to evidence based strategies designed to treat treatment refractory major depressive disorder.



Bipolar I disorder can cause dramatic mood swings (episode). Manic episode is a medical emergency. Manic patients have terrible judgment and get themselves into all sorts of interpersonal, financial, legal, and sexual trouble. The combination of grandiosity, impulsivity, delusions, and heightened energy can lead to fatal car accidents, “flying” off a roof, quick intimacy with dangerous strangers, or lethal drug overdose. Admission to a hospital is often necessary for clearer diagnosis, for beginning the treatment, and (most important) for safety.


Bipolar I disorder is mental disorder characterized by the periods of one or more elevated mood episodes called manic episodes and periods of depressive mood episodes.  The manic episode is the hallmark of bipolar I disorder.

Diagnostic prototype

The world is the patient’s oyster. Everything feels so smooth, so easy, so great, and so vivid. Colors are brighter, food is more delicious, sex is more intense, jokes are funnier. The patient is flying high with expansive ideas, booming confidence and dauntless energy. His mind is racing, his speech is pressured and punning, and his body is in perpetual motion. There is nothing he can’t do, and the usual limitations in life no longer apply. There seems no need for sleep or eating, or for the routines of the everyday. Impulses are unleashed— wild shopping sprees, reckless investing, expansive new projects, intense new relationships, fast cars, adventurous drugs, restless travel. Eventually, the euphoria morphs from high spirits into impatient irritability (especially when other people refuse to join the party). Increased energy merges into restless agitation, then dissolves into utter exhaustion; expansive thoughts can become psychotic delusions. At the end of every Manic Episode, there is an inevitable crash with a bruising collapse into depression.

Video link: https://www.youtube.com/watch?v=o4Gp2iMELzA (video illustration)


 Core Symptoms (Manic Episode) 

A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 1 week and present most of the day, nearly every day (or any duration if hospitalization is necessary).

Euphoric or Irritable Mood & Increased Energy

Is a state of abnormally elevated arousal, affect, and energy level, a state of heightened activation with enhanced affective expression together with lability of affect. The heightened mood can be either euphoric or irritable.  Usually as the mania intensifies, irritability can be more pronounced and result in violence or anxiety.


Additional Symptoms Necessary for the Diagnosis  

  • Inflated self-esteem or grandiosity.
  • Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
  • More talkative than usual or pressure to keep talking.
  • Flight of ideas or subjective experience that thoughts are racing.
  • Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli), as reported or observed.
  • Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation (i.e., purposeless non-goal-directed activity).
  • Excessive involvement in activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments).


Conditions that need to be ruled out

  • The episode is not attributable to the physiological effects of a substance or another medical condition.


 Additional Validated Rating Scales

Mood Disorder Questionnaire (MDQ)

Young Mania Rating Scale (YMRS)

Altman Self-Rating Mania Scale (ASRM)

Bech-Rafaelsen Mania Rating Scale (MAS)



  1. Course Specifiers: Current or most recent episode (manic, hypomanic, depressed)
  2. Severity Specifiers: Mild, moderate, severe, with psychotic features, in partial remission, in full remission.
  3. Additional Specifiers: With anxious distress; With mixed features; With melancholic features; With atypical features; With mood-congruent psychotic features; With mood-incongruent psychotic features; With catatonia; With peripartum onset; With seasonal pattern

Epidemiological factors

Prevalence: 0.6 to 1 % (twelve months)

Predominant age: mean age at onset is 18 years.

Predominant gender: none

Course of illness: recurrent (in more than 90%)

Bipolar I disorder has an early onset and lifelong high risk of recurrence.  Early course is characterized by equal number of manic and depressive episodes. Later course is dominated by high rates of depressive episodes.  Low rates of fully sustained recovery and high rates of incomplete remission leads to considerable chronicity and disability. The suicide risk is 15–20-fold higher than in the general population. Bipolar I disorder is complex and can present with a wide constellation of symptoms. These can be separated into 4 major domains: (1) manic mood and behavior; (2) dysphoric or negative mood and behavior; (3) psychotic symptoms; and (4) cognitive symptoms. Manic mood and behavior is characterized by euphoria, grandiosity, pressured speech, impulsivity, excessive libido, recklessness, social intrusiveness, and diminished need for sleep. Dysphoric or negative mood and behavior is characterized by depression, anxiety, irritability, hostility, and violence or suicide. Psychotic symptoms include delusions and hallucinations. Cognitive symptoms include racing thoughts, distractibility, disorganization, and inattentiveness.



It is estimated that an adult who has developed bipolar disorder loses 12 years of a healthy life, 14 years of working life and that their life expectancy is reduced by
9 years.  Employment problems and divorce/separation were twice as common in patients with bipolar I disorder than in general population.  25–50% attempt suicide and 15% die by suicide.


Prognosis is depended upon

Age of onset

Number of prior episodes

Full and sustained recovery

Adherence to treatment plan



Genetic and epigenetic factors influence multiple signaling cell systems leading to vulnerability and impaired neural plasticity.  Loss of GABAergic interneurons and dysfunction of retino-hypothalamic pathway lead to dysregulation of dopaminergic mesolimbic pathway and circadian rhythm abnormality.  The main risk factors are family history (1st-degree relatives are 7 × more likely to develop bipolar I disorder than the general population), major life stressors (especially loss of parent or spouse), substance abuse and sleep disruptors.


Frequent comorbid conditions

Substance abuse (60%),


Anxiety disorders, and

Eating disorders


Differential Diagnosis

Other psychiatric considerations: Unipolar depression ± psychotic features, schizophrenia, schizoaffective disorder, personality disorders (particularly antisocial, borderline, histrionic, and narcissistic).

Medical considerations: Epilepsy (e.g., temporal lobe), brain tumor, infection (e.g., AIDS, syphilis), stroke, endocrine (e.g., thyroid disease), multiple sclerosis.

Substance-induced considerations: Stimulants, steroids, antidepressants, others.

In children, consider ADHD and ODD.


Test and other evaluations


Drug/Alcohol screen with each presentation

Dementia workup if new onset in seniors

Consider brain imaging (CT, MRI) with initial onset of mania to rule out organic cause (e.g., tumor, infection, or stroke), especially with onset in elderly and if psychosis is present.


General plan for assessment and treatment

  • Assessment of Symptoms, signs and Dysfunctions (Impairments)
  • Diagnosing Bipolar I Disorder (based on current or past history of manic episode, early onset and frequent mood episodes, common family history, uneven life course, and non-response or erratic response to antidepressants).
  • Evaluation of Suicidal Risk
  • Diagnosing Comorbid psychiatric and medical conditions
  • Tests and other evaluations
  • Establishing goals of treatment
  • Choosing the best treatment intervention
  • Monitoring response to treatment


Treatment goals

The main goal of treatment is to ensure mood stabilization in patients with bipolar disorder.  This can be achieved by controlling the acute symptoms of bipolar disorder and in the long term preventing relapse.  It is also important to ensure that patients adhere to treatment and that any comorbid conditions are managed effectively.


Biopsychosocial Treatment Model

BIOLOGICAL-Brain/Body Based

Pharmacotherapy is the first line treatment both for acute phase, relapse prevention and maintenance.  Antidepressants should be avoided. Mood stabilizers are treatment of choice for long term treatment. Primary mood stabilizers are lithium, valproate, carbamazepine and lamotrigine. Administer medications once daily whenever possible. Noncompliance stems from lack of insight, side effects and inconvenience.

Neurostimulation therapies (ECT, BLT, TMS for acute phase)

Nutrition (anti-inflammatory diet, vitamin B12, Folate, D3, omega-3 fatty acids)


Elimination of substances of abuse (alcohol, tobacco, caffeine, others)

Sleep hygiene (extremely important for relapse and recurrence prevention)

SOCIAL-Relationship Based

Interpersonal and Social Rhythm Therapy (IPSRT)

Family therapy


Bibliotherapy (Psychoeducation, Guided Self-Help)

Pleasurable Activities –Behavioral activation

Cognitive Behavioral Therapy


Duration of treatment

Long-term maintenance with mood stabilizers (primarily lithium or valproate) is recommended due to almost universal risk for recurrent manic or depressive episodes.  Ongoing psychoeducation of patient and family ensures the collaborative approach to treatment, recognition of early signs of relapse and modification of life style necessary for mood stabilization. Avoidance of mood dysregulators, regular sleep and rest, practicing stress-reduction methods, establishment of daily routines and even change of career should be considered.



The concept of schizophrenia has frequently changed, both in name (Dementia Praecox) and in core symptomatology.   The current (DSM-5) classification of schizophrenia is characterized by the marked heterogeneity, multiple dimensions of psychopathology, prominent mood symptoms, emphasis on psychosis (positive symptoms) and de- emphasis of catatonia.  Persistent psychotic manifestations is accompanied by variable cognitive dysfunction and profound psychosocial impairment.



Schizophrenia is severe chronic mental disorder that generally affects mental functions and behavior. It is associated with a variable course, and outcomes range from complete recovery to severe disability. The most prominent characteristics of schizophrenia are hallucinations, delusions, and disorganization, which may lead to dangerous or bizarre behaviors. More insidious are so-called negative symptoms, such as social withdrawal and diminished emotional engagement, and cognitive impairments that can impair social and occupational functioning.


Diagnostic prototype

Unlike major depressive disorder and bipolar I disorder where it was relatively easy to describe diagnostic prototype, that is not the case with schizophrenia due to variability of presentation and overlaps with many other disorders.

Video link: https://www.youtube.com/watch?v=iGH7hGkkMrU (video illustration)


 Core symptoms

Disorganized thinking (formal thought disorder), fragmentation of the logical, progressive, and goal-directed speech. The individual may switch from one topic to another (derailment or loose associations). Answers to questions may be obliquely related or completely unrelated (tangentiality). Rarely, speech may be so severely disorganized that it is nearly incomprehensible and resembles receptive aphasia in its linguistic disorganization (incoherence or “word salad”).
Negative symptoms are reduction in normal function. Two negative symptoms are particularly prominent in schizophrenia: diminished emotional expression and avolition. Diminished emotional expression includes reductions in the expression of emotions in the face, eye contact, intonation of speech (prosody), and movements of the hand, head, and face that normally give an emotional emphasis to speech. Avolition is a decrease in motivated self-initiated purposeful activities.
Grossly disorganized or abnormal motor behavior may manifest itself in a variety of ways, ranging from childlike “silliness” to unpredictable agitation. Problems may be noted in any form of goal-directed behavior, leading to difficulties in performing activities of daily living.
Hallucinations are perception-like experiences that occur without an external stimulus. They are vivid and clear, with the full force and impact of normal perceptions, and not under voluntary control. They may occur in any sensory modality, but auditory hallucinations are the most common in schizophrenia (voices conversing among themselves or commenting on the patient).
Delusions are fixed beliefs that are not amenable to change considering conflicting evidence. Their content may include a variety of themes (the most common are persecutory and referential).


Additional Symptoms Supporting the Diagnosis  

Inappropriate affect (e.g., laughing in the absence of an appropriate stimulus);

Dysphoric mood that can take the form of depression, anxiety, or anger;

Depersonalization, derealization, and somatic concerns.

Cognitive deficits

Lack of “insight” includes unawareness of symptoms of schizophrenia (i.e. anosognosia).

Hostility and aggression


Conditions that need to be ruled out

Schizoaffective disorder and depressive or bipolar disorder with psychotic features

Symptoms are not attributable to the physiological effects of a substance or another medical condition.


Additional Validated Rating scales

Brief Psychiatric Rating Scale

Positive and Negative Symptoms Scale (PANSS)



  1. Course Specifiers: Single episode, Multiple episodes, Continuous
  2. Severity Specifiers: Mild, moderate, severe, in partial remission, in full remission.
  3. Additional Specifiers: With catatonia


Epidemiological factors

Incidence: 15.2 new cases per 100,000

Prevalence: 1% (life-time)

Age of onset: early- to mid-20s for males and in the late-20s for females


  • Premorbid Phase

Stable social and cognitive deficits

Frequent subtle neurological abnormalities

  • Prodromal Phase

Lack of stability

Worsening positive and negative symptoms

Deteriorating course of psychosocial impairment

  • Acute Phase

Onset of frank psychosis with recurrent exacerbations and remissions

Ongoing functional decline

  • Chronic (Residual) Phase

Deficits and symptoms reach a level of stability

Course of schizophrenia is characterized by exacerbations and remissions, with varying recovery between the episodes.  Exacerbations are triggered by stress, nonadherence to treatment, substance abuse. Positive symptoms tend to become less severe and negative symptoms more prominent. Cognitive symptoms are generally stable. Mood symptoms vary in severity in partial association with psychotic symptoms.



Individuals with schizophrenia exhibit increased mortality, high risk of suicide, increased rates of a range of comorbid medical and psychiatric illnesses, reduced likelihood of employment, and impairments in quality of life. Mortality rates double the general population. Lifespan is reduced by approximately 15–20 years.  Among males, suicide is the leading cause of death.  Among females, cardiovascular disease is number one killer.


Prognosis is depended upon

Good prognostic signs are later onset, presence of precipitating factor, good premorbid functioning, presence of mood symptoms, family history of mood disorder rather than psychotic disorder, being married, good support system, absence of negative symptoms, female gender.  There are a sizable number of individuals with highly successful careers who have recovered from schizophrenia. One of the most prominent advocate for “spreading the word” about high functioning patients is USC Law Professor Elyn Saks.  She can be seen and listened at: https://www.youtube.com/watch?v=h7WM6XFkxWw.

Poor prognostic signs are: insidious onset at young age with poor premorbid functioning, family history of schizophrenia, negative symptoms, neurological signs, history of prenatal trauma, poor response to treatment with multiple hospitalizations.



Over 150 genes appear to contribute to schizophrenia risk. Implicated are genes that regulate neuronal migration, synaptogenesis, cellular adhesion, and neurite outgrowth, synaptic DA availability, glutamate and DA neurotransmission and nicotinic activity. Patients with schizophrenia also have increased rates of genome-wide DNA microduplications and epigenetic changes, including disruptions in DNA methylation patterns in various brain regions. Prominent perinatal factors are: advanced paternal age (40 years or older), toxoplasma gondii antibodies, maternal infections, prenatal nutritional deprivation, complications during childbirth and winter or spring birth. Socioenvironmental factors are: international migrants, urban populations of ethnic minorities.  Perinatal and genetic factors can cause disruption in the developing brain that can lead to schizophrenia as one of potential clinical outcomes. In this manner, schizophrenia is considered neurodevelopmental disorder that leads to micro and macro structural, neurochemical, immune and other pathophysiological changes.


Frequent comorbid conditions

Over half of individuals with schizophrenia have tobacco use disorder.

Rates of obsessive-compulsive disorder and panic disorder are elevated in individuals with schizophrenia.

Schizotypal or paranoid personality disorder may sometimes precede the onset of schizophrenia.


Differential Diagnosis

Major depressive or bipolar disorder with psychotic or catatonic features

Schizoaffective disorder

Schizophreniform disorder and brief psychotic disorder

Delusional disorder

Schizotypal personality disorder

Obsessive-compulsive disorder and body dysmorphic disorder

Posttraumatic stress disorder

Autism spectrum disorder or communication disorders

Alcohol Related Psychosis

Cocaine-Related Psychiatric Disorders

Mental Disorders Secondary to General Medical Conditions


Test and other evaluations

All patients with new-onset psychosis would benefit from:

Complete blood count

Comprehensive metabolic panel

Thyroid-stimulating hormone and reflex to free thyroxine


Urine screen for drugs of abuse

Urine pregnancy test for all women of childbearing age

Vitamin B12 levels

Red blood cell (RBC) folate

Fasting lipid panel

Fasting glucose levels


Treponemal antibody enzyme immunoassay

Lyme titer

Erythrocyte sedimentation rate

Antinuclear antibody


HIV serology

Chest X ray (to aid in detection of sarcoidosis or other pulmonary disease)

Magnetic resonance imaging (MRI) of brain without contrast


General plan for assessment and treatment

  • Assessment of symptoms, signs and dysfunctions (impairments)
  • Diagnosing Schizophrenia (the cornerstone of diagnosis is the clinical examination of the patient, with review of symptoms cross-sectionally and historically. Positive diagnosis is based on DSM-5 criteria including exclusion other disorders /medical, substance-induced, psychiatric/ that can mimic schizophrenia. No disease specific biomarkers (genetic, imaging, neurophysiological, laboratory) are available at the present time for positive diagnosis).
  • Evaluation of Suicidal Risk
  • Diagnosing Comorbid psychiatric and medical conditions
  • Tests and other evaluations
  • Establishing goals of treatment
  • Choosing the best treatment intervention
  • Monitoring response to treatment

Treatment goals

  • Reduce or eliminate symptoms
  • Prevent relapse
  • Enhance adaptive skills
  • Reduce disease burden


Biopsychosocial Treatment Model

BIOLOGICAL-Brain/Body Based

Pharmacotherapy with antipsychotic drugs is the first line treatment both for acute phase, relapse prevention and maintenance. Clozapine is indicated for treatment resistant schizophrenia and for reducing the risk of recurrent suicidal behavior in schizophrenia or schizoaffective disorder.  ECT is recommended if clozapine is ineffective or cannot to be used.

Nutrition (anti-inflammatory diet, vitamin B12, Folate, D3, omega-3 fatty acids)


Elimination of substances of abuse (alcohol, tobacco, caffeine, others)

Sleep hygiene

SOCIAL-Relationship Based

Social skills training

Assertive community treatment

Vocational rehabilitation


Psychoeducation and coping-oriented interventions

Cognitive Behavioral Therapy

Cognitive remediation (for cognitive impairment)



Duration of treatment

Early intervention program with Coordinated Specialty Care (CSC), for people with first episode psychosis (FEP), has become a US health policy priority. CSC promotes shared decision making and uses a team of specialists who work with the client to create a personal treatment plan. The goal is to link the individual with a CSC team as soon as possible after psychotic symptoms begin. There are many different programs that are considered CSC: those include (but are not limited to) the Early Assessment and Support Alliance (EASA) in Oregon, NAVIGATE, OnTrackNY, the Specialized Treatment Early in Psychosis (STEP) Program in New Haven (CT), and the RAISE Connection Program (Maryland).  The main rational for these programs is that longer periods of untreated psychosis are associated with poorer outcomes. Continuous long-term treatment with antipsychotics is recommended because relapse is far more likely when medications are stopped (approximately 80% within 1 year).



Individuals who suffer from Posttraumatic stress disorder (PTSD) endure distressing aspects of the traumatic event, with vivid emotional immediacy and high intensity.  They constantly re-live the trauma in the present and organize their lives to contain the persistent effects of the traumatic experience.  They are unable to distance themselves emotionally from their traumatic experiences, which are ever-present, powerful, and dominant.  Most PTSD patients have frequent, intrusive and distressing recollection of the traumatic events during the daytime or in nightmares. They respond to remote reminders of the event by unnecessary, involuntary and uncontrollable alarm, and defensively avoid external and internal stimuli reminiscent of the trauma.



Posttraumatic stress disorder is a syndrome consisting of an enduring, pathological manifestation of both conditioned and unconditioned fear response resulting from exposure to real or threatened serious injury or sexual assault.


Diagnostic prototype

Patient has experienced or witnessed a traumatic event that elicited intense feelings of fear, helplessness, or horror. He persistently reexperiences the event through intrusive thoughts, mental images, or dreams related to the trauma as well as through flashbacks, illusions, hallucinatory images, or a sense that the event is occurring again.  He may experience intense psychological distress or physiological arousal when “triggered” by cues that resemble or symbolize the event.  He tries to avoid stimuli, thoughts, feelings, places, people, or conversations that might remind him of the event.  At times, he may also “shut down,” and experience an emotional numbing, feelings of detachment or estrangement from others, or diminished interest or participation in significant activities. He has difficulty falling or staying asleep, difficulty concentrating, exaggerated startle response, hypersensitivity to possible signs of danger, or irritability with outbursts of anger.

Video link: https://www.youtube.com/watch?v=KEmck4J64QA (video illustration)

Core Symptoms

Persistent avoidance of stimuli associated with the traumatic event(s), beginning after the traumatic event(s) occurred by avoidance of or efforts to avoid distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s); avoidance of or efforts to avoid external reminders (people, places, conversations, activities, objects, situations) that arouse distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s).
Re-experiencing the trauma either through recurrent, involuntary, and intrusive distressing memories of the traumatic event(s); or recurrent distressing dreams in which the content and/or affect of the dream are related to the traumatic event(s); or dissociative reactions (e.g., flashbacks) in which the individual feels or acts as if the traumatic event(s) were recurring; or intense or prolonged psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event(s); or marked physiological reactions to internal or external cues that symbolize or resemble an aspect of the traumatic event(s).
Negative alterations in cognitions and mood associated with the traumatic event(s) as evidenced by inability to remember an important aspect of the traumatic event(s);  persistent and exaggerated negative beliefs or expectations about oneself, others, or the world;  persistent, distorted cognitions about the cause or consequences of the traumatic event(s) that lead the individual to blame him-/herself or others; persistent negative emotional state (e.g., fear, horror, anger, guilt, or shame); markedly diminished interest or participation in significant activities; feelings of detachment or estrangement from others; persistent inability to experience positive emotions.
Marked alterations in arousal and reactivity associated with the traumatic event(s)in the form of irritable behavior and angry outbursts; reckless or self-destructive behavior; hypervigilance; exaggerated startle response; problems with concentration; sleep disturbance.
Traumatic event relates to exposure to actual or threatened death, serious injury, or sexual violence by either directly experiencing the traumatic event; or witnessing, in person, the event as it occurred to others; or learning that the traumatic event occurred to a close family member or close friend; or experiencing repeated or extreme exposure to aversive details of the traumatic event as part of the job.


Additional Symptoms Supporting the Diagnosis  

Patients with PTSD often present with somatic symptoms such as:

Gastrointestinal symptoms

Cardiovascular symptoms

Neurological symptoms

Musculoskeletal symptoms


Low back pain

Respiratory symptoms


Conditions that need to be ruled out

Other trauma and stressor related disorders

Persistent complex bereavement disorder

Anxiety disorders

Dissociative disorders

Psychotic disorders

Traumatic brain injury


Symptoms attributable to the physiological effects of a substance or another medical condition.


Additional Validated Rating scales

Clinician Administered PTSD Scale (CAPS)

The National Stressful Events Survey PTSD Short Scale (NSESSS)

PTSD Checklist for DSM-5 (PCL-5)



Course Specifiers: Acute (less than 3 months), or Chronic (more than 3 months)

Severity Specifiers:  Mild, moderate, severe, in partial remission, in full remission.

Additional Specifiers: With dissociative symptoms, With delayed expression


Epidemiological factors

Prevalence: 8.7% (life-time); 3.5% (12-month)

Age of onset: at any age, beginning after the first year of life

Predominant gender: females > males (4:1)


PTSD symptoms usually present within the first 3 months following the traumatic event.

Less frequently, symptoms onset may be delayed for months or years after the traumatic event.

Symptoms of PTSD may persist for months or years following the traumatic event.

Approximately 50% of all cases of PTSD are chronic (last more than 3 months).



Individuals with PTSD exhibit higher rates of diabetes, cardiovascular disease, autoimmune diseases, hypertension, and dementia.  Increased rates of psychiatric hospitalization, unemployment, poverty, and suicide are reported.  Additional diagnoses of depressive, substance use, and anxiety disorders are relatively common.




30 percent of the variance in the risk for PTSD is determined by genes alone. Pretrauma risk factors indicated above create sensitivity (intermediate phenotype) for enhanced fear conditioning related to traumatic event.  Consolidation of fear due to multiple brain mechanisms in amygdala, hippocampus and medial prefrontal cortex is the crucial step in the development of PTSD.  Expression of fear (PTSD symptoms) is related to processes of generalization, impaired inhibition, lack of extinction and discrimination of fear conditioning.


Frequent comorbid conditions

Majority w/PTSD have other diagnoses: ~80-90%

Depressive disorders

Panic disorder and GAD

Substance use disorders

Somatic symptom and related disorders


Differential Diagnosis

Adjustment Disorder

Persistent complex bereavement disorder

Other mental disorders that may occur after exposure to an extreme stressor (e.g. Brief psychotic disorder or MDD)

Obsessive-compulsive disorder

Panic disorder

Generalized anxiety disorder

Dissociative disorder

Psychotic disorders

Traumatic brain injury



Test and other evaluations

No tests or evaluations are indicated unless specific differential diagnostic concerns are taken into considerations. For example, urine screen for drugs of abuse, or  magnetic resonance imaging (MRI) of brain without contrast for TBI.


General plan for assessment and treatment

  • Assessment of symptoms, signs and dysfunctions (impairments)
  • Diagnosing PTSD (Diagnosis can be based on a clinical interview or a structured diagnostic interview such as the Clinician-Administered PTSD Scale (CAPS). It can be helpful to administer a self-report questionnaire such as the PTSD Checklist for DSM-5 (PCL-5). Positive diagnosis is based on DSM-5 criteria including exclusion other disorders /medical, substance-induced, psychiatric/. No disease specific biomarkers (genetic, imaging, neurophysiological, laboratory) are available now for positive diagnosis).
  • Evaluation of Suicidal Risk
  • Diagnosing Comorbid psychiatric and medical conditions
  • Tests and other evaluations
  • Establishing goals of treatment
  • Choosing the best treatment intervention
  • Monitoring response to treatment


Treatment goals

  • Reduce or eliminate symptoms
  • Prevent relapse
  • Enhance adaptive skills
  • Reduce disease burden


Biopsychosocial Treatment Model


Prolonged exposure therapy (treatment of choice)

Cognitive Processing Therapy (treatment of choice for sexual assault)

Eye movement desensitization and reprocessing

Stress inoculation training


Art therapy

Virtual reality

Spiritual practices

BIOLOGICAL-Brain/Body Based

The pharmacotherapy trials in PTSD have shown smaller effect sizes (0.3 to 0.8) than psychological interventions (>1.0). Selective serotonin reuptake inhibitors, such as fluoxetine, sertraline, and paroxetine, and serotonin norepinephrine reuptake inhibitors, such as venlafaxine, have demonstrated efficacy in reducing PTSD symptoms and are considered first-line medication treatments for PTSD. However, antidepressants alone are not usually effective in treating the insomnia and nightmares associated with PTSD. Prazosin, trazodone, eszopiclone, are options in treating insomnia and nightmares associated with PTSD. Several studies have demonstrated the efficacy of prazosin (2 to 20 mg per day), an alpha one–adrenergic blocker in reducing nightmares, and hyperarousal related to PTSD.

Nutrition (anti-inflammatory diet, vitamin B12, Folate, D3, omega-3 fatty acids)


Elimination of substances of abuse (alcohol, tobacco, caffeine, others)

Sleep hygiene


Tai chi

SOCIAL-Relationship Based

Family therapy

Group therapy

Social skills training

Vocational rehabilitation

Animal-assisted therapy


 Duration of treatment

Active treatment should occur until symptoms have abated. In addition to monitoring symptoms and social and occupational functioning, assessment for the emergence of suicidal ideation or substance abuse needs to be ongoing.



Social anxiety disorder is one of the most prevalent mental disorders, with an early onset and is often chronic.  More than 90% of persons with the disorder report psychosocial impairments (e.g., increased risk of dropping out of school, reduced workplace productivity and quality of life), and more than one third report severe impairments. However, only 35% of persons with a lifelong social anxiety disorder receive treatment specifically for this disorder. Social anxiety disorder is often mistaken for shyness and remains both underrecognized and undertreated.



Persistent and excessive fear of being judged and criticized by others in social and performance situations.


Diagnostic prototype

The patient reports feeling very anxious when giving a presentation, taking an examination, or meeting an authority figure. In these situations, he has palpitations, tremors, blushing, and sweating, and he is fearful that he will embarrass himself. He reports having few social contacts and avoids going to parties and making phone calls, but he feels lonely. His anxieties started during his teenage years and have increased considerably since he started attending a university.

Video link: https://www.youtube.com/watch?v=CsUbdl3QwpA (video illustration)


Core Symptoms

Marked fear is typically manifested in social interactions (e.g., having a conversation, meeting unfamiliar people), being observed (e.g., eating or drinking), and performing in front of others (e.g., giving a speech).


Additional Symptoms Necessary for the Diagnosis

 The individual fears that he or she will act in a way or show anxiety symptoms that will be negatively evaluated (i.e., will be humiliating or embarrassing; will lead to rejection or offend others).

The social situations almost always provoke fear or anxiety.

The social situations are avoided or endured with intense fear or anxiety.

The fear or anxiety is out of proportion to the actual threat posed by the social situation and to the sociocultural context.

Physical symptoms often include excessive blushing, excess sweating, trembling, palpitations, and nausea. Stammering may be present, along with rapid speech. Panic attacks can also occur under intense fear and discomfort.


Conditions that need to be ruled out

The fear, anxiety, or avoidance due to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition.

The fear, anxiety, or avoidance are symptoms of another mental disorder, such as panic disorder, body dysmorphic disorder, or autism spectrum disorder.


Rating scales

Severity Measure for Social Anxiety Disorder (Social Phobia)—Adult

Social Phobia Inventory (SPIN)

Liebowitz Social Anxiety Scale (LSAS)

Social Interaction Anxiety Scale (SIAS)


Epidemiological factors

Prevalence: 13.3% (life-time); 7% (12-month)

Age of onset: 75% of individuals have an age at onset between 8 and 15 years

Predominant gender: females > males (2:1)

Course:  30% of individuals with social anxiety disorder experience remission of symptoms within 1 year, and about 50% experience remission within a few years. For approximately 60% of individuals without a specific treatment for social anxiety disorder, the course takes several years or longer.



Extreme avoidance behavior (i.e., avoiding contact with others and being unable to maintain employment) sometimes complicates this condition.

School refusal is a common complication of social anxiety disorder.

Substance abuse, particularly the abuse of alcohol, sedatives, or narcotics, can also complicate treatment.


Prognosis is depended upon

A significant number of people who develop social anxiety disorder in adolescence may recover before reaching adulthood. However, if social anxiety disorder has persisted into adulthood, the chance of recovery in the absence of treatment is unlikely.



Heritability estimates are 25 to 50%.

Stressful social events in early life (for example, being bullied, familial abuse, public embarrassment or one’s mind going blank during a public performance) are commonly reported by people with social anxiety disorder.

Parental modelling of fear and avoidance in social situations plus an overprotective parenting style have both been linked to the development of the condition.

Sociability is closely tied to dopamine neurotransmission which points to the role of dopamine in social anxiety disorder.

Some evidence suggests dysfunction in serotonin neurotransmission.

Norepinephrine and glutamate may be over-active in social anxiety disorder, and the inhibitory transmitter GABA may be under-active in the thalamus.

Individuals with social anxiety disorder have been found to have a hypersensitive amygdala in relation to social threat cues.

The anterior cingulate cortex might be involved in the experience of “social pain”.


Frequent comorbid conditions

SAD shows a high degree of co-occurrence (66%) with other psychiatric disorders,

most commonly with depressive and anxiety disorders, in particular generalized anxiety disorder.

Avoidant personality disorder rates range from 25% to 89%.

One-fifth of patients with social anxiety disorder also suffer from substance use disorders.


Differential Diagnosis

Normative shyness


Panic disorder

Generalized anxiety disorder

Separation anxiety disorder

Specific phobias

Selective mutism

Major depressive disorder

Body dysmorphic disorder

Delusional disorder

Autism spectrum disorder

Avoidant personality disorder

Oppositional defiant disorder


Test and other evaluations

No tests or evaluations are indicated unless specific differential diagnostic concerns are taken into considerations.


General plan for assessment and treatment

  • Assessment of symptoms, signs and dysfunctions (impairments)
  • Diagnosing SAD (Diagnosis can be based on a clinical interview and validated rating scales. Positive diagnosis is based on DSM-5 criteria including exclusion of other disorders /medical, substance-induced, psychiatric/. No disease specific biomarkers (genetic, imaging, neurophysiological, laboratory) are available now for positive diagnosis).
  • Evaluation of Suicidal Risk
  • Diagnosing Comorbid psychiatric and medical conditions
  • Tests and other evaluations
  • Establishing goals of treatment
  • Choosing the best treatment intervention
  • Monitoring response to treatment


Treatment goals

  • Reduce or eliminate symptoms
  • Prevent relapse
  • Enhance adaptive skills
  • Reduce disease burden


Biopsychosocial Treatment Model


Cognitive-Behavioral therapy (Cognitive restructuring and Exposure therapy)

Mindfulness and Acceptance-Based Therapies

BIOLOGICAL-Brain/Body Based

The pharmacotherapy options include SSRIs, venlafaxine, MAOI, beta-adrenergic blockers, gabapentin, buspirone, benzodiazepine, atypical antipsychotics.

Relaxation techniques (reduction of sympathetic nervous system arousal)

Elimination of substances of abuse (alcohol, tobacco, caffeine, others)

Sleep hygiene

SOCIAL-Relationship Based

Group therapy

Social skills training


Duration of treatment

Psychological and Social Based treatments are usually short-term (3-6 months).

Pharmacotherapy requires longer duration (6-12 months) for prevention of relapse.




Panic disorder can be a severe and disabling condition.  It could be difficult to assess and diagnose when it presents acutely, as many symptoms may also be experienced with physical illness. Those who experience panic disorder often present repeatedly to their primary care provider or local emergency department with worrying episodes of multiple symptoms that the patient may ascribe to life-threatening illness.



Panic disorder is characterized by the spontaneous and unexpected occurrence of panic attacks, the frequency of which can vary from several attacks per day to only a few attacks per year. Panic attacks are defined as a period of intense fear in which 4 of 13 defined symptoms develop abruptly and peak rapidly less than 10 minutes from symptom onset.


Diagnostic prototype

Suddenly, and seemingly for no reason, the person experiences stark terror along with air hunger, racing heart, dizziness, shaking hands, sweating, a weird feeling of pins and needles in fingers and toes, and a clenching of hands and feet. Fear that something even more catastrophic is about to happen soon is overwhelming — perhaps fainting or throwing up, having a heart attack, going crazy, or even dying. Sometimes the world feels unreal, and the person has an uncanny sense of not being himself. The panic attack is brief and ends almost as suddenly as it began. At first the attacks are not predictably connected to environment triggers, but over time the situations where they have previously occurred may become conditioned cues that provoke new attacks (at least some of the time). The person often then begins to avoid these situations. Places that prevent ready escape or would cause embarrassment are the ones most likely to be avoided.

Video link: https://www.youtube.com/watch?v=iB6O1UEp4GI (video illustration)


Core Symptoms

A panic attack is an abrupt surge of intense fear or intense discomfort that reaches a peak within minutes, and during which time four (or more) of the following symptoms occur: Palpitations, pounding heart, or accelerated heart rate; Sweating; Trembling or shaking; Sensations of shortness of breath or smothering; Feelings of choking; Chest pain or discomfort; Nausea or abdominal distress; Feeling dizzy, unsteady, light-headed, or faint; Chills or heat sensations; Paresthesias (numbness or tingling sensations); Derealization (feelings of unreality) or depersonalization (being detached from oneself); Fear of losing control or “going crazy.”; Fear of dying.


Additional Symptoms Necessary for the Diagnosis:

At least one of the attacks has been followed by 1 month (or more) of one or both of the following:

  • Persistent concern or worry about additional panic attacks or their consequences (e.g., losing control, having a heart attack, “going crazy”).
  • A significant maladaptive change in behavior related to the attacks (e.g., behaviors designed to avoid having panic attacks, such as avoidance of exercise or unfamiliar situations).


Conditions that need to be ruled out

The fear, anxiety, or avoidance due to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition (e.g., hyperthyroidism, cardiopulmonary disorders).

The fear, anxiety, or avoidance are symptoms of another mental disorder, such as the panic attacks in response to feared social situations, as in social anxiety disorder; in response to circumscribed phobic objects or situations, as in specific phobia; in response to obsessions, as in obsessive-compulsive disorder; in response to reminders of traumatic events, as in posttraumatic stress disorder; or in response to separation from attachment figures, as in separation anxiety disorder.


Rating scales

Severity Measure for Panic Disorder—Adult

Panic Disorder Severity Scale (PDSS)


Epidemiological factors

Prevalence: 2-6% (life-time); 2-3% (12-month)

Age of onset: 20-24 years of age

Predominant gender: females > males (2:1)

Course:  The usual course, if untreated, is chronic but waxing and waning. Some individuals may have episodic outbreaks with years of remission in between, and others may have continuous severe symptomatology. The course of panic disorder typically is complicated by a range of other disorders, in particular other anxiety disorders, depressive disorders, and substance use disorders.



Panic disorder is associated with high levels of social, occupational, and physical disability; considerable economic costs; and the highest number of medical visits among the anxiety disorders.

The risk of coronary artery disease in patients with panic disorder is nearly doubled.

The suicide rate in individuals with panic disorder is also many times higher than the general population.


Prognosis is depended upon

Patients with good premorbid functioning and a brief duration of symptoms tend to have a good prognosis. About 10-20% of patients continue to have significant symptoms due to severe illness at the time of the initial assessment, high interpersonal sensitivity, low social class, separation from a parent by death during early life, divorce, and unmarried status.



Heritability estimates are around 43%.

Panic attacks are mediated by neurobiological alteration in “fear network” in the brain that involves the amygdala, hypothalamus, and brainstem centers. The corticostriatal-thalamocortical (CSTC) circuitry is believed to mediate worry, interacting with the more fear-specific circuit in the amygdala.  Projections from the amygdala to the hypothalamus mediate autonomic and endocrine responses to fear.

Heightened anxiety sensitivity (the belief that anxiety-related body sensations are harmful) may be acquired from recurrent direct aversive experiences (e.g., childhood maltreatment, physical illness such as asthma), vicarious observations (e.g., significant illnesses or deaths among family members), or parental reinforcement or modeling of distressed reactions to bodily sensations.


Frequent comorbid conditions

98% of panic disorder patients had at least one comorbid lifetime psychiatric disorder.

Major depressive disorder, other anxiety disorders, and alcohol use disorders are the most common comorbid disorders


Differential Diagnosis

Agoraphobia (often co-exists).

Social anxiety disorder (often co-exists).

Anxiety disorders, including generalized anxiety disorder (may co-exist).

Adjustment disorders.

Bipolar disorder.

Depressive disorders

Dissociative disorders.

Factitious illness.

Somatic symptom and related disorder.

Obsessive-compulsive disorder.

Specific phobic disorders.

Post-traumatic stress disorder.

Stimulant-drug misuse (including caffeine-related illness).



Carcinoid syndrome.

Hypoglycemic episodes (possibly due to insulinoma in those not using insulin/oral hypoglycemic agents).

Paroxysmal cardiac dysrhythmia.

Mitral valve prolapse.

Myocardial infarction.

Recurrent small pulmonary emboli.

Epileptiform disorders, particularly temporal lobe epilepsy.

Withdrawal from alcohol/sedatives/opiates.

Paroxysmal vestibular disorders – e.g. Meniere’s disease.


Test and other evaluations

Serum electrolytes to exclude hypokalemia and acidosis

Serum glucose to exclude hypoglycemia

Cardiac enzymes in patients suspected of acute coronary syndromes

Serum hemoglobin in patients with near-syncope

Thyroid-stimulating hormone (TSH) in patients suspected of hyperthyroidism

Urine toxicology screen for amphetamines, cannabis, cocaine, and phencyclidine in patients suspected of intoxication

D-dimer assay to exclude pulmonary embolism

Comprehensive workup (if indicated) involves: ECG, EEG, MRI, Holter monitor, 24-hour urine catecholamines.


General plan for assessment and treatment

  • Assessment of symptoms, signs and dysfunctions (impairments)
  • Diagnosing Panic disorder (Diagnosis can be based on a clinical interview and validated rating scales. Positive diagnosis is based on DSM-5 criteria including exclusion of other disorders /medical, substance-induced, psychiatric/. No disease specific biomarkers (genetic, imaging, neurophysiological, laboratory) are available now for positive diagnosis).
  • Evaluation of Suicidal Risk
  • Diagnosing Comorbid psychiatric and medical conditions
  • Tests and other evaluations
  • Establishing goals of treatment
  • Choosing the best treatment intervention
  • Monitoring response to treatment


Treatment goals

  • Reduce or eliminate symptoms
  • Prevent relapse
  • Enhance adaptive skills
  • Reduce disease burden


Biopsychosocial Treatment Model


Cognitive-Behavioral therapy (Psychoeducation, Cognitive restructuring and Interoceptive exposure)

Panic-Focused Psychodynamic Psychotherapy

BIOLOGICAL-Brain/Body Based

The pharmacotherapy options include Selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), TCAs, and benzodiazepines.

Relaxation techniques (reduction of sympathetic nervous system arousal)

Elimination of substances of abuse (alcohol, tobacco, caffeine, others)

SOCIAL-Relationship Based

No evidence-based intervention


Duration of treatment

Psychological treatments are usually short-term (3-6 months).

Pharmacotherapy requires longer duration (6-12 months) for prevention of relapse.