Category: Mental Health History

On This Day … 30 March

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People (Births)

  • 1882 – Melanie Klein, Jewish Austrian-English psychologist and author (d. 1960).

People (Deaths)

  • 1873 – Bénédict Morel, Austrian-French psychiatrist and physician (b. 1809).

Melanie Klein

Melanie Klein (née Reizes; 30 March 1882 to 22 September 1960) was an Austrian-British author and psychoanalyst known for her work in child analysis. She was the primary figure in the development of object relations theory. Klein suggested that pre-verbal existential anxiety in infancy catalysed the formation of the unconscious, resulting in the unconscious splitting of the world into good and bad idealisations. In her theory, how the child resolves that split depends on the constitution of the child and the character of nurturing the child experiences; the quality of resolution can inform the presence, absence, and/or type of distresses a person experiences later in life.

Contributions to Psychoanalysis

Klein was one of the first to use traditional psychoanalysis with young children. She was innovative in both her techniques (such as working with children using toys) and her theories on infant development. Gaining the respect of those in the academic community, Klein established a highly influential training program in psychoanalysis.

By observing and analysing the play and interactions of children, Klein built onto the work of Freud’s unconscious mind. Her dive into the unconscious mind of the infant yielded the findings of the early Oedipus complex, as well as the developmental roots of the superego.

Klein’s theoretical work incorporates Freud’s belief in the existence of the death pulsation, reflecting the notion that all living organisms are inherently drawn toward an “inorganic” state, and therefore, somehow, towards death. In psychological terms, Eros (properly, the life pulsation), the postulated sustaining and uniting principle of life, is thereby presumed to have a companion force, Thanatos (death pulsation), which seeks to terminate and disintegrate life. Both Freud and Klein regarded these “biomental” forces as the foundations of the psyche. These primary unconscious forces, whose mental matrix is the id, spark the ego – the experiencing self – into activity. Id, ego and superego, to be sure, were merely shorthand terms (similar to the instincts) referring to highly complex and mostly uncharted psychodynamic operations.

Benedict Morel

Bénédict Augustin Morel (22 November 1809 to 30 March 1873) was a French psychiatrist born in Vienna, Austria. He was an influential figure in the field of degeneration theory during the mid-19th century.

Morel received his education in Paris, and while a student, supplemented his income by teaching English and German classes. In 1839 he earned his medical doctorate, and two years later became an assistant to psychiatrist Jean-Pierre Falret (1794-1870) at the Salpêtrière in Paris.

Morel’s interest in psychiatry was further enhanced in the mid-1840s when he visited several mental institutions throughout Europe. In 1848 he was appointed director of the Asile d’Aliénés de Maréville at Nancy. Here he introduced reforms towards the welfare of the mentally ill, in particular liberalisation of restraining practices. At the Maréville asylum he studied the mentally handicapped, researching their family histories and investigating aspects such as poverty and childhood physical illnesses. In 1856 he was appointed director of the mental asylum at Saint-Yon in Rouen.

Morel, influenced by various pre-Darwinian theories of evolution, particularly those that attributed a powerful role to acclimation, saw mental deficiency as the end stage of a process of mental deterioration. In the 1850s, he developed a theory of “degeneration” in regards to mental problems that take place from early life to adulthood. In 1857 he published Traité des dégénérescences physiques, intellectuelles et morales de l’espèce humaine et des causes qui produisent ces variétés maladives, a treatise in which he explains the nature, causes, and indications of human degeneration. Morel looked for answers to mental illness in heredity, although later on he believed that alcohol and drug usage could also be important factors in the course of mental decline.

What is Avoidant Personality Disorder?

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Introduction

Avoidant personality disorder (AvPD) is a Cluster C personality disorder in which the main coping mechanism of those affected is avoidance of feared stimuli.

Those affected display a pattern of severe social anxiety, social inhibition, feelings of inadequacy and inferiority, extreme sensitivity to negative evaluation and rejection, and avoidance of social interaction despite a strong desire for intimacy.

People with AvPD often consider themselves to be socially inept or personally unappealing and avoid social interaction for fear of being ridiculed, humiliated, rejected, or disliked. They often avoid becoming involved with others unless they are certain they will be liked.

Childhood emotional neglect (in particular, the rejection of a child by one or both parents) and peer group rejection are associated with an increased risk for its development; however, it is possible for AvPD to occur without any notable history of abuse or neglect.

Brief History

The avoidant personality has been described in several sources as far back as the early 1900s, although it was not so named for some time. Swiss psychiatrist Eugen Bleuler described patients who exhibited signs of avoidant personality disorder in his 1911 work Dementia Praecox: Or the Group of Schizophrenias. Avoidant and schizoid patterns were frequently confused or referred to synonymously until Kretschmer (1921), in providing the first relatively complete description, developed a distinction.

Signs and Symptoms

Avoidant individuals are preoccupied with their own shortcomings and form relationships with others only if they believe they will not be rejected. They often view themselves with contempt, while showing a decreased ability to identify traits within themselves that are generally considered as positive within their societies. Loss and social rejection are so painful that these individuals will choose to be alone rather than risk trying to connect with others.

Some with this disorder fantasize about idealized, accepting and affectionate relationships because of their desire to belong. They often feel themselves unworthy of the relationships they desire, and shame themselves from ever attempting to begin them. If they do manage to form relationships, it is also common for them to pre-emptively abandon them out of fear of the relationship failing.

Individuals with the disorder tend to describe themselves as uneasy, anxious, lonely, unwanted and isolated from others. They often choose jobs of isolation in which they do not have to interact with others regularly. Avoidant individuals also avoid performing activities in public spaces for fear of embarrassing themselves in front of others.

Symptoms include:

  • Extreme shyness or anxiety in social situations, though the person feels a strong desire for close relationships;
  • Heightened attachment-related anxiety, which may include a fear of abandonment; and
  • Substance abuse and/or dependence.

Comorbidity

AvPD is reported to be especially prevalent in people with anxiety disorders, although estimates of comorbidity vary widely due to differences in (among others) diagnostic instruments. Research suggests that approximately 10-50% of people who have panic disorder with agoraphobia have avoidant personality disorder, as well as about 20-40% of people who have social anxiety disorder. In addition to this, AvPD is more prevalent in people who have comorbid social anxiety disorder and generalised anxiety disorder (GAD) than in those who have only one of the aforementioned conditions.

Some studies report prevalence rates of up to 45% among people with GAD and up to 56% of those with obsessive-compulsive disorder. Posttraumatic stress disorder is also commonly comorbid with AvPD.

Avoidants are prone to self-loathing and, in certain cases, self-harm. In particular, avoidants who have comorbid PTSD have the highest rates of engagement in self-harming behaviour, outweighing even those with borderline personality disorder (with or without PTSD). Substance use disorders are also common in individuals with AvPD – particularly in regard to alcohol, benzodiazepines and heroin – and may significantly affect a patient’s prognosis.

Earlier theorists proposed a personality disorder with a combination of features from borderline personality disorder and avoidant personality disorder, called “avoidant-borderline mixed personality” (AvPD/BPD).

Causes

Causes of AvPD are not clearly defined, but appear to be influenced by a combination of social, genetic and psychological factors. The disorder may be related to temperamental factors that are inherited.

Specifically, various anxiety disorders in childhood and adolescence have been associated with a temperament characterised by behavioural inhibition, including features of being shy, fearful and withdrawn in new situations. These inherited characteristics may give an individual a genetic predisposition towards AvPD.

Childhood emotional neglect and peer group rejection are both associated with an increased risk for the development of AvPD. Some researchers believe a combination of high-sensory-processing sensitivity coupled with adverse childhood experiences may heighten the risk of an individual developing AvPD.

Subtypes

Millon

Psychologist Theodore Millon notes that because most patients present a mixed picture of symptoms, their personality disorder tends to be a blend of a major personality disorder type with one or

more secondary personality disorder types. He identified four adult subtypes of AvPD as outlined below.

SubtypePersonality Traits/Features
Phobic Avoidant (including dependent features)General apprehensiveness displaced with avoidable tangible precipitant; qualms and disquietude symbolised by a repugnant and specific dreadful object or circumstances.
Conflicted Avoidant (including negativistic features)Internal discord and dissension; fears dependence; unsettled; unreconciled within self; hesitating, confused, tormented, paroxysmic, embittered; and unresolvable angst.
Hypersensitive Avoidant (including paranoid features)Intensely wary and suspicious; alternatively panicky, terrified, edgy, and timorous, then thin-skinned, high-strung, petulant, and prickly.
Self-Deserting Avoidant (including depressive features)Blocks or fragments self-awareness; discards painful images and memories; casts away untenable thoughts and impulses; ultimately jettisons self (suicidal).

Others

In 1993, Lynn E. Alden and Martha J. Capreol proposed two other subtypes of avoidant personality disorder, as outlined below.

SubtypePersonality Traits/Features
Cold-AvoidantCharacterised by an inability to experience and express positive emotion towards others.
Exploitable-AvoidantCharacterised by an inability to express anger towards others or to resist coercion from others. May be at risk for abuse by others.

Diagnosis

ICD

The World Health Organisation’s ICD-10 lists avoidant personality disorder as anxious (avoidant) personality disorder (F60.6).

It is characterised by the presence of at least four of the following:

  1. Persistent and pervasive feelings of tension and apprehension.
  2. Belief that one is socially inept, personally unappealing, or inferior to others.
  3. Excessive preoccupation with being criticised or rejected in social situations.
  4. Unwillingness to become involved with people unless certain of being liked.
  5. Restrictions in lifestyle because of need to have physical security.
  6. Avoidance of social or occupational activities that involve significant interpersonal contact because of fear of criticism, disapproval, or rejection.

Associated features may include hypersensitivity to rejection and criticism.

It is a requirement of ICD-10 that all personality disorder diagnoses also satisfy a set of general personality disorder criteria.

DSM

The Diagnostic and Statistical Manual of Mental Disorders (DSM) of the APA also has an avoidant personality disorder diagnosis (301.82). It refers to a widespread pattern of inhibition around people, feeling inadequate and being very sensitive to negative evaluation. Symptoms begin by early adulthood and occur in a range of situations.

Four of the following seven specific symptoms should be present:

  1. Avoids occupational activities that involve significant interpersonal contact, because of fears of criticism, disapproval, or rejection.
  2. Is unwilling to get involved with people unless certain of being liked.
  3. Shows restraint within intimate relationships because of the fear of being shamed or ridiculed.
  4. Is preoccupied with being criticised or rejected in social situations.
  5. Is inhibited in new interpersonal situations because of feelings of inadequacy.
  6. Views self as socially inept, personally unappealing, or inferior to others.
  7. Is unusually reluctant to take personal risk or to engage in any new activities because they may prove embarrassing.

Differential Diagnosis

In contrast to social anxiety disorder, a diagnosis of AvPD also requires that the general criteria for a personality disorder are met.

According to the DSM-5, avoidant personality disorder must be differentiated from similar personality disorders such as dependent, paranoid, schizoid, and schizotypal. But these can also occur together; this is particularly likely for AvPD and dependent personality disorder. Thus, if criteria for more than one personality disorder are met, all can be diagnosed.

There is also an overlap between avoidant and schizoid personality traits and AvPD may have a relationship to the schizophrenia spectrum.

Epidemiology

Data from the 2001-2002 National Epidemiologic Survey on Alcohol and Related Conditions indicates a prevalence of 2.36% in the US general population. It appears to occur with equal frequency in males and females. In one study, it was seen in 14.7% of psychiatric outpatients.

Criticism

There is controversy as to whether avoidant personality disorder (AvPD) is distinct from generalised social anxiety disorder. Both have similar diagnostic criteria and may share a similar causation, subjective experience, course, treatment and identical underlying personality features, such as shyness.

It is contended by some that they are merely different conceptualisations of the same disorder, where avoidant personality disorder may represent the more severe form. In particular, those with AvPD experience not only more severe social phobia symptoms, but are also more depressed and more functionally impaired than patients with generalised social phobia alone. But they show no differences in social skills or performance on an impromptu speech. Another difference is that social phobia is the fear of social circumstances whereas AvPD is better described as an aversion to intimacy in relationships.

Treatment

Treatment of avoidant personality disorder can employ various techniques, such as social skills training, psychotherapy, cognitive therapy, and exposure treatment to gradually increase social contacts, group therapy for practicing social skills, and sometimes drug therapy.

A key issue in treatment is gaining and keeping the patient’s trust since people with an avoidant personality disorder will often start to avoid treatment sessions if they distrust the therapist or fear rejection. The primary purpose of both individual therapy and social skills group training is for individuals with an avoidant personality disorder to begin challenging their exaggerated negative beliefs about themselves.

Significant improvement in the symptoms of personality disorders is possible, with the help of treatment and individual effort.

Prognosis

Being a personality disorder, which is usually chronic and has long-lasting mental conditions, an avoidant personality disorder is not expected to improve with time without treatment. Given that it is a poorly studied personality disorder and in light of prevalence rates, societal costs, and the current state of research, AvPD qualifies as a neglected disorder.

On This Day … 28 March

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People (Births)

  • 1955 – John Alderdice, Baron Alderdice, Northern Irish psychiatrist and politician, 1st Speaker of the Northern Ireland Assembly.

John Alderdice

John Thomas Alderdice, Baron Alderdice (born 28 March 1955 is a Northern Ireland politician.

He was Speaker of the Northern Ireland Assembly 1998–2004, leader of the Alliance Party of Northern Ireland 1987-1998, and since 1996 has sat in the House of Lords as a Liberal Democrat.

John was educated at Ballymena Academy and the Queen’s University Belfast (QUB) where he studied medicine and qualified in 1978. In 1977 he married Joan Hill, with whom he has two sons and one daughter. He worked part-time as a consultant psychiatrist in psychotherapy in the NHS from 1988 until he retired from psychiatric practice in 2010. He also lectured at Queen’s University’s Faculty of Medicine between 1991 and 1999.

Alderdice claims a distant relationship to John King, a 19th-century Australian explorer and the sole survivor of the Burke and Wills expedition.

On This Day … 27 March

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People (Deaths)

  • 1938 – William Stern, German-American psychologist and philosopher (b. 1871).
  • 1946 – Karl Groos, German psychologist and philosopher (b. 1861).
  • 1998 – David McClelland, American psychologist and academic (b. 1917).

William Stern

William Stern (April 29, 1871 to March 27, 1938), born Louis William Stern, was a German psychologist and philosopher. He is known for the development of personalistic psychology, which placed emphasis on the individual by examining measurable personality traits as well as the interaction of those traits within each person to create the self.

Stern also coined the term intelligence quotient, or IQ, and invented the tone variator as a new way to study human perception of sound. Stern studied psychology and philosophy under Hermann Ebbinghaus at the University of Berlin, and quickly moved on to teach at the University of Breslau. Later he was appointed to the position of professor at the University of Hamburg.

Over the course of his career, Stern wrote many books pioneering new fields in psychology such as differential psychology, critical personalism, forensic psychology, and intelligence testing. Stern was also a pioneer in the field of child psychology. Working with his wife, Clara Joeesephy Stern, the couple kept meticulous diaries detailing the lives of their 3 children for 18 years. He used these journals to write several books that offered an unprecedented look into the psychological development of children over time.

Karl Groos

Karl Groos (10 December 1861 to 27 March 1946, in Tübingen) was a philosopher and psychologist who proposed an evolutionary instrumentalist theory of play. His 1898 book on The Play of Animals suggested that play is a preparation for later life.

Groos was full Professor of philosophy in Gießen, Basel and 1911-1929 in Tübingen.

His main idea was that play is basically useful, and so it can be explained by the normal process of evolution by natural selection. When animals ‘play’ they are practising basic instincts, such as fighting, for survival. This is translated from the original as “pre-tuning”. Despite this insight, Groos’ work is seldom read today, and his connection of play with aesthetics has been termed “misguided”. Another area of study was the psychology of literature, including statistical analysis.

Among his scholars is the German philosopher Willy Moog (1888-1935) (doctorate on Goethe supervised by Karl Groos in Gießen 1909).

David McClelland

David Clarence McClelland (20 May 1917 to 27 March 1998) was an American psychologist, noted for his work on motivation Need Theory. He published a number of works between the 1950s and the 1990s and developed new scoring systems for the Thematic Apperception Test (TAT) and its descendants.

McClelland is credited with developing Achievement Motivation Theory, commonly referred to as “need for achievement” or n-achievement theory. A Review of General Psychology survey published in 2002, ranked McClelland as the 15th most cited psychologist of the 20th century.

What is Biological Psychiatry?

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Introduction

Biological psychiatry or biopsychiatry is an approach to psychiatry that aims to understand mental disorder in terms of the biological function of the nervous system. It is interdisciplinary in its approach and draws on sciences such as neuroscience, psychopharmacology, biochemistry, genetics, epigenetics and physiology to investigate the biological bases of behaviour and psychopathology. Biopsychiatry is the branch of medicine which deals with the study of the biological function of the nervous system in mental disorders.

There is some overlap with neurology, which focuses on disorders where gross or visible pathology of the nervous system is apparent, such as epilepsy, cerebral palsy, encephalitis, neuritis, Parkinson’s disease and multiple sclerosis. There is also some overlap with neuropsychiatry, which typically deals with behavioral disturbances in the context of apparent brain disorder. In contrast biological psychiatry describes the basic principles and then delves deeper into various disorders. It is structured to follow the organisation of the DSM-IV, psychiatry’s primary diagnostic and classification guide. The contributions of this field explore functional neuroanatomy, imaging, and neuropsychology and pharmacotherapeutic possibilities for depression, anxiety and mood disorders, substance abuse and eating disorders, schizophrenia and psychotic disorders, and cognitive and personality disorders.

Biological psychiatry and other approaches to mental illness are not mutually exclusive, but may simply attempt to deal with the phenomena at different levels of explanation. Because of the focus on the biological function of the nervous system, however, biological psychiatry has been particularly important in developing and prescribing drug-based treatments for mental disorders.

In practice, however, psychiatrists may advocate both medication and psychological therapies when treating mental illness. The therapy is more likely to be conducted by clinical psychologists, psychotherapists, occupational therapists or other mental health workers who are more specialised and trained in non-drug approaches.

The history of the field extends back to the ancient Greek physician Hippocrates, but the phrase biological psychiatry was first used in peer-reviewed scientific literature in 1953. The phrase is more commonly used in the United States than in some other countries such as the UK. However the term “biological psychiatry” is sometimes used as a phrase of disparagement in controversial dispute.

Brief History

Early 20th Century

Sigmund Freud was originally focused on the biological causes of mental illness. Freud’s professor and mentor, Ernst Wilhelm von Brücke, strongly believed that thought and behaviour were determined by purely biological factors. Freud initially accepted this and was convinced that certain drugs (particularly cocaine) functioned as antidepressants. He spent many years trying to “reduce” personality to neurology, a cause he later gave up on before developing his now well-known psychoanalytic theories.

Nearly 100 years ago, Harvey Cushing, the father of neurosurgery, noted that pituitary gland problems often cause mental health disorders. He wondered whether the depression and anxiety he observed in patients with pituitary disorders were caused by hormonal abnormalities, the physical tumour itself, or both.

Mid 20th Century

An important point in modern history of biological psychiatry was the discovery of modern antipsychotic and antidepressant drugs. Chlorpromazine (also known as Thorazine), an antipsychotic, was first synthesized in 1950. In 1952, iproniazid, a drug being trialled against tuberculosis, was serendipitously discovered to have anti-depressant effects, leading to the development of monoamine oxidase inhibitors (MAOIs) as the first class of antidepressants. In 1959 imipramine, the first tricyclic antidepressant, was developed. Research into the action of these drugs led to the first modern biological theory of mental health disorders called the catecholamine theory, later broadened to the monoamine theory, which included serotonin. These were popularly called the “chemical imbalance” theory of mental health disorders.

Late 20th Century

Starting with fluoxetine (marketed as Prozac) in 1988, a series of monoamine-based antidepressant medications belonging to the class of selective serotonin reuptake inhibitors were approved. These were no more effective than earlier antidepressants, but generally had fewer side effects. Most operate on the same principle, which is modulation of monoamines (neurotransmitters) in the neuronal synapse. Some drugs modulate a single neurotransmitter (typically serotonin). Others affect multiple neurotransmitters, called dual action or multiple action drugs. They are no more effective clinically than single action versions. That most antidepressants invoke the same biochemical method of action may explain why they are each similarly effective in rough terms. Recent research indicates antidepressants often work but are less effective than previously thought.

Problems with Catecholamine/Monoamine Hypotheses

The monoamine hypothesis was compelling, especially based on apparently successful clinical results with early antidepressant drugs, but even at the time there were discrepant findings. Only a minority of patients given the serotonin-depleting drug reserpine became depressed; in fact reserpine even acted as an antidepressant in many cases. This was inconsistent with the initial monoamine theory which said depression was caused by neurotransmitter deficiency.

Another problem was the time lag between antidepressant biological action and therapeutic benefit. Studies showed the neurotransmitter changes occurred within hours, yet therapeutic benefit took weeks.

To explain these behaviours, more recent modifications of the monoamine theory describe a synaptic adaptation process which takes place over several weeks. Yet this alone does not appear to explain all of the therapeutic effects.

Scope and Detailed Definition

Biological psychiatry is a branch of psychiatry where the focus is chiefly on researching and understanding the biological basis of major mental disorders such as unipolar and bipolar affective (mood) disorders, schizophrenia and organic mental disorders such as Alzheimer’s disease. This knowledge has been gained using imaging techniques, psychopharmacology, neuroimmunochemistry and so on. Discovering the detailed interplay between neurotransmitters and the understanding of the neurotransmitter fingerprint of psychiatric drugs such as clozapine has been a helpful result of the research.

On a research level, it includes all possible biological bases of behaviour – biochemical, genetic, physiological, neurological and anatomical. On a clinical level, it includes various therapies, such as drugs, diet, avoidance of environmental contaminants, exercise, and alleviation of the adverse effects of life stress, all of which can cause measurable biochemical changes. The biological psychiatrist views all of these as possible aetiologies of or remedies for mental health disorders.

However, the biological psychiatrist typically does not discount talk therapies. Medical psychiatric training generally includes psychotherapy and biological approaches. Accordingly, psychiatrists are usually comfortable with a dual approach: “psychotherapeutic methods […] are as indispensable as psychopharmacotherapy in a modern psychiatric clinic”.

Basis for Biological Psychiatry

Sigmund Freud developed psychotherapy in the early 1900s, and through the 1950s this technique was prominent in treating mental health disorders.

However, in the late 1950s, the first modern antipsychotic and antidepressant drugs were developed: chlorpromazine (also known as Thorazine), the first widely used antipsychotic, was synthesized in 1950, and iproniazid, one of the first antidepressants, was first synthesized in 1957. In 1959 imipramine, the first tricyclic antidepressant, was developed.

Based significantly on clinical observations of the above drug results, in 1965 the seminal paper “The catecholamine hypothesis of affective disorders” was published. It articulated the “chemical imbalance” hypothesis of mental health disorders, especially depression. It formed much of the conceptual basis for the modern era in biological psychiatry.

The hypothesis has been extensively revised since its advent in 1965. More recent research points to deeper underlying biological mechanisms as the possible basis for several mental health disorders.

Modern brain imaging techniques allow non-invasive examination of neural function in patients with mental health disorders, however this is currently experimental. With some disorders it appears the proper imaging equipment can reliably detect certain neurobiological problems associated with a specific disorder. If further studies corroborate these experimental results, future diagnosis of certain mental health disorders could be expedited using such methods.

Another source of data indicating a significant biological aspect of some mental health disorders is twin studies. Identical twins have the same nuclear DNA, so carefully constructed studies may indicate the relative importance of environmental and genetic factors on the development of a particular mental health disorder.

The results from this research and the associated hypotheses form the basis for biological psychiatry and the treatment approaches in a clinical setting.

Scope of Clinical Biological Psychiatric Treatment

Since various biological factors can affect mood and behaviour, psychiatrists often evaluate these before initiating further treatment. For example, dysfunction of the thyroid gland may mimic a major depressive episode, or hypoglycaemia (low blood sugar) may mimic psychosis.

While pharmacological treatments are used to treat many mental disorders, other non-drug biological treatments are used as well, ranging from changes in diet and exercise to transcranial magnetic stimulation and electroconvulsive therapy. Types of non-biological treatments such as cognitive therapy, behavioural therapy, and psychodynamic psychotherapy are often used in conjunction with biological therapies. Biopsychosocial models of mental illness are widely in use, and psychological and social factors play a large role in mental disorders, even those with an organic basis such as schizophrenia.

Diagnostic Process

Correct diagnosis is important for mental health disorders, otherwise the condition could worsen, resulting in a negative impact on both the patient and the healthcare system. Another problem with misdiagnosis is that a treatment for one condition might exacerbate other conditions. In other cases apparent mental health disorders could be a side effect of a serious biological problem such as concussion, brain tumour, or hormonal abnormality, which could require medical or surgical intervention.

Examples of Biologic Treatments

  • Seasonal affective disorder: light therapy, SSRIs (Like fluoxetine and paroxetine).
  • Clinical depression: SSRIs, serotonin-norepinephrine reuptake inhibitors (venlafaxine), dopamine reuptake inhibitors: (bupropion), tricyclic antidepressants, monoamine oxidase inhibitors, electroconvulsive therapy, transcranial magnetic stimulation, fish oil, St. John’s wort.
  • Bipolar disorder: lithium carbonate, antipsychotics (like olanzapine or quetiapine), anticonvulsants (like valproic acid, lamotrigine and topiramate).
  • Schizophrenia: antipsychotics such as haloperidol, clozapine, olanzapine, risperidone and quetiapine.
  • Generalized anxiety disorder: SSRIs, benzodiazepines, buspirone.
  • Obsessive-compulsive disorder: tricyclic antidepressants, SSRIs.
  • ADHD: clonidine, D-amphetamine, methamphetamine, and methylphenidate.

Latest Biological Hypotheses of Mental Health Disorders

New research indicates different biological mechanisms may underlie some mental health disorders, only indirectly related to neurotransmitters and the monoamine chemical imbalance hypothesis.

Recent research indicates a biological “final common pathway” may exist which both electroconvulsive therapy and most current antidepressant drugs have in common. These investigations show recurrent depression may be a neurodegenerative disorder, disrupting the structure and function of brain cells, destroying nerve cell connections, even killing certain brain cells, and precipitating a decline in overall cognitive function.

In this new biological psychiatry viewpoint, neuronal plasticity is a key element. Increasing evidence points to various mental health disorders as a neurophysiological problem which inhibits neuronal plasticity.

This is called the neurogenic hypothesis of depression. It promises to explain pharmacological antidepressant action, including the time lag from taking the drug to therapeutic onset, why downregulation (not just upregulation) of neurotransmitters can help depression, why stress often precipitates mood disorders, and why selective modulation of different neurotransmitters can help depression. It may also explain the neurobiological mechanism of other non-drug effects on mood, including exercise, diet and metabolism. By identifying the neurobiological “final common pathway” into which most antidepressants funnel, it may allow rational design of new medications which target only that pathway. This could yield drugs which have fewer side effects, are more effective and have quicker therapeutic onset.

There is significant evidence that oxidative stress plays a role in schizophrenia.

Criticism

A number of patients, activists, and psychiatrists dispute biological psychiatry as a scientific concept or as having a proper empirical basis, for example arguing that there are no known biomarkers for recognized psychiatric conditions. This position has been represented in academic journals such as The Journal of Mind and Behaviour and Ethical Human Psychology and Psychiatry, which publishes material specifically countering “the idea that emotional distress is due to an underlying organic disease.” Alternative theories and models instead view mental disorders as non-biomedical and might explain it in terms of, for example, emotional reactions to negative life circumstances or to acute trauma.

Fields such as social psychiatry, clinical psychology, and sociology may offer non-biomedical accounts of mental distress and disorder for certain ailments and are sometimes critical of biopsychiatry. Social critics believe biopsychiatry fails to satisfy the scientific method because they believe there is no testable biological evidence of mental disorders. Thus, these critics view biological psychiatry as a pseudoscience attempting to portray psychiatry as a biological science.

R.D. Laing argued that attributing mental disorders to biophysical factors was often flawed due to the diagnostic procedure. The “complaint” is often made by a family member, not the patient, the “history” provided by someone other than patient, and the “examination” consists of observing strange, incomprehensible behaviour. Ancillary tests (EEG, PET) are often done after diagnosis, when treatment has begun, which makes the tests non-blind and incurs possible confirmation bias. The psychiatrist Thomas Szasz commented frequently on the limitations of the medical approach to psychiatry and argued that mental illnesses are medicalised problems in living.

Silvano Arieti, while approving of the use of medication in some cases of schizophrenia, preferred intensive psychotherapy without medication if possible. He was also known for approving the use of electroconvulsive therapy on those with disorganised schizophrenia in order to make them reachable by psychotherapy. The views he expressed in Interpretation of Schizophrenia are nowadays known as the trauma model of mental disorders, an alternative to the biopsychiatric model.

On This Day … 26 March

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People (Births)

  • 1905 – Viktor Frankl, Austrian neurologist and psychiatrist (d. 1997).

People (Deaths)

  • 2014 – Roger Birkman, American psychologist and author (b. 1919).
  • 2015 – Tomas Tranströmer, Swedish poet, translator, and psychologist Nobel Prize laureate (b. 1931).

Viktor Frankl

Viktor Emil Frankl (26 March 1905 to 02 September 1997) was an Austrian neurologist, psychiatrist, philosopher, author, and Holocaust survivor.

He was the founder of logotherapy, a school of psychotherapy which describes a search for a life meaning as the central human motivational force. Logotherapy is part of existential and humanistic psychology theories.

Frankl published 39 books. The autobiographical Man’s Search for Meaning, a best-selling book, is based on his experiences in various Nazi concentration camps.

Roger Birkman

Roger Winfred Birkman (01 February 1919 to 26 March 2014) was an American organisational psychologist. He was the creator of The Birkman Method, a workplace psychological assessment. Birkman received his Ph.D. in psychology in 1961 from the University of Texas at Austin. He was the founder and chairman of the board of Birkman International, Inc.

The Birkman Method

The Birkman Method is an online personality, social perception, and occupational interest assessment consisting of ten scales describing occupational preferences (Interests), 11 scales describing “effective behaviours” (Usual behaviours) and 11 scales describing interpersonal and environmental expectations (Needs or Expectations). A corresponding set of 11 scale values was derived to describe “less than effective” behaviours (Stress behaviours). Occupational profiling consists of 22 job families with more than 200 corresponding job titles all connected to O*Net.

The construction and comparative analysis of the Birkman Method is designed to provide insight into what specifically drives a person’s behaviour, with the goal of creating greater choice and more self-responsibility. It attempts to measure social behaviours, underlying expectations of interpersonal and task actions, potential stress reactions to unmet expectations, occupational preferences and organisational strengths. It is empirically supported by reliability and validity studies, including studies using classical test theory (CTT) and item response theory (IRT). The Birkman Method has 3 different types of assessments available.

Tomas Tranströmer

Tomas Gösta Tranströmer 15 April 1931 to 26 March 2015) was a Swedish poet, psychologist and translator. His poems captured the long Swedish winters, the rhythm of the seasons and the palpable, atmospheric beauty of nature. Tranströmer’s work is also characterised by a sense of mystery and wonder underlying the routine of everyday life, a quality which often gives his poems a religious dimension. He has been described as a Christian poet.

Tranströmer is acclaimed as one of the most important Scandinavian writers since the Second World War. Critics praised his poetry for its accessibility, even in translation. His poetry has been translated into over 60 languages. He was the recipient of the 1990 Neustadt International Prize for Literature and the 2011 Nobel Prize in Literature.

What is Treatment-Resistant Depression?

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Introduction

Treatment-resistant depression (TRD) is a term used in clinical psychiatry to describe a condition that affects people with major depressive disorder (MDD) who do not respond adequately to a course of appropriate antidepressant medication within a certain time.

Typical definitions of TRD vary, and they do not include a resistance to psychological therapies. Inadequate response has traditionally been defined as no clinical response whatsoever (e.g. no improvement in depressive symptoms). However, many clinicians consider a response inadequate if the person does not achieve full remission of symptoms. People with treatment-resistant depression who do not adequately respond to antidepressant treatment are sometimes referred to as pseudoresistant. Some factors that contribute to inadequate treatment are: early discontinuation of treatment, insufficient dosage of medication, patient noncompliance, misdiagnosis, and concurrent psychiatric disorders. Cases of treatment-resistant depression may also be referred to by which medications people with TRD are resistant to (e.g.: SSRI-resistant). In TRD adding further treatments such as psychotherapy, lithium, or aripiprazole is weakly supported as of 2019.

Refer to Atypical Depression and Masked Depression.

Risk Factors

Comorbid Psychiatric Disorders

Comorbid psychiatric disorders commonly go undetected in the treatment of depression. If left untreated, the symptoms of these disorders can interfere with both evaluation and treatment. Anxiety disorders are one of the most common disorder types associated with treatment-resistant depression. The two disorders commonly co-exist, and have some similar symptoms. Some studies have shown that patients with both MDD and panic disorder are the most likely to be nonresponsive to treatment. Substance abuse may also be a predictor of treatment-resistant depression. It may cause depressed patients to be noncompliant in their treatment, and the effects of certain substances can worsen the effects of depression. Other psychiatric disorders that may predict treatment-resistant depression include attention deficit hyperactivity disorder, personality disorders, obsessive compulsive disorder, and eating disorders.

Comorbid Medical Disorders

Some people who are diagnosed with treatment-resistant depression may have an underlying undiagnosed health condition that is causing or contributing to their depression. Endocrine disorders like hypothyroidism, Cushing’s disease, and Addison’s disease are among the most commonly identified as contributing to depression. Others include diabetes, coronary artery disease, cancer, HIV, and Parkinson’s disease. Another factor is that medications used to treat comorbid medical disorders may lessen the effectiveness of antidepressants or cause depression symptoms.

Features of Depression

People with depression who also display psychotic symptoms such as delusions or hallucinations are more likely to be treatment resistant. Another depressive feature that has been associated with poor response to treatment is longer duration of depressive episodes. Finally, people with more severe depression and those who are suicidal are more likely to be nonresponsive to antidepressant treatment.

Treatment

There are three basic categories of drug treatment that can be used when a medication course is found to be ineffective. One option is to switch the patient to a different medication. Another option is to add a medication to the patient’s current treatment. This can include combination therapy: the combination of two different types of antidepressants, or augmentation therapy: the addition of a non-antidepressant medication that may increase the effectiveness of the antidepressant.

Medication

Antidepressants

Dose Increase

Increasing the dosage of an antidepressant is a common strategy to treat depression that does not respond after adequate treatment duration. Practitioners who use this strategy will usually increase the dose until the person reports intolerable side effects, symptoms are eliminated, or the dose is increased to the limit of what is considered safe.

Switching Antidepressants

Studies have shown a wide variability in the effectiveness of switching antidepressants, with anywhere from 25-70% of people responding to a different antidepressant. There is support for the effectiveness of switching people to a different SSRI; 50% of people that were non-responsive after taking one SSRI were responsive after taking a second type. Switching people with TRD to a different class of antidepressants may also be effective. People who are non-responsive after taking an SSRI may respond to moclobemide or tricyclic antidepressant, bupropion or an MAOI.

However, the more antidepressants an individual had already tried, the less likely they were to benefit from a new antidepressant trial.

Some off label antidepressants are low dose ketamine and highly serotonergic catecholamines (including very controlled use of MDMA in the treatment of PTSD and crippling depression/anxiety). For lethargic syndromes, dysthymia, or caffeine-resistant amotivation, a dopaminergic stimulant such as methlyphenidate, or even 2.5 mg dextroamphetamine can be helpful.

Primarily dopaminergic or norepinephrine releasing stimulants, in low doses, have been used especially in the past, or in conjunction with a multidisciplinary therapy approach, although more targeted and “mild” agents, including modafinil and atomoxetine are considered first line for both childhood and adult lethargy and inattention disorders, due to their virtually non-existent abuse potential (limited to one or two cases per 10,000), and higher selectivity, safety, and thus slightly broader therapeutic index. When depression is related or co-morbid to an inattention disorder, often ADHD, then both can be carefully managed with the same first line stimulant medication, typically both methylphenidate and lisdexamphetamine.

Other Medications

Medications that have been shown to be effective in people with treatment-resistant depression include lithium, triiodothyronine, benzodiazepines, atypical antipsychotics, and stimulants. Adding lithium may be effective for people taking some types of antidepressants; it does not appear to be effective in patients taking SSRIs. Triiodothyroxine (T3) is a type of thyroid hormone and has been associated with improvement in mood and depression symptoms. Benzodiazepines may improve treatment-resistant depression by decreasing the adverse side effects caused by some antidepressants and therefore increasing patient compliance. Since the entry of olanzapine into psychopharmacology, anecdotal evidence suggests that many psychiatrists have been adding low dose olanzapine to antidepressants and other atypical antipsychotics such as aripiprazole and quetiapine. Eli Lilly, the company that sells both olanzapine and fluoxetine individually, has also released a combination formulation which contains olanzapine and fluoxetine in a single capsule. Some low to moderate quality evidence points to success in the short term (8-12 weeks) using mianserin (or antipsychotics cariprazine, olanzapine, quetiapine or ziprasidone) to augment antidepressant medications.

These have shown promise in treating refractory depression but come with serious side effects. Stimulants such as amphetamines and methylphenidate have also been tested with positive results but have potential for abuse. However, stimulants have been shown to be effective for the unyielding depressed combined lacking addictive personality traits or heart problems.

Ketamine has been tested as a rapid-acting antidepressant for treatment-resistant depression in bipolar disorder, and major depressive disorder.

Research

A 2016 placebo randomised controlled trial (RCT) evaluated the rapid antidepressant effects of the psychedelic ayahuasca in treatment-resistant depression with positive outcome.

Physical Psychiatric Treatments

Electroconvulsive Therapy

Electroconvulsive therapy is generally only considered as a treatment option in severe cases of treatment-resistant depression. It is used when medication has repeatedly failed to improve symptoms, and usually when the patient’s symptoms are so severe that they have been hospitalised. Electroconvulsive therapy has been found to reduce thoughts of suicide and relieve depressive symptoms. It is associated with an increase in glial cell line derived neurotrophic factor.

rTMS

rTMS (repetitive transcranial magnetic stimulation) is gradually becoming recognised as a valuable therapeutic option in treatment-resistant depression. A number of randomised placebo-controlled trials have compared real versus sham rTMS. These trials have consistently demonstrated the efficacy of this treatment against major depression. There have also been a number of meta-analyses of RCTs confirming the efficacy of rTMS in treatment-resistant major depression, as well as naturalistic studies showing its effectiveness in “real world” clinical settings.

dTMS

dTMS (deep transcranial magnetic stimulation) is a continuation of the same idea as rTMS, but with the hope that deeper stimulation of subcortical areas of the brain leads to increased effect. A 2015 systematic review and health technology assessment found lacking evidence in order to recommend the method over either ECT or rTMS because so few studies had been published.

Psychotherapy

There is sparse evidence on the effectiveness of psychotherapy in cases of treatment-resistant depression. However, a review of the literature suggests that it may be an effective treatment option. Psychotherapy may be effective in people with TRD because it can help relieve stress that may contribute to depressive symptoms.

A Cochrane systematic review has shown that psychological therapies (including cognitive behavioural therapy, dialectal behavioural therapy, interpersonal therapy and intensive short-term dynamic psychotherapy) added to usual care (with antidepressants) can be beneficial for depressive symptoms and for response and remission rates over the short term (up to six months) for patients with TRD. Medium‐ (7-12 months) and long‐term (longer than 12 months) effects seem similarly beneficial. Psychological therapies added to usual care (antidepressants) seem as acceptable as usual care alone.

Outcomes

Treatment-resistant depression is associated with more instances of relapse than depression that is responsive to treatment. One study showed that as many as 80% of people with TRD who needed more than one course of treatment relapsed within a year. Treatment-resistant depression has also been associated with lower long-term quality of life.

Another study saw just 8 of 124 patients in remission after two years of regular treatment with therapy and medicines.

Epidemiology

Treatment-resistance is relatively common in people with MDD. Rates of total remission following antidepressant treatment are only 50.4%. In cases of depression treated by a primary care physician, 32% of people partially responded to treatment and 45% did not respond at all.

What is Masked Depression?

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Introduction

Masked depression (MD) was a proposed form of atypical depression in which somatic symptoms or behavioural disturbances dominate the clinical picture and disguise the underlying affective disorder.

The concept (as of March 2021) is not currently supported by the mental health profession.

Refer to Atypical Depression and Treatment-Resistant Depression.

Clinical Manifestations

Somatic manifestations of MD are distinguished by an extreme diversity and include headaches, back pain, abdominal pain etc. Pathological behaviour masking depression may take the form of compulsive gambling, compulsive work, changes in arousal or orgasmic function, decreased libido or, on the contrary, impulsive sexual behaviour, alcoholism, or drug addiction.

Dispute about the Concept

MD has been variously described as “depression sine (without) depression” (K. Schneider, 1925), “latent” depression (Lange J., 1928), “vegetative depression” (R. Lemke, 1949) “hidden” or “masked” depression (Lopez Ibor J.J. [es], 1972; Kielholz J.J., 1983; Pichot P.; Hasson J., 1973), “larvate” or “somatisation depression” (Gayral L., 1972), “depressive equivalents” etc. Most investigators, especially those in the German-speaking countries, assumed masked depression (German: die larvierte Depression) to be endogenous depression. The term was largely used in the 1970s and 1980s, but at the end of the 20th century there was a decline in interest in the study of masked depression. Today this diagnosis does not play a significant clinical or scientific role.

Epidemiology

MD is supposed to be a common clinical phenomenon. According to some authors, masked depression is as frequent as overt depression. Although masked depression can be found at any age, it has been observed more commonly after mid-life.

Making the diagnosis and the management of MD in clinical practice are complicated by the fact that the individual who has MD is unaware of their mental illness. Patients with MD are reluctant to associate their physical symptoms with an affective disorder and refuse mental health care. As a rule, these patients attribute their disturbances to physical illness, seek medical care for them, and report only somatic complaints to their medical professional, with the consequence that many of such depressions are not recognised or are misdiagnosed and mistreated Estimates of depressed patients who are correctly identified and treated range from 5% to 60%. Recent data show that about 10% of people who consult a medical professional for any reason originally suffer from affective disorders disguised by physical symptoms.

Official Diagnostic Status

Current classifications: ICD-10 and DSM-5 do not contain the term “masked depression”.

Some Ukrainian psychiatrists claim that MD is to be qualified as “depression with somatic symptoms” (F 3x.01), according to ICD-10. This means that those who struggle with masked depression often have more physical symptoms such as back pain, abdominal pain, headaches, and even pain during sexual activity or painful periods.

For those with more clinical depression, while they still may have physical symptoms, their symptoms are usually more mental or emotional. This includes feelings of helplessness, extreme and/or persisting sadness, numbness, tiredness, drowsiness, exhaustion, and even suicidal thoughts or feelings.

Diagnostic Criteria

Affective disorders in patients with MD can only be detected by means of a clinician-administered diagnostic interview. Organic exclusion rules and other criteria are used in making the diagnosis of MD. Some physical symptoms of masked depression include general aches, pains including headache, backache, musculoskeletal aches, and other nonpainful symptoms such as changes in appetite and libido, lack of energy, sleep disturbance, dizziness, palpitations, dyspnoea, and gastrointestinal tract disturbances.

What is Atypical Depression?

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Introduction

Atypical depression as it has been known in the DSM IV, is depression that shares many of the typical symptoms of the psychiatric syndromes of major depression or dysthymia but is characterised by improved mood in response to positive events.

In contrast to atypical depression, people with melancholic depression generally do not experience an improved mood in response to normally pleasurable events. Atypical depression also features significant weight gain or an increased appetite, hypersomnia, a heavy sensation in the limbs, and interpersonal rejection sensitivity that results in significant social or occupational impairment.

Despite its name, “atypical” depression does not mean it is uncommon or unusual. The reason for its name is twofold: it was identified with its “unique” symptoms subsequent to the identification of melancholic depression and its responses to the two different classes of antidepressants that were available at the time were different from melancholic depression (i.e. monoamine oxidase inhibitors (MAOIs) had clinically significant benefits for atypical depression, while tricyclics did not).

Atypical depression is four times more common in females than in males. Individuals with atypical features tend to report an earlier age of onset (e.g. while in high school) of their depressive episodes, which also tend to be more chronic and only have partial remission between episodes. Younger individuals may be more likely to have atypical features, whereas older individuals may more often have episodes with melancholic features. Atypical depression has high comorbidity of anxiety disorders, carries more risk of suicidal behaviour, and has distinct personality psychopathology and biological traits.

Atypical depression is more common in individuals with bipolar I, bipolar II, cyclothymia and seasonal affective disorder. Depressive episodes in bipolar disorder tend to have atypical features, as does depression with seasonal patterns.

Refer to Masked Depression and Treatment-Resistant Depression.

Pathophysiology

Significant overlap between atypical and other forms of depression have been observed, though studies suggest there are differentiating factors within the various pathophysiological models of depression. In the endocrine model, evidence suggests the HPA axis is hyperactive in melancholic depression, and hypoactive in atypical depression. Atypical depression can be differentiated from melancholic depression via verbal fluency tests and psychomotor speed tests. Although both show impairment in several areas such as visuospatial memory and verbal fluency, melancholic patients tend to show more impairment than atypical depressed patients.

Furthermore, regarding the inflammatory theory of depression, inflammatory blood markers (cytokines) appear to be more elevated in atypical depression when compared to non-atypical depression.

Diagnosis

The diagnosis of atypical depression is based on the criteria stated in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). The DSM-5 defines atypical depression as a subtype of major depressive disorder that presents with “atypical features”, characterised by:

  • Mood reactivity (i.e., mood brightens in response to actual or potential positive events)
  • At least two of the following:
    • Significant weight gain or increase in appetite (hyperphagia);
    • Hypersomnia (sleeping too much, as opposed to the insomnia present in melancholic depression);
    • Leaden paralysis (i.e., heavy feeling resulting in difficulty moving the arms or legs);
    • Long-standing pattern of interpersonal rejection sensitivity (not limited to episodes of mood disturbance) that results in significant social or occupational impairment.

Criteria are not met for With Melancholic Features or With Catatonic Features during the same episode.

Treatment

Due to the differences in clinical presentation between atypical depression and melancholic depression, studies were conducted in the 1980s and 1990s to assess the therapeutic responsiveness of the available antidepressant pharmacotherapy in this subset of patients. Currently, antidepressants such as SSRIs, SNRIs, NRIs, and mirtazapine are considered the best medications to treat atypical depression due to efficacy and fewer side effects than previous treatments. Bupropion, a norepinephrine reuptake inhibitor, may be uniquely suited to treat the atypical depression symptoms of lethargy and increased appetite in adults. Modafinil is sometimes used successfully as an off-label treatment option.

Before the year 2000, monoamine oxidase inhibitors (MAOIs) were shown to be of superior efficacy compared to other antidepressants for the treatment of atypical depression, and were used as first-line treatment for this clinical presentation. This class of medication fell in popularity with the advent of the aforementioned selective agents, due to concerns of interaction with tyramine-rich foods (such as some aged cheese, certain types of wine, tap beer and fava beans) causing a hypertensive crisis and some – but not all – sympathomimetic drugs, as well as the risk of serotonin syndrome when concomitantly used with serotonin reuptake agents. Despite these concerns, they are still used in treatment-resistant cases, when other options have been exhausted, and usually show greater rates of remission compared to previous pharmacotherapies. They are also generally better tolerated by many patients. There are also newer selective and reversible MAOIs, such as moclobemide, which carry a much lower risk of tyramine potentiation and have fewer interactions with other drugs.

Tricyclic antidepressants (TCAs) were also used prior to the year 2000 for atypical depression, but were not as efficacious as MAOIs, and have fallen out of favour with prescribers due to the less tolerable side effects of TCAs and more adequate therapies being available.

Some evidence supports that psychotherapy such as cognitive behavioural therapy (CBT) has equal efficacy to MAOI. These are talk therapy sessions with psychiatrists to help the individual identify troubling thoughts or experiences that may have affected their mental state, and develop corresponding coping mechanisms for each identified issue.

No robust guidelines for the treatment of atypical depression currently exist.

Epidemiology

True prevalence of atypical depression is difficult to determine. Several studies conducted in patients diagnosed with a depressive disorder show that about 40% exhibit atypical symptoms, with four times more instances found in female patients. Research also supports that atypical depression tends to have an earlier onset, with teenagers and young adults more likely to exhibit atypical depression than older patients. Patients with atypical depression have shown to have higher rates of neglect and abuse in their childhood as well as alcohol and drug disorders in their family. Overall, rejection sensitivity is the most common symptom, and due to some studies forgoing this criterion, there is concern for underestimation of prevalence.

Research

In general, atypical depression tends to cause greater functional impairment than other forms of depression. Atypical depression is a chronic syndrome that tends to begin earlier in life than other forms of depression – usually beginning in the teenage years. Similarly, patients with atypical depression are more likely to suffer from personality disorders and anxiety disorders such as borderline personality disorder, avoidant personality disorder, generalised anxiety disorder, obsessive-compulsive disorder, and bipolar disorder.

Recent research suggests that young people are more likely to suffer from hypersomnia while older people are more likely to suffer from polyphagia.

Medication response differs between chronic atypical depression and acute melancholic depression. Some studies suggest that the older class of antidepressants, MAOIs, may be more effective at treating atypical depression. While the more modern SSRIs and SNRIs are usually quite effective in this illness, the tricyclic antidepressants typically are not. The wakefulness-promoting agent modafinil has shown considerable effect in combating atypical depression, maintaining this effect even after discontinuation of treatment. Antidepressant response can often be enhanced with supplemental medications, such as buspirone, bupropion, or aripiprazole. Psychotherapy, whether alone or in combination with medication, is also an effective treatment in individual and group settings.

On This Day … 25 March

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People (Deaths)

Milton H. Erickson

Milton Hyland Erickson (05 December 1901 to 25 March 1980) was an American psychiatrist and psychologist specialising in medical hypnosis and family therapy.

He was founding president of the American Society for Clinical Hypnosis and a fellow of the American Psychiatric Association, the American Psychological Association, and the American Psychopathological Association.

He is noted for his approach to the unconscious mind as creative and solution-generating. He is also noted for influencing brief therapy, strategic family therapy, family systems therapy, solution focused brief therapy, and neuro-linguistic programming.