Mental Health History – Page 70 – Mental Health Matters

What is a Panic Attack?

Published on 02/03/202102/03/2021 by Andrew Marshall4 Comments

Introduction

Panic attacks are sudden periods of intense fear that may include palpitations, sweating, shaking, shortness of breath, numbness, or a feeling of impending doom. The maximum degree of symptoms occurs within minutes. Typically they last for about 30 minutes but the duration can vary from seconds to hours. There may be a fear of losing control or chest pain. Panic attacks themselves are not dangerous physically.

Panic attacks can occur due to several disorders including panic disorder, social anxiety disorder, post-traumatic stress disorder, drug use disorder, depression, and medical problems. They can either be triggered or occur unexpectedly. Smoking, caffeine, and psychological stress increase the risk of having a panic attack. Before diagnosis, conditions that produce similar symptoms should be ruled out, such as hyperthyroidism, hyperparathyroidism, heart disease, lung disease, drug use, and dysautonomia.

Treatment of panic attacks should be directed at the underlying cause. In those with frequent attacks, counselling or medications may be used. Breathing training and muscle relaxation techniques may also help. Those affected are at a higher risk of suicide.

Signs and Symptoms

People with panic attacks often report a fear of dying or heart attack, flashing vision, faintness or nausea, numbness throughout the body, heavy breathing and hyperventilation, or loss of body control. Some people also suffer from tunnel vision, mostly due to blood flow leaving the head to more critical parts of the body in defence. These feelings may provoke a strong urge to escape or flee the place where the attack began (a consequence of the “fight-or-flight response”, in which the hormone causing this response is released in significant amounts). This response floods the body with hormones, particularly epinephrine (adrenaline), which aid it in defending against harm.

A panic attack can result when up-regulation by the sympathetic nervous system (SNS) is not moderated by the parasympathetic nervous system (PNS). The most common symptoms include trembling, dyspnoea (shortness of breath), heart palpitations, chest pain (or chest tightness), hot flashes, cold flashes, burning sensations (particularly in the facial or neck area), sweating, nausea, dizziness (or slight vertigo), light-headedness, heavy-headedness, hyperventilation, paraesthesia’s’ (tingling sensations), sensations of choking or smothering, difficulty moving, depersonalisation and/or derealization. These physical symptoms are interpreted with alarm in people prone to panic attacks. This results in increased anxiety and forms a positive feedback loop.

Shortness of breath and chest pain are the predominant symptoms. People experiencing a panic attack may incorrectly attribute them to a heart attack and thus seek treatment in an emergency room. Because chest pain and shortness of breath are hallmark symptoms of cardiovascular illnesses, including unstable angina and myocardial infarction (heart attack), a diagnosis of exclusion (ruling out other conditions) must be performed before diagnosing a panic attack. It is especially important to do this for people whose mental health and heart health statuses are unknown. This can be done using an electrocardiogram and mental health assessments.

Panic attacks are distinguished from other forms of anxiety by their intensity and their sudden, episodic nature. They are often experienced in conjunction with anxiety disorders and other psychological conditions, although panic attacks are not generally indicative of a mental disorder.

Causes

There are long-term, biological, environmental, and social causes of panic attacks. In 1993, Fava et al. proposed a staging method of understanding the origins of disorders. The first stage in developing a disorder involves predisposing factors, such as genetics, personality, and a lack of well-being. Panic disorder often occurs in early adulthood, although it may appear at any age. It occurs more frequently in women and more often in people with above-average intelligence. Various twin studies where one identical twin has an anxiety disorder have reported a high incidence of the other twin also having an anxiety disorder diagnosis.

Biological causes may include obsessive-compulsive disorder, postural orthostatic tachycardia syndrome, post-traumatic stress disorder, hypoglycaemia, hyperthyroidism, Wilson’s disease, mitral valve prolapse, pheochromocytoma, and inner ear disturbances (labyrinthitis). Dysregulation of the norepinephrine system in the locus coeruleus, an area of the brain stem, has been linked to panic attacks.

Panic attacks may also occur due to short-term stressors. Significant personal loss, including an emotional attachment to a romantic partner, life transitions, and significant life changes may all trigger a panic attack to occur. A person with an anxious temperament, excessive need for reassurance, hypochondriacal fears, overcautious view of the world, and cumulative stress have been correlated with panic attacks. In adolescents, social transitions may also be a cause.

People will often experience panic attacks as a direct result of exposure to an object/situation that they have a phobia for. Panic attacks may also become situationally-bound when certain situations are associated with panic due to previously experiencing an attack in that particular situation. People may also have a cognitive or behavioural predisposition to having panic attacks in certain situations.

Some maintaining causes include avoidance of panic-provoking situations or environments, anxious/negative self-talk (“what-if” thinking), mistaken beliefs (“these symptoms are harmful and/or dangerous”), and withheld feelings.

Hyperventilation syndrome may occur when a person breathes from the chest, which can lead to over-breathing (exhaling excessive carbon dioxide related to the amount of oxygen in one’s bloodstream). Hyperventilation syndrome can cause respiratory alkalosis and hypocapnia. This syndrome often involves prominent mouth breathing as well. This causes a cluster of symptoms, including rapid heartbeat, dizziness, and lightheadedness, which can trigger panic attacks.

Panic attacks may also be caused by substances. Discontinuation or marked reduction in the dose of a substance such as a drug (drug withdrawal), for example, an antidepressant (antidepressant discontinuation syndrome), can cause a panic attack. According to the Harvard Mental Health Letter, “the most commonly reported side effects of smoking marijuana are anxiety and panic attacks. Studies report that about 20% to 30% of recreational users experience such problems after smoking marijuana.” Cigarette smoking is another substance that has been linked to panic attacks.

A common denominator of current psychiatric approaches to panic disorder is that no real danger exists, and the person’s anxiety is inappropriate.

Panic Disorder

Refer to Panic Disorder.

People who have repeated, persistent attacks or feel severe anxiety about having another attack are said to have panic disorder. Panic disorder is strikingly different from other types of anxiety disorders in that panic attacks are often sudden and unprovoked. However, panic attacks experienced by those with panic disorder may also be linked to or heightened by certain places or situations, making daily life difficult.

Agoraphobia

Refer to Agoraphobia and Hikikomori.

Agoraphobia is an anxiety disorder that primarily consists of the fear of experiencing a difficult or embarrassing situation from which the sufferer cannot escape. Panic attacks are commonly linked to agoraphobia and the fear of not being able to escape a bad situation. As the result, severe sufferers of agoraphobia may become confined to their homes, experiencing difficulty traveling from this “safe place”. The word “agoraphobia” is an English adoption of the Greek words agora (αγορά) and Phobos (φόβος). The term “agora” refers to the place where ancient Greeks used to gather and talk about issues of the city, so it applies to any or all public places; however, the essence of agoraphobia is a fear of panic attacks especially if they occur in public as the victim may feel like he or she has no escape. In the case of agoraphobia caused by a social phobia or social anxiety, sufferers may be very embarrassed by having a panic attack publicly in the first place. This translation is the reason for the common misconception that agoraphobia is a fear of open spaces, and is not clinically accurate. Agoraphobia, as described in this manner, is a symptom professionals check for when making a diagnosis of panic disorder. In Japan, people who exhibit extreme agoraphobia to the point of becoming unwilling or unable to leave their homes are referred to as Hikikomori. The phenomena in general is known by the same name, and it is estimated that roughly half a million Japanese youths are Hikikomori.

People who have had a panic attack in certain situations may develop irrational fears, called phobias, of these situations and begin to avoid them. Eventually, the pattern of avoidance and level of anxiety about another attack may reach the point where individuals with panic disorder are unable to drive or even step out of the house. At this stage, the person is said to have panic disorder with agoraphobia.

Experimentally Induced

Panic attack symptoms can be experimentally induced in the laboratory by various means. Among them, for research purposes, by administering a bolus injection of the neuropeptide cholecystokinin-tetrapeptide (CCK-4). Various animal models of panic attacks have been experimentally studied.

Neurotransmitter Imbalances

Many neurotransmitters are affected when the body is under the increased stress and anxiety that accompany a panic attack. Some include serotonin, GABA (gamma-aminobutyric acid), dopamine, norepinephrine, and glutamate. More research into how these neurotransmitters interact with one another during a panic attack is needed to make any solid conclusions, however.

An increase of serotonin in certain pathways of the brain seems to be correlated with reduced anxiety. More evidence that suggests serotonin plays a role in anxiety is that people who take SSRIs tend to feel a reduction of anxiety when their brain has more serotonin available to use.

The main inhibitory neurotransmitter in the central nervous system (CNS) is GABA. Most of the pathways that use GABA tend to reduce anxiety immediately.

Dopamine’s role in anxiety is not well understood. Some antipsychotic medications that affect dopamine production have been proven to treat anxiety. However, this may be attributed to dopamine’s tendency to increase feelings of self-efficacy and confidence, which indirectly reduces anxiety.

Many physical symptoms of anxiety, such as rapid heart rate and hand tremors, are regulated by norepinephrine. Drugs that counteract norepinephrine’s effect may be effective in reducing the physical symptoms of a panic attack. Nevertheless, some drugs that increase ‘background’ norepinephrine levels such as tricyclics and SNRIs are effective for the long-term treatment of panic attacks, possibly by blunting the norepinephrine spikes associated with panic attacks.

Because glutamate is the primary excitatory neurotransmitter involved in the central nervous system (CNS), it can be found in almost every neural pathway in the body. Glutamate is likely involved in conditioning, which is the process by which certain fears are formed, and extinction, which is the elimination of those fears.

Pathophysiology

The symptoms of a panic attack may cause the person to feel that their body is failing. The symptoms can be understood as follows. First, there is frequently the sudden onset of fear with little provoking stimulus. This leads to a release of adrenaline (epinephrine) which brings about the fight-or-flight response when the body prepares for strenuous physical activity. This leads to an increased heart rate (tachycardia), rapid breathing (hyperventilation) which may be perceived as shortness of breath (dyspnoea), and sweating. Because strenuous activity rarely ensues, the hyperventilation leads to a drop in carbon dioxide levels in the lungs and then in the blood. This leads to shifts in blood pH (respiratory alkalosis or hypocapnia), causing compensatory metabolic acidosis activating chemosensing mechanisms that translate this pH shift into autonomic and respiratory responses.

Moreover, this hypocapnia and release of adrenaline during a panic attack cause vasoconstriction resulting in slightly less blood flow to the head which causes dizziness and lightheadedness. A panic attack can cause blood sugar to be drawn away from the brain and toward the major muscles. Neuroimaging suggests heightened activity in the amygdala, thalamus, hypothalamus, and brainstem regions including the periaqueductal gray, parabrachial nucleus, and Locus coeruleus. In particular, the amygdala has been suggested to have a critical role. The combination of increased activity in the amygdala (fear centre) and brainstem along with decreased blood flow and blood sugar in the brain can lead to decreased activity in the prefrontal cortex (PFC) region of the brain. There is evidence that having an anxiety disorder increases the risk of cardiovascular disease (CVD). Those affected also have a reduction in heart rate variability.

Cardiovascular Disease

People who have been diagnosed with panic disorder have approximately double the risk of coronary heart disease. Certain stress responses to depression also have been shown to increase the risk and those diagnosed with both depression and panic disorder are nearly three times more at risk.

Diagnosis

DSM-5 diagnostic criteria for a panic attack include a discrete period of intense fear or discomfort, in which four (or more) of the following symptoms developed abruptly and reached a peak within minutes:

Palpitations, and/or accelerated heart rate.
Sweating.
Trembling or shaking.
Sensations of shortness of breath or being smothered.
Feeling of choking.
Chest pain or discomfort.
Nausea or abdominal distress.
Feeling dizzy, unsteady, lightheaded, or faint.
Derealization (feelings of unreality) or depersonalisation (being detached from oneself).
Fear of losing control or going insane.
Sense of impending doom.
Paraesthesia’s (numbness or tingling sensations).
Chills or hot flashes..

In DSM-5, culture-specific symptoms (e.g., tinnitus, neck soreness, headache, and uncontrollable screaming or crying) may be seen. Such symptoms should not count as one of the four required symptoms.

Some or all of these symptoms can be found in the presence of a pheochromocytoma.

Screening tools such as the Panic Disorder Severity Scale can be used to detect possible cases of disorder and suggest the need for a formal diagnostic assessment.

Treatment

Panic disorder can be effectively treated with a variety of interventions, including psychological therapies and medication. Cognitive-behavioural therapy (CBT) has the most complete and longest duration of effect, followed by specific selective serotonin reuptake inhibitors (SSRIs). A 2009 review found positive results from therapy and medication and a much better result when the two were combined.

Lifestyle Changes

Caffeine may cause or exacerbate panic anxiety. Anxiety can temporarily increase during withdrawal from caffeine and various other drugs.

Increased and regimented aerobic exercise such as running has been shown to have a positive effect on combating panic anxiety. There is evidence that suggests that this effect is correlated to the release of exercise-induced endorphins and the subsequent reduction of the stress hormone cortisol.

There remains a chance of panic symptoms becoming triggered or being made worse due to increased respiration rate that occurs during aerobic exercise. This increased respiration rate can lead to hyperventilation and hyperventilation syndrome, which mimics symptoms of a heart attack, thus inducing a panic attack. The benefits of incorporating an exercise regimen have shown the best results when paced accordingly.

Muscle relaxation techniques are useful to some individuals. These can be learned using recordings, videos, or books. While muscle relaxation has proved to be less effective than CBT in controlled trials, many people still find at least temporary relief from muscle relaxation.

Breathing Exercises

In the great majority of cases, hyperventilation is involved, exacerbating the effects of the panic attack. Breathing retraining exercise helps to rebalance the oxygen and CO2 levels in the blood.

David D. Burns recommends breathing exercises for those suffering from anxiety. One such breathing exercise is a 5-2-5 count. Using the stomach (or diaphragm) – and not the chest – inhale (feel the stomach come out, as opposed to the chest expanding) for 5 seconds. As the maximal point at inhalation is reached, hold the breath for 2 seconds. Then slowly exhale, over 5 seconds. Repeat this cycle twice and then breathe ‘normally’ for 5 cycles (1 cycle = 1 inhale + 1 exhale). The point is to focus on breathing and relax the heart rate. Regular diaphragmatic breathing may be achieved by extending the out-breath by counting or humming.

Although breathing into a paper bag was a common recommendation for short-term treatment of symptoms of an acute panic attack, it has been criticised as inferior to measured breathing, potentially worsening the panic attack and possibly reducing needed blood oxygen. While the paper bag technique increases needed carbon dioxide and so reduces symptoms, it may excessively lower oxygen levels in the bloodstream.

Capnometry, which provides exhaled CO2 levels, may help guide breathing.

Therapy

According to the American Psychological Association, “most specialists agree that a combination of cognitive and behavioural therapies are the best treatment for panic disorder. Medication might also be appropriate in some cases.” The first part of therapy is largely informational; many people are greatly helped by simply understanding exactly what panic disorder is and how many others suffer from it. Many people who suffer from panic disorder are worried that their panic attacks mean they are “going crazy” or that the panic might induce a heart attack. Cognitive restructuring helps people replace those thoughts with more realistic, positive ways of viewing the attacks. Avoidance behaviour is one of the key aspects that prevent people with frequent panic attacks from functioning healthily. Exposure therapy, which includes repeated and prolonged confrontation with feared situations and body sensations, helps weaken anxiety responses to these external and internal stimuli and reinforce realistic ways of viewing panic symptoms.

In deeper level psychoanalytic approaches, in particular object relations theory, panic attacks are frequently associated with splitting (psychology), paranoid-schizoid and depressive positions, and paranoid anxiety. They are often found comorbid with borderline personality disorder and child sexual abuse. Paranoid anxiety may reach the level of a persecutory anxiety state.

Meditation may also be helpful in the treatment of panic disorders. There was a meta-analysis of the comorbidity of panic disorders and agoraphobia. It used exposure therapy to treat patients over a period. Hundreds of patients were used in these studies and they all met the DSM-IV criteria for both of these disorders. A result was that 32% of patients had a panic episode after treatment. They concluded that the use of exposure therapy has lasting efficacy for a client who is living with a panic disorder and agoraphobia.

The efficacy of group therapy treatment over conventional individual therapy for people with panic disorder with or without agoraphobia appears similar.

Medication

Medication options for panic attacks typically include benzodiazepines and antidepressants. Benzodiazepines are being prescribed less often because of their potential side effects, such as dependence, fatigue, slurred speech, and memory loss. Antidepressant treatments for panic attacks include selective serotonin reuptake inhibitors (SSRIs), serotonin noradrenaline reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), and MAO inhibitors (MAOIs). SSRIs in particular tend to be the first drug treatment used to treat panic attacks. Selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants appear similar for short-term efficacy.

SSRIs carry a relatively low risk since they are not associated with much tolerance or dependence, and are difficult to overdose with. TCAs are similar to SSRIs in their many advantages but come with more common side effects such as weight gain and cognitive disturbances. They are also easier to overdose on. MAOIs are generally suggested for patients who have not responded to other forms of treatment.

While the use of drugs in treating panic attacks can be very successful, it is generally recommended that people also be in some form of therapy, such as CBT. Drug treatments are usually used throughout the duration of panic attack symptoms and discontinued after the patient has been free of symptoms for at least six months. It is usually safest to withdraw from these drugs gradually while undergoing therapy. While drug treatment seems promising for children and adolescents, they are at an increased risk of suicide while taking these medications and their well-being should be monitored closely.

Prognosis

Roughly one-third are treatment-resistant. These people continue to have panic attacks and various other panic disorder symptoms after receiving treatment.

Many people being treated for panic attacks begin to experience limited symptom attacks. These panic attacks are less comprehensive, with fewer than four bodily symptoms being experienced.

It is not unusual to experience only one or two symptoms at a time, such as vibrations in their legs, shortness of breath, or an intense wave of heat traveling up their bodies, which is not similar to hot flashes due to oestrogen shortage. Some symptoms, such as vibrations in the legs, are sufficiently different from any normal sensation that they indicate a panic disorder. Other symptoms on the list can occur in people who may or may not have panic disorder. Panic disorder does not require four or more symptoms to all be present at the same time. Causeless panic and racing heartbeat are sufficient to indicate a panic attack.

Epidemiology

In Europe, about 3% of the population has a panic attack in a given year while in the United States they affect about 11%. They are more common in females than in males. They often begin during puberty or early adulthood. Children and older people are less commonly affected. A meta-analysis was conducted on data collected about twin studies and family studies on the link between genes and panic disorder. The researchers also examined the possibility of a link to phobias, obsessive-compulsive disorder (OCD), and generalised anxiety disorder. The researchers used a database called MEDLINE to accumulate their data. The results concluded that the aforementioned disorders have a genetic component and are inherited or passed down through genes. For the non-phobias, the likelihood of inheriting is 30-40%, and for the phobias, it was 50-60%.

What is Object Relations Theory?

Published on 02/02/2021 by Andrew Marshall16 Comments

Introduction

Object relations theory in psychoanalytic psychology is the process of developing a psyche in relation to others in the childhood environment. It designates theories or aspects of theories that are concerned with the exploration of relationships between real and external people as well as internal images and the relations found in them. It maintains that the infant’s relationship with the mother primarily determines the formation of its personality in adult life. Particularly, the need for attachment is the bedrock of the development of the self or the psychic organisation that creates the sense of identity.

The Theory

While object relations theory is based on psychodynamic theory, it modified it so that the role of biological drives in the formation of adult personality received less emphasis. The theory suggests that the way people relate to others and situations in their adult lives is shaped by family experiences during infancy. For example, an adult who experienced neglect or abuse in infancy would expect similar behaviour from others who remind them of the neglectful or abusive parent from their past. These images of people and events turn into objects in the unconscious that the “self” carries into adulthood, and they are used by the unconscious to predict people’s behaviour in their social relationships and interactions.

The first “object” in someone is usually an internalised image of one’s mother. Internal objects are formed by the patterns in one’s experience of being taken care of as a baby, which may or may not be accurate representations of the actual, external caretakers. Objects are usually internalised images of one’s mother, father, or primary caregiver, although they could also consist of parts of a person such as an infant relating to the breast or things in one’s inner world (one’s internalised image of others). Later experiences can reshape these early patterns, but objects often continue to exert a strong influence throughout life. Objects are initially comprehended in the infant mind by their functions and are termed part objects. The breast that feeds the hungry infant is the “good breast”, while a hungry infant that finds no breast is in relation to the “bad breast”. With a “good enough” facilitating environment, part object functions eventually transform into a comprehension of whole objects. This corresponds with the ability to tolerate ambiguity, to see that both the “good” and the “bad” breast are a part of the same mother figure.

Brief History

The initial line of thought emerged in 1917 with Ferenczi and, early in the 1930s, Sullivan, coiner of the term “interpersonal”. British psychologists Melanie Klein, Donald Winnicott, Harry Guntrip, Scott Stuart, and others extended object relations theory during the 1940s and 1950s. Ronald Fairbairn in 1952 independently formulated his theory of object relations.

The term has been used in many different contexts, which led to different connotations and denotations. While Fairbairn popularised the term “object relations”, Melanie Klein’s work tends to be most commonly identified with the terms “object relations theory” and “British object relations”, at least in contemporary North America, though the influence of ‘what is known as the British independent perspective, which argued that the primary motivation of the child is object seeking rather than drive gratification’, is becoming increasingly recognised. Klein felt that the psychodynamic battleground that Freud proposed occurs very early in life, during infancy. Furthermore, its origins are different from those that Freud proposed. The interactions between infant and mother are so deep and intense that they form the focus of the infant’s structure of drives. Some of these interactions provoke anger and frustration; others provoke strong emotions of dependence as the child begins to recognise the mother is more than a breast from which to feed. These reactions threaten to overwhelm the individuality of the infant. The way in which the infant resolves the conflict, Klein believed, is reflected in the adult’s personality.

Freud originally identified people in a subject’s environment with the term “object” to identify people as the object of drives. Fairbairn took a radical departure from Freud by positing that humans were not seeking satisfaction of the drive, but actually seek the satisfaction that comes in being in relation to real others. Klein and Fairbairn were working along similar lines, but unlike Fairbairn, Klein always held that she was not departing from Freudian theory, but simply elaborating early developmental phenomena consistent with Freudian theory.

Within the London psychoanalytic community, a conflict of loyalties took place between Klein and object relations theory (sometimes referred to as “id psychology”), and Anna Freud and ego psychology. In America, Anna Freud heavily influenced American psychoanalysis in the 1940s, 1950s, and 1960s. American ego psychology was furthered in the works of Hartmann, Kris, Loewenstein, Rapaport, Erikson, Jacobson, and Mahler. In London, those who refused to choose sides were termed the “middle school,” whose members included Michael Balint and D.W. Winnicott. A certain division developed in England between the school of Anna Freud and that of Melanie Klein, which later influenced psychoanalytic politics worldwide. Klein was popularised in South America while A. Freud garnered an American allegiance.

Fairbairn revised much of Freud’s model of the mind. He identified how people who were abused as children internalise that experience. Fairbairn’s “moral defence” is the tendency seen in survivors of abuse to take all the bad upon themselves, each believing he is morally bad so his caretaker object can be regarded as good. This is a use of splitting as a defence to maintain an attachment relationship in an unsafe world. Fairbairn introduced a four-year-old girl with a broken arm to a doctor friend of his. He told the little girl that they were going to find her a new mommy. “Oh no!” the girl cried. “I want my real mommy.” “You mean the mommy that broke your arm?” Fairbairn asked. “I was bad,” the girl replied. She needed to believe that her love object (mother) was all good, so that she could believe she would one day receive the love and nurturing she needed. If she accepted her mother was bad, then she would be bereft and alone in the world, an intolerable state. She used the Moral Defence to make herself bad, but preserve her mother’s goodness.

Kleinian Object Relations Theory

Unconscious Phantasy

Klein termed the psychological aspect of instinct unconscious phantasy (deliberately spelled with ‘ph’ to distinguish it from the word ‘fantasy’). Phantasy is a given of psychic life which moves outward towards the world. These image-potentials are given a priority with the drives and eventually allow the development of more complex states of mental life. Unconscious phantasy in the infant’s emerging mental life is modified by the environment as the infant has contact with reality.

From the moment the infant starts interacting with the outer world, he is engaged in testing his phantasies in a reality setting. I want to suggest that the origin of thought lies in this process of testing phantasy against reality; that is, that thought is not only contrasted with phantasy, but based on it and derived from it.

The role of unconscious phantasy is essential in the development of a capacity for thinking. In Bion’s terms, the phantasy image is a preconception that will not be a thought until experience combines with a realisation in the world of experience. The preconception and realization combine to take form as a concept that can be thought. The classic example of this is the infant’s observed rooting for the nipple in the first hours of life. The instinctual rooting is the preconception. The provision of the nipple provides the realisation in the world of experience, and through time, with repeated experience, the preconception and realisation combined to create the concept. Mental capacity builds upon previous experience as the environment and infant interact.

The first bodily experiences begin to build up the first memories, and external realities are progressively woven into the texture of phantasy. Before long, the child’s phantasies are able to draw upon plastic images as well as sensations – visual, auditory, kinaesthetic, touch, taste, smell images, etc. And these plastic images and dramatic representations of phantasy are progressively elaborated along with articulated perceptions of the external world.

With adequate care, the infant is able to tolerate increasing awareness of experience which is underlain by unconscious phantasy and leads to attainment of consecutive developmental achievements, “the positions” in Kleinian theory.

Projective Identification

As a specific term, projective identification is introduced by Klein in “Notes on some schizoid mechanisms.”

[Projection] helps the ego to overcome anxiety by ridding it of danger and badness. Introjection of the good object is also used by the ego as a defence against anxiety. . . .The processes of splitting off parts of the self and projecting them into objects are thus of vital importance for normal development as well as for abnormal object-relation. The effect of introjection on object relations is equally important. The introjection of the good object, first of all the mother’s breast, is a precondition for normal development . . . It comes to form a focal point in the ego and makes for cohesiveness of the ego. . . . I suggest for these processes the term ‘projective identification’.

Klein imagined this function as a defence which contributes to the normal development of the infant, including ego structure and the development of object relations. The introjection of the good breast provides a location where one can hide from persecution, an early step in developing a capacity to self-soothe.

Ogden identifies four functions that projective identification may serve. As in the traditional Kleinian model, it serves as a defence. Projective identification serves as a mode of communication. It is a form of object relations, and “a pathway for psychological change.” As a form of object relationship, projective identification is a way of relating with others who are not seen as entirely separate from the individual. Instead, this relating takes place “between the stage of the subjective object and that of true object relatedness”.

The Paranoid-Schizoid and Depressive Positions

The positions of Kleinian theory, underlain by unconscious phantasy, are stages in the normal development of ego and object relationships, each with its own characteristic defences and organizational structure. The paranoid-schizoid and depressive positions occur in the pre-oedipal, oral phase of development.

In contrast to Fairbairn and later Guntrip, Klein believed that both good and bad objects are introjected by the infant, the internalisation of good objects being essential to the development of healthy ego function. Klein conceptualised the depressive position as “the most mature form of psychological organisation”, which continues to develop throughout the life span.

The depressive position occurs during the second quarter of the first year. Prior to that the infant is in the paranoid-schizoid position, which is characterised by persecutory anxieties and the mechanisms of splitting, projection, introjection, and omnipotence – which includes idealising and denial – to defend against these anxieties. Depressive and paranoid-schizoid modes of experience continue to intermingle throughout the first few years of childhood.

Paranoid-Schizoid Position

The paranoid-schizoid position is characterised by part object relationships. Part objects are a function of splitting, which takes place in phantasy. At this developmental stage, experience can only be perceived as all good or all bad. As part objects, it is the function that is identified by the experiencing self, rather than whole and autonomous others. The hungry infant desires the good breast who feeds it. Should that breast appear, it is the good breast. If the breast does not appear, the hungry and now frustrated infant, in its distress, has destructive phantasies dominated by oral aggression towards the bad, hallucinated breast.

Klein notes that in splitting the object, the ego is also split. The infant who phantasies destruction of the bad breast is not the same infant that takes in the good breast, at least not until obtaining the depressive position, at which point good and bad can be tolerated simultaneously in the same person and the capacity for remorse and reparation ensue.

The anxieties of the paranoid schizoid position are of a persecutory nature, fear of the ego’s annihilation. Splitting allows good to stay separate from bad. Projection is an attempt to eject the bad in order to control through omnipotent mastery. Splitting is never fully effective, according to Klein, as the ego tends towards integration.

Depressive Position

Klein saw the depressive position as an important developmental milestone that continues to mature throughout the life span. The splitting and part object relations that characterise the earlier phase are succeeded by the capacity to perceive that the other who frustrates is also the one who gratifies. Schizoid defences are still in evidence, but feelings of guilt, grief, and the desire for reparation gain dominance in the developing mind.

In the depressive position, the infant is able to experience others as whole, which radically alters object relationships from the earlier phase. “Before the depressive position, a good object is not in any way the same thing as a bad object. It is only in the depressive position that polar qualities can be seen as different aspects of the same object.” Increasing nearness of good and bad brings a corresponding integration of ego.

In a development which Grotstein terms the “primal split”, the infant becomes aware of separateness from the mother. This awareness allows guilt to arise in response to the infant’s previous aggressive phantasies when bad was split from good. The mother’s temporary absences allow for continuous restoration of her “as an image of representation” in the infant mind. Symbolic thought may now arise, and can only emerge once access to the depressive position has been obtained. With the awareness of the primal split, a space is created in which the symbol, the symbolised, and the experiencing subject coexist. History, subjectivity, interiority, and empathy all become possible.

The anxieties characteristic of the depressive position shift from a fear of being destroyed to a fear of destroying others. In fact or phantasy, one now realises the capacity to harm or drive away a person who one ambivalently loves. The defences characteristic of the depressive position include the manic defences, repression and reparation. The manic defences are the same defences evidenced in the paranoid-schizoid position, but now mobilised to protect the mind from depressive anxiety. As the depressive position brings about an increasing integration in the ego, earlier defences change in character, becoming less intense and allowing for in increased awareness of psychic reality.

In working through depressive anxiety, projections are withdrawn, allowing the other more autonomy, reality, and a separate existence. The infant, whose destructive phantasies were directed towards the bad mother who frustrated, now begins to realise that bad and good, frustrating and satiating, it is always the same mother. Unconscious guilt for destructive phantasies arises in response to the continuing love and attention provided by caretakers.

[As] fears of losing the loved one become active, a very important step is made in the development. These feelings of guilt and distress now enter as a new element into the emotion of love. They become an inherent part of love, and influence it profoundly both in quality and quantity.

From this developmental milestone come a capacity for sympathy, responsibility to and concern for others, and an ability to identify with the subjective experience of people one cares about. With the withdrawal of the destructive projections, repression of the aggressive impulses takes place. The child allows caretakers a more separate existence, which facilitates increasing differentiation of inner and outer reality. Omnipotence is lessened, which corresponds to a decrease in guilt and the fear of loss.

When all goes well, the developing child is able to comprehend that external others are autonomous people with their own needs and subjectivity.

Previously, extended absences of the object (the good breast, the mother) was experienced as persecutory, and, according to the theory of unconscious phantasy, the persecuted infant phantasies destruction of the bad object. The good object who then arrives is not the object which did not arrive. Likewise, the infant who destroyed the bad object is not the infant who loves the good object.

In phantasy, the good internal mother can be psychically destroyed by the aggressive impulses. It is crucial that the real parental figures are around to demonstrate the continuity of their love. In this way, the child perceives that what happens to good objects in phantasy does not happen to them in reality. Psychic reality is allowed to evolve as a place separate from the literalness of the physical world.

Through repeated experience with good enough parenting, the internal image that the child has of external others, that is the child’s internal object, is modified by experience and the image transforms, merging experiences of good and bad which becomes more similar to the real object (e.g. the mother, who can be both good and bad). In Freudian terms, the pleasure principle is modified by the reality principle.

Melanie Klein saw this surfacing from the depressive position as a prerequisite for social life. Moreover, she viewed the establishment of an inside and an outside world as the start of interpersonal relationships.

Klein argued that people who never succeed in working through the depressive position in their childhood will, as a result, continue to struggle with this problem in adult life. For example: the cause that a person may maintain suffering from intense guilt feelings over the death of a loved one, may be found in the unworked- through depressive position. The guilt is there because of a lack of differentiation between phantasy and reality. It also functions as a defence mechanism to defend the self against unbearable feelings of sadness and sorrow, and the internal object of the loved one against the unbearable rage of the self, which, it is feared, could destroy the internal object forever.

Further Thinking Regarding the Positions

Wilfred Bion articulates the dynamic nature of the positions, a point emphasised by Thomas Ogden, and expanded by John Steiner in terms of ‘”The equilibrium between the paranoid-schizoid and the depressive positions”‘. Ogden and James Grotstein have continued to explore early infantile states of mind, and incorporating the work of Donald Meltzer, Ester Bick and others, postulate a position preceding the paranoid-schizoid. Grotstein, following Bion, also hypothesizes a transcendent position which emerges following attainment of the depressive position. This aspect of both Ogden and Grotstein’s work remains controversial for many within classical object relations theory.

Death Drive

Sigmund Freud developed the concept object relation to describe or emphasize that bodily drives satisfy their need through a medium, an object, on a specific focus. The central thesis in Melanie Klein’s object relations theory was that objects play a decisive role in the development of a subject and can be either part-objects or whole-objects, i.e. a single organ (a mother’s breast) or a whole person (a mother). Consequently, both a mother or just the mother’s breast can be the focus of satisfaction for a drive. Furthermore, according to traditional psychoanalysis, there are at least two types of drives, the libido (mythical counterpart: Eros), and the death drive, mortido (mythical counterpart: Thanatos). Thus, the objects can be receivers of both love and hate, the affective effects of the libido and the death drive.

Ronald Fairbairn’s Six Ego Positions

Fairbairn posited six ego positions or inner voices, or 3 pairs:

The Whole Ego relating to the Good Object, is the healthy inner child relating to the patient and nurturing inner parent.
- This is the part of the inner world that object relations therapists try to expand and grow.
The Antilibidinal Ego relating to the Bad Object, is the depressed, angry or hopeless inner child relating to the rejecting or neglectful inner parent.
- Whenever someone speaks in a tantrum-like way they are speaking from the Antilibidinal Ego, and they are speaking to the Bad Object.
- Whenever someone is overly critical and harshly judgmental they are speaking from the Bad Object part of their personality, and are speaking to the Antilibidinal Ego (hopeless inner child).
The Libidinal Ego relating to the Exciting Object, is the gullible and overly hopeful inner child relating to the exciting over-promising inner parent.
- Whenever a person goes back to their cheating or abusive spouse they are operating from their Libidinal Ego and relating to the Exciting Object in their inner worlds.
- Whenever they are in an addiction they are treating whatever they are addicted to as if it were an Exciting Object.

The Fairbairnian object relations therapist imagines that all interactions between the client and the therapist are occurring in the client’s inner object relations world, in one of the three dyads. If the client thinks the therapist is wise and compassionate the therapist sees this as an interaction between the client’s Libidinal Ego and Exciting Object. If the client is angry at the therapist for not meeting the client’s needs, the therapist might see it as an interaction between the client’s Antilibidinal Ego and the Bad Object. The therapist might ask the client if this particular interaction reminds the client of something from childhood.

The Fairbairnian object relations therapist also uses his/her own emotional reactions as therapeutic cues. If the therapist is feeling irritated at the client, or bored, he/she might interpret that as a re-enactment of the Antilibidinal Ego and the Bad Object, with the therapist cast in the role of Bad Object. If the therapist can patiently be an empathic therapist through the client’s re-enactment, then the client has a new experience to incorporate into their inner object world, hopefully expanding their inner picture of their Good Object. Cure is seen as the client being able to receive from their inner Good Object often enough to have a more stable peaceful life.

The Fairbairnian object relations Therapist also uses their mistakes in the therapy. If the therapist has absent mindedly made a mistake that hurts the client, the therapist admits the mistake, and empathizes with the client’s pain, but instead of apologising, the therapist asks: How did this mistake in therapy re-enact a childhood scene?

Numerous research studies have found that most all models of psychotherapy are equally helpful, the difference mainly being the quality of the individual therapist, not the theory the therapist subscribes to. Object Relations Theory attempts to explain this phenomenon via the theory of the Good Object. If a therapist can be patient and empathic, most clients improve their functioning in their world. The client carries with them a picture of the empathic therapist that helps them cope with the stressors of daily life, regardless of what theory of psychology they subscribe to.

Continuing Developments in the Theory

Attachment theory, researched by John Bowlby and others, has continued to deepen our understanding of early object relationships. While a different strain of psychoanalytic theory and research, the findings in attachment studies have continued to support the validity of the developmental progressions described in object relations. Recent decades in developmental psychological research, for example on the onset of a “theory of mind” in children, has suggested that the formation of the mental world is enabled by the infant-parent interpersonal interaction which was the main thesis of British object-relations tradition (e.g. Fairbairn, 1952).

While object relations theory grew out of psychoanalysis, it has been applied to the general fields of psychiatry and psychotherapy by such authors as N. Gregory Hamilton and Glen O. Gabbard. In making object relations theory more useful as a general psychology N. Gregory Hamilton added the specific ego functions to Otto F. Kernberg’s concept of object relations units.

What is Neuroscience?

Published on 02/01/2021 by Andrew Marshall7 Comments

Introduction

Neuroscience (or neurobiology) is the scientific study of the nervous system. It is a multidisciplinary science that combines physiology, anatomy, molecular biology, developmental biology, cytology, mathematical modelling, and psychology to understand the fundamental and emergent properties of neurons and neural circuits. The understanding of the biological basis of learning, memory, behaviour, perception, and consciousness has been described by Eric Kandel as the “ultimate challenge” of the biological sciences.

The scope of neuroscience has broadened over time to include different approaches used to study the nervous system at different scales and the techniques used by neuroscientists have expanded enormously, from molecular and cellular studies of individual neurons to imaging of sensory, motor and cognitive tasks in the brain.

Brief History

The earliest study of the nervous system dates to ancient Egypt. Trepanation, the surgical practice of either drilling or scraping a hole into the skull for the purpose of curing head injuries or mental disorders, or relieving cranial pressure, was first recorded during the Neolithic period. Manuscripts dating to 1700 BC indicate that the Egyptians had some knowledge about symptoms of brain damage.

Early views on the function of the brain regarded it to be a “cranial stuffing” of sorts. In Egypt, from the late Middle Kingdom onwards, the brain was regularly removed in preparation for mummification. It was believed at the time that the heart was the seat of intelligence. According to Herodotus, the first step of mummification was to “take a crooked piece of iron, and with it draw out the brain through the nostrils, thus getting rid of a portion, while the skull is cleared of the rest by rinsing with drugs.”

The view that the heart was the source of consciousness was not challenged until the time of the Greek physician Hippocrates. He believed that the brain was not only involved with sensation – since most specialised organs (e.g. eyes, ears, tongue) are located in the head near the brain – but was also the seat of intelligence. Plato also speculated that the brain was the seat of the rational part of the soul. Aristotle, however, believed the heart was the centre of intelligence and that the brain regulated the amount of heat from the heart. This view was generally accepted until the Roman physician Galen, a follower of Hippocrates and physician to Roman gladiators, observed that his patients lost their mental faculties when they had sustained damage to their brains.

Abulcasis, Averroes, Avicenna, Avenzoar, and Maimonides, active in the Medieval Muslim world, described a number of medical problems related to the brain. In Renaissance Europe, Vesalius (1514-1564), René Descartes (1596-1650), Thomas Willis (1621-1675) and Jan Swammerdam (1637-1680) also made several contributions to neuroscience.

Luigi Galvani’s pioneering work in the late 1700s set the stage for studying the electrical excitability of muscles and neurons. In the first half of the 19th century, Jean Pierre Flourens pioneered the experimental method of carrying out localised lesions of the brain in living animals describing their effects on motricity, sensibility and behaviour. In 1843 Emil du Bois-Reymond demonstrated the electrical nature of the nerve signal, whose speed Hermann von Helmholtz proceeded to measure, and in 1875 Richard Caton found electrical phenomena in the cerebral hemispheres of rabbits and monkeys. Adolf Beck published in 1890 similar observations of spontaneous electrical activity of the brain of rabbits and dogs. Studies of the brain became more sophisticated after the invention of the microscope and the development of a staining procedure by Camillo Golgi during the late 1890s. The procedure used a silver chromate salt to reveal the intricate structures of individual neurons. His technique was used by Santiago Ramón y Cajal and led to the formation of the neuron doctrine, the hypothesis that the functional unit of the brain is the neuron. Golgi and Ramón y Cajal shared the Nobel Prize in Physiology or Medicine in 1906 for their extensive observations, descriptions, and categorizations of neurons throughout the brain.

In parallel with this research, work with brain-damaged patients by Paul Broca suggested that certain regions of the brain were responsible for certain functions. At the time, Broca’s findings were seen as a confirmation of Franz Joseph Gall’s theory that language was localised and that certain psychological functions were localised in specific areas of the cerebral cortex. The localisation of function hypothesis was supported by observations of epileptic patients conducted by John Hughlings Jackson, who correctly inferred the organisation of the motor cortex by watching the progression of seizures through the body. Carl Wernicke further developed the theory of the specialisation of specific brain structures in language comprehension and production. Modern research through neuroimaging techniques, still uses the Brodmann cerebral cytoarchitectonic map (referring to study of cell structure) anatomical definitions from this era in continuing to show that distinct areas of the cortex are activated in the execution of specific tasks.

During the 20th century, neuroscience began to be recognised as a distinct academic discipline in its own right, rather than as studies of the nervous system within other disciplines. Eric Kandel and collaborators have cited David Rioch, Francis O. Schmitt, and Stephen Kuffler as having played critical roles in establishing the field. Rioch originated the integration of basic anatomical and physiological research with clinical psychiatry at the Walter Reed Army Institute of Research, starting in the 1950s. During the same period, Schmitt established a neuroscience research programme within the Biology Department at the Massachusetts Institute of Technology, bringing together biology, chemistry, physics, and mathematics. The first freestanding neuroscience department (then called Psychobiology) was founded in 1964 at the University of California, Irvine by James L. McGaugh. This was followed by the Department of Neurobiology at Harvard Medical School, which was founded in 1966 by Stephen Kuffler.

The understanding of neurons and of nervous system function became increasingly precise and molecular during the 20th century. For example, in 1952, Alan Lloyd Hodgkin and Andrew Huxley presented a mathematical model for transmission of electrical signals in neurons of the giant axon of a squid, which they called “action potentials”, and how they are initiated and propagated, known as the Hodgkin-Huxley model. In 1961–1962, Richard FitzHugh and J. Nagumo simplified Hodgkin-Huxley, in what is called the FitzHugh-Nagumo model. In 1962, Bernard Katz modelled neurotransmission across the space between neurons known as synapses. Beginning in 1966, Eric Kandel and collaborators examined biochemical changes in neurons associated with learning and memory storage in Aplysia. In 1981 Catherine Morris and Harold Lecar combined these models in the Morris-Lecar model. Such increasingly quantitative work gave rise to numerous biological neuron models and models of neural computation.

As a result of the increasing interest about the nervous system, several prominent neuroscience organizations have been formed to provide a forum to all neuroscientist during the 20th century. For example, the International Brain Research Organisation was founded in 1961, the International Society for Neurochemistry in 1963, the European Brain and Behaviour Society in 1968, and the Society for Neuroscience in 1969. Recently, the application of neuroscience research results has also given rise to applied disciplines as neuroeconomics, neuroeducation, neuroethics, and neurolaw.

Over time, brain research has gone through philosophical, experimental, and theoretical phases, with work on brain simulation predicted to be important in the future.

Modern Neuroscience

The scientific study of the nervous system increased significantly during the second half of the twentieth century, principally due to advances in molecular biology, electrophysiology, and computational neuroscience. This has allowed neuroscientists to study the nervous system in all its aspects: how it is structured, how it works, how it develops, how it malfunctions, and how it can be changed.

For example, it has become possible to understand, in much detail, the complex processes occurring within a single neuron. Neurons are cells specialised for communication. They are able to communicate with neurons and other cell types through specialised junctions called synapses, at which electrical or electrochemical signals can be transmitted from one cell to another. Many neurons extrude a long thin filament of axoplasm called an axon, which may extend to distant parts of the body and are capable of rapidly carrying electrical signals, influencing the activity of other neurons, muscles, or glands at their termination points. A nervous system emerges from the assemblage of neurons that are connected to each other.

The vertebrate nervous system can be split into two parts: the central nervous system (defined as the brain and spinal cord), and the peripheral nervous system. In many species – including all vertebrates – the nervous system is the most complex organ system in the body, with most of the complexity residing in the brain. The human brain alone contains around one hundred billion neurons and one hundred trillion synapses; it consists of thousands of distinguishable substructures, connected to each other in synaptic networks whose intricacies have only begun to be unravelled. At least one out of three of the approximately 20,000 genes belonging to the human genome is expressed mainly in the brain.

Due to the high degree of plasticity of the human brain, the structure of its synapses and their resulting functions change throughout life.

Making sense of the nervous system’s dynamic complexity is a formidable research challenge. Ultimately, neuroscientists would like to understand every aspect of the nervous system, including how it works, how it develops, how it malfunctions, and how it can be altered or repaired. Analysis of the nervous system is therefore performed at multiple levels, ranging from the molecular and cellular levels to the systems and cognitive levels. The specific topics that form the main foci of research change over time, driven by an ever-expanding base of knowledge and the availability of increasingly sophisticated technical methods. Improvements in technology have been the primary drivers of progress. Developments in electron microscopy, computer science, electronics, functional neuroimaging, and genetics and genomics have all been major drivers of progress.

Molecular and Cellular Neuroscience

Basic questions addressed in molecular neuroscience include the mechanisms by which neurons express and respond to molecular signals and how axons form complex connectivity patterns. At this level, tools from molecular biology and genetics are used to understand how neurons develop and how genetic changes affect biological functions. The morphology, molecular identity, and physiological characteristics of neurons and how they relate to different types of behaviour are also of considerable interest.

Questions addressed in cellular neuroscience include the mechanisms of how neurons process signals physiologically and electrochemically. These questions include how signals are processed by neurites and somas and how neurotransmitters and electrical signals are used to process information in a neuron. Neurites are thin extensions from a neuronal cell body, consisting of dendrites (specialised to receive synaptic inputs from other neurons) and axons (specialised to conduct nerve impulses called action potentials). Somas are the cell bodies of the neurons and contain the nucleus.

Another major area of cellular neuroscience is the investigation of the development of the nervous system. Questions include the patterning and regionalisation of the nervous system, neural stem cells, differentiation of neurons and glia (neurogenesis and gliogenesis), neuronal migration, axonal and dendritic development, trophic interactions, and synapse formation.

Computational neurogenetic modelling is concerned with the development of dynamic neuronal models for modelling brain functions with respect to genes and dynamic interactions between genes.

Neural Circuits and Systems

Questions in systems neuroscience include how neural circuits are formed and used anatomically and physiologically to produce functions such as reflexes, multisensory integration, motor coordination, circadian rhythms, emotional responses, learning, and memory. In other words, they address how these neural circuits function in large-scale brain networks, and the mechanisms through which behaviours are generated. For example, systems level analysis addresses questions concerning specific sensory and motor modalities: how does vision work? How do songbirds learn new songs and bats localize with ultrasound? How does the somatosensory system process tactile information? The related fields of neuroethology and neuropsychology address the question of how neural substrates underlie specific animal and human behaviours. Neuroendocrinology and psychoneuroimmunology examine interactions between the nervous system and the endocrine and immune systems, respectively. Despite many advancements, the way that networks of neurons perform complex cognitive processes and behaviours is still poorly understood.

Cognitive and Behavioural Neuroscience

Cognitive neuroscience addresses the questions of how psychological functions are produced by neural circuitry. The emergence of powerful new measurement techniques such as neuroimaging (e.g. fMRI, PET, SPECT), EEG, MEG, electrophysiology, optogenetics and human genetic analysis combined with sophisticated experimental techniques from cognitive psychology allows neuroscientists and psychologists to address abstract questions such as how cognition and emotion are mapped to specific neural substrates. Although many studies still hold a reductionist stance looking for the neurobiological basis of cognitive phenomena, recent research shows that there is an interesting interplay between neuroscientific findings and conceptual research, soliciting and integrating both perspectives. For example, neuroscience research on empathy solicited an interesting interdisciplinary debate involving philosophy, psychology and psychopathology. Moreover, the neuroscientific identification of multiple memory systems related to different brain areas has challenged the idea of memory as a literal reproduction of the past, supporting a view of memory as a generative, constructive and dynamic process.

Neuroscience is also allied with the social and behavioural sciences as well as nascent interdisciplinary fields such as neuroeconomics, decision theory, social neuroscience, and neuromarketing to address complex questions about interactions of the brain with its environment. A study into consumer responses for example uses EEG to investigate neural correlates associated with narrative transportation into stories about energy efficiency.

Computational Neuroscience

Questions in computational neuroscience can span a wide range of levels of traditional analysis, such as development, structure, and cognitive functions of the brain. Research in this field utilises mathematical models, theoretical analysis, and computer simulation to describe and verify biologically plausible neurons and nervous systems. For example, biological neuron models are mathematical descriptions of spiking neurons which can be used to describe both the behaviour of single neurons as well as the dynamics of neural networks. Computational neuroscience is often referred to as theoretical neuroscience.

Nanoparticles in medicine are versatile in treating neurological disorders showing promising results in mediating drug transport across the blood brain barrier. Implementing nanoparticles in antiepileptic drugs enhances their medical efficacy by increasing bioavailability in the bloodstream, as well as offering a measure of control in release time concentration. Although nanoparticles can assist therapeutic drugs by adjusting physical properties to achieve desirable effects, inadvertent increases in toxicity often occur in preliminary drug trials. Furthermore, production of nanomedicine for drug trials is economically consuming, hindering progress in their implementation. Computational models in nanoneuroscience provide alternatives to study the efficacy of nanotechnology-based medicines in neurological disorders while mitigating potential side effects and development costs.

Nanomaterials often operate at length scales between classical and quantum regimes. Due to the associated uncertainties at the length scales that nanomaterials operate, it is difficult to predict their behaviour prior to in vivo studies. Classically, the physical processes which occur throughout neurons are analogous to electrical circuits. Designers focus on such analogies and model brain activity as a neural circuit. Success in computational modelling of neurons have led to the development of stereochemical models that accurately predict acetylcholine receptor-based synapses operating at microsecond time scales.

Ultrafine nanoneedles for cellular manipulations are thinner than the smallest single walled carbon nanotubes. Computational quantum chemistry is used to design ultrafine nanomaterials with highly symmetrical structures to optimise geometry, reactivity and stability.

Behaviour of nanomaterials are dominated by long ranged non-bonding interactions. Electrochemical processes that occur throughout the brain generate an electric field which can inadvertently affect the behaviour of some nanomaterials. Molecular dynamics simulations can mitigate the development phase of nanomaterials as well as prevent neural toxicity of nanomaterials following in vivo clinical trials. Testing nanomaterials using molecular dynamics optimizes nano characteristics for therapeutic purposes by testing different environment conditions, nanomaterial shape fabrications, nanomaterial surface properties, etc without the need for in vivo experimentation. Flexibility in molecular dynamic simulations allows medical practitioners to personalise treatment. Nanoparticle related data from translational nanoinformatics links neurological patient specific data to predict treatment response.

Nano-Neurotechnology

The visualization of neuronal activity is of key importance in the study of neurology. Nano-imaging tools with nanoscale resolution help in these areas. These optical imaging tools are PALM and STORM which helps visualise nanoscale objects within cells. Pampaloni states that, so far, these imaging tools revealed the dynamic behaviour and organisation of the actin cytoskeleton inside the cells, which will assist in understanding how neurons probe their involvement during neuronal outgrowth and in response to injury, and how they differentiate axonal processes and characterisation of receptor clustering and stoichiometry at the plasma inside the synapses, which are critical for understanding how synapses respond to changes in neuronal activity. These past works focused on devices for stimulation or inhibition of neural activity, but the crucial aspect is the ability for the device to simultaneously monitor neural activity. The major aspect that is to be improved in the nano imaging tools is the effective collection of the light as a major problem is that biological tissue are dispersive media that do not allow a straightforward propagation and control of light. These devices use nanoneedle and nanowire (NWs) for probing and stimulation.

NWs are artificial nano- or micro-sized “needles” that can provide high-fidelity electrophysiological recordings if used as microscopic electrodes for neuronal recordings. NWs are an attractive as they are highly functional structures that offer unique electronic properties that are affected by biological/chemical species adsorbed on their surface; mostly the conductivity. This conductivity variance depending on chemical species present allows enhanced sensing performances. NWs are also able to act as non-invasive and highly local probes. These versatility of NWs makes it optimal for interfacing with neurons due to the fact that the contact length along the axon (or the dendrite projection crossing a NW) is just about 20 nm.

Neuroscience and Medicine

Neurology, psychiatry, neurosurgery, psychosurgery, anesthesiology and pain medicine, neuropathology, neuroradiology, ophthalmology, otolaryngology, clinical neurophysiology, addiction medicine, and sleep medicine are some medical specialties that specifically address the diseases of the nervous system. These terms also refer to clinical disciplines involving diagnosis and treatment of these diseases.

Neurology works with diseases of the central and peripheral nervous systems, such as amyotrophic lateral sclerosis (ALS) and stroke, and their medical treatment. Psychiatry focuses on affective, behavioural, cognitive, and perceptual disorders. Anaesthesiology focuses on perception of pain, and pharmacologic alteration of consciousness. Neuropathology focuses upon the classification and underlying pathogenic mechanisms of central and peripheral nervous system and muscle diseases, with an emphasis on morphologic, microscopic, and chemically observable alterations. Neurosurgery and psychosurgery work primarily with surgical treatment of diseases of the central and peripheral nervous systems.

Translational Research

Recently, the boundaries between various specialties have blurred, as they are all influenced by basic research in neuroscience. For example, brain imaging enables objective biological insight into mental illnesses, which can lead to faster diagnosis, more accurate prognosis, and improved monitoring of patient progress over time.

Integrative neuroscience describes the effort to combine models and information from multiple levels of research to develop a coherent model of the nervous system. For example, brain imaging coupled with physiological numerical models and theories of fundamental mechanisms may shed light on psychiatric disorders.

Nanoneuroscience

One of the main goals of nanoneuroscience is to gain a detailed understanding of how the nervous system operates and, thus, how neurons organise themselves in the brain. Consequently, creating drugs and devices that are able to cross the blood brain barrier (BBB) are essential to allow for detailed imaging and diagnoses. The blood brain barrier functions as a highly specialised semipermeable membrane surrounding the brain, preventing harmful molecules that may be dissolved in the circulation blood from entering the central nervous system.

The main two hurdles for drug-delivering molecules to access the brain are size (must have a molecular weight < 400 Da) and lipid solubility. Physicians hope to circumvent difficulties in accessing the central nervous system through viral gene therapy. This often involves direct injection into the patient’s brain or cerebral spinal fluid. The drawback of this therapy is that it is invasive and carries a high risk factor due to the necessity of surgery for the treatment to be administered. Because of this, only 3.6% of clinical trials in this field have progressed to stage III since the concept of gene therapy was developed in the 1980s.

Another proposed way to cross the BBB is through temporary intentional disruption of the barrier. This method was first inspired by certain pathological conditions that were discovered to break down this barrier by themselves, such as Alzheimer’s disease, Parkinson’s disease, stroke, and seizure conditions.

Nanoparticles are unique from macromolecules because their surface properties are dependent on their size, allowing for strategic manipulation of these properties (or, “programming”) by scientists that would not be possible otherwise. Likewise, nanoparticle shape can also be varied to give a different set of characteristics based on the surface area to volume ratio of the particle.

Nanoparticles have promising therapeutic effects when treating neurodegenerative diseases. Oxygen reactive polymer (ORP) is a nano-platform programmed to react with oxygen and has been shown to detect and reduce the presence of reactive oxygen species (ROS) formed immediately after traumatic brain injuries. Nanoparticles have also been employed as a “neuroprotective” measure, as is the case with Alzheimer’s disease and stroke models. Alzheimer’s disease results in toxic aggregates of the amyloid beta protein formed in the brain. In one study, gold nanoparticles were programmed to attach themselves to these aggregates and were successful in breaking them up. Likewise, with ischemic stroke models, cells in the affected region of the brain undergo apoptosis, dramatically reducing blood flow to important parts of the brain and often resulting in death or severe mental and physical changes. Platinum nanoparticles have been shown to act as ROS, serving as “biological antioxidants” and significantly reducing oxidation in the brain as a result of stroke. Nanoparticles can also lead to neurotoxicity and cause permanent BBB damage either from brain oedema or from unrelated molecules crossing the BBB and causing brain damage. This proves further long term in vivo studies are needed to gain enough understanding to allow for successful clinical trials.

One of the most common nano-based drug delivery platforms is liposome-based delivery. They are both lipid-soluble and nano-scale and thus are permitted through a fully functioning BBB. Additionally, lipids themselves are biological molecules, making them highly biocompatible, which in turn lowers the risk of cell toxicity. The bilayer that is formed allows the molecule to fully encapsulate any drug, protecting it while it is travelling through the body. One drawback to shielding the drug from the outside cells is that it no longer has specificity, and requires coupling to extra antibodies to be able to target a biological site. Due to their low stability, liposome-based nanoparticles for drug delivery have a short shelf life.

Targeted therapy using magnetic nanoparticles (MNPs) is also a popular topic of research and has led to several stage III clinical trials. Invasiveness is not an issue here because a magnetic force can be applied from the outside of a patient’s body to interact and direct the MNPs. This strategy has been proven successful in delivering Brain-derived neurotropic factor, a naturally occurring gene thought to promote neurorehabilitation, across the BBB.

Major Branches

Modern neuroscience education and research activities can be very roughly categorised into the following major branches, based on the subject and scale of the system in examination as well as distinct experimental or curricular approaches. Individual neuroscientists, however, often work on questions that span several distinct subfields.

Branch	Description
Affective Neuroscience	Affective neuroscience is the study of the neural mechanisms involved in emotion, typically through experimentation on animal models.
Behavioural Neuroscience	Behavioural neuroscience (also known as biological psychology, physiological psychology, biopsychology, or psychobiology) is the application of the principles of biology to the study of genetic, physiological, and developmental mechanisms of behaviour in humans and non-human animals.
Cellular Neuroscience	Cellular neuroscience is the study of neurons at a cellular level including morphology and physiological properties.
Clinical Neuroscience	The scientific study of the biological mechanisms that underlie the disorders and diseases of the nervous system.
Cognitive Neuroscience	Cognitive neuroscience is the study of the biological mechanisms underlying cognition.
Computational Neuroscience	Computational neuroscience is the theoretical study of the nervous system.
Cultural Neuroscience	Cultural neuroscience is the study of how cultural values, practices and beliefs shape and are shaped by the mind, brain and genes across multiple timescales.
Developmental Neuroscience	Developmental neuroscience studies the processes that generate, shape, and reshape the nervous system and seeks to describe the cellular basis of neural development to address underlying mechanisms.
Evolutionary Neuroscience	Evolutionary neuroscience studies the evolution of nervous systems.
Molecular Neuroscience	Molecular neuroscience studies the nervous system with molecular biology, molecular genetics, protein chemistry, and related methodologies.
Neural Neuroscience	Neural engineering uses engineering techniques to interact with, understand, repair, replace, or enhance neural systems.
Neuroanatomy	Neuroanatomy is the study of the anatomy of nervous systems.
Neurochemistry	Neurochemistry is the study of how neurochemicals interact and influence the function of neurons.
Neuroethology	Neuroethology is the study of the neural basis of non-human animals behaviour.
Neurogastronomy	Neurogastronomy is the study of flavour and how it affects sensation, cognition, and memory.
Neurogenetics	Neurogenetics is the study of the genetical basis of the development and function of the nervous system.
Neuroimaging	Neuroimaging includes the use of various techniques to either directly or indirectly image the structure and function of the brain.
Neuroimmunology	Neuroimmunology is concerned with the interactions between the nervous and the immune system.
Neuroinformatics	Neuroinformatics is a discipline within bioinformatics that conducts the organisation of neuroscience data and application of computational models and analytical tools.
Neurolinguistics	Neurolinguistics is the study of the neural mechanisms in the human brain that control the comprehension, production, and acquisition of language.
Neurophysics	Neurophysics deals with the development of physical experimental tools to gain information about the brain.
Neurophysiology	Neurophysiology is the study of the functioning of the nervous system, generally using physiological techniques that include measurement and stimulation with electrodes or optically with ion- or voltage-sensitive dyes or light-sensitive channels.
Neuropsychology	Neuropsychology is a discipline that resides under the umbrellas of both psychology and neuroscience, and is involved in activities in the arenas of both basic science and applied science. In psychology, it is most closely associated with biopsychology, clinical psychology, cognitive psychology, and developmental psychology. In neuroscience, it is most closely associated with the cognitive, behavioural, social, and affective neuroscience areas. In the applied and medical domain, it is related to neurology and psychiatry.
Paleoneurobiology	Paleoneurobiology is a field which combines techniques used in palaeontology and archaeology to study brain evolution, especially that of the human brain.
Social Neuroscience	Social neuroscience is an interdisciplinary field devoted to understanding how biological systems implement social processes and behaviour, and to using biological concepts and methods to inform and refine theories of social processes and behaviour.
Systems Neuroscience	Systems neuroscience is the study of the function of neural circuits and systems.

Neuroscience Organisations

The largest professional neuroscience organisation is the Society for Neuroscience (SFN), which is based in the United States but includes many members from other countries. Since its founding in 1969 the SFN has grown steadily: as of 2010 it recorded 40,290 members from 83 different countries. Annual meetings, held each year in a different American city, draw attendance from researchers, postdoctoral fellows, graduate students, and undergraduates, as well as educational institutions, funding agencies, publishers, and hundreds of businesses that supply products used in research.

Other major organisations devoted to neuroscience include the International Brain Research Organisation (IBRO), which holds its meetings in a country from a different part of the world each year, and the Federation of European Neuroscience Societies (FENS), which holds a meeting in a different European city every two years. FENS comprises a set of 32 national-level organisations, including the British Neuroscience Association, the German Neuroscience Society (Neurowissenschaftliche Gesellschaft), and the French Société des Neurosciences. The first National Honour Society in Neuroscience, Nu Rho Psi, was founded in 2006. Numerous youth neuroscience societies which support undergraduates, graduates and early career researchers also exist, like Project Encephalon.

In 2013, the BRAIN Initiative was announced in the US. An International Brain Initiative was created in 2017, currently integrated by more than seven national-level brain research initiatives (US, Europe, Allen Institute, Japan, China, Australia, Canada, Korea, Israel) spanning four continents.

Public Education and Outreach

In addition to conducting traditional research in laboratory settings, neuroscientists have also been involved in the promotion of awareness and knowledge about the nervous system among the general public and government officials. Such promotions have been done by both individual neuroscientists and large organisations. For example, individual neuroscientists have promoted neuroscience education among young students by organising the International Brain Bee, which is an academic competition for high school or secondary school students worldwide. In the United States, large organisations such as the Society for Neuroscience have promoted neuroscience education by developing a primer called Brain Facts, collaborating with public school teachers to develop Neuroscience Core Concepts for K-12 teachers and students, and cosponsoring a campaign with the Dana Foundation called Brain Awareness Week to increase public awareness about the progress and benefits of brain research. In Canada, the CIHR Canadian National Brain Bee is held annually at McMaster University.

Neuroscience educators formed Faculty for Undergraduate Neuroscience (FUN) in 1992 to share best practices and provide travel awards for undergraduates presenting at Society for Neuroscience meetings.

Finally, neuroscientists have also collaborated with other education experts to study and refine educational techniques to optimise learning among students, an emerging field called educational neuroscience. Federal agencies in the United States, such as the National Institute of Health (NIH) and National Science Foundation (NSF), have also funded research that pertains to best practices in teaching and learning of neuroscience concepts.

On This Day … 01 February

Published on 02/01/202101/30/2021 by Andrew MarshallLeave a comment

People (Births)

1846 – G. Stanley Hall, American psychologist and academic (d. 1924).

G. Stanley Hall

Granville Stanley Hall (01 February 1846 to 24 April 1924) was a pioneering American psychologist and educator. His interests focused on childhood development and evolutionary theory. Hall was the first president of the American Psychological Association and the first president of Clark University. A Review of General Psychology survey, published in 2002, ranked Hall as the 72nd most cited psychologist of the 20th century, in a tie with Lewis Terman.

New Discipline of Psychology

In 1887, Hall founded the American Journal of Psychology, and in 1892 was appointed as the first president of the American Psychological Association. In 1889 he was named the first president of Clark University, a post he filled until 1920. During his 31 years as president, Hall remained intellectually active. He was instrumental in the development of educational psychology, and attempted to determine the effect adolescence has on education. He was also responsible for inviting Sigmund Freud and Carl Jung to visit and deliver a lecture series in 1909 at the Clark Conference. Hall promised Freud an honorary degree from Clark University in exchange. Hall and Freud shared the same beliefs on sex and adolescence. This was Freud’s first and only visit to America and the biggest conference held at Clark University. It was also the most controversial conference, given that Freud’s research was based on theories that Hall’s colleagues criticised as non-scientific.

In 1888, when he was tapped for the Clark presidency from the faculty of Johns Hopkins University, the 44 year-old Hall was already well on his way to eminence in the then emerging field of psychology. His establishment of experimental laboratories at Johns Hopkins, the first in the discipline, quickly became the measure of the fully modern psychology department. Over his 32 years as a scholar/teacher president at Clark, he had an influence over the future shape of the field of psychology.

What attracted some to Hall and his ideas, and alienated others, were his “music man” propensities. He was the promoter, the impresario par excellence. Hall could “put on a party”, as he did with the extraordinary celebrations in 1899 and 1909, on the occasions of the 10th and 20th anniversaries of the opening of Clark University. He did so with an incomparable sense of daring – inviting major figures with unconventional, unpopular, or even scandalous ideas, and then promoting them with the press. He seemed always to be founding new journals or scholarly associations to disseminate his ideas and those of scholars whose perspectives were consistent with his own. Among his creations were the widely respected American Journal of Psychology and the American Psychological Association. He also helped found the Association of American Universities. Ross described this side of Hall as journalist, entrepreneur, and preacher.

In 1917, Hall published a book on religious psychology, Jesus the Christ in the Light of Psychology. The book was written in two volumes to define Jesus Christ in psychological terms. Hall thoroughly discussed all that is written about Christ, and the probable mental mechanisms of Christ and all of those who believed in him and wrote about him. He analyses the myths, the magic, etc., built up about the name and life of Christ. He dissects the parables and discusses the miracles, the death and the resurrection of Jesus. He endeavours to reduce all possible expressions or trends which he finds in Jesus and his followers to their genetic origins, and with that aid in comparative psychology, especially the knowledge of anthropology and childhood tendencies, he points out here and there certain universal trends which are at the bottom of it all. This was his least successful work. In 1922, at the age of 78, he published the book Senescence, a book on aging.

Darwin’s theory of evolution and Ernst Haeckel’s recapitulation theory were large influences on Hall’s career. These ideas prompted Hall to examine aspects of childhood development in order to learn about the inheritance of behaviour. The subjective character of these studies made their validation impossible. He believed that as children develop, their mental capabilities resemble those of their ancestors and so they develop over a lifetime the same way that species develop over eons. Hall believed that the process of recapitulation could be sped up through education and force children to reach modern standards of mental capabilities in a shorter length of time. His work also delved into controversial portrayals of the differences between women and men, as well as the concept of racial eugenics. While Hall was a proponent of racial eugenics, his views were less severe in terms of creating and keeping distinct separations between races. Hall believed in giving “lower races” a chance to accept and adapt to “superior civilisation”. Hall even commended high ranking African Americans in society as being “exception to the Negro’s diminished evolutionary inheritance”. Hall viewed civilisation in a similar fashion he viewed biological development. Humans must allow civilisation to “run its natural evolution”. Hall saw those who did not accept the superior civilisation as being primitive “savages”. Hall viewed these civilisations in a similar fashion as he viewed children, stating that “their faults and their virtues are those of childhood and youth”. Hall believed that men and women should be separated into their own schools during puberty because it allowed them to be able to grow within their own gender. Women could be educated with motherhood in mind and the men could be educated in more hands-on projects, helping them to become leaders of their homes. Hall believed that schools with both sexes limited the way they could learn and softened the boys earlier than they should be. “It is a period of equilibrium, but with the onset of puberty the equilibrium is disturbed and new tendencies arise. Modifications in the reproductive organs take place and bring about secondary sexual characteristics. Extroversion gives way slowly to introversion, and more definitely social instincts begin to play an increasing role.”

Hall was also influenced by Jean-Baptiste Lamarck and his theory of evolution. Hall found the idea of passing on memories from parent to offspring was a plausible mode of inheritance.

Anomalistic Psychology

Hall was one of the founding members and a vice President of the American Society for Psychical Research. The early members of the society were sceptical of paranormal phenomena. Hall took a psychological approach to psychical phenomena. By 1890 he had resigned from the society. He became an outspoken critic of parapsychology.

Hall was an early psychologist in the field of anomalistic psychology. Hall and his assistant Amy Tanner from Clark University were notable debunkers of spiritualism and carried out psychological and physiological tests on mediums. Tanner published Studies in Spiritism (1910) with an introduction by Hall. The book documented the tests carried out by Hall and Tanner in the séance sittings held with the medium Leonora Piper. Hall and Tanner had proven by tests that the personalities of Piper were fictitious creations and not discarnate spirits.

Legacy and Honours

Hall contributed a large amount of work in understand adolescent development, some of which still holds true today. Hall observed that males tend to have an increase in sensation seeking and aggression during adolescence. Hall also observed an increase in crime rates during the adolescent years.[11] He noted that in terms of aggression there are two types; relational aggression and physical aggression. Relational aggression relates to gossiping, rumour spreading, and exclusions of others. Hall noted that relational aggression occurs more frequently in females while physical aggression occurs more often in males.

Much of the mark that Hall left behind was from his expansion of psychology as a field in the United States. He did a lot of work to bring psychology to the United States as a legitimate form of study and science. He began the first journal dedicated only to psychology in the United States of America, called the American Journal of Psychology. He was also the first president of the American Psychological Association. All of the work that Hall did in the field of psychology and for psychology in the United States of America allowed for all the other psychologists to follow in his foot steps and to become psychologists in the United States. Without the effort from Hall it could have taken many more years for psychology to become a field in the United States.

The World War II Liberty Ship SS Granville S. Hall was named in his honour.

What is Major Depressive Disorder?

Published on 01/30/2021 by Andrew Marshall102 Comments

Introduction

Major depressive disorder (MDD), also known simply as depression, is a mental disorder characterised by at least two weeks of pervasive low mood. Low self-esteem, loss of interest in normally enjoyable activities, low energy, and pain without a clear cause are common symptoms. Those affected may also occasionally have delusions or hallucinations. Some people have periods of depression separated by years, while others nearly always have symptoms present. Major depression is more severe and lasts longer than sadness, which is a normal part of life.

The diagnosis of MDD is based on the person’s reported experiences and a mental status examination. There is no laboratory test for the disorder, but testing may be done to rule out physical conditions that can cause similar symptoms. Those with MDD are typically treated with counselling and antidepressant medication. Medication appears to be effective, but the effect may only be significant in the most severely depressed. Types of counselling used include cognitive behavioural therapy (CBT) and interpersonal therapy, and electroconvulsive therapy (ECT) may be considered if other measures are not effective. Hospitalisation may be necessary in cases with a risk of harm to self and may occasionally occur against a person’s wishes.

The most common time of onset is in a person’s 20s and 30s, with females affected about twice as often as males. MDD affected approximately 163 million people (2% of the world’s population) in 2017. The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France. Lifetime rates are higher in the developed world (15%) compared to the developing world (11%). The disorder causes the second-most years lived with disability, after lower back pain.

The term MDD was introduced by a group of US clinicians in the mid-1970s. The cause of MDD is believed to be a combination of genetic, environmental, and psychological factors, with about 40% of the risk related to genetics. Risk factors include a family history of the condition, major life changes, certain medications, chronic health problems, and substance abuse. It can negatively affect a person’s personal life, work life, or education as well as sleeping, eating habits, and general health. Those currently or previously affected with the disorder may be stigmatised.

Not to be confused with Depression (Mood).

Brief History

The Ancient Greek physician Hippocrates described a syndrome of melancholia as a distinct disease with particular mental and physical symptoms; he characterised all “fears and despondencies, if they last a long time” as being symptomatic of the ailment. It was a similar but far broader concept than today’s depression; prominence was given to a clustering of the symptoms of sadness, dejection, and despondency, and often fear, anger, delusions and obsessions were included.

The term depression itself was derived from the Latin verb deprimere, “to press down”. From the 14th century, “to depress” meant to subjugate or to bring down in spirits. It was used in 1665 in English author Richard Baker’s Chronicle to refer to someone having “a great depression of spirit”, and by English author Samuel Johnson in a similar sense in 1753. The term also came into use in physiology and economics. An early usage referring to a psychiatric symptom was by French psychiatrist Louis Delasiauve in 1856, and by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function. Since Aristotle, melancholia had been associated with men of learning and intellectual brilliance, a hazard of contemplation and creativity. The newer concept abandoned these associations and through the 19th century, became more associated with women.

Although melancholia remained the dominant diagnostic term, depression gained increasing currency in medical treatises and was a synonym by the end of the century; German psychiatrist Emil Kraepelin may have been the first to use it as the overarching term, referring to different kinds of melancholia as depressive states.

Sigmund Freud likened the state of melancholia to mourning in his 1917 paper Mourning and Melancholia. He theorized that objective loss, such as the loss of a valued relationship through death or a romantic break-up, results in subjective loss as well; the depressed individual has identified with the object of affection through an unconscious, narcissistic process called the libidinal cathexis of the ego. Such loss results in severe melancholic symptoms more profound than mourning; not only is the outside world viewed negatively but the ego itself is compromised. The patient’s decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness. He also emphasized early life experiences as a predisposing factor. Adolf Meyer put forward a mixed social and biological framework emphasizing reactions in the context of an individual’s life, and argued that the term depression should be used instead of melancholia. The first version of the DSM (DSM-I, 1952) contained depressive reaction and the DSM-II (1968) depressive neurosis, defined as an excessive reaction to internal conflict or an identifiable event, and also included a depressive type of manic-depressive psychosis within Major affective disorders.

In the mid-20th century, researchers theorised that depression was caused by a chemical imbalance in neurotransmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpine and isoniazid in altering monoamine neurotransmitter levels and affecting depressive symptoms. The chemical imbalance theory has never been proven.

The term unipolar (along with the related term bipolar) was coined by the neurologist and psychiatrist Karl Kleist, and subsequently used by his disciples Edda Neele and Karl Leonhard.

The term Major depressive disorder was introduced by a group of US clinicians in the mid-1970s as part of proposals for diagnostic criteria based on patterns of symptoms (called the “Research Diagnostic Criteria”, building on earlier Feighner Criteria), and was incorporated into the DSM-III in 1980. The American Psychiatric Association added “major depressive disorder” to the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), as a split of the previous depressive neurosis in the DSM-II, which also encompassed the conditions now known as dysthymia and adjustment disorder with depressed mood. To maintain consistency the ICD-10 used the same criteria, with only minor alterations, but using the DSM diagnostic threshold to mark a mild depressive episode, adding higher threshold categories for moderate and severe episodes. The ancient idea of melancholia still survives in the notion of a melancholic subtype.

The new definitions of depression were widely accepted, albeit with some conflicting findings and views. There have been some continued empirically based arguments for a return to the diagnosis of melancholia. There has been some criticism of the expansion of coverage of the diagnosis, related to the development and promotion of antidepressants and the biological model since the late 1950s.

Epidemiology

MDD affected approximately 163 million people in 2017 (2% of the global population). The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France. In most countries the number of people who have depression during their lives falls within an 8-18% range. In North America, the probability of having a major depressive episode within a year-long period is 3-5% for males and 8-10% for females. Major depression is about twice as common in women as in men, although it is unclear why this is so, and whether factors unaccounted for are contributing to this. The relative increase in occurrence is related to pubertal development rather than chronological age, reaches adult ratios between the ages of 15 and 18, and appears associated with psychosocial more than hormonal factors. As of 2017, depression is the third most common worldwide cause of disability among both sexes, following low back pain and headache.

People are most likely to develop their first depressive episode between the ages of 30 and 40, and there is a second, smaller peak of incidence between ages 50 and 60. The risk of major depression is increased with neurological conditions such as stroke, Parkinson’s disease, or multiple sclerosis, and during the first year after childbirth. It is also more common after cardiovascular illnesses, and is related more to those with a poor cardiac disease outcome than to a better one. Studies conflict on the prevalence of depression in the elderly, but most data suggest there is a reduction in this age group. Depressive disorders are more common in urban populations than in rural ones and the prevalence is increased in groups with poorer socioeconomic factors, e.g. homelessness.

Signs and Symptoms

Major depression significantly affects a person’s family and personal relationships, work or school life, sleeping and eating habits, and general health. Its impact on functioning and well-being has been compared to that of other chronic medical conditions, such as diabetes.

A person having a major depressive episode usually exhibits a low mood, which pervades all aspects of life, and an inability to experience pleasure in previously enjoyable activities. Depressed people may be preoccupied with – or ruminate over – thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness or hopelessness. In severe cases, depressed people may have symptoms of psychosis. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant. Other symptoms of depression include poor concentration and memory (especially in those with melancholic or psychotic features), withdrawal from social situations and activities, reduced sex drive, irritability, and thoughts of death or suicide. Insomnia is common among the depressed. In the typical pattern, a person wakes very early and cannot get back to sleep. Hypersomnia, or oversleeping, can also happen. Some antidepressants may also cause insomnia due to their stimulating effect.

A depressed person may report multiple physical symptoms such as fatigue, headaches, or digestive problems; physical complaints are the most common presenting problem in developing countries, according to the World Health Organisation’s (WHO’s) criteria for depression. Appetite often decreases, with resulting weight loss, although increased appetite and weight gain occasionally occur. Family and friends may notice that the person’s behaviour is either agitated or lethargic. Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness, and a more noticeable slowing of movements.

Depressed children may often display an irritable mood rather than a depressed one, and show varying symptoms depending on age and situation. Most lose interest in school and show a decline in academic performance. They may be described as clingy, demanding, dependent, or insecure. Diagnosis may be delayed or missed when symptoms are interpreted as “normal moodiness.”

Associated Conditions

Major depression frequently co-occurs with other psychiatric problems. The 1990-1992 National Comorbidity Survey (US) reports that half of those with major depression also have lifetime anxiety and its associated disorders such as generalised anxiety disorder. Anxiety symptoms can have a major impact on the course of a depressive illness, with delayed recovery, increased risk of relapse, greater disability and increased suicide attempts. There are increased rates of alcohol and drug abuse and particularly dependence, and around a third of individuals diagnosed with attention deficit hyperactivity disorder (ADHD) develop comorbid depression. Post-traumatic stress disorder and depression often co-occur. Depression may also coexist with ADHD, complicating the diagnosis and treatment of both. Depression is also frequently comorbid with alcohol abuse and personality disorders. Depression can also be exacerbated during particular months (usually winter) for those with seasonal affective disorder. While overuse of digital media has been associated with depressive symptoms, digital media may also be utilised in some situations to improve mood.

Depression and pain often co-occur. One or more pain symptoms are present in 65% of depressed patients, and anywhere from 5 to 85% of patients with pain will be suffering from depression, depending on the setting; there is a lower prevalence in general practice, and higher in specialty clinics. The diagnosis of depression is often delayed or missed, and the outcome can worsen if the depression is noticed but completely misunderstood.

Depression is also associated with a 1.5- to 2-fold increased risk of cardiovascular disease, independent of other known risk factors, and is itself linked directly or indirectly to risk factors such as smoking and obesity. People with major depression are less likely to follow medical recommendations for treating and preventing cardiovascular disorders, which further increases their risk of medical complications. In addition, cardiologists may not recognise underlying depression that complicates a cardiovascular problem under their care.

Depression often coexists with physical disorders common among the elderly, such as stroke, other cardiovascular diseases, Parkinson’s disease, and chronic obstructive pulmonary disease.

Cause(s)

The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression. The diathesis-stress model specifies that depression results when a pre-existing vulnerability, or diathesis, is activated by stressful life events. The pre-existing vulnerability can be either genetic, implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.

Childhood abuse, either physical, sexual or psychological, are all risk factors for depression, among other psychiatric issues that co-occur such as anxiety and drug abuse. Childhood trauma also correlates with severity of depression, lack of response to treatment and length of illness. However, some are more susceptible to developing mental illness such as depression after trauma, and various genes have been suggested to control susceptibility.

Genetics

Family and twin studies find that nearly 40% of individual differences in risk for major depressive disorder can be explained by genetic factors. Like most psychiatric disorders, major depressive disorder is likely to be influenced by many individual genetic changes. In 2018, a genome-wide association study discovered 44 variants in the genome linked to risk for major depression. This was followed by a 2019 study that found 102 variants in the genome linked to depression.

The 5-HTTLPR, or serotonin transporter promoter gene’s short allele has been associated with increased risk of depression. However, since the 1990s, results have been inconsistent, with three recent reviews finding an effect and two finding none. Other genes that have been linked to a gene-environment interaction include CRHR1, FKBP5 and BDNF, the first two of which are related to the stress reaction of the HPA axis, and the latter of which is involved in neurogenesis. There is no conclusive effects of candidate gene on depression, either alone or in combination with life stress. Research focusing on specific candidate genes has been criticised for its tendency to generate false positive findings. There are also other efforts to examine interactions between life stress and polygenic risk for depression.

Other Health Problems

Depression may also come secondary to a chronic or terminal medical condition, such as HIV/AIDS or asthma, and may be labelled “secondary depression.” It is unknown whether the underlying diseases induce depression through effect on quality of life, of through shared aetiologies (such as degeneration of the basal ganglia in Parkinson’s disease or immune dysregulation in asthma). Depression may also be iatrogenic (the result of healthcare), such as drug-induced depression. Therapies associated with depression include interferons, beta-blockers, isotretinoin, contraceptives, cardiac agents, anticonvulsants, antimigraine drugs, antipsychotics, and hormonal agents such as gonadotropin-releasing hormone agonist. Drug abuse in early age is also associated with increased risk of developing depression later in life. Depression that occurs as a result of pregnancy is called postpartum depression, and is thought to be the result of hormonal changes associated with pregnancy. Seasonal affective disorder, a type of depression associated with seasonal changes in sunlight, is thought to be the result of decreased sunlight.

Pathophysiology

The pathophysiology of depression is not yet understood, but the current theories centre around monoaminergic systems, the circadian rhythm, immunological dysfunction, HPA axis dysfunction and structural or functional abnormalities of emotional circuits.

The monoamine theory, derived from the efficacy of monoaminergic drugs in treating depression, was the dominant theory until recently. The theory postulates that insufficient activity of monoamine neurotransmitters is the primary cause of depression. Evidence for the monoamine theory comes from multiple areas. Firstly, acute depletion of tryptophan, a necessary precursor of serotonin, a monoamine, can cause depression in those in remission or relatives of depressed patients; this suggests that decreased serotonergic neurotransmission is important in depression. Secondly, the correlation between depression risk and polymorphisms in the 5-HTTLPR gene, which codes for serotonin receptors, suggests a link. Third, decreased size of the locus coeruleus, decreased activity of tyrosine hydroxylase, increased density of alpha-2 adrenergic receptor, and evidence from rat models suggest decreased adrenergic neurotransmission in depression. Furthermore, decreased levels of homovanillic acid, altered response to dextroamphetamine, responses of depressive symptoms to dopamine receptor agonists, decreased dopamine receptor D1 binding in the striatum, and polymorphism of dopamine receptor genes implicate dopamine, another monoamine, in depression. Lastly, increased activity of monoamine oxidase, which degrades monoamines, has been associated with depression. However, this theory is inconsistent with the fact that serotonin depletion does not cause depression in healthy persons, the fact that antidepressants instantly increase levels of monoamines but take weeks to work, and the existence of atypical antidepressants which can be effective despite not targeting this pathway. One proposed explanation for the therapeutic lag, and further support for the deficiency of monoamines, is a desensitisation of self-inhibition in raphe nuclei by the increased serotonin mediated by antidepressants. However, disinhibition of the dorsal raphe has been proposed to occur as a result of decreased serotonergic activity in tryptophan depletion, resulting in a depressed state mediated by increased serotonin. Further countering the monoamine hypothesis is the fact that rats with lesions of the dorsal raphe are not more depressive than controls, the finding of increased jugular 5-HIAA in depressed patients that normalised with SSRI treatment, and the preference for carbohydrates in depressed patients. Already limited, the monoamine hypothesis has been further oversimplified when presented to the general public.

Immune system abnormalities have been observed, including increased levels of cytokines involved in generating sickness behaviour (which shares overlap with depression). The effectiveness of nonsteroidal anti-inflammatory drugs (NSAIDs) and cytokine inhibitors in treating depression, and normalization of cytokine levels after successful treatment further suggest immune system abnormalities in depression.

HPA axis abnormalities have been suggested in depression given the association of CRHR1 with depression and the increased frequency of dexamethasone test non-suppression in depressed patients. However, this abnormality is not adequate as a diagnosis tool, because its sensitivity is only 44%. These stress-related abnormalities have been hypothesized to be the cause of hippocampal volume reductions seen in depressed patients. Furthermore, a meta-analysis yielded decreased dexamethasone suppression, and increased response to psychological stressors. Further abnormal results have been obscured with the cortisol awakening response, with increased response being associated with depression.

Theories unifying neuroimaging findings have been proposed. The first model proposed is the “Limbic Cortical Model”, which involves hyperactivity of the ventral paralimbic regions and hypoactivity of frontal regulatory regions in emotional processing. Another model, the “Corito-Striatal model”, suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures results in depression. Another model proposes hyperactivity of salience structures in identifying negative stimuli, and hypoactivity of cortical regulatory structures resulting in a negative emotional bias and depression, consistent with emotional bias studies.

Diagnosis

Clinical Assessment

A diagnostic assessment may be conducted by a suitably trained general practitioner, or by a psychiatrist or psychologist, who records the person’s current circumstances, biographical history, current symptoms, family history, and alcohol and drug use. The assessment also includes a mental state examination, which is an assessment of the person’s current mood and thought content, in particular the presence of themes of hopelessness or pessimism, self-harm or suicide, and an absence of positive thoughts or plans. Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely to primary-care clinicians. This issue is even more marked in developing countries. Rating scales are not used to diagnose depression, but they provide an indication of the severity of symptoms for a time period, so a person who scores above a given cut-off point can be more thoroughly evaluated for a depressive disorder diagnosis. Several rating scales are used for this purpose; these include the Hamilton Rating Scale for Depression, the Beck Depression Inventory[90] or the Suicide Behaviours Questionnaire-Revised.

Primary-care physicians and other non-psychiatrist physicians have more difficulty with under-recognition and undertreatment of depression compared to psychiatric physicians, in part because of the physical symptoms that often accompany depression, in addition to many potential patient, provider, and system barriers. A review found that non-psychiatrist physicians miss about two-thirds of cases, though this has improved somewhat in more recent studies.

Before diagnosing major depressive disorder, a doctor generally performs a medical examination and selected investigations to rule out other causes of symptoms. These include blood tests measuring TSH and thyroxine to exclude hypothyroidism; basic electrolytes and serum calcium to rule out a metabolic disturbance; and a full blood count including ESR to rule out a systemic infection or chronic disease. Adverse affective reactions to medications or alcohol misuse are often ruled out, as well. Testosterone levels may be evaluated to diagnose hypogonadism, a cause of depression in men. Vitamin D levels might be evaluated, as low levels of vitamin D have been associated with greater risk for depression.

Subjective cognitive complaints appear in older depressed people, but they can also be indicative of the onset of a dementing disorder, such as Alzheimer’s disease. Cognitive testing and brain imaging can help distinguish depression from dementia. A CT scan can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms. No biological tests confirm major depression. In general, investigations are not repeated for a subsequent episode unless there is a medical indication.

DSM and ICD Criteria

The most widely used criteria for diagnosing depressive conditions are found in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM) and the WHO’s International Statistical Classification of Diseases and Related Health Problems (ICD) which uses the name depressive episode for a single episode and recurrent depressive disorder for repeated episodes. The latter system is typically used in European countries, while the former is used in the US and many other non-European nations, and the authors of both have worked towards conforming one with the other.

Both DSM-5 and ICD-10 mark out typical (main) depressive symptoms. ICD-10 defines three typical depressive symptoms (depressed mood, anhedonia, and reduced energy), two of which should be present to determine the depressive disorder diagnosis. According to DSM-5, there are two main depressive symptoms- a depressed mood and loss of interest/pleasure in activities (anhedonia). These symptoms, as well as five out of the nine more specific symptoms listed, must frequently occur for more than two weeks (to the extent in which it impairs functioning) for the diagnosis.

MDD is classified as a mood disorder in DSM-5. The diagnosis hinges on the presence of single or recurrent major depressive episodes. Further qualifiers are used to classify both the episode itself and the course of the disorder. The category Unspecified Depressive Disorder is diagnosed if the depressive episode’s manifestation does not meet the criteria for a major depressive episode. The ICD-10 system does not use the term major depressive disorder but lists very similar criteria for the diagnosis of a depressive episode (mild, moderate or severe); the term recurrent may be added if there have been multiple episodes without mania.

Major Depressive Episode

A major depressive episode (MDE) is characterised by the presence of a severely depressed mood that persists for at least two weeks.

Episodes may be isolated or recurrent and are categorised as mild (few symptoms in excess of minimum criteria), moderate, or severe (marked impact on social or occupational functioning). An episode with psychotic features – commonly referred to as psychotic depression – is automatically rated as severe. If the patient has had an episode of mania or markedly elevated mood, a diagnosis of bipolar disorder is made instead. Depression without mania is sometimes referred to as unipolar because the mood remains at one emotional state or “pole”.

DSM-IV-TR excludes cases where the symptoms are a result of bereavement, although it is possible for normal bereavement to evolve into a depressive episode if the mood persists and the characteristic features of a MDE develop. The criteria were criticised because they do not take into account any other aspects of the personal and social context in which depression can occur. In addition, some studies have found little empirical support for the DSM-IV cut-off criteria, indicating they are a diagnostic convention imposed on a continuum of depressive symptoms of varying severity and duration. Bereavement is no longer an exclusion criterion in DSM-5, and it is now up to the clinician to distinguish between normal reactions to a loss and MDD. Excluded are a range of related diagnoses, including:

Dysthymia, which involves a chronic but milder mood disturbance;
Recurrent brief depression, consisting of briefer depressive episodes;
Minor depressive disorder, whereby only some symptoms of major depression are present; and
Adjustment disorder with depressed mood, which denotes low mood resulting from a psychological response to an identifiable event or stressor.

Three new depressive disorders were added to the DSM-5:

Disruptive mood dysregulation disorder, classified by significant childhood irritability and tantrums;
Premenstrual dysphoric disorder (PMDD), causing periods of anxiety, depression, or irritability in the week or two before a woman’s menstruation, and
Persistent depressive disorder.

Subtypes

The DSM-5 recognises six further subtypes of MDD, called specifiers, in addition to noting the length, severity and presence of psychotic features:

Melancholic depression:
- This is characterised by a loss of pleasure in most or all activities, a failure of reactivity to pleasurable stimuli, a quality of depressed mood more pronounced than that of grief or loss, a worsening of symptoms in the morning hours, early-morning waking, psychomotor retardation, excessive weight loss (not to be confused with anorexia nervosa), or excessive guilt.
Atypical depression:
- This is characterised by mood reactivity (paradoxical anhedonia) and positivity, significant weight gain or increased appetite (comfort eating), excessive sleep or sleepiness (hypersomnia), a sensation of heaviness in limbs known as leaden paralysis, and significant social impairment as a consequence of hypersensitivity to perceived interpersonal rejection.
Catatonic depression:
- This is a rare and severe form of major depression involving disturbances of motor behaviour and other symptoms.
- Here, the person is mute and almost stuporous, and either remains immobile or exhibits purposeless or even bizarre movements.
- Catatonic symptoms also occur in schizophrenia or in manic episodes, or may be caused by neuroleptic malignant syndrome.
Depression with anxious distress:
- This was added into the DSM-V as a means to emphasize the common co-occurrence between depression or mania and anxiety, as well as the risk of suicide of depressed individuals with anxiety.
- Specifying in such a way can also help with the prognosis of those diagnosed with a depressive or bipolar disorder.
Depression with peri-partum onset:
- This refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth or while a woman is pregnant.
- DSM-IV-TR used the classification “postpartum depression,” but this was changed in order to not exclude cases of depressed woman during pregnancy.
- Depression with peripartum onset has an incidence rate of 10-15% among new mothers.
- The DSM-V mandates that, in order to qualify as depression with peripartum onset, onset occur during pregnancy or within one month of delivery.
- It has been said that postpartum depression can last as long as three months.
Seasonal affective disorder (SAD):
- This is a form of depression in which depressive episodes come on in the autumn or winter, and resolve in spring.
- The diagnosis is made if at least two episodes have occurred in colder months with none at other times, over a two-year period or longer.

Differential Diagnosis

Refer to Differential Diagnoses of Depression.

To confirm MDD as the most likely diagnosis, other potential diagnoses must be considered, including dysthymia, adjustment disorder with depressed mood, or bipolar disorder. Dysthymia is a chronic, milder mood disturbance in which a person reports a low mood almost daily over a span of at least two years. The symptoms are not as severe as those for major depression, although people with dysthymia are vulnerable to secondary episodes of major depression (sometimes referred to as double depression). Adjustment disorder with depressed mood is a mood disturbance appearing as a psychological response to an identifiable event or stressor, in which the resulting emotional or behavioural symptoms are significant but do not meet the criteria for a MDE. Bipolar disorder, also known as manic–depressive disorder, is a condition in which depressive phases alternate with periods of mania or hypomania. Although depression is currently categorised as a separate disorder, there is ongoing debate because individuals diagnosed with major depression often experience some hypomanic symptoms, indicating a mood disorder continuum. Further differential diagnoses involve chronic fatigue syndrome.

Other disorders need to be ruled out before diagnosing major depressive disorder. They include depressions due to physical illness, medications, and substance abuse. Depression due to physical illness is diagnosed as a mood disorder due to a general medical condition. This condition is determined based on history, laboratory findings, or physical examination. When the depression is caused by a medication, drug of abuse, or exposure to a toxin, it is then diagnosed as a specific mood disorder (previously called substance-induced mood disorder in the DSM-IV-TR).

Screening and Prevention

Since 2016, the United States Preventive Services Task Force (USPSTF) has recommended screening for depression among those over the age 12; a 2005 Cochrane review found that the routine use of screening questionnaires has little effect on detection or treatment.

Preventive efforts may result in decreases in rates of the condition of between 22 and 38%. Eating large amounts of fish may also reduce the risk.

Behavioural interventions, such as interpersonal therapy and cognitive-behavioural therapy, are effective at preventing new onset depression. Because such interventions appear to be most effective when delivered to individuals or small groups, it has been suggested that they may be able to reach their large target audience most efficiently through the Internet.

However, an earlier meta-analysis found preventive programmes with a competence-enhancing component to be superior to behaviour-oriented programmes overall, and found behavioural programmes to be particularly unhelpful for older people, for whom social support programmes were uniquely beneficial. In addition, the programs that best prevented depression comprised more than eight sessions, each lasting between 60 and 90 minutes, were provided by a combination of lay and professional workers, had a high-quality research design, reported attrition rates, and had a well-defined intervention.

The Netherlands mental health care system provides preventive interventions, such as the “Coping with Depression” course (CWD) for people with sub-threshold depression. The course is claimed to be the most successful of psychoeducational interventions for the treatment and prevention of depression (both for its adaptability to various populations and its results), with a risk reduction of 38% in major depression and an efficacy as a treatment comparing favourably to other psychotherapies.

Management

The three most common treatments for depression are psychotherapy, medication, and electroconvulsive therapy. Psychotherapy is the treatment of choice (over medication) for people under 18. The UK National Institute for Health and Care Excellence (NICE) 2004 guidelines indicate that antidepressants should not be used for the initial treatment of mild depression because the risk-benefit ratio is poor. The guidelines recommend that antidepressants treatment in combination with psychosocial interventions should be considered for:

People with a history of moderate or severe depression.
Those with mild depression that has been present for a long period.
As a second line treatment for mild depression that persists after other interventions.
As a first line treatment for moderate or severe depression.

The guidelines further note that antidepressant treatment should be continued for at least six months to reduce the risk of relapse, and that SSRIs are better tolerated than tricyclic antidepressants.

American Psychiatric Association treatment guidelines recommend that initial treatment should be individually tailored based on factors including severity of symptoms, co-existing disorders, prior treatment experience, and patient preference. Options may include pharmacotherapy, psychotherapy, exercise, electroconvulsive therapy (ECT), transcranial magnetic stimulation (TMS) or light therapy. Antidepressant medication is recommended as an initial treatment choice in people with mild, moderate, or severe major depression, and should be given to all patients with severe depression unless ECT is planned. There is evidence that collaborative care by a team of health care practitioners produces better results than routine single-practitioner care.

Treatment options are much more limited in developing countries, where access to mental health staff, medication, and psychotherapy is often difficult. Development of mental health services is minimal in many countries; depression is viewed as a phenomenon of the developed world despite evidence to the contrary, and not as an inherently life-threatening condition. A 2014 Cochrane review found insufficient evidence to determine the effectiveness of psychological versus medical therapy in children.

Lifestyle

Physical exercise is recommended for management of mild depression, and has a moderate effect on symptoms. Exercise has also been found to be effective for (unipolar) major depression. It is equivalent to the use of medications or psychological therapies in most people. In older people it does appear to decrease depression. Exercise may be recommended to people who are willing, motivated, and physically healthy enough to participate in an exercise programme as treatment.

There is a small amount of evidence that skipping a night’s sleep may improve depressive symptoms, with the effects usually showing up within a day. This effect is usually temporary. Besides sleepiness, this method can cause a side effect of mania or hypomania.

In observational studies, smoking cessation has benefits in depression as large as or larger than those of medications.

Besides exercise, sleep and diet may play a role in depression, and interventions in these areas may be an effective add-on to conventional methods.

Talking Therapies

Talking therapy (psychotherapy) can be delivered to individuals, groups, or families by mental health professionals. A 2017 review found that cognitive behavioural therapy appears to be similar to antidepressant medication in terms of effect. A 2012 review found psychotherapy to be better than no treatment but not other treatments. With more complex and chronic forms of depression, a combination of medication and psychotherapy may be used. There is moderate-quality evidence that psychological therapies are a useful addition to standard antidepressant treatment of treatment-resistant depression in the short term.

Psychotherapy has been shown to be effective in older people. Successful psychotherapy appears to reduce the recurrence of depression even after it has been stopped or replaced by occasional booster sessions.

Cognitive Behavioural Therapy

Cognitive behavioural therapy (CBT) currently has the most research evidence for the treatment of depression in children and adolescents, and CBT and interpersonal psychotherapy (IPT) are preferred therapies for adolescent depression. In people under 18, according to the National Institute for Health and Clinical Excellence, medication should be offered only in conjunction with a psychological therapy, such as CBT, interpersonal therapy, or family therapy. CBT has also been shown to reduce the number of sick days taken by people with depression, when used in conjunction with primary care.

The most-studied form of psychotherapy for depression is CBT, which teaches clients to challenge self-defeating, but enduring ways of thinking (cognitions) and change counter-productive behaviours. Research beginning in the mid-1990s suggested that CBT could perform as well as or better than antidepressants in patients with moderate to severe depression. CBT may be effective in depressed adolescents, although its effects on severe episodes are not definitively known. Several variables predict success for cognitive behavioural therapy in adolescents: higher levels of rational thoughts, less hopelessness, fewer negative thoughts, and fewer cognitive distortions. CBT is particularly beneficial in preventing relapse.

CBT and occupational programmes (including modification of work activities and assistance) have been shown to be effective in reducing sick days taken by workers with depression.

Variants

Several variants of CBT have been used in those with depression, the most notable being rational emotive behaviour therapy (REBT), and mindfulness-based cognitive therapy. Mindfulness-based stress reduction programmes may reduce depression symptoms. Mindfulness programmes also appear to be a promising intervention in youth.

Psychoanalysis

Psychoanalysis is a school of thought, founded by Sigmund Freud, which emphasizes the resolution of unconscious mental conflicts. Psychoanalytic techniques are used by some practitioners to treat clients presenting with major depression. A more widely practiced therapy, called psychodynamic psychotherapy, is in the tradition of psychoanalysis but less intensive, meeting once or twice a week. It also tends to focus more on the person’s immediate problems, and has an additional social and interpersonal focus. In a meta-analysis of three controlled trials of Short Psychodynamic Supportive Psychotherapy, this modification was found to be as effective as medication for mild to moderate depression.

Antidepressants

Conflicting results have arisen from studies that look at the effectiveness of antidepressants in people with acute, mild to moderate depression. Stronger evidence supports the usefulness of antidepressants in the treatment of depression that is chronic (dysthymia) or severe.

While small benefits were found, researchers Irving Kirsch and Thomas Moore state they may be due to issues with the trials rather than a true effect of the medication. In a later publication, Kirsch concluded that the overall effect of new-generation antidepressant medication is below recommended criteria for clinical significance. Similar results were obtained in a meta-analysis by Fornier.

A review commissioned by the National Institute for Health and Care Excellence (UK) concluded that there is strong evidence that selective serotonin reuptake inhibitors (SSRIs), such as escitalopram, paroxetine, and sertraline, have greater efficacy than placebo on achieving a 50% reduction in depression scores in moderate and severe major depression, and that there is some evidence for a similar effect in mild depression. Similarly, a Cochrane systematic review of clinical trials of the generic tricyclic antidepressant amitriptyline concluded that there is strong evidence that its efficacy is superior to placebo.

A 2019 Cochrane review on the combined use of antidepressants plus benzodiazepines demonstrated improved effectiveness when compared to antidepressants alone; however, these effects were not maintained in the acute or continuous phase. The benefits of adding a benzodiazepine should be balanced against possible harms and other alternative treatment strategies when antidepressant mono-therapy is considered inadequate.

In 2014, the US Food and Drug Administration published a systematic review of all antidepressant maintenance trials submitted to the agency between 1985 and 2012. The authors concluded that maintenance treatment reduced the risk of relapse by 52% compared to placebo, and that this effect was primarily due to recurrent depression in the placebo group rather than a drug withdrawal effect.

To find the most effective antidepressant medication with minimal side-effects, the dosages can be adjusted, and if necessary, combinations of different classes of antidepressants can be tried. Response rates to the first antidepressant administered range from 50 to 75%, and it can take at least six to eight weeks from the start of medication to improvement. Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimise the chance of recurrence, and even up to one year of continuation is recommended. People with chronic depression may need to take medication indefinitely to avoid relapse.

SSRIs are the primary medications prescribed, owing to their relatively mild side-effects, and because they are less toxic in overdose than other antidepressants. People who do not respond to one SSRI can be switched to another antidepressant, and this results in improvement in almost 50% of cases. Another option is to switch to the atypical antidepressant bupropion. Venlafaxine, an antidepressant with a different mechanism of action, may be modestly more effective than SSRIs. However, venlafaxine is not recommended in the UK as a first-line treatment because of evidence suggesting its risks may outweigh benefits, and it is specifically discouraged in children and adolescents.

For children, some research has supported the use of the SSRI antidepressant fluoxetine. The benefit however appears to be slight in children, while other antidepressants have not been shown to be effective. Medications are not recommended in children with mild disease. There is also insufficient evidence to determine effectiveness in those with depression complicated by dementia. Any antidepressant can cause low blood sodium levels; nevertheless, it has been reported more often with SSRIs. It is not uncommon for SSRIs to cause or worsen insomnia; the sedating atypical antidepressant mirtazapine can be used in such cases.

Irreversible monoamine oxidase inhibitors, an older class of antidepressants, have been plagued by potentially life-threatening dietary and drug interactions. They are still used only rarely, although newer and better-tolerated agents of this class have been developed. The safety profile is different with reversible monoamine oxidase inhibitors, such as moclobemide, where the risk of serious dietary interactions is negligible and dietary restrictions are less strict.

It is unclear whether antidepressants affect a person’s risk of suicide. For children, adolescents, and probably young adults between 18 and 24 years old, there is a higher risk of both suicidal ideations and suicidal behaviour in those treated with SSRIs. For adults, it is unclear whether SSRIs affect the risk of suicidality. One review found no connection; another an increased risk; and a third no risk in those 25-65 years old and a decreased risk in those more than 65. A black box warning was introduced in the United States in 2007 on SSRIs and other antidepressant medications due to the increased risk of suicide in patients younger than 24 years old. Similar precautionary notice revisions were implemented by the Japanese Ministry of Health.

Other Medications

There is some evidence that omega-3 fatty acids fish oil supplements containing high levels of eicosapentaenoic acid (EPA) to docosahexaenoic acid (DHA) are effective in the treatment of, but not the prevention of major depression. However, a Cochrane review determined there was insufficient high quality evidence to suggest omega-3 fatty acids were effective in depression. There is limited evidence that vitamin D supplementation is of value in alleviating the symptoms of depression in individuals who are vitamin D-deficient. There is some preliminary evidence that COX-2 inhibitors, such as celecoxib, have a beneficial effect on major depression. Lithium appears effective at lowering the risk of suicide in those with bipolar disorder and unipolar depression to nearly the same levels as the general population. There is a narrow range of effective and safe dosages of lithium thus close monitoring may be needed. Low-dose thyroid hormone may be added to existing antidepressants to treat persistent depression symptoms in people who have tried multiple courses of medication. Limited evidence suggests stimulants, such as amphetamine and modafinil, may be effective in the short term, or as adjuvant therapy. Also, it is suggested that folate supplements may have a role in depression management. There is tentative evidence for benefit from testosterone in males.

Electroconvulsive Therapy

Electroconvulsive therapy (ECT) is a standard psychiatric treatment in which seizures are electrically induced in patients to provide relief from psychiatric illnesses. ECT is used with informed consent as a last line of intervention for major depressive disorder.

A round of ECT is effective for about 50% of people with treatment-resistant major depressive disorder, whether it is unipolar or bipolar. Follow-up treatment is still poorly studied, but about half of people who respond relapse within twelve months.

Aside from effects in the brain, the general physical risks of ECT are similar to those of brief general anaesthesia. Immediately following treatment, the most common adverse effects are confusion and memory loss. ECT is considered one of the least harmful treatment options available for severely depressed pregnant women.

A usual course of ECT involves multiple administrations, typically given two or three times per week, until the patient is no longer suffering symptoms. ECT is administered under anaesthesia with a muscle relaxant. Electroconvulsive therapy can differ in its application in three ways: electrode placement, frequency of treatments, and the electrical waveform of the stimulus. These three forms of application have significant differences in both adverse side effects and symptom remission. After treatment, drug therapy is usually continued, and some patients receive maintenance ECT.

ECT appears to work in the short term via an anticonvulsant effect mostly in the frontal lobes, and longer term via neurotrophic effects primarily in the medial temporal lobe.

Transcranial Magnetic Stimulation

Transcranial magnetic stimulation (TMS) or deep transcranial magnetic stimulation is a non-invasive method used to stimulate small regions of the brain. TMS was approved by the FDA for treatment-resistant major depressive disorder (trMDD) in 2008 and as of 2014 evidence supports that it is probably effective. The American Psychiatric Association the Canadian Network for Mood and Anxiety Disorders, and the Royal Australia and New Zealand College of Psychiatrists have endorsed TMS for trMDD.

Transcranial Direct Current Stimulation

Transcranial direct current stimulation (tDCS) is another non-invasive method used to stimulate small regions of the brain with the help of a weak electric current. Increasing evidence has been gathered for its efficiency as a depression treatment. A meta-analysis was published in 2020 summarising results across nine studies (572 participants) concluded that active tDCS was significantly superior to sham for response (30.9% vs. 18.9%, respectively), remission (19.9% vs. 11.7%) and depression improvement. According to a 2016 meta analysis, 34% of tDCS-treated patients showed at least 50% symptom reduction compared to 19% sham-treated across 6 randomised controlled trials.

Light Therapy

Bright light therapy reduces depression symptom severity, with benefit for both seasonal affective disorder and for non-seasonal depression, and an effect similar to those for conventional antidepressants. For non-seasonal depression, adding light therapy to the standard antidepressant treatment was not effective. For non-seasonal depression, where light was used mostly in combination with antidepressants or wake therapy, a moderate effect was found, with response better than control treatment in high-quality studies, in studies that applied morning light treatment, and with people who respond to total or partial sleep deprivation. Both analyses noted poor quality, short duration, and small size of most of the reviewed studies.

Other

There is insufficient evidence for Reiki and dance movement therapy in depression.

As of 2019 cannabis is specifically not recommended as a treatment.

Prognosis

Major depressive episodes often resolve over time whether or not they are treated. Outpatients on a waiting list show a 10-15% reduction in symptoms within a few months, with approximately 20% no longer meeting the full criteria for a depressive disorder. The median duration of an episode has been estimated to be 23 weeks, with the highest rate of recovery in the first three months.

Studies have shown that 80% of those suffering from their first major depressive episode will have at least one more depression during their life, with a lifetime average of 4 episodes. Other general population studies indicate that around half those who have an episode recover (whether treated or not) and remain well, while the other half will have at least one more, and around 15% of those experience chronic recurrence. Studies recruiting from selective inpatient sources suggest lower recovery and higher chronicity, while studies of mostly outpatients show that nearly all recover, with a median episode duration of 11 months. Around 90% of those with severe or psychotic depression, most of whom also meet criteria for other mental disorders, experience recurrence.

A high proportion of people who experience full symptomatic remission still have at least one not fully resolved symptom after treatment. Recurrence or chronicity is more likely if symptoms have not fully resolved with treatment. Current guidelines recommend continuing antidepressants for four to six months after remission to prevent relapse. Evidence from many randomised controlled trials indicate continuing antidepressant medications after recovery can reduce the chance of relapse by 70% (41% on placebo vs. 18% on antidepressant). The preventive effect probably lasts for at least the first 36 months of use.

People experiencing repeated episodes of depression require ongoing treatment in order to prevent more severe, long-term depression. In some cases, people must take medications for the rest of their lives.

Cases when outcome is poor are associated with inappropriate treatment, severe initial symptoms including psychosis, early age of onset, previous episodes, incomplete recovery after one year of treatment, pre-existing severe mental or medical disorder, and family dysfunction.

Depressed individuals have a shorter life expectancy than those without depression, in part because depressed patients are at risk of dying of suicide. They also have a higher rate of dying from other causes, being more susceptible to medical conditions such as heart disease. Up to 60% of people who die of suicide have a mood disorder such as major depression, and the risk is especially high if a person has a marked sense of hopelessness or has both depression and borderline personality disorder. About 2-8% of adults with major depression die by suicide, and about 50% of people who die by suicide had depression or another mood disorder. The lifetime risk of suicide associated with a diagnosis of major depression in the US is estimated at 3.4%, which averages two highly disparate figures of almost 7% for men and 1% for women (although suicide attempts are more frequent in women). The estimate is substantially lower than a previously accepted figure of 15%, which had been derived from older studies of hospitalised patients.

Major depression is currently the leading cause of disease burden in North America and other high-income countries, and the fourth-leading cause worldwide. In the year 2030, it is predicted to be the second-leading cause of disease burden worldwide after HIV, according to the WHO. Delay or failure in seeking treatment after relapse and the failure of health professionals to provide treatment are two barriers to reducing disability.

Depression may affect people’s ability to work. The combination of usual clinical care and support with return to work (like working less hours or changing tasks) probably reduces sick leave by 15%, and leads to fewer depressive symptoms and improved work capacity, reducing sick leave by an annual average of 25 days per year. Helping depressed people return to work without a connection to clinical care has not been shown to have an effect on sick leave days. Additional psychological interventions (such as online CBT) leads to fewer sick days compared to standard management only. Streamlining care or adding specific providers for depression care may help to reduce sick leave.

Society and Culture

Terminology

The term “depression” is used in a number of different ways. It is often used to mean this syndrome but may refer to other mood disorders or simply to a low mood. People’s conceptualisations of depression vary widely, both within and among cultures. “Because of the lack of scientific certainty,” one commentator has observed, “the debate over depression turns on questions of language. What we call it – ‘disease,’ ‘disorder,’ ‘state of mind’ – affects how we view, diagnose, and treat it.” There are cultural differences in the extent to which serious depression is considered an illness requiring personal professional treatment, or is an indicator of something else, such as the need to address social or moral problems, the result of biological imbalances, or a reflection of individual differences in the understanding of distress that may reinforce feelings of powerlessness, and emotional struggle.

The diagnosis is less common in some countries, such as China. It has been argued that the Chinese traditionally deny or somatise emotional depression (although since the early 1980s, the Chinese denial of depression may have modified). Alternatively, it may be that Western cultures reframe and elevate some expressions of human distress to disorder status. Australian professor Gordon Parker and others have argued that the Western concept of depression “medicalises” sadness or misery. Similarly, Hungarian-American psychiatrist Thomas Szasz and others argue that depression is a metaphorical illness that is inappropriately regarded as an actual disease. There has also been concern that the DSM, as well as the field of descriptive psychiatry that employs it, tends to reify abstract phenomena such as depression, which may in fact be social constructs. American archetypal psychologist James Hillman writes that depression can be healthy for the soul, insofar as “it brings refuge, limitation, focus, gravity, weight, and humble powerlessness.” Hillman argues that therapeutic attempts to eliminate depression echo the Christian theme of resurrection, but have the unfortunate effect of demonising a soulful state of being.

Stigma

Historical figures were often reluctant to discuss or seek treatment for depression due to social stigma about the condition, or due to ignorance of diagnosis or treatments. Nevertheless, analysis or interpretation of letters, journals, artwork, writings, or statements of family and friends of some historical personalities has led to the presumption that they may have had some form of depression. People who may have had depression include English author Mary Shelley, American-British writer Henry James, and American president Abraham Lincoln. Some well-known contemporary people with possible depression include Canadian songwriter Leonard Cohen and American playwright and novelist Tennessee Williams. Some pioneering psychologists, such as Americans William James and John B. Watson, dealt with their own depression.

There has been a continuing discussion of whether neurological disorders and mood disorders may be linked to creativity, a discussion that goes back to Aristotelian times. British literature gives many examples of reflections on depression. English philosopher John Stuart Mill experienced a several-months-long period of what he called “a dull state of nerves”, when one is “unsusceptible to enjoyment or pleasurable excitement; one of those moods when what is pleasure at other times, becomes insipid or indifferent”. He quoted English poet Samuel Taylor Coleridge’s “Dejection” as a perfect description of his case: “A grief without a pang, void, dark and drear, / A drowsy, stifled, unimpassioned grief, / Which finds no natural outlet or relief / In word, or sigh, or tear.” English writer Samuel Johnson used the term “the black dog” in the 1780s to describe his own depression, and it was subsequently popularised by depression sufferer former British Prime Minister Sir Winston Churchill.

Social stigma of major depression is widespread, and contact with mental health services reduces this only slightly. Public opinions on treatment differ markedly to those of health professionals; alternative treatments are held to be more helpful than pharmacological ones, which are viewed poorly. In the UK, the Royal College of Psychiatrists and the Royal College of General Practitioners conducted a joint Five-year Defeat Depression campaign to educate and reduce stigma from 1992 to 1996; a MORI study conducted afterwards showed a small positive change in public attitudes to depression and treatment.

Elderly

Depression is especially common among those over 65 years of age and increases in frequency beyond this age. In addition, the risk of depression increases in relation to the frailty of the individual. Depression is one of the most important factors which negatively impact quality of life in adults, as well as the elderly. Both symptoms and treatment among the elderly differ from those of the rest of the population.

As with many other diseases, it is common among the elderly not to present with classical depressive symptoms. Diagnosis and treatment is further complicated in that the elderly are often simultaneously treated with a number of other drugs, and often have other concurrent diseases. Treatment differs in that studies of SSRIs have shown lesser and often inadequate effects among the elderly, while other drugs, such as duloxetine (a serotonin-norepinephrine reuptake inhibitor), with more clear effects have adverse effects, such as dizziness, dryness of the mouth, diarrhoea and constipation, which can be especially difficult to handle among the elderly.

Problem solving therapy was, as of 2015, the only psychological therapy with proven effect, and can be likened to a simpler form of CBT. However, elderly with depression are seldom offered any psychological treatment, and the evidence proving other treatments effective is incomplete. ECT has been used in the elderly, and register-studies suggest it is effective, although less so as compared to the rest of the population. The risks involved with treatment of depression among the elderly as opposed to benefits are not entirely clear.

Research

MRI scans of patients with depression have revealed a number of differences in brain structure compared to those who are not depressed. Meta-analyses of neuroimaging studies in major depression reported that, compared to controls, depressed patients had increased volume of the lateral ventricles and adrenal gland and smaller volumes of the basal ganglia, thalamus, hippocampus, and frontal lobe (including the orbitofrontal cortex and gyrus rectus). Hyperintensities have been associated with patients with a late age of onset, and have led to the development of the theory of vascular depression.

Trials are looking at the effects of botulinum toxins on depression. The idea is that the drug is used to make the person look less frowning and that this stops the negative facial feedback from the face. In 2015 results showed, however, that the partly positive effects that had been observed until then could have been due to placebo effects.

In 2018-2019, the US Food and Drug Administration (FDA) granted Breakthrough therapy designation to Compass Pathways and, separately, Usona Institute. Compass is a for-profit company studying psilocybin for treatment-resistant depression; Usona is a non-profit organisation studying psilocybin for major depressive disorder more broadly.

Animals Models

Models of depression in animals for the purpose of study include iatrogenic depression models (such as drug-induced), forced swim tests, tail suspension test, and learned helplessness models. Criteria frequently used to assess depression in animals include expression of despair, neurovegetative changes, and anhedonia, as many other criteria for depression are untestable in animals, such as guilt and suicidality.

What is Learned Optimism?

Published on 01/29/2021 by Andrew Marshall1 Comment

Introduction

Learned optimism is the idea in positive psychology that a talent for joy, like any other, can be cultivated.

In contrast with learned helplessness, optimism is learned by consciously challenging any negative self talk.

Overview

Learned optimism was defined by Martin Seligman and published in his 1990 book, Learned Optimism. The benefits of an optimistic outlook are many: Optimists are higher achievers and have better overall health. Pessimism, on the other hand, is much more common; pessimists are more likely to give up in the face of adversity or to suffer from depression. Seligman invites pessimists to learn to be optimists by thinking about their reactions to adversity in a new way. The resulting optimism – one that grew from pessimism – is a learned optimism. The optimist’s outlook on failure can thus be summarised as “What happened was an unlucky situation (not personal), and really just a setback (not permanent) for this one, of many, goals (not pervasive)”.

Other differences exist between pessimists and optimists in terms of explanatory style:

Permanence:
- Optimistic people believe bad events to be more temporary than permanent and bounce back quickly from failure, whereas others may take longer periods to recover or may never recover.
- They also believe good things happen for reasons that are permanent, rather than seeing the transient nature of positive events.
- Optimists point to specific temporary causes for negative events; pessimists point to permanent causes.
Pervasiveness:
- Optimistic people compartmentalise helplessness, whereas pessimistic people assume that failure in one area of life means failure in life as a whole.
- Optimistic people also allow good events to brighten every area of their lives rather than just the particular area in which the event occurred.
Personalisation:
- Optimists blame bad events on causes outside of themselves, whereas pessimists blame themselves for events that occur.
- Optimists are therefore generally more confident.
- Optimists also quickly internalise positive events while pessimists externalise them.

History

Seligman came to the concept of learned optimism through a scientific study of learned helplessness, the idea that a certain reoccurring negative event is out of the person’s control. As he was performing tests to study helplessness further, he began to wonder why some people resisted helplessness-conditioning. He noticed that, while some subjects blamed themselves for negative outcomes, others blamed the experiment for setting them up to fail.

Seligman shifted his focus to attempting to discover what it is that keeps some people from ever becoming helpless. The answer was optimism. Using his knowledge about conditioning people to be helpless in the lab, he shifted his focus to conditioning people to be optimists. The result of these experiments led to defining the processes of learning optimism.

Research

In a study completed by Martin Seligman and Gregory Buchanan at the University of Pennsylvania and published by the American Psychological Association, learned optimism techniques were found to significantly reduce depression in a class of college freshmen. As incoming students to the university, a survey determined the most pessimistic students and they were invited to participate in the study. They were randomly assigned, half to attend a 16-hour workshop on the techniques of learning optimism, and half were the control group. In an 18-month follow up, 32% of the control group suffered moderate to severe depression and 15% suffered moderate to severe anxiety disorder, whereas only 22% of the workshop participants were depressed and 7% had anxiety issues. Those who participated in the learned optimism workshop also reported fewer health problems over the 18-month period of the study than those students in the control group.

A study done by Peter Schulman at the Wharton School, published in the Journal of Selling and Sales Management, looked to determine the effects of applying learned optimism in business. After measuring the optimism levels of an insurance sales force, it was determined that the optimistic sales people sold 35% more, and identified pessimists were two times more likely to quit in the first year than optimists. As a result of his studies, he recommends testing sales job candidates for optimism levels to fit them to appropriate positions, training employees in learned optimism techniques, and designing an organisation overall to have attainable goals set and good support from management.

Finally, a study conducted by Mark Ylvisaker of the College of Saint Rose and Timothy Feeney of the Wildwood Institute looked at children with executive function impairment. The children had brain functioning impairments affecting motor skills, memory, or the ability to focus. Learned optimism was not taught to the children themselves, but rather to their caretakers, who often are more likely to feel helpless than optimistic in regards to caring for the child. It was found that learned optimism in caretakers of children with brain damage actually led the children to develop more functioning than children without optimistic caretakers. Thus Ylvisaker concludes that the optimism of professional rehabilitators can affect the results of their clients.

Seligman’s Method of Learning Optimism

According to Martin Seligman, anyone can learn optimism. Whether currently an optimist or a pessimist, benefits can be gained from exposure to the process of learned optimism to improve response to both big and small adversities. A learned optimism test (developed by Seligman) is used to determine an individual’s base level of optimism. Being in the more pessimistic categories means that learning optimism has a chance of preventing depression, helping the person achieve more, and improve physical health.

Seligman’s process of learning optimism consists of a simple method to train a new way of responding to adversity, specifically, by learning to talk themselves through personal defeat. It begins with the Ellis ABC model of adversity, belief, and consequence. Adversity is the event that happens, Belief is how that adversity is interpreted, and Consequences are the feelings and actions that result from the beliefs. This is demonstrated in the example below:

Adversity: Someone cuts you off in traffic.
Belief: You think, “I can’t believe that idiot was so rude and selfish!”
Consequence: You are overcome with anger, yelling profanity at the other driver.

In the journey to learning optimism, emphasis is placed on first understanding one’s current reaction to and interpretation of adversity. Learners are asked to keep a journal for two days in which they note small adverse events and the beliefs and consequences that followed. Next the learner returns to the journal to highlight pessimism (e.g. pervasiveness: “it doomed me…”) in their written descriptions of the events.

To the ABC model, Seligman adds:

“D” (Disputation):
- Disputation centres on generating counter-evidence to any of the following: the negative beliefs in general, the causes of the event, or the implications.
- D also means reminding oneself of any potential usefulness of moving on from the adversity.
- Disputation for the above traffic example might sound like this: “I am overreacting. I don’t know what situation he is in. Maybe he is on his way to his daughter’s piano recital and is running late. I’m sure I have cut people off before without meaning to, so I should really cut him a break. I am not in a hurry anyway.”
- Over time, responses like this are predicted to change feelings to be more hopeful and positive.
“E” (Energisation):
- Successful disputation leads to energisation, the E in the ABCDE model.
- One is energised, and should indeed try to actively celebrate, the positive feelings and sense of accomplishment that come from successful disputation of negative beliefs.
- Disputation and Energisation (celebration) are the keys to Seligman’s method.

Teaching children learned optimism by guiding them through the ABCDE techniques can help children to better deal with adversity they encounter in their lives. If children are taught early then the thought process of disputation is claimed to become ingrained in them. They do not, then, have to focus on being optimistic, but rather optimism becomes automatic and leads to a more positive life for the child.

Applications

If learnable, optimism techniques could be practical in life. They are used today in many areas such as parenting, business, therapy, and education.

Business would benefit from more optimistic workers, as they are more successful. Seligman’s focus in business is on ‘the personal wall’ that is each individual worker’s set-point of discouragement. Putting the ABCDE model into practice attempts to allow workers to respond to this ‘wall’ with a readiness to conquer rather than to feel dejected. The Attributional Style Questionnaire is often used to measure optimism of job candidates during the interview process by asking the participant to write down causes for situational failures. Participants attributions may be used to help understand if the candidate will be a high or low performer in his/her projected role based on his level of optimism.

Learned optimism has been used to combat depression during cognitive behavioural therapy. This is based on the idea that patients may be depressed in part because they have a pessimistic outlook. Rather than perceiving adversity as a constant thing that cannot be overcome, and taking personal blame for that adversity, patients come out of cognitive behavioural therapy with the belief that they can control how they respond to adversity. A shift toward optimism is a shift away from depression.

Criticism

Martin Seligman’s learned optimism now orients the US armed services’ psychological stance. Keith Ablow, a frequent guest on Fox News, blamed this in part for the actions of the US soldier accused of killing 16 civilians in Afghanistan. He wrote (under the Fox News banner) that soldiers are “taught to deny stress and trauma, and false bravado is actually encouraged, under the banner of ‘resilience.’ It’s a bad, bad idea that pushes soldiers to ‘fake good’ until they fall apart. And, then, the system continues to withhold needed care, particularly of a psychotherapeutic, insight-oriented variety.”

What is Learned Helplessness?

Published on 01/29/202101/29/2021 by Andrew Marshall2 Comments

Introduction

Learned helplessness is behaviour exhibited by a subject after enduring repeated aversive stimuli beyond their control. It was initially thought to be caused from the subject’s acceptance of their powerlessness: discontinuing attempts to escape or avoid the aversive stimulus, even when such alternatives are unambiguously presented. Upon exhibiting such behaviour, the subject was said to have acquired learned helplessness.

Over the past few decades, neuroscience has provided insight into learned helplessness and shown that the original theory actually had it backwards: the brain’s default state is to assume that control is not present, and the presence of “helpfulness” is what is actually learned.

In humans, learned helplessness is related to the concept of self-efficacy; the individual’s belief in their innate ability to achieve goals. Learned helplessness theory is the view that clinical depression and related mental illnesses may result from such real or perceived absence of control over the outcome of a situation.

Refer to Learned Optimism.

Foundation of Research and Theory

Early Experiments

American psychologist Martin Seligman initiated research on learned helplessness in 1967 at the University of Pennsylvania as an extension of his interest in depression. This research was later expanded through experiments by Seligman and others. One of the first was an experiment by Seligman & Maier:

In Part 1 of this study, three groups of dogs were placed in harnesses.
- Group 1 dogs were simply put in a harness for a period of time and were later released.
- Groups 2 and 3 consisted of “yoked pairs”.
- Dogs in Group 2 were given electric shocks at random times, which the dog could end by pressing a lever.
- Each dog in Group 3 was paired with a Group 2 dog; whenever a Group 2 dog got a shock, its paired dog in Group 3 got a shock of the same intensity and duration, but its lever did not stop the shock.
- To a dog in Group 3, it seemed that the shock ended at random, because it was their paired dog in Group 2 that was causing it to stop.
- Thus, for Group 3 dogs, the shock was “inescapable”.
In Part 2 of the experiment the same three groups of dogs were tested in a shuttle-box apparatus (a chamber containing two rectangular compartments divided by a barrier a few inches high).
- All of the dogs could escape shocks on one side of the box by jumping over a low partition to the other side.
- The dogs in Groups 1 and 2 quickly learned this task and escaped the shock.
- Most of the Group 3 dogs – which had previously learned that nothing they did had any effect on shocks – simply lay down passively and whined when they were shocked.

In a second experiment later that year with new groups of dogs, Overmier and Seligman ruled out the possibility that, instead of learned helplessness, the Group 3 dogs failed to avert in the second part of the test because they had learned some behaviour that interfered with “escape”. To prevent such interfering behaviour, Group 3 dogs were immobilised with a paralysing drug (curare), and underwent a procedure similar to that in Part 1 of the Seligman and Maier experiment. When tested as before in Part 2, these Group 3 dogs exhibited helplessness as before. This result serves as an indicator for the ruling out of the interference hypothesis.

From these experiments, it was thought that there was to be only one cure for helplessness. In Seligman’s hypothesis, the dogs do not try to escape because they expect that nothing they do will stop the shock. To change this expectation, experimenters physically picked up the dogs and moved their legs, replicating the actions the dogs would need to take in order to escape from the electrified grid. This had to be done at least twice before the dogs would start wilfully jumping over the barrier on their own. In contrast, threats, rewards, and observed demonstrations had no effect on the “helpless” Group 3 dogs.

Later Experiments

Later experiments have served to confirm the depressive effect of feeling a lack of control over an aversive stimulus. For example, in one experiment, humans performed mental tasks in the presence of distracting noise. Those who could use a switch to turn off the noise rarely bothered to do so, yet they performed better than those who could not turn off the noise. Simply being aware of this option was enough to substantially counteract the noise effect. In 2011, an animal study found that animals with control over stressful stimuli exhibited changes in the excitability of certain neurons in the prefrontal cortex. Animals that lacked control failed to exhibit this neural effect and showed signs consistent with learned helplessness and social anxiety.

Expanded Theories

Research has found that a human’s reaction to feeling a lack of control differs both between individuals and between situations, i.e. learned helplessness sometimes remains specific to one situation but at other times generalises across situations. Such variations are not explained by the original theory of learned helplessness, and an influential view is that such variations depend on an individual’s attributional or explanatory style. According to this view, how someone interprets or explains adverse events affects their likelihood of acquiring learned helplessness and subsequent depression. For example, people with pessimistic explanatory style tend to see negative events as permanent (“it will never change”), personal (“it’s my fault”), and pervasive (“I can’t do anything correctly”), and are likely to suffer from learned helplessness and depression.

Bernard Weiner proposed a detailed account of the attributional approach to learned helplessness. His attribution theory includes the dimensions of globality/specificity, stability/instability, and internality/externality:

A global attribution occurs when the individual believes that the cause of negative events is consistent across different contexts.
- A specific attribution occurs when the individual believes that the cause of a negative event is unique to a particular situation.
A stable attribution occurs when the individual believes the cause to be consistent across time.
- An unstable attribution occurs when the individual thinks that the cause is specific to one point in time.
An external attribution assigns causality to situational or external factors,
- while an internal attribution assigns causality to factors within the person.

Research has shown that those with an internal, stable, and global attributional style for negative events can be more at risk for a depressive reaction to failure experiences.

Neurobiological Perspective

Research has shown that increased 5-HT (serotonin) activity in the dorsal raphe nucleus plays a critical role in learned helplessness. Other key brain regions that are involved with the expression of helpless behaviour include the basolateral amygdala, central nucleus of the amygdala and bed nucleus of the stria terminalis. Activity in medial prefrontal cortex, dorsal hippocampus, septum and hypothalamus has also been observed during states of helplessness.

In the article, “Exercise, Learned Helplessness, and the Stress-Resistant Brain”, Benjamin N. Greenwood and Monika Fleshner discuss how exercise might prevent stress-related disorders such as anxiety and depression. They show evidence that running wheel exercise prevents learned helplessness behaviours in rats. They suggest that the amount of exercise may not be as important as simply exercising at all. The article also discusses the neurocircuitry of learned helplessness, the role of serotonin (or 5-HT), and the exercise-associated neural adaptations that may contribute to the stress-resistant brain. However, the authors finally conclude that:

“The underlying neurobiological mechanisms of this effect, however, remain unknown. Identifying the mechanisms by which exercise prevents learned helplessness could shed light on the complex neurobiology of depression and anxiety and potentially lead to novel strategies for the prevention of stress-related mood disorders”.

Health Implications

People who perceive events as uncontrollable show a variety of symptoms that threaten their mental and physical well-being. They experience stress, they often show disruption of emotions demonstrating passivity or aggressiveness, and they can also have difficulty performing cognitive tasks such as problem-solving. They are less likely to change unhealthy patterns of behaviour, causing them, for example, to neglect diet, exercise, and medical treatment.

Depression

Abnormal and cognitive psychologists have found a strong correlation between depression-like symptoms and learned helplessness in laboratory animals.

Young adults and middle-aged parents with a pessimistic explanatory style often suffer from depression. They tend to be poor at problem-solving and cognitive restructuring, and also tend to demonstrate poor job satisfaction and interpersonal relationships in the workplace. Those with a pessimistic style also tend to have weakened immune systems, having not only increased vulnerability to minor ailments (e.g. cold, fever) and major illness (e.g. heart attack, cancers), but also poorer recovery from health problems.

Social Impact

Learned helplessness can be a factor in a wide range of social situations.

In emotionally abusive relationships, the victim often develops learned helplessness.
- This occurs when the victim confronts or tries to leave the abuser only to have the abuser dismiss or trivialise the victim’s feelings, pretend to care but not change, or impede the victim from leaving.
The motivational effect of learned helplessness is often seen in the classroom.
- Students who repeatedly fail may conclude that they are incapable of improving their performance, and this attribution keeps them from trying to succeed, which results in increased helplessness, continued failure, loss of self-esteem and other social consequences.
Child abuse by neglect can be a manifestation of learned helplessness.
- For example, when parents believe they are incapable of stopping an infant’s crying, they may simply give up trying to do anything for the child.
Those who are extremely shy or anxious in social situations may become passive due to feelings of helplessness.
- Gotlib and Beatty (1985) found that people who cite helplessness in social settings may be viewed poorly by others, which tends to reinforce the passivity.
Aging individuals may respond with helplessness to the deaths of friends and family members, the loss of jobs and income, and the development of age-related health problems.
- This may cause them to neglect their medical care, financial affairs, and other important needs.
According to Cox et al., Abramson, Devine, and Hollon (2012), learned helplessness is a key factor in depression that is caused by inescapable prejudice (i.e. “deprejudice”).
- Thus: “Helplessness born in the face of inescapable prejudice matches the helplessness born in the face of inescapable shocks.”
According to Ruby K. Payne’s book A Framework for Understanding Poverty, treatment of the poor can lead to a cycle of poverty, a culture of poverty, and generational poverty.
- This type of learned helplessness is passed from parents to children.
- People who embrace this mentality feel there is no way to escape poverty and so one must live in the moment and not plan for the future, trapping families in poverty.

Social problems resulting from learned helplessness may seem unavoidable to those entrenched. However, there are various ways to reduce or prevent it. When induced in experimental settings, learned helplessness has been shown to resolve itself with the passage of time. People can be immunized against the perception that events are uncontrollable by increasing their awareness of previous experiences, when they were able to effect a desired outcome. Cognitive therapy can be used to show people that their actions do make a difference and bolster their self-esteem.

Extensions

Cognitive scientist and usability engineer Donald Norman used learned helplessness to explain why people blame themselves when they have a difficult time using simple objects in their environment.

The UK educationalist Phil Bagge describes it as a learning avoidance strategy caused by prior failure and the positive reinforcement of avoidance such as asking teachers or peers to explain and consequently do the work. It shows itself as sweet helplessness or aggressive helplessness often seen in challenging problem solving contexts, such as learning to use a new computer programming language.

The US sociologist Harrison White has suggested in his book Identity and Control that the notion of learned helplessness can be extended beyond psychology into the realm of social action. When a culture or political identity fails to achieve desired goals, perceptions of collective ability suffer.

Emergence under Torture

Studies on learned helplessness served as the basis for developing enhanced interrogation techniques. In CIA interrogation manuals, learned helplessness is characterised as “apathy” which may result from prolonged use of coercive techniques which result in a “debility-dependency-dread” state in the subject, “If the debility-dependency-dread state is unduly prolonged, however, the arrestee may sink into a defensive apathy from which it is hard to arouse him.”

What is the Journal of the American Psychoanalytic Association?

Published on 01/29/2021 by Andrew MarshallLeave a comment

Introduction

The Journal of the American Psychoanalytic Association is a bi-monthly peer-reviewed healthcare journal covering all aspects of psychoanalysis and is the official journal of the American Psychoanalytic Association.

Details

1953 to present.
Bi-monthly.
English language.

Abstracting and Indexing

Journal of the American Psychoanalytic Association is abstracted and indexed in, among other databases: SCOPUS, and the Social Sciences Citation Index.

According to the Journal Citation Reports, the journal has a 2017 impact factor of 0.538, ranking it 4th out of 12 journals in the category “Psychology, Psychoanalysis”, and 130th out of 142 journals in the category “Psychiatry (SSCI)”.

Website

Sage Publications (US, Publisher): https://journals.sagepub.com/home/apa.
American Psychoanalytic Association.

On This Day … 28 January

Published on 01/28/202101/24/2021 by Andrew MarshallLeave a comment

People (Deaths)

1971 – Donald Winnicott, English paediatrician and psychoanalyst (b. 1896).

Donald Winnicott

Donald Woods Winnicott FRCP (07 April 1896 to 25 January 1971) was an English paediatrician and psychoanalyst who was especially influential in the field of object relations theory and developmental psychology. He was a leading member of the British Independent Group of the British Psychoanalytical Society, President of the British Psychoanalytical Society twice (1956-1959 and 1965-1968), and a close associate of Marion Milner.

Winnicott is best known for his ideas on the true self and false self, the “good enough” parent, and borrowed from his second wife, Clare Winnicott, arguably his chief professional collaborator, the notion of the transitional object. He wrote several books, including Playing and Reality, and over 200 papers.

Career

Winnicott completed his medical studies in 1920, and in 1923, the same year as his marriage to the artist Alice Buxton Winnicott (born Taylor). She was a potter and they married on 07 July 1923 in St Mary’s Church, Frensham. Alice had “severe psychological difficulties” and Winnicott arranged for her, and his own therapy, to address the difficulties this condition created. He obtained a post as physician at the Paddington Green Children’s Hospital in London, where he was to work as a paediatrician and child psychoanalyst for 40 years. In 1923 he began a ten-year psychoanalysis with James Strachey, and in 1927 he began training as an analytic candidate. Strachey discussed Winnicott’s case with his wife Alix Strachey, apparently reporting that Winnicott’s sex life was affected by his anxieties. Winnicott’s second analysis, beginning in 1936, was with Joan Riviere.

Winnicott rose to prominence as a psychoanalyst just as the followers of Anna Freud were in conflict with those of Melanie Klein for the right to be called Sigmund Freud’s “true intellectual heirs”. Out of the Controversial discussions during World War II, a compromise was reached with three more-or-less amicable groups within the psychoanalytic movement: the “Freudians”, the “Kleinians”, and the “Middle Group” of the British Psychoanalytical Society (the latter being called the “Independent Group”), to which Winnicott belonged, along with Ronald Fairbairn, Michael Balint, Masud Khan, John Bowlby, Marion Milner, and Margaret Little.

During the Second World War, Winnicott served as consultant paediatrician to the children’s evacuation programme. During the war, he met and worked with Clare Britton, a psychiatric social worker who became his colleague in treating children displaced from their homes by wartime evacuation. Winnicott was lecturing after the war and Janet Quigley and Isa Benzie of the BBC asked him to give over sixty talks on the radio between 1943 and 1966. His first series of talks in 1943 was titled “Happy Children.” As a result of the success of these talks, Quigley offered him total control over the content of his talks but this soon became more consultative as Quigley advised him on the correct pitch.

After the war, he also saw patients in his private practice. Among contemporaries influenced by Winnicott was R.D. Laing, who wrote to Winnicott in 1958 acknowledging his help.

Winnicott divorced his first wife in 1949 and married Clare Britton (1907-1984) in 1951. A keen observer of children as a social worker and a psychoanalyst in her own right, she had an important influence on the development of his theories and likely acted as midwife to his prolific publications after they met.

Except for one book published in 1931 (Clinical Notes on Disorders of Childhood), all of Winnicott’s books were published after 1944, including The Ordinary Devoted Mother and Her Baby (1949), The Child and the Family (1957), Playing and Reality (1971), and Holding and Interpretation: Fragment of an Analysis (1986).

Winnicott died on 25 January 1971, following the last of a series of heart attacks and was cremated in London. Clare Winnicott oversaw the posthumous publication of several of his works.

What is Integrative Psychotherapy?

Published on 01/27/2021 by Andrew Marshall1 Comment

Introduction

Integrative psychotherapy is the integration of elements from different schools of psychotherapy in the treatment of a client.

Integrative psychotherapy may also refer to the psychotherapeutic process of integrating the personality: uniting the “affective, cognitive, behavioural, and physiological systems within a person”.

Background

Initially, Sigmund Freud developed a talking cure called psychoanalysis; then he wrote about his therapy and popularised psychoanalysis. After Freud, many different disciplines splintered off. Some of the more common therapies include: psychodynamic psychotherapy, transactional analysis, cognitive behavioural therapy, gestalt therapy, body psychotherapy, family systems therapy, person-centred psychotherapy, and existential therapy. Hundreds of different theories of psychotherapy are practiced (Norcross, 2005, p.5).

A new therapy is born in several stages. After being trained in an existing school of psychotherapy, the therapist begins to practice. Then, after follow up training in other schools, the therapist may combine the different theories as a basis of a new practice. Then, some practitioners write about their new approach and label this approach with a new name.

A pragmatic or a theoretical approach can be taken when fusing schools of psychotherapy. Pragmatic practitioners blend a few strands of theory from a few schools as well as various techniques; such practitioners are sometimes called eclectic psychotherapists and are primarily concerned with what works. Alternatively, other therapists consider themselves to be more theoretically grounded as they blend their theories; they are called integrative psychotherapists and are not only concerned with what works, but why it works (Norcross, 2005, p.8).

For example, an eclectic therapist might experience a change in their client after administering a particular technique and be satisfied with a positive result. In contrast, an integrative therapist is curious about the “why and how” of the change as well. A theoretical emphasis is important: for example, the client may only have been trying to please the therapist and was adapting to the therapist rather than becoming more fully empowered in themselves.

Different Routes to Integration

The most recent edition of the Handbook of Psychotherapy Integration (Norcross & Goldfried, 2005) recognized four general routes to integration: common factors, technical eclecticism, theoretical integration, and assimilative integration (Norcross, 2005).

Common Factors

The first route to integration is called common factors and “seeks to determine the core ingredients that different therapies share in common” (Norcross, 2005, p.9). The advantage of a common factors approach is the emphasis on therapeutic actions that have been demonstrated to be effective. The disadvantage is that common factors may overlook specific techniques that have been developed within particular theories. Common factors have been described by Jerome Frank (Frank & Frank, 1991), Bruce Wampold (Wampold & Imel, 2015), and Miller, Duncan and Hubble (2005). Common factors theory asserts it is precisely the factors common to the most psychotherapies that make any psychotherapy successful.

Some psychologists have converged on the conclusion that a wide variety of different psychotherapies can be integrated via their common ability to trigger the neurobiological mechanism of memory reconsolidation in such a way as to lead to deconsolidation (Ecker, Ticic & Hulley 2012; Lane et al. 2015; Welling 2012 – but for a more hesitant view of the role of memory reconsolidation in psychotherapy see the objections in some of the invited comments in: Lane et al. 2015).

Technical Eclecticism

The second route to integration is technical eclecticism which is designed “to improve our ability to select the best treatment for the person and the problem…guided primarily by data on what has worked best for others in the past” (Norcross, 2005, p.8). The advantage of technical eclecticism is that it encourages the use of diverse strategies without being hindered by theoretical differences. A disadvantage is that there may not be a clear conceptual framework describing how techniques drawn from divergent theories might fit together. The most well known model of technical eclectic psychotherapy is Arnold Lazarus’ (2005) multimodal therapy. Another model of technical eclecticism is Larry E. Beutler and colleagues’ systematic treatment selection (Beutler, Consoli, & Lane, 2005).

Theoretical Integration

The third route to integration commonly recognised in the literature is theoretical integration in which “two or more therapies are integrated in the hope that the result will be better than the constituent therapies alone” (Norcross, 2005, p.8). Some models of theoretical integration focus on combining and synthesizing a small number of theories at a deep level, whereas others describe the relationship between several systems of psychotherapy. One prominent example of theoretical synthesis is Paul Wachtel’s model of cyclical psychodynamics that integrates psychodynamic, behavioural, and family systems theories (Wachtel, Kruk, & McKinney, 2005). Another example of synthesis is Anthony Ryle’s model of cognitive analytic therapy, integrating ideas from psychoanalytic object relations theory and cognitive psychotherapy (Ryle, 2005). Another model of theoretical integration is specifically called integral psychotherapy (Forman, 2010; Ingersoll & Zeitler, 2010). The most notable model describing the relationship between several different theories is the transtheoretical model (Prochaska & DiClemente, 2005).

Assimilative Integration

Assimilative integration is the fourth route and acknowledges that most psychotherapists select a theoretical orientation that serves as their foundation but, with experience, incorporate ideas and strategies from other sources into their practice. “This mode of integration favours a firm grounding in any one system of psychotherapy, but with a willingness to incorporate or assimilate, in a considered fashion, perspectives or practices from other schools” (Messer, 1992, p.151). Some counsellors may prefer the security of one foundational theory as they begin the process of integrative exploration. Formal models of assimilative integration have been described based on a psychodynamic foundation (Frank, 1999; Stricker & Gold, 2005) and based on cognitive behavioural therapy (Castonguay, Newman, Borkovec, Holtforth, & Maramba, 2005).

Govrin (2015) pointed out a form of integration, which he called “integration by conversion”, whereby theorists import into their own system of psychotherapy a foreign and quite alien concept, but they give the concept a new meaning that allows them to claim that the newly imported concept was really an integral part of their original system of psychotherapy, even if the imported concept significantly changes the original system. Govrin gave as two examples Heinz Kohut’s novel emphasis on empathy in psychoanalysis in the 1970s and the novel emphasis on mindfulness and acceptance in “third-wave” cognitive behavioural therapy in the 1990s to 2000s.

Other Models that Combine Routes

In addition to well-established approaches that fit into the five routes mentioned above, there are newer models that combine aspects of the traditional routes.

Clara E. Hill’s (2014) three-stage model of helping skills encourages counsellors to emphasize skills from different theories during different stages of helping. Hill’s model might be considered a combination of theoretical integration and technical eclecticism. The first stage is the exploration stage. This is based on client-centred therapy. The second stage is entitled insight. Interventions used in this stage are based on psychoanalytic therapy. The last stage, the action stage, is based on behavioural therapy.

Good and Beitman (2006) described an integrative approach highlighting both core components of effective therapy and specific techniques designed to target clients’ particular areas of concern. This approach can be described as an integration of common factors and technical eclecticism.

Multitheoretical psychotherapy (Brooks-Harris, 2008) is an integrative model that combines elements of technical eclecticism and theoretical integration. Therapists are encouraged to make intentional choices about combining theories and intervention strategies.

An approach called integral psychotherapy (Forman, 2010; Ingersoll & Zeitler, 2010) is grounded in the work of theoretical psychologist and philosopher Ken Wilber (2000), who integrates insights from contemplative and meditative traditions. Integral theory is a meta-theory that recognises that reality can be organised from four major perspectives: subjective, intersubjective, objective, and interobjective. Various psychotherapies typically ground themselves in one these four foundational perspectives, often minimising the others. Integral psychotherapy includes all four. For example, psychotherapeutic integration using this model would include subjective approaches (cognitive, existential), intersubjective approaches (interpersonal, object relations, multicultural), objective approaches (behavioural, pharmacological), and interobjective approaches (systems science). By understanding that each of these four basic perspectives all simultaneously co-occur, each can be seen as essential to a comprehensive view of the life of the client. Integral theory also includes a stage model that suggests that various psychotherapies seek to address issues arising from different stages of psychological development (Wilber, 2000).

The generic term, integrative psychotherapy, can be used to describe any multi-modal approach which combines therapies. For example, an effective form of treatment for some clients is psychodynamic psychotherapy combined with hypnotherapy. Kraft & Kraft (2007) gave a detailed account of this treatment with a 54-year-old female client with refractory IBS in a setting of a phobic anxiety state. The client made a full recovery and this was maintained at the follow-up a year later.

Comparison with Eclecticism

In Integrative and Eclectic Counselling and Psychotherapy (Woolfe & Palmer, 2000, pp.55 & 256), the authors make clear the distinction between integrative and eclectic psychotherapy approaches: “Integration suggests that the elements are part of one combined approach to theory and practice, as opposed to eclecticism which draws ad hoc from several approaches in the approach to a particular case.” Psychotherapy’s eclectic practitioners are not bound by the theories, dogma, conventions or methodology of any one particular school. Instead, they may use what they believe or feel or experience tells them will work best, either in general or suiting the often immediate needs of individual clients; and working within their own preferences and capabilities as practitioners (Norcross & Goldfried, 2005, pp.3-23).

References

Beutler, L.E., Consoli, A.J. & Lane, G. (2005). Systematic treatment selection and prescriptive psychotherapy: an integrative eclectic approach. In J.C. Norcross & M.R. Goldfried (Eds.), Handbook of Psychotherapy Integration (2nd Ed, pp.121-143). New York: Oxford.
Brooks-Harris, J.E. (2008). Integrative Multitheoretical Psychotherapy. Boston: Houghton-Mifflin.
Castonguay, L.G., Newman, M.G., Borkovec, T.D., Holtforth, M.G. & Maramba, G.G. (2005). Cognitive-behavioral assimilative integration. In J.C. Norcross & M.R. Goldfried (Eds.), Handbook of Psychotherapy Integration (2nd Ed, pp.241-260). New York: Oxford.
Ecker, B., Ticic, R. & Hulley, L. (2012). Unlocking the Emotional Brain: Eliminating Symptoms at Their Roots Using Memory Reconsolidation. New York: Routledge.
Forman, M.D. (2010). A Guide to Integral Psychotherapy: Complexity, Integration, and Spirituality in Practice. Albany, NY: SUNY Press.
Frank, J.D. & Frank, J.B. (1991). Persuasion and Healing: A Comparative Study of Psychotherapy (3rd Ed). Baltimore, MD: Johns Hopkins University.
Frank, K.A. (1999). Psychoanalytic Participation: Action, Interaction, and Integration. Mahwah, NJ: Analytic Press.
Good, G.E. & Beitman, B.D. (2006). Counseling and Psychotherapy Essentials: Integrating Theories, Skills, and Practices. New York: W.W. Norton.
Govrin, A. (2015). Blurring the threat of ‘otherness’: integration by conversion in psychoanalysis and CBT. Journal of Psychotherapy Integration. 26(1), pp.78-90.
Hill, C.E. (2014). Helping Skills: Facilitating Exploration, Insight, and Action. 4th Ed. Washington, DC: American Psychological Association.
Ingersoll, E. & Zeitler, D. (2010). Integral Psychotherapy: Inside Out/Outside In. Albany, NY: SUNY Press.
Kraft T. & Kraft D. (2007). Irritable bowel syndrome: symptomatic treatment approaches versus integrative psychotherapy. Contemporary Hypnosis, 24(4), pp.161-177.
Lane, R.D., Ryan, L., Nadel, L. & Greenberg, L.S. (2015). Memory reconsolidation, emotional arousal and the process of change in psychotherapy: new insights from brain science. Behavioral and Brain Sciences, 38, pp.e1.
Lazarus, A.A. (2005). Multimodal therapy. In J.C. Norcross & M.R. Goldfried (Eds), Handbook of Psychotherapy Integration. 2nd Ed. pp.105-120). New York: Oxford.
Messer, S.B. (1992). A critical examination of belief structures in integrative and eclectic psychotherapy. In J.C. Norcross, & M. R. Goldfried, (Eds), Handbook of Psychotherapy Integration (pp.130-165). New York: Basic Books.
Miller, S.D., Duncan, B.L. & Hubble, M.A. (2005). Outcome-informed clinical work. In J.C. Norcross, & M.R. Goldfried (Eds.), Handbook of Psychotherapy Integration (2nd Ed, pp. 84-102). New York: Oxford.
Norcross, J.C. (2005). A primer on psychotherapy integration. In J.C. Norcross & M.R. Goldfried (Eds), Handbook of Psychotherapy Integration (2nd Ed, pp.3-23). New York: Oxford.
Norcross, J.C. & Goldfried, M.R. (Eds) (2005). Handbook of Psychotherapy Integration (2nd Ed). New York: Oxford.
Prochaska, J.O. & DiClemente, C.C. (2005). The transtheoretical approach. In J.C. Norcross & M.R. Goldfried (Eds), Handbook of Psychotherapy Integration (2nd Ed, pp.147-171). New York: Oxford.
Ryle, A. (2005). Cognitive analytic therapy. In J.C. Norcross & M.R. Goldfried (Eds), Handbook of Psychotherapy Integration (2nd Ed, pp.196-217). New York: Oxford.
Stricker, G. & Gold, J. (2005). Assimilative psychodynamic psychotherapy. In J.C. Norcross & M.R. Goldfried (Eds.), Handbook of Psychotherapy Integration (2nd Ed, pp.221-240). New York: Oxford.
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