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What is a Spectrum Disorder?

Introduction

A spectrum disorder is a mental disorder that includes a range of linked conditions, sometimes also extending to include singular symptoms and traits.

The different elements of a spectrum either have a similar appearance or are thought to be caused by the same underlying mechanism. In either case, a spectrum approach is taken because there appears to be “not a unitary disorder but rather a syndrome composed of subgroups”. The spectrum may represent a range of severity, comprising relatively “severe” mental disorders through to relatively “mild and nonclinical deficits”.

In some cases, a spectrum approach joins together conditions that were previously considered separately. A notable example of this trend is the autism spectrum, where conditions on this spectrum may now all be referred to as autism spectrum disorders. A spectrum approach may also expand the type or the severity of issues which are included, which may lessen the gap with other diagnoses or with what is considered “normal”. Proponents of this approach argue that it is in line with evidence of gradations in the type or severity of symptoms in the general population.

Origin

The term spectrum was originally used in physics to indicate an apparent qualitative distinction arising from a quantitative continuum (i.e. a series of distinct colours experienced when a beam of white light is dispersed by a prism according to wavelength). Isaac Newton first used the word spectrum (Latin for “appearance” or “apparition”) in print in 1671, in describing his experiments in optics.

The term was first used by analogy in psychiatry with a slightly different connotation, to identify a group of conditions that is qualitatively distinct in appearance but believed to be related from an underlying pathogenic point of view. It has been noted that for clinicians trained after the publication of DSM-III (1980), the spectrum concept in psychiatry may be relatively new, but that it has a long and distinguished history that dates back to Emil Kraepelin and beyond. A dimensional concept was proposed by Ernst Kretschmer in 1921 for schizophrenia (schizothymic – schizoid – schizophrenic) and for affective disorders (cyclothymic temperament – cycloid ‘psychopathy’ – manic-depressive disorder), as well as by Eugen Bleuler in 1922. The term “spectrum” was first used in psychiatry in 1968 in regard to a postulated schizophrenia spectrum, at that time meaning a linking together of what were then called “schizoid personalities”, in people diagnosed with schizophrenia and their genetic relatives (refer to Seymour S. Kety).

For different investigators, the hypothetical common disease-causing link has been of a different nature.

A spectrum approach generally overlays or extends a categorical approach, which today is most associated with the Diagnostic and Statistical Manual of Mental Disorders (DSM) and International Statistical Classification of Diseases (ICD). In these diagnostic guides, disorders are considered present if there is a certain combination and number of symptoms. Gradations of present versus absent are not allowed, although there may be subtypes of severity within a category. The categories are also polythetic, because a constellation of symptoms is laid out and different patterns of them can qualify for the same diagnosis. These categories are aids important for our practical purposes such as providing specific labels to facilitate payments for mental health professionals. They have been described as clearly worded, with observable criteria, and therefore an advance over some previous models for research purposes.

A spectrum approach sometimes starts with the nuclear, classic DSM diagnostic criteria for a disorder (or may join together several disorders), and then include an additional broad range of issues such as temperaments or traits, lifestyle, behavioural patterns, and personality characteristics.

In addition, the term ‘spectrum’ may be used interchangeably with continuum, although the latter goes further in suggesting a direct straight line with no significant discontinuities. Under some continuum models, there are no set types or categories at all, only different dimensions along which everyone varies (hence a dimensional approach).

An example can be found in personality or temperament models. For example, a model that was derived from linguistic expressions of individual differences is subdivided into the Big Five personality traits, where everyone can be assigned a score along each of the five dimensions. This is by contrast to models of ‘personality types’ or temperament, where some have a certain type and some do not. Similarly, in the classification of mental disorders, a dimensional approach, which is being considered for the DSM-V, would involve everyone having a score on personality trait measures. A categorical approach would only look for the presence or absence of certain clusters of symptoms, perhaps with some cut-off points for severity for some symptoms only, and as a result diagnose some people with personality disorders.

A spectrum approach, by comparison, suggests that although there is a common underlying link, which could be continuous, particular sets of individuals present with particular patterns of symptoms (i.e. syndrome or subtype), reminiscent of the visible spectrum of distinct colours after refraction of light by a prism.

It has been argued that within the data used to develop the DSM system there is a large literature leading to the conclusion that a spectrum classification provides a better perspective on phenomenology (appearance and experience) of psychopathology (mental difficulties) than a categorical classification system. However, the term has a varied history, meaning one thing when referring to a schizophrenia spectrum and another when referring to bipolar or obsessive-compulsive disorder spectrum, for example.

Types of Spectrum

The widely used DSM and ICD manuals are generally limited to categorical diagnoses. However, some categories include a range of subtypes which vary from the main diagnosis in clinical presentation or typical severity. Some categories could be considered subsyndromal (not meeting criteria for the full diagnosis) subtypes. In addition, many of the categories include a ‘not otherwise specified’ subtype, where enough symptoms are present but not in the main recognized pattern; in some categories this is the most common diagnosis.

Spectrum concepts used in research or clinical practice include the following.

Anxiety, Stress, and Dissociation

Several types of spectrum are in use in these areas, some of which are being considered in the DSM-5.

NameOutline
Generalised Anxiety SpectrumThis spectrum has been defined by duration of symptoms: a type lasting over six months (a DSM-IV criterion), over one month (DSM-III), or lasting two weeks or less (though may recur), and also isolated anxiety symptoms not meeting criteria for any type.
Social Anxiety SpectrumThis has been defined to span shyness to social anxiety disorder, including typical and atypical presentations, isolated signs and symptoms, and elements of avoidant personality disorder.
Panic-Agoraphobia SpectrumDue to the heterogeneity (diversity) found in individual clinical presentations of panic disorder and agoraphobia, attempts have been made to identify symptom clusters in addition to those included in the DSM diagnoses, including through the development of a dimensional questionnaire measure.
Post-Traumatic Stress Spectrum (or Trauma and Loss Spectrum)Work in this area has sought to go beyond the DSM category and consider in more detail a spectrum of severity of symptoms (rather than just presence or absence for diagnostic purposes), as well as a spectrum in terms of the nature of the stressor (e.g. the traumatic incident) and a spectrum of how people respond to trauma. This identifies a significant amount of symptoms and impairment below threshold for DSM diagnosis but nevertheless important, and potentially also present in other disorders a person might be diagnosed with.
Depersonalisation-Derealisation SpectrumAlthough the DSM identifies only a chronic and severe form of depersonalisation disorder, and the ICD a ‘depersonalisation-derealisation syndrome’, a spectrum of severity has long been identified, including short-lasting episodes commonly experienced in the general population and often associated with other disorders.

Obsessions and Compulsions

An obsessive-compulsive spectrum: This can include a wide range of disorders from Tourette syndrome to the hypochondrias, as well as forms of eating disorder, itself a spectrum of related conditions.

General Developmental Disorders

An autistic spectrum: In its simplest form this joins together autism and Asperger syndrome, and can additionally include other pervasive developmental disorders (PDD). These include PDD ‘not otherwise specified’ (including ‘atypical autism’), as well as Rett syndrome and childhood disintegrative disorder (CDD). The first three of these disorders are commonly called the autism spectrum disorders; the last two disorders are much rarer, and are sometimes placed in the autism spectrum and sometimes not. The merging of these disorders is based on findings that the symptom profiles are similar, such that individuals are better differentiated by clinical specifiers (i.e. dimensions of severity, such as extent of social communication difficulties or how fixed or restricted behaviours or interests are) and associated features (e.g. known genetic disorders, epilepsy, intellectual disabilities). The term specific developmental disorders is reserved for categorising particular specific learning disabilities and developmental disorders affecting coordination.

Psychosis

Refer to Psychosis.

The schizophrenia spectrum or psychotic spectrum: There are numerous psychotic spectrum disorders already in the DSM, many involving reality distortion. These include:

There are also traits identified in first degree relatives of those diagnosed with schizophrenia associated with the spectrum. Other spectrum approaches include more specific individual phenomena which may also occur in non-clinical forms in the general population, such as some paranoid beliefs or hearing voices. Some researchers have also proposed that avoidant personality disorder and related social anxiety traits should be considered part of a schizophrenia spectrum. Psychosis accompanied by mood disorder may be included as a schizophrenia spectrum disorder, or may be classed separately as below.

Schizoaffective Disorders

A schizoaffective spectrum: This spectrum refers to features of both psychosis (hallucinations, delusions, thought disorder etc.) and mood disorder (see below). The DSM has, on the one hand, a category of schizoaffective disorder (which may be more affective (mood) or more schizophrenic), and on the other hand psychotic bipolar disorder and psychotic depression categories. A spectrum approach joins these together and may additionally include specific clinical variables and outcomes, which initial research suggested may not be particularly well captured by the different diagnostic categories except at the extremes.

Schizophrenia-Like Personality Disorders

Schizoid personality disorder, schizotypal personality disorder and paranoid personality disorder can be considered ‘schizophrenia-like personality disorders’ because of their links to the schizophrenia spectrum.

Mood

A mood disorder (affective) spectrum or bipolar spectrum or depressive spectrum. These approaches have expanded out in different directions. On the one hand, work on major depressive disorder has identified a spectrum of subcategories and sub-threshold symptoms that are prevalent, recurrent and associated with treatment needs. People are found to move between the subtypes and the main diagnostic type over time, suggesting a spectrum. This spectrum can include already recognised categories of minor depressive disorder, ‘melancholic depression‘ and various kinds of atypical depression.

In another direction, numerous links and overlaps have been found between major depressive disorder and bipolar syndromes, including mixed states (simultaneous depression and mania or hypomania). Hypomanic (‘below manic’) and more rarely manic signs and symptoms have been found in a significant number of cases of major depressive disorder, suggesting not a categorical distinction but a dimension of frequency that is higher in bipolar II and higher again in bipolar I. In addition, numerous subtypes of bipolar have been proposed beyond the types already in the DSM (which includes a milder form called cyclothymia). These extra subgroups have been defined in terms of more detailed gradations of mood severity, or the rapidity of cycling, or the extent or nature of psychotic symptoms. Furthermore, due to shared characteristics between some types of bipolar disorder and borderline personality disorder, some researchers have suggested they may both lie on a spectrum of affective disorders, although others see more links to post-trauma syndromes.

Substance Use

A spectrum of drug use, drug abuse and substance dependence: One spectrum of this type, adopted by the Health Officers Council of British Columbia in 2005, does not employ loaded terms and distinctions such as “use” vs. “abuse”, but explicitly recognises a spectrum ranging from potentially beneficial to chronic dependence. The model includes the role not just of the individual but of society, culture and availability of substances. In concert with the identified spectrum of drug use, a spectrum of policy approaches was identified which depended partly on whether the drug in question was available in a legal, for-profit commercial economy, or at the other of the spectrum only in a criminal/prohibition, black-market economy. In addition, a standardised questionnaire has been developed in psychiatry based on a spectrum concept of substance use.

Paraphilias and Obsessions

The interpretative key of ‘spectrum,’ developed from the concept of ‘related disorders,’ has been considered also in paraphilias.

Paraphilic behaviour is triggered by thoughts or urges that are psychopathologically close to obsessive impulsive area. Hollander (1996) includes in the obsessive-compulsive spectrum, neurological obsessive disorders, body-perception-related disorders and impulsivity-compulsivity disorders. In this continuum from impulsivity to compulsivity it is particularly hard to find a clear borderline between the two entities.

On this point of view, paraphilias represent such as sexual behaviours due to a high impulsivity-compulsivity drive. It is difficult to distinguish impulsivity from compulsivity: sometimes paraphilic behaviours are prone to achieve pleasure (desire or fantasy), in some other cases these attitudes are merely expressions of anxiety, and the behavioural perversion is an attempt to reduce anxiety. In the last case, the pleasure gained is short in time and is followed by a new increase in anxiety levels, such as it can be seen in an obsessive patient after he performs his compulsion.

Eibl-Eibelsfeldt (1984) underlines a female sexual arousal condition during flight and fear reactions. Some women, with masochistic traits, can reach orgasm in such conditions.

Broad Spectrum Approach

Various higher-level types of spectrum have also been proposed, that subsume conditions into fewer but broader overarching groups.

One psychological model based on factor analysis, originating from developmental studies but also applied to adults, posits that many disorders fall on either an “internalising” spectrum (characterised by negative affectivity; subdivides into a “distress” subspectrum and a “fear” subspectrum) or an “externalising” spectrum (characterised by negative affectivity plus disinhibition). These spectra are hypothetically linked to underlying variation in some of the big five personality traits. Another theoretical model proposes that the dimensions of fear and anger, defined in a broad sense, underlie a broad spectrum of mood, behavioural and personality disorders. In this model, different combinations of excessive or deficient fear and anger correspond to different neuropsychological temperament types hypothesized to underlie the spectrum of disorders.

Similar approaches refer to the overall ‘architecture’ or ‘meta-structure’, particularly in relation to the development of the DSM or ICD systems. Five proposed meta-structure groupings were recently proposed in this way, based on views and evidence relating to risk factors and clinical presentation. The clusters of disorder that emerged were described as:

  • Neurocognitive (identified mainly by neural substrate abnormalities);
  • Neurodevelopmental (identified mainly by early and continuing cognitive deficits);
  • Psychosis (identified mainly by clinical features and biomarkers for information processing deficits);
  • Emotional (identified mainly by being preceded by a temperament of negative emotionality); and
  • Externalising (identified mainly be being preceded by disinhibition).

However, the analysis was not necessarily able to validate one arrangement over others. From a psychological point of view, it has been suggested that the underlying phenomena are too complex, inter-related and continuous – with too poorly understood a biological or environmental basis – to expect that everything can be mapped into a set of categories for all purposes. In this context the overall system of classification is to some extent arbitrary, and could be thought of as a user interface which may need to satisfy different purposes.

An Overview of the Biology of Obsessive-Compulsive Disorder

Introduction

The biology of obsessive-compulsive disorder (OCD) refers biologically based theories about the mechanism of OCD.

Cognitive models generally fall into the category of executive dysfunction or modulatory control. Neuroanatomically, functional and structural neuroimaging studies implicate the prefrontal cortex (PFC), basal ganglia (BG), insula, and posterior cingulate cortex (PCC). Genetic and neurochemical studies implicate glutamate and monoamine neurotransmitters, especially serotonin and dopamine.

Refer to Obsessive-Compulsive Spectrum.

Neuroanatomy

Models

The cortico-basal ganglia-thalamo-cortical loop (CBGTC) model is based on the observation that the basal ganglia loops related to the OFC and ACC are implicated in OCD by neuroimaging studies, although the directionality of volumetric and functional changes is not consistent. Causal evidence from OCD secondary to neuropsychiatric disorders supports the CBGTC model. Obsessions may arise from failure of the circuit to gate information that is normally implicitly processed, leading to representation in explicit processing systems such as the dlPFC and hippocampus, and thereby resulting in obsessions.

Abnormal affect in OCD has been hypothesized to result from dysfunction in the OFC, ventral striatum, and amygdala. OCD is characterised by high levels of anxiety, high rates of comorbidity with major depressive disorder, and blunted response to reward. This is reflected by reduced amygdala and ventral striatum response to positive stimuli, and elevated amygdala response to fearful stimuli. Furthermore, deep brain stimulation of the nucleus accumbens is an effective treatment of OCD, and symptom improvement correlates with reduced binding of dopamine receptors. The reduced binding, due to the ability of the radioligand tracers to be displaced by endogenous dopamine, is taken to reflect increased basal dopamine release. Affective dysregulation due to blunted reward, and elevated fear sensitivity may promote compulsivity by assigning excessive motivational salience to avoidance behaviour.

The ventral striatum is important in action selection, and receives inputs from the medial OFC that signal various aspects of value for stimulus association outcomes. By assigning abnormal values to certain behaviours, OFC may lead to compulsive behaviour through modulating action selection in the ventral striatum. A number of abnormalities have been found in the OFC, including reduced volume, increased resting state activity, and reduced activity during cognitive tasks. The difference between resting and cognitive paradigms may be due to increased signal to noise ratio, a possible mechanism of aberrant valuation. OFC-striatum connectivity also predicts symptom severity, although the opposite has been found in some studies.

Besides abnormal valuation of stimuli or tasks, compulsions may be driven by dysfunction in error monitoring that leads to excessive uncertainty.

OCD has also been conceptualised as resulting from dysfunction in response inhibition, and fear extinction. While hyperactivation of the OFC as a whole during resting is observed in OCD, hyperactivation of the lateral OFC and hypoactivation of the mOFC is seen. This is congruent with the localization of fear/avoidance behaviours to the lOFC and emotional regulation to the mOFC. Hyperactivity of the dACC during monitoring task, along with hyperactivity of the lOFC and amygadala may all contribute to generating obsessions, reduced regulation by the mOFC may enable them.

One model suggests that obsessions do not drive compulsions, but are rather byproducts of compulsions, as evidenced by some studies reporting excessive reliance on habit. Dysfunctional habit based learning may be a driver behind neuroimaging studies of memory reporting increased hippocampus activity. The conscious processing of information that is normally implicitly processing may be the underlying cause of obsessions.

Functional Neuroimaging

Functional neuroimaging studies have implicated multiple regions in OCD. Symptom provocation is associated with increased likelihood of activation in the bilateral orbitofrontal cortex (OFC), right anterior PFC, left dorsolateral prefrontal cortex (dlPFC), bilateral anterior cingulate cortex (ACC), left precuneus, right premotor cortex, left superior temporal gyrus (STG), bilateral external globus pallidus, left hippocampus, right insula, left caudate, right posterior cingulate cortex (PCC), and right superior parietal lobule. The medial portion of the orbitofrontal cortex connects with the paralimbic-limbic system, including the insular cortex, cingulate gryus, amygdala, and hypothalamus. This area is involved in encoding the representation of the value of an expected outcome, which is used to anticipate positive and negative consequences that are likely to follow a given action. During affective tasks hyperactivation has been observed in the ACC, insula and head of the caudate and putamen, regions implicated in salience, arousal, and habit. Hypoactivation during affective tasks is observed in the medial prefrontal cortex (mPFC) and posterior caudate, which are implicated in behavioural and cognitive control. During non-affective tasks, hyperactivation has been observed in the precuneus and PCC, while hypoactivation has been observed in the pallidum, ventral anterior thalamus and posterior caudate. An older meta analysis found hyperactivity in the OFC and ACC. An ALE meta analysis of various functional neuroimaging paradigms observed various abnormalities during Go/no go, interference, and task switching paradigms. Decreased likelihood of activation in right putamen and cerebellum was reported during Go/no go. During interference tasks, likelihood of activation was reported in the left superior frontal gyrus, right precentral gyrus, and left cingulate gyrus, to be decreased, and in the right caudate to be increased. Task switching was associated with extensive decreased likelihood of activation in the middle, medial, inferior, superior frontal gyri, caudate, cingulate and precuneus. A separate ALE meta analysis found consistent abnormalities in orbitofrontal, striatal, lateral frontal, anterior cingulate, middle occipital and parietal, and cerebellar regions.

Structural Neuroimaging

Differences in grey matter, white matter and structural connectivity have been observed in OCD. One meta-analysis reported grey matter increases in the bilateral lenticular nuclei, and grey matter decreases in the ACC (anterior cingulate cortex) and mPFC (medial prefrontal cortex).[14] Another meta-analysis reported that global volumes are not decreased, but the left ACC and OFC demonstrate decreased volume, while the thalamus but not basal ganglia have increased volumes. An ALE meta analysis found increased grey matter in the left postcentral gyrus, middle frontal region, putamen, thalamus, left ACC, and culmen, while decreased grey matter was reported in the right temporal gyrus and left insula extending to the inferior frontal gyrus.

Overlapping abnormalities in white matter volume and diffusivity have been reported. Increased white matter volume and decreased Fractional anisotropy has been observed in anterior midline tracts, interpreted as indicating increased crossings. However, given these effects were most pronounced in medicated adults, it is possible that medication plays a role An ALE meta analysis has observed increased FA in the superior longitudinal fasiculus and corpus callosum, and decreased FA in inferior longitudinal and cingulum fibres.

Neurochemistry

Glutamate, an excitatory neurotransmitter has been implicated in OCD. MRS studies have observed decreased Glx (glutamate, glutamine and GABA) in the striatum. However, increased Glx has been reported in the ACC. Furthermore, increased cerebrospinal fluid (CSF) glutamate and glycine have been found. Various preclinical models have supported glutamate signalling dysfunction in OCD, and treatment with glutamatergic agents such as the glutamate-inhibiting riluzole has been reported to be efficacious.

Reduced dopamine D1 receptors and dopamine D2 receptors in the striatum have been reported in people with OCD, along with both increased and decreased reports of dopamine transporter (DAT) binding. While antipsychotics are sometimes used to treat refractory OCD, they frequently fail in treating or exacerbate OCD symptoms. Treatment with deep brain stimulation is effective in OCD, and response correlates with increased dopamine in the nucleus accumbens. Combined this evidence suggests that OCD may be associated with both increased and decreased dopamine signalling, or that a unidirectional model may not be adequate.

Drug challenge studies have implicated 5-HT2A and 5-HT2A in OCD. Administration of meta-Chlorophenylpiperazine (mCPP), a non selective serotonin (5-HT) release and receptor agonist with a preference for 5-HT2C has been reported to exacerbate OCD symptoms. Psilocybin, a 5-HT2C, 5-HT2A and 5-HT1A receptor agonist has been associated with acute improvement of OCD symptoms. In vivo neuroimaging has found abnormalities with 5-HT2A and serotonin transporter (5-HTT). Inconsistent binding potentials have been observed for 5-HT2A, with both decreased and increased and binding potentials being reported. Inconsistent results have been reported in with respect to 5-HTT as well, with increased, decreased and no changes being reported.

Oestrogen and OCD

Aromatase is an enzyme expressed in several gonadic tissue sites. It is the rate limiting step in the conversion of androgens to oestrogen. This conversion can significantly impact oestrogen levels in brain areas. These OCD-linked effects have been demonstrated by Aromatase knockout mice (ArKO), who lack a functional enzyme to convert androgens to oestrogen. This ArKO knockout strategy has provided a model to examine the physiological impact of lower than normal amounts of oestrogen.

Studies with ArKO mice have been used to show that varying levels of oestrogen affect the onset of OCD behaviours. Lower amounts of oestrogen are associated with an increase of OCD behaviours in males more than females.

Variation in oestrogen can lead to increased levels of OCD symptoms within women as well. The disorder itself has a later onset in women, and tends to show two distinct peaks of onset. The first peak occurs around puberty and the second around the age of childbearing. These peaks correlate with time periods where oestrogen levels are highest in women.

What is the Obsessive-Compulsive Spectrum?

Introduction

The obsessive-compulsive spectrum is a model of medical classification where various psychiatric, neurological and/or medical conditions are described as existing on a spectrum of conditions related to obsessive-compulsive disorder (OCD).

Refer to An Overview of the Biology of Obsessive-Compulsive Disorder.

“The disorders are thought to lie on a spectrum from impulsive to compulsive where impulsivity is said to persist due to deficits in the ability to inhibit repetitive behavior with known negative consequences, while compulsivity persists as a consequence of deficits in recognizing completion of tasks.”

OCD is a mental disorder characterised by obsessions and/or compulsions. An obsession is defined as “a recurring thought, image, or urge that the individual cannot control”. Compulsion can be described as a “ritualistic behaviour that the person feels compelled to perform”. The model suggests that many conditions overlap with OCD in symptomatic profile, demographics, family history, neurobiology, comorbidity, clinical course and response to various pharmacotherapies. Conditions described as being on the spectrum are sometimes referred to as obsessive-compulsive spectrum disorders.

Conditions

The following conditions have been hypothesized by various researchers as existing on the spectrum:

However, recently there is a growing support for proposals to narrow down this spectrum to only include body dysmorphic disorder, hypochondriasis, tic disorders, and trichotillomania.

Body Dysmorphic Disorder

Refer to Body Dysmorphic Disorder.

Body dysmorphic disorder is defined by an obsession with an imagined defect in physical appearance, and compulsive rituals in an attempt to conceal the perceived defect. Typical complaints include perceived facial flaws, perceived deformities of body parts and body size abnormalities. Some compulsive behaviours observed include mirror checking, ritualised application of makeup to hide the perceived flaw, excessive hair combing or cutting, excessive physician visits and plastic surgery. Body dysmorphic disorder is not gender specific and onset usually occurs in teens and young adults.

Hypochondriasis

Hypochondriasis is excessive preoccupancy or worry about having a serious illness. These thoughts cause a person a great deal of anxiety and stress. The prevalence of this disorder is the same for men and women. Hypochondriasis is normally recognised in early adult age. Those that suffer with hypochondriasis are constantly thinking of their body functions, minor bumps and bruises as well as body images. Hypochondriacs go to numerous outpatient facilities for confirmation of their own diagnosis. Hypochondriasis is the belief that something is wrong but it is not known to be a delusion.

Tic Disorders

Tourette’s syndrome is a neurological disorder characterised by recurrent involuntary movements (motor tics) and involuntary noises (vocal tics). The reason Tourette’s syndrome and other tic disorders are being considered for placement in the obsessive compulsive spectrum is because of the phenomenology and co-morbidity of the disorders with obsessive compulsive disorder. Within the population of patients with OCD up to 40% have a history of a tic disorder and 60% of people with Tourette’s syndrome have obsessions and/or compulsions. Plus 30% of people with Tourette’s syndrome have clinically diagnosable OCD. Course of illness is another factor that suggests correlation because it has been found that tics displayed in childhood are a predictor of obsessive and compulsive symptoms in late adolescence and early adulthood. However, the association of Tourette’s and tic disorders with OCD is challenged by neuropsychology and pharmaceutical treatment. Whereas OCD is treated with SSRI, tics are treated with dopamine blockers and alpha-2 agonists.

Trichotillomania

Refer to Trichotillomania.

Trichotillomania is an impulse control disorder which causes an individual to pull out their hair from various parts of their body without a purpose. The cause for trichotillomania remains unknown. Like OCD, trichotillomania isn’t a nervous condition but stress can trigger this habit. For some people pulling their hair out of boredom is normal, but that isn’t the case for someone that is dealing with trichotillomania. Emotions do not affect the behaviour but these behaviours are more prevalent in those that suffer with depression. Review articles recommend behavioural interventions such as habit reversal training and decoupling.

On This Day … 18 January

People (Births)

  • 1932 – Robert Anton Wilson, American psychologist, author, poet, and playwright (d. 2007).

Robert Anton Wilson

Robert Anton Wilson (born Robert Edward Wilson; 18 January 1932 to 11 January 2007) was an American author, futurist, and self-described agnostic mystic. Recognised within Discordianism as an Episkopos, pope and saint, Wilson helped publicize Discordianism through his writings and interviews.

Wilson described his work as an “attempt to break down conditioned associations, to look at the world in a new way, with many models recognized as models or maps, and no one model elevated to the truth”. His goal was “to try to get people into a state of generalized agnosticism, not agnosticism about God alone but agnosticism about everything.”

In addition to writing several science-fiction novels, Wilson also wrote non-fiction books on extrasensory perception, mental telepathy, metaphysics, paranormal experiences, conspiracy theory, sex, drugs and what Wilson himself called “quantum psychology”.

Following a career in journalism and as an editor, notably for Playboy, Wilson emerged as a major countercultural figure in the mid-1970s, comparable to one of his co-authors, Timothy Leary, as well as Terence McKenna.

What is Nefazodone?

Introduction

Nefazodone, sold formerly under the brand names Serzone, Dutonin, and Nefadar among others, is an atypical antidepressant which was first marketed by Bristol-Myers Squibb (BMS) in 1994 but has since largely been discontinued.

BMS withdrew it from the market by 2004 due to decreasing sales due to the rare incidence of severe liver damage and the onset of generic competition. The incidence of severe liver damage is approximately 1 in every 250,000 to 300,000 patient-years. Generic versions were introduced in 2003.

Nefazodone is a phenylpiperazine compound and is related to trazodone. It has been described as a serotonin antagonist and reuptake inhibitor (SARI) due to its combined actions as a potent serotonin 5-HT2A receptor and 5-HT2C receptor antagonist and weak serotonin-norepinephrine-dopamine reuptake inhibitor (SNDRI).

Brief History

Nefazodone was discovered by scientists at Bristol-Myers Squibb (BMS) who were seeking to improve on trazodone by reducing its sedating qualities.

BMS obtained marketing approvals worldwide for nefazodone in 1994. It was marketed in the US under the brand name Serzone and in Europe under the brand name Dutonin.

In 2002, the US Food and Drug Administration (FDA) obligated BMS to add a black box warning about potential fatal liver toxicity to the drug label. Worldwide sales in 2002 were $409 million.

In 2003 Public Citizen filed a citizen petition asking the FDA to withdraw the marketing authorisation in the US, and in early 2004 the organisation sued the FDA to attempt to force withdrawal of the drug. The FDA issued a response to the petition in June 2004 and filed a motion to dismiss, and Public Citizen withdrew the suit.

Generic versions were introduced in the US in 2003 and Health Canada withdrew the marketing authorization that year.

Sales of nefazodone were about $100 million in 2003. By that time it was also being marketed under the additional brand names Serzonil, Nefadar, and Rulivan.

In April 2004, BMS announced that it was going discontinue the sale of Serzone in the US in June 2004 and said that this was due to declining sales. By that time BMS had already withdrawn the drug from the market in Europe, Australia, New Zealand and Canada.

As of 2012 generic nefazodone was available in the US.

Medical Uses

Nefazodone is used to treat major depressive disorder, aggressive behaviour, and panic disorder.

Available Forms

Nefazodone is available as 50 mg, 100 mg, 150 mg, 200 mg, and 250 mg tablets for oral ingestion.

Side Effects

Nefazodone can cause severe liver damage, leading to a need for liver transplant, and death. The incidence of severe liver damage is approximately 1 in every 250,000 to 300,000 patient-years. By the time that it started to be withdrawn in 2003, nefazodone had been associated with at least 53 cases of liver injury, with 11 deaths, in the United States, and 51 cases of liver toxicity, with 2 cases of liver transplantation, in Canada. In a Canadian study which found 32 cases in 2002, it was noted that databases like that used in the study tended to include only a small proportion of suspected drug reactions.

Common and mild side effects of nefazodone reported in clinical trials more often than placebo include dry mouth (25%), sleepiness (25%), nausea (22%), dizziness (17%), blurred vision (16%), weakness (11%), lightheadedness (10%), confusion (7%), and orthostatic hypotension (5%). Rare and serious adverse reactions may include allergic reactions, fainting, painful/prolonged erection, and jaundice.

Nefazodone is not especially associated with increased appetite and weight gain.

Interactions

Nefazodone is a potent inhibitor of CYP3A4, and may interact adversely with many commonly used medications that are metabolized by CYP3A4.

Pharmacology

Pharmacodynamics

Nefazodone acts primarily as a potent antagonist of the serotonin 5-HT2A receptor and to a lesser extent of the serotonin 5-HT2C receptor. It also has high affinity for the α1-adrenergic receptor and serotonin 5-HT1A receptor, and relatively lower affinity for the α2-adrenergic receptor and dopamine D2 receptor. Nefazodone has low but significant affinity for the serotonin, norepinephrine, and dopamine transporters as well, and therefore acts as a weak serotonin-norepinephrine-dopamine reuptake inhibitor (SNDRI). It has low but potentially significant affinity for the histamine H1 receptor, where it is an antagonist, and hence may have some antihistamine activity. Nefazodone has negligible activity at muscarinic acetylcholine receptors, and accordingly, has no anticholinergic effects.

Pharmacokinetics

The bioavailability of nefazodone is low and variable, about 20%. Its plasma protein binding is approximately 99%, but it is bound loosely.

Nefazodone is metabolized in the liver, with the main enzyme involved thought to be CYP3A4. The drug has at least four active metabolites, which include hydroxynefazodone, para-hydroxynefazodone, triazoledione, and meta-chlorophenylpiperazine. Nefazodone has a short elimination half-life of about 2 to 4 hours. Its metabolite hydroxynefazodone similarly has an elimination half-life of about 1.5 to 4 hours, whereas the elimination half-lives of triazoledione and mCPP are longer at around 18 hours and 4 to 8 hours, respectively. Due to its long elimination half-life, triazole is the major metabolite and predominates in the circulation during nefazodone treatment, with plasma levels that are 4 to 10 times higher than those of nefazodone itself. Conversely, hydroxynefazodone levels are about 40% of those of nefazodone at steady state. Plasma levels of mCPP are very low at about 7% of those of nefazodone; hence, mCPP is only a minor metabolite. mCPP is thought to be formed from nefazodone specifically by CYP2D6.

The ratios of brain-to-plasma concentrations of mCPP to nefazodone are 47:1 in mice and 10:1 in rats, suggesting that brain exposure to mCPP may be much higher than plasma exposure. Conversely, hydroxynefazodone levels in the brain are 10% of those in plasma in rats. As such, in spite of its relatively low plasma concentrations, brain exposure to mCPP may be substantial, whereas that of hydroxynefazodone may be minimal.

Chemistry

Nefazodone is a phenylpiperazine; it is an alpha-phenoxyl derivative of etoperidone which in turn was a derivative of trazodone.

Society and Culture

Generic Names

Nefazodone is the generic name of the drug and its INN and BAN, while néfazodone is its DCF and nefazodone hydrochloride is its USAN and USP.

Brand Names

Nefazodone has been marketed under a number of brand names including Dutonin (AT, ES, IE, UK), Menfazona (ES), Nefadar (CH, DE, NO, SE), Nefazodone BMS (AT), Nefazodone Hydrochloride Teva (US), Reseril (IT), Rulivan (ES), and Serzone (AU, CA, US). As of 2017, it remains available only on a limited basis as Nefazodone Hydrochloride Teva in the United States.

Research

The use of nefazodone to prevent migraine has been studied, due to its antagonistic effects on the 5-HT2A and 5-HT2C receptors.

What is the National Alliance on Mental Illness?

Introduction

The National Alliance on Mental Illness (NAMI) is a United States-based advocacy group originally founded as a grassroots group by family members of people diagnosed with mental illness.

NAMI identifies its mission as “providing advocacy, education, support and public awareness so that all individuals and families affected by mental illness can build better lives” and its vision as “a world where all people affected by mental illness live healthy, fulfilling lives supported by a community that cares”. NAMI offers classes and trainings for people living with mental illnesses, their families, community members, and professionals, including what is termed psychoeducation, or education about mental illness. NAMI holds regular events which combine fundraising for the organization and education, including Mental Illness Awareness Week and NAMIWalks.

Headquartered in Arlington, Virginia, NAMI has around 1,000 state and local affiliates and is represented in all 50 US states, Washington, D.C., and Puerto Rico. NAMI is funded primarily through pharmaceutical company donations. Additional funding comes from individual donors, as well as sponsorships and grants. NAMI publishes a magazine around twice a year called The Advocate. NAMI also runs a HelpLine five days a week, which is funded in part by pharmaceutical companies Janssen and Lundbeck.

Brief History

NAMI was founded in Madison, Wisconsin, by Harriet Shetler and Beverly Young. The two women both had sons diagnosed with schizophrenia, and “were tired of being blamed for their sons’ mental illness”. Unhappy with the lack of services available and the treatment of those living with mental illness, the women sought out others with similar concerns. The first meeting held to address these issues in mental health led to the formation of the National Alliance for the Mentally Ill in 1979. In 1997, the legal name was changed to the acronym NAMI by a vote of the membership due to concerns that the name National Alliance for the Mentally Ill did not use person-first language. In 2005, the meaning of NAMI was changed to the backronym National Alliance on Mental Illness.

Mission

NAMI identifies its mission as to promote recovery by preserving and strengthening family relationships “affected by mental illness”. NAMI’s programmes and services include education, support groups, informational publications, and presentations. Although originally focused primarily on family members, in more recent years NAMI has moved toward trying to include people diagnosed with mental illness as well (although activists have criticised these efforts). In addition, NAMI has a strong focus on discriminatory attitudes and behaviours about mental illness (what they term stigma); another identified goal is “to increase public and professional understanding”, and “to improve the mental health system”.

Structure

The National Alliance on Mental Illness is a 501(c)(3) non-profit run by a board of directors who are elected by membership. NAMI National is the umbrella organisation; state and local affiliates operate semi-independently, in an attempt to more accurately represent those in the surrounding communities. Since 2015, NAMI has been using a four-year strategic plan which expires in 2019.

The national chief executive officer from 2014-2019 was Mary Giliberti, who resigned on 24 April 2019. She was immediately preceded by Michael Fitzpatrick. Gilberti, who has a law degree from Yale University and clerked for Judge Phyllis A. Kravitch. Before coming to NAMI, Giliberti worked as a senior attorney at Bazelon Centre for Mental Health Law for almost ten years and the Senate Health, Education, Labour, and Pensions Committee from 2008 to 2014. She worked for NAMI National during this time as the director of public policy and advocacy for federal and state issues. In 2017, she was “appointed by the Secretary of the U.S. Department of Health and Human Service (HHS) to serve as one of 14 non-federal members of HHS’ Interdepartmental Serious Mental Illness Coordinating Committee.”

National and state NAMI organisations function to provide Governance, Public Education, Political Advocacy, and management of NAMI’s Educational Programmes. At the local level, the local NAMI chapters also provide assistance in obtaining mental health resources, scheduling and administration of NAMI’s programmes, and hosting local meetings and events for NAMI members.

In February 2020, NAMI Sioux Falls has merged with the South Dakota Office. The move was a result of a decision by the national NAMI office.

Partnerships

In 2017, NAMI partnered with Alpha Kappa Alpha (since 2015), Instagram, tumblr, Women’s Health, Fox Sports, Stanley Centre for Psychiatric Research at Broad Institute, Jack and Jill of America, The Jed Foundation, and Lokai. Celebrity partnerships included Utkarsh Ambudkar, Maria Bamford, Andrea Barber, AJ Brooks, Sterling K. Brown, Corinne Foxx, Naomi Judd, Dawn McCoy, Stefania Owen, Alessandra Torresani, Wil Wheaton, DeWanda Wise, and Chris Wood.

Philosophy and Positions

NAMI generally endorses a medical model approach to mental illnesses, and previously was a major proponent of terming them “serious brain disorders” during the “decade of the brain”. NAMI endorses the term anosognosia, or “that someone is unaware of their own mental health condition or that they can’t perceive their condition accurately”. While NAMI previously referred to mental illnesses as “serious brain disorders”, current advice on their “How we talk about NAMI” page recommends against this language.

Programmes

NAMI programmes are generally in the area of support and education for individuals and families, often for no cost. The programmes are set up through local NAMI Affiliate organisations, with different programmes varying in their targeted audience.

NAMI Family-to-Family

The NAMI Family-to-Family Education Programme is a free eight-week course targeted toward family and friends of individuals with mental illness, providing education from a medical model perspective of mental illness. Originally offered as a twelve-week programme, but updated to a shorter model in 2020, the courses are taught by a NAMI-trained family member of a person diagnosed with a psychiatric disorder. Family-to-Family is taught in 44 states, and two provinces in Canada. The programme was developed by clinical psychologist Joyce Burland. Facilitators are required to teach material from the curriculum without alteration.

Purpose

The Family-to-Family programme provides general information about mental illness and how it is currently treated from a medical model perspective. The programmes cover mental illnesses including schizophrenia, depression, bipolar disorder, etc., as well as the indications and side effects of medications. Family-to-Family takes a biologically-based approach to explaining mental illness and its treatments.

According to the NAMI website, Family-to-Family programme states its goals as teaching coping and advocacy skills, providing mutual support, how to “handle a crisis”, “information on mental health conditions and how they affect the brain”, and locating resources in the community

Evidence Base

The NAMI Family-to-Family programme has initial research evidence; one randomised clinical trial showed gains in empowerment, increases in problem solving and reductions in participant anxiety scores following the class; these changes persisted at 6 month follow up. These studies confirm an earlier finding that Family-to-Family graduates describe a permanent transformation in the understanding and engagement with mental illness in themselves and their family. Because a randomized controlled trial is at risk of poor external validity by mechanism of self-selection, Dixon and colleges sought out to strengthen the evidence base by confirming the benefits attributed to Family-to-Family with a subset of individuals who declined participation during initial studies.

The NAMI Family-to-Family programme was found to increase self efficacy in family members involved in caring for a family member with schizophrenia while reducing subjective burden and need for information. In light of recent research, Family-to-Family was added to the SAMHSA National Registry of Evidence-Based Programmes and Practices (NREPP), although as of January 2018 this database and designation has been eliminated by SAMHSA.

NAMI Peer-to-Peer

The NAMI Peer-to-Peer is an eight-week educational programme aimed at adults diagnosed with a mental illness. The NAMI Peer-to-Peer programme describes the course as a holistic approach to recovery through lectures, discussions, interactive exercises, and teaching stress management techniques. The programme provides information about biological explanations of mental illness, symptoms, and personal experiences. The programme also includes information about interacting with healthcare providers as well as decision making and stress reducing skills. The Peer-to-Peer philosophy is advertised as being centred around certain values such as individuality, autonomy, and unconditional positive regard. The programme is also available in Spanish.

Preliminary studies have suggested Peer-to-Peer provided many of its purported benefits (e.g. self-empowerment, disorder management, confidence). Peer interventions in general have been studied more extensively, having been found to increase social adjustment.

NAMI In Our Own Voice

The NAMI In Our Own Voice (IOOV) programme started as a mental health consumer education program for people living with schizophrenia in 1996, and was further developed to IOOV with grant funding from Eli Lily & Co. in 2002. The programme was based on the idea that those successfully living with mental illness were experts in a sense, and sharing their stories would benefit those with similar struggles. The programme approached this by relaying the idea that recovery is possible, attempting to build confidence and self-esteem. Because of the initial success of the programme and positive reception, IOOV also took on the role of public advocacy.

NAMI In Our Own Voice involves two trained speakers presenting personal experiences related to mental illness, in front of an audience. Unlike the majority of NAMI’s programmes, IOOV consists of a single presentation educating groups of individuals with the acknowledgement many are likely unfamiliar with mental illness. The programme’s aims include raising awareness regarding NAMI and mental illness in general, addressing stigma, and empowering those affected by mental illness. Other than those directly affected by mental illness, In Our Own Voice often educates groups of individuals like law enforcement, politicians, and students.

In Our Own Voice has been shown to be superior at reducing self stigmatisation of families when compared to clinician led education. Research into the effectiveness of the NAMI In Our Own Voice programme has shown the programme also can be of benefit to Graduate level therapists and adolescents. A 2016 study evaluating IOOV in California found significant reductions in desire for social distancing after attending an IOOV presentation, although no validated measures were used in the evaluation.

NAMI Basics

The NAMI Basics Programme is a six-session course for parents or other primary caregivers of children and adolescents living with mental illness. NAMI Basics is conceptually similar to NAMI Family-to-Family in that it aims to educate families, but recognises providing care for a child living with mental illness presents unique challenges in parenting, and that mental illness in children typically manifest differently than in adults. Because of the development of the brain and nervous system throughout childhood and adolescence, information regarding mental illness biology and its presentation is fundamentally different from with adults. The NAMI Basics programme has a relatively short time course to accommodate parents’ difficulty in attending because of their caregiver status.

NAMI Connection

The NAMI Connection Recovery Support Group Programme is a weekly support group for adults living with mental illness. The programme is for adults 18+ diagnosed with mental illness and groups are usually weekly for 90 minutes. The support groups are led by trained facilitators who identify as having experienced mental illness themselves.

NAMI On Campus

NAMI On Campus is an initiative for university students to start NAMI On Campus organisations within their respective universities. NAMI On Campus was started to address the mental health issues of college-aged students. Adolescence and early adulthood are periods where the onset of mental illness is common, with 75% of mental illnesses beginning by age 24. When asked what barriers, if any, prevented them from gaining support and treatment, surveys found stigma to be the number one barrier.

Ending the Silence

This 50-minute or one hour programme is available for students, school staff, and family members. It involves two presenters: one who shares educational information and one who is a young adult living well in recovery who shares their personal story. This programme has been shown to improve the mental health knowledge of middle- and high school students.

In 2017, Former Second Lady of the United States Tipper Gore gave a $1 million donation to the Ending the Silence programme.

Funding

NAMI receives funding from both private and public sources, including corporations, federal agencies, foundations and individuals. NAMI maintains that it is committed to avoiding conflicts of interest and does not endorse nor support any specific service or treatment. Records of NAMI’s quarterly grants and contributions since 2009 are freely available on its website.

In 2017, NAMI had a 16% increase in overall revenue.

NAMIWalks

The 2017 annual report noted “$11.3 million raised across the country by 68,000 participants.”

Criticism

The funding of NAMI by multiple pharmaceutical companies was reported by the investigative magazine Mother Jones in 1999, including that an Eli Lilly & Company executive was then “on loan” to NAMI working out of NAMI headquarters.

During a 2009 investigation into the drug industry’s influence on the practice of medicine, US Senator Chuck Grassley (R-IA) sent letters to NAMI and about a dozen other influential disease and patient advocacy organisations asking about their ties to drug and device makers. The investigation confirmed pharmaceutical companies provided a majority of NAMI’s funding, a finding which led to NAMI releasing documents listing donations over $5,000.

Dr. Peter Breggin refers to NAMI as an “AstroTurf lobbying organisation” of the “psychopharmaceutical complex”.

On This Day … 17 January

People (Births)

  • 1881 – Harry Price, English psychologist and author (d. 1948).
  • 1887 – Ola Raknes, Norwegian psychoanalyst and philologist (d. 1975).
  • 1945 – Anne Cutler, Australian psychologist and academic.

Harry Price

Harry Price (17 January 1881 to 29 March 1948) was a British psychic researcher and author, who gained public prominence for his investigations into psychical phenomena and his exposing fraudulent spiritualist mediums.

He is best known for his well-publicised investigation of the purportedly haunted Borley Rectory in Essex, England.

Ola Raknes

Ola Raknes (17 January 1887 to 28 January 1975) was a Norwegian psychologist, philologist and non-fiction writer.

Born in Bergen, Norway, he was internationally known as a psychoanalyst in the Reichian tradition. He has been described as someone who spent his entire life working with the conveying of ideas through many languages and between different epistemological systems of reference, science and religion (Dannevig, 1975). For large portions of his life he was actively contributing to the public discourse in Norway. He has also been credited for his contributions to strengthening and enriching the Nynorsk language and its use in the public sphere.

Raknes was known as a thorough philologist and a controversial therapist. Internationally he was known as one of Wilhelm Reich’s closest students and defenders.

Anne Cutler

(Elizabeth) Anne Cutler (born 1945 in Melbourne) FRS, FBA, FASSA is a Research Professor at the MARCS Institute for Brain, Behaviour and Development, Western Sydney University and Emeritus Director of the Max Planck Institute for Psycholinguistics in Nijmegen.

After studying languages and psychology in Melbourne, Berlin and Bonn, Anne Cutler embraced psycholinguistics when it emerged as an independent field, going on to complete her PhD in the discipline at the University of Texas at Austin.

On This Day … 15 January

People (Births)

  • 1842 – Josef Breuer, Austrian physician and psychiatrist (d. 1925).
  • 1877 – Lewis Terman, American psychologist, eugenicist, and academic (d. 1956).
  • 1958 – Boris Tadić, Serbian psychologist and politician, 16th President of Serbia.

Josef Breuer

Josef Breuer (15 January 1842 to 20 June 1925) was a distinguished physician who made key discoveries in neurophysiology, and whose work in the 1880s with his patient Bertha Pappenheim, known as Anna O., developed the talking cure (cathartic method) and laid the foundation to psychoanalysis as developed by his protégé Sigmund Freud.

Lewis Terman

Lewis Madison Terman (15 January 1877 to 21 December 1956) was an American psychologist and author. He was noted as a pioneer in educational psychology in the early 20th century at the Stanford Graduate School of Education.

He is best known for his revision of the Stanford-Binet Intelligence Scales and for initiating the longitudinal study of children with high IQs called the Genetic Studies of Genius. He was a prominent eugenicist and was a member of the Human Betterment Foundation. He also served as president of the American Psychological Association. A Review of General Psychology survey, published in 2002, ranked Terman as the 72nd most cited psychologist of the 20th century, in a tie with G. Stanley Hall.

Boris Tadic

Boris Tadić (born 15 January 1958) is a Serbian politician who served as the president of Serbia from 2004 to 2012.

Tadić was a member of the Democratic Party since its establishment in 1990, and has been their president from 2004 until 2012. After the downfall of Milošević, he was appointed in the government as the Minister of Telecommunications of the Federal Republic of Yugoslavia and would later serve as the first Minister of Defence of Serbia and Montenegro before being elected as the president in 2004. He was re-elected for his second term in 2008. Following his defeat in the 2012 presidential election and poor party ratings, he stepped down in November 2012, to take the position of the party’s Honorary President. After a split with the new leadership in January 2014, Tadić left the Democratic Party and formed his own New Democratic Party (later renamed Social Democratic Party) for the 2014 parliamentary election.

Tadić strongly advocates close ties with the European Union (EU) and Serbia’s European integration. During his presidency, the EU has abolished visas for Serbian citizens traveling to the Schengen Area countries, Serbian government signed the Stabilisation and Association Agreement (SAA) and received an EU candidate status, as well as, Serbia has completed obligations to the International Criminal Tribunal for the former Yugoslavia (ICTY). He became the first Serbian head of state or head of government to visit the Srebrenica Genocide Memorial and he launched an initiative for the Serbian parliament to adopt a resolution condemning the Srebrenica massacre. The period of a coalition government led by the Tadić’s Democratic Party was characterized by the challenges of the Kosovo declaration of independence and the global financial crisis, leading to low rates of economic growth. He is widely regarded as a pro-Western leader, who also favours balanced relations with Russia, the United States and the EU.

What is Malignant Narcissism?

Introduction

Malignant narcissism is a psychological syndrome comprising an extreme mix of narcissism, antisocial behaviour, aggression, and sadism.

Grandiose, and always ready to raise hostility levels, the malignant narcissist undermines families and organisations in which they are involved, and dehumanises the people with whom they associate.

Malignant narcissism is a hypothetical, experimental diagnostic category. Narcissistic personality disorder (NPD) is found in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), while malignant narcissism is not. As a hypothetical syndrome, malignant narcissism could include aspects of NPD alongside a mix of antisocial, paranoid and sadistic personality disorder traits. The importance of malignant narcissism and of projection as a defence mechanism has been confirmed in paranoia, as well as “the patient’s vulnerability to malignant narcissistic regression”.

Brief History

The social psychologist Erich Fromm first coined the term “malignant narcissism” in 1964, describing it as a “severe mental sickness” representing “the quintessence of evil”. He characterised the condition as “the most severe pathology and the root of the most vicious destructiveness and inhumanity”. Edith Weigert (1967) saw malignant narcissism as a “regressive escape from frustration by distortion and denial of reality”, while Herbert Rosenfeld (1971) described it as “a disturbing form of narcissistic personality where grandiosity is built around aggression and the destructive aspects of the self become idealized.”

On 11 May 1968, psychoanalyst Otto Kernberg presented his paper Factors in the Psychoanalytic Treatment of Narcissistic Personalities, from the work of the Psychotherapy Research Project of The Menninger Foundation, at the 55th Annual Meeting of the American Psychoanalytic Association in Boston.[6] Kernberg’s paper was first published in hard copy on 01 January 1970. In Kernberg’s 1968 paper, first published in 1970 in the Journal of the American Psychoanalytic Association (JAPA), the word ‘malignant’ does not appear once, while ‘pathological’ or ‘pathologically’ appears 25 times.

Developing these ideas further, Kernberg pointed out that the antisocial personality was fundamentally narcissistic and without morality. Malignant narcissism includes a sadistic element creating, in essence, a sadistic psychopath. In his article, “malignant narcissism” and psychopathy are employed interchangeably. Kernberg first proposed malignant narcissism as a psychiatric diagnosis in 1984. So far it has not been accepted in any of the medical manuals, such as the ICD-10 or the DSM-5.

Kernberg described malignant narcissism as a syndrome characterised by a NPD, antisocial features, paranoid traits, and egosyntonic aggression. Other symptoms may include an absence of conscience, a psychological need for power, and a sense of importance (grandiosity). Psychoanalyst George H. Pollock wrote in 1978: “The malignant narcissist is presented as pathologically grandiose, lacking in conscience and behavioral regulation with characteristic demonstrations of joyful cruelty and sadism”. Of note, M. Scott Peck uses malignant narcissism as a way to explain evil.

Kernberg believed that malignant narcissism should be considered part of a spectrum of pathological narcissism, which he saw as ranging from Hervey M. Cleckley’s antisocial character (what is now referred to as psychopathy or antisocial personality) at the high end of severity, through malignant narcissism, and then to narcissistic personality disorder at the low end. So according to Kernberg’s hierarchy, psychopathy trumps malignant narcissism as a more extreme form of pathological narcissism. Malignant narcissism can be distinguished from psychopathy, according to Kernberg, because of the malignant narcissist’s capacity to internalise “both aggressive and idealized superego precursors, leading to the idealization of the aggressive, sadistic features of the pathological grandiose self of these patients”.

According to Kernberg, the psychopath’s paranoid stance against external influences makes him or her unwilling to internalise even the values of the “aggressor”, while malignant narcissists “have the capacity to admire powerful people, and can depend on sadistic and powerful but reliable parental images”. Malignant narcissists, in contrast to psychopaths, are also said to be capable of developing:

“some identification with other powerful idealized figures as part of a cohesive ‘gang’…which permits at least some loyalty and good object relations to be internalized… Some of them may present rationalized antisocial behavior – for example, as leaders of sadistic gangs or terrorist groups…with the capacity for loyalty to their own comrades.”

Psychopathy

The terms malignant narcissist and psychopath are sometimes used interchangeably because there is little to clinically separate the two. Individuals with narcissistic personality disorder, malignant narcissism, and psychopathy all display similar traits which are outlined in the Hare Psychopathy Checklist. The test has 20 items scored on a three-point scale, with a rating of:

  • 0 if it does not apply at all;
  • 1 if there is a partial match or mixed information; and
  • 2 if there is a reasonably good match.

With a maximum score of 40, the cut-off for the label of psychopathy is 30 in the US and 25 in the UK. High scores are positively associated with measures of impulsivity and aggression, Machiavellianism, persistent criminal behaviour, and negatively associated with measures of empathy and affiliation.

Malignant narcissism is highlighted as a key area in the study of mass murder, sexual, and serial murder.

Contrast with Narcissism

The primary difference between narcissism and malignant narcissism is that malignant narcissism includes comorbid features of other personality disorders and thus consists of a broader range of symptoms than pathological narcissism (NPD). In the term “malignant narcissism”, the word “malignant” is used in the sense of the word described by the Merriam-Webster Dictionary as “passionately and relentlessly malevolent: aggressively malicious”. In malignant narcissism, NPD is accompanied by additional symptoms of antisocial, paranoid and sadistic personality disorders. While a person with NPD will deliberately damage other people in pursuit of their own selfish desires, they may regret and will in some circumstances show remorse for doing so. Because traits of antisocial personality disorder are present in malignant narcissism, the “malignant narcissist” suffers from a more pervasive lack of empathy than someone with NPD alone and will lack feelings of guilt or remorse for the damage they cause. Since sadism is often considered a feature of malignant narcissism, an individual with the syndrome may not only lack feelings of guilt or remorse for hurting others but may even derive pleasure from the gratuitous infliction of mental or physical pain on others. These traits were formerly codified in the DSM-III under sadistic personality disorder (SPD).

Therapy

Typically in the analysis of the malignant narcissist, “the patient attempts to triumph over the analyst by destroying the analysis and himself or herself” – an extreme version of what Jacques Lacan described as “that resistance of the amour-propre… which is often expressed thus: ‘I can’t bear the thought of being freed by anyone other than myself'”.

What is the Term: ‘Kick the Cat’?

Introduction

Kick the cat (or kick the dog) is a metaphor used to describe how a relatively high-ranking person in an organisation or family displaces (see below) their frustrations by abusing a lower-ranking person, who may in turn take it out on their own subordinate.

Displacement

In psychology, displacement is an unconscious defence mechanism whereby the mind substitutes either a new aim or a new object for goals felt in their original form to be dangerous or unacceptable.

Origin of the Idiom

The term has been used at least since the 19th century. According to author John Bradshaw, humans were far more cruel to cats at that time, to the extent that kicking one was not perceived to be unusual and hence entered the language as a popular idiom.

The concept was reinforced in British culture by a scene in the Blackadder episode Nob and Nobility in which Edmund Blackadder kicks the cat when annoyed, and the cat bites the mouse, and the mouse bites Baldrick.

In current usage, the name envisions a scenario where an angry or frustrated employee comes home from work looking for some way to take out his anger, but the only thing present is the cat. He physically abuses it as a means of relieving his frustration, despite the cat playing no part in causing it.

Workplace or Family Dynamics

Kicking the cat is commonly used to describe the behaviour of staff abusing co-workers or subordinates as a mechanism to relieve stress. This behaviour can result in a chain reaction, where a higher-ranking member of the company abuses their subordinate, who takes it out on their own subordinate, and so on down the line. This domino effect can also be seen in family dynamics, where the father yells at the mother who yells at the older child who yells at the younger child who yells at the pet.

Blaming others can lead to kicking the dog where individuals in a hierarchy blame their immediate subordinate, and this propagates down a hierarchy until the lowest rung (the “dog”). A 2009 experimental study has shown that blaming can be contagious even for uninvolved onlookers.

Psychological Theories

According to Psychology Today, “Anger and frustration in one part of life can lead us to lash out at innocent people (or pets) in another.” The technical term for this kind of behaviour is “displaced aggression”.

Kicking the cat is looked upon unfavourably and viewed as a sign of poor anger management. According to author Steve Sonderman, “Men funnel 90 percent of their emotions through anger” and may “kick the cat” as a substitute for grief, anxiety or other emotions. Psychology author Raj Persaud suggests that people “kick the cat” as a means of catharsis because they fear expressing their full emotions to the peers and colleagues.