Tag: Psychosis

What is Dopamine Supersensitivity Psychosis?

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Introduction

Dopamine supersensitivity psychosis is a hypothesis that attempts to explain the phenomenon in which psychosis (e.g. having hallucinations, which can mean hearing or seeing things that other people do not see or hear) occurs despite treatment with escalating doses of antipsychotics. Dopamine supersensitivity may be caused by the dopamine receptor D2 antagonising effect of antipsychotics, causing a compensatory increase in D2 receptors within the brain that sensitizes neurons to endogenous release of the neurotransmitter dopamine. Because psychosis is thought to be mediated—at least in part—by the activity of dopamine at D2 receptors, the activity of dopamine in the presence of supersensitivity may paradoxically give rise to worsening psychotic symptoms despite antipsychotic treatment at a given dose. This phenomenon may co-occur with tardive dyskinesia, a rare movement disorder that may also be due to dopamine supersensitivity.

Brief History

When supersensitivity psychosis was explored in 1978, a featured concern was increasing resistance to medication, requiring higher doses or not responding to higher doses. Some articles use the term tardive psychosis to reference to this specific concept. However, articles have disputed its validity. The condition has been discovered in very few people. Palmstierna asserts that tardive psychosis is a combination of “several different and not necessarily correlated phenomena related to neuroleptic treatment of schizophrenia.”

Mechanism

Dopamine supersensitivity psychosis may occur due to upregulation of dopamine 2 receptors (D2). The D2 receptor is the primary target of almost all antipsychotics, which oppose the action of the neurotransmitter dopamine at this receptor. The antagonising or “blockade” of D2 by antipsychotics may cause neurons, a type of cell within the brain, to undergo compensatory changes to make up for the loss of activity at D2 receptors. The D2 signalling pathway within neurons is complex, and involves multiple enzymes and other secondary messengers. It may be the case that, in response to antipsychotics, neurons increase the production of D2 receptors (upregulation), thereby sensitizing the neuron to dopamine. However, this is likely an oversimplification, as—despite differences in sensitivity to dopamine of around 3-fold in people that have taken antipsychotics chronically, there is a disproportionately low increase in the amount of D2 receptors in the brain in these people (around 1.4-fold in the striatum of the brain in people with schizophrenia). Other hypotheses include increases in the “active” D2 receptors (termed D2High) relative to the “inactive” conformation (D2Low).

The result is dopamine supersensitivity. It is thought that the psychotic symptoms within schizophrenia are primarily due to overactive dopamine activity in the mesolimbic area of the brain. Therefore, dopamine supersensitivity may reduce the effect of antipsychotics and increase the brain’s response to endogenous dopamine, leading to worsening psychosis.

Tardive dyskinesia, a type of rare movement disorder that can be caused by antipsychotics, may also be caused by dopamine receptor sensitization. This may explain why, for people with tardive dyskinesia, increasing the dose of the antipsychotic may temporarily improve symptoms.

Diagnosis

The original criteria for dopamine supersensitivity psychosis were the following:

A. Continuous use of antipsychotics for at least 3 months.
B. One of the following:

  1. Rebound psychosis within 6 weeks of a change (e.g. dose reduction, or antipsychotic switching) in an oral antipsychotic regimen or 3 months for long-acting injectable antipsychotics
  2. Tolerance to antipsychotic effects (requiring escalating doses, even beyond what has controlled symptoms in the past)
  3. Presence of tardive dyskinesia (which should occur when antipsychotics are withdrawn, and improve or disappear when antipsychotics are restarted)

Differential Diagnosis

It may sometimes be impossible to distinguish dopamine supersensitivity psychosis from psychosis that occurs “naturally” in the course of a primary psychotic disorder like schizophrenia, including cases in which the person was not taking their antipsychotic medication. Even in the presence of an alternative aetiology, or when it is impossible to determine the precise aetiology for a psychotic episode, it is possible that dopamine supersensitivity psychosis can play a role in the presentation. Recognising the possible role of dopamine supersensitivity psychosis in a psychotic episode has implications for how to best manage someone’s antipsychotic therapy.

Society and Culture

Dopamine supersensitivity is often dismissed as an inconsequential factor in the progression of psychotic disorders by psychiatrists in the medical literature. The dopamine supersensitivity hypothesis was discussed by investigative journalist and author Robert Whitaker in his book Anatomy of an Epidemic, published in 2010.

Research

As of 2017, much of the evidence for dopamine supersensitivity psychosis comes from studies performed in animals. There is still a need for robust, human research.

In a cohort study of people taking chronic antipsychotic therapy with either schizophrenia or schizoaffective disorder that presented for psychiatric care due to a relapse of their psychotic symptoms without a clear precipitating cause (e.g. new or worsening substance abuse, evidence of nonadherence to antipsychotics), 39% of the sample met the authors’ checklist for dopamine supersensitivity psychosis. The people that met the criteria were more likely than others to have worse symptoms when their psychosis returned (relapsed), have residual psychotic symptoms, had overall worse health outcomes at 6-month follow-ups, and were more likely to live in residential care.

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What is the Dopamine Hypothesis of Schizophrenia?

Published on by Andrew Marshall1 Comment

Introduction

The dopamine hypothesis of schizophrenia or the dopamine hypothesis of psychosis is a model that attributes the positive symptoms of schizophrenia to a disturbed and hyperactive dopaminergic signal transduction.

The model draws evidence from the observation that a large number of antipsychotics have dopamine-receptor antagonistic effects. The theory, however, does not posit dopamine overabundance as a complete explanation for schizophrenia. Rather, the overactivation of D2 receptors, specifically, is one effect of the global chemical synaptic dysregulation observed in this disorder.

Refer to Glutamate Hypothesis of Schizophrenia.

Introduction

Some researchers have suggested that dopamine systems in the mesolimbic pathway may contribute to the ‘positive symptoms’ of schizophrenia, whereas problems concerning dopamine function within the mesocortical pathway may be responsible for the ‘negative symptoms’, such as avolition and alogia. Abnormal expression, thus distribution of the D2 receptor between these areas and the rest of the brain may also be implicated in schizophrenia, specifically in the acute phase. A relative excess of these receptors within the limbic system means Broca’s area, which can produce illogical language, has an abnormal connection to Wernicke’s area, which comprehends language but does not create it. Note that variation in distribution is observed within individuals, so abnormalities of this characteristic likely play a significant role in all psychological illnesses. Individual alterations are produced by differences within glutamatergic pathways within the limbic system, which are also implicated in other psychotic syndromes. Among the alterations of both synaptic and global structure, the most significant abnormalities are observed in the uncinate fasciculus and the cingulate cortex. The combination of these creates a profound dissymmetry of prefrontal inhibitory signaling, shifted positively towards the dominant side. Eventually, the cingulate gyrus becomes atrophied towards the anterior, due to long-term depression (LTD) and long-term potentiation (LTP) from the abnormally strong signals transversely across the brain. This, combined with a relative deficit in GABAergic input to Wernicke’s area, shifts the balance of bilateral communication across the corpus callosum posteriorly. Through this mechanism, hemispherical communication becomes highly shifted towards the left/dominant posterior. As such, spontaneous language from Broca’s can propagate through the limbic system to the tertiary auditory cortex. This retrograde signalling to the temporal lobes that results in the parietal lobes not recognising it as internal results in the auditory hallucinations typical of chronic schizophrenia.

In addition, significant cortical grey matter volume reductions are observed in this disorder. Specifically, the right hemisphere atrophies more, while both sides show a marked decrease in frontal and posterior volume. This indicates that abnormal synaptic plasticity occurs, where certain feedback loops become so potentiated, others receive little glutaminergic transmission. This is a direct result of the abnormal dopaminergic input to the striatum, thus (indirectly) disinhibition of thalamic activity. The excitatory nature of dopaminergic transmission means the glutamate hypothesis of schizophrenia is inextricably intertwined with this altered functioning. 5-HT also regulates monoamine neurotransmitters, including dopaminergic transmission. Specifically, the 5-HT2A receptor regulates cortical input to the basal ganglia and many typical and atypical antipsychotics are antagonists at this receptor. Several antipsychotics are also antagonists at the 5-HT2C receptor, leading to dopamine release in the structures where 5-HT2C is expressed; striatum, prefrontal cortex, nucleus accumbens, amygdala, hippocampus (all structures indicated in this disease), and currently thought to be a reason why antipsychotics with 5HT2C antagonistic properties improves negative symptoms. More research is needed to explain the exact nature of the altered chemical transmission in this disorder.

Recent evidence on a variety of animal models of psychosis, such as sensitization of animal behaviour by amphetamine, or phencyclidine (PCP, Angel Dust), or excess steroids, or by removing various genes (COMT, DBH, GPRK6, RGS9, RIIbeta), or making brain lesions in newborn animals, or delivering animals abnormally by Caesarian section, all induce a marked behavioural supersensitivity to dopamine and a marked rise in the number of dopamine D2 receptors in the high-affinity state for dopamine. This latter work implies that there are multiple genes and neuronal pathways that can lead to psychosis and that all these multiple psychosis pathways converge via the high-affinity state of the D2 receptor, the common target for all antipsychotics, typical or atypical. Combined with less inhibitory signalling from the thalamus and other basal ganglic structures, from hyoptrophy the abnormal activation of the cingulate cortex, specifically around Broca’s and Wernicke’s areas, abnormal D2 agonism can facilitate the self-reinforcing, illogical patterns of language found in such patients. In schizophrenia, this feedback loop has progressed, which produced the widespread neural atrophy characteristic of this disease. Patients on neuroleptic or antipsychotic medication have significantly less atrophy within these crucial areas. As such, early medical intervention is crucial in preventing the advancement of these profound deficits in bilateral communication at the root of all psychotic disorders. Advanced, chronic schizophrenia can not respond even to clozapine, regarded as the most effective antipsychotic, as such, a cure for highly advanced schizophrenia is likely impossible through the use of any modern antipsychotics, so the value of early intervention cannot be stressed enough.

Discussion

Evidence for the Dopamine Hypothesis

Stimulants such as amphetamine, and cocaine increase the levels of dopamine in the brain and can cause symptoms of psychosis, particularly after large doses or prolonged use. This is often referred to as “amphetamine psychosis” or “cocaine psychosis,” but may produce experiences virtually indistinguishable from the positive symptoms associated with schizophrenia. Similarly, those treated with dopamine enhancing levodopa for Parkinson’s disease can experience psychotic side effects mimicking the symptoms of schizophrenia. Up to 75% of patients with schizophrenia have increased signs and symptoms of their psychosis upon challenge with moderate doses of methylphenidate or amphetamine or other dopamine-like compounds, all given at doses at which control normal volunteers do not have any psychologically disturbing effects.

Some functional neuroimaging studies have also shown that, after taking amphetamine, patients diagnosed with schizophrenia show greater levels of dopamine release (particularly in the striatum) than non-psychotic individuals. However, the acute effects of dopamine stimulants include euphoria, alertness and over-confidence; these symptoms are more reminiscent of mania than schizophrenia. Since the 2000s, several PET studies have confirmed an altered synthesis capacity of dopamine in the nigrostriatal system demonstrating a dopaminergic dysregulation.

A group of drugs called the phenothiazines, including antipsychotics such as chlorpromazine, has been found to antagonise dopamine binding (particularly at receptors known as D2 dopamine receptors) and reduce positive psychotic symptoms. This observation was subsequently extended to other antipsychotic drug classes, such as butyrophenones including haloperidol. The link was strengthened by experiments in the 1970s which suggested that the binding affinity of antipsychotic drugs for D2 dopamine receptors seemed to be inversely proportional to their therapeutic dose. This correlation, suggesting that receptor binding is causally related to therapeutic potency, was reported by two laboratories in 1976.

People with Schizophrenia appear to have a high rate of self-medication with nicotine; the therapeutic effect likely occurs through dopamine modulation by nicotinic acetylcholine receptors.

However, there was controversy and conflicting findings over whether post-mortem findings resulted from drug tolerance to chronic antipsychotic treatment. Compared to the success of post-mortem studies in finding profound changes of dopamine receptors, imaging studies using SPECT and PET methods in drug naïve patients have generally failed to find any difference in dopamine D2 receptor density compared to controls. Comparable findings in longitudinal studies show: ” Particular emphasis is given to methodological limitations in the existing literature, including lack of reliability data, clinical heterogeneity among studies, and inadequate study designs and statistic,” suggestions are made for improving future longitudinal neuroimaging studies of treatment effects in schizophrenia A recent review of imaging studies in schizophrenia shows confidence in the techniques, while discussing such operator error. In 2007 one report said, “During the last decade, results of brain imaging studies by use of PET and SPECT in schizophrenic patients showed a clear dysregulation of the dopaminergic system.”

Recent findings from meta-analyses suggest that there may be a small elevation in dopamine D2 receptors in drug-free patients with schizophrenia, but the degree of overlap between patients and controls makes it unlikely that this is clinically meaningful. While the review by Laruelle acknowledged more sites were found using methylspiperone, it discussed the theoretical reasons behind such an increase (including the monomer-dimer equilibrium) and called for more work to be done to ‘characterise’ the differences. In addition, newer antipsychotic medication (called atypical antipsychotic medication) can be as potent as older medication (called typical antipsychotic medication) while also affecting serotonin function and having somewhat less of a dopamine blocking effect. In addition, dopamine pathway dysfunction has not been reliably shown to correlate with symptom onset or severity. HVA levels correlate trendwise to symptoms severity. During the application of debrisoquin, this correlation becomes significant.

Giving a more precise explanation of this discrepancy in D2 receptor has been attempted by a significant minority. Radioligand imaging measurements involve the monomer and dimer ratio, and the ‘cooperativity’ model. Cooperativitiy is a chemical function in the study of enzymes. Dopamine receptors interact with their own kind, or other receptors to form higher order receptors such as dimers, via the mechanism of cooperativity. Philip Seeman has said: “In schizophrenia, therefore, the density of [11C] methylspiperone sites rises, reflecting an increase in monomers, while the density of [11C] raclopride sites remains the same, indicating that the total population of D2 monomers and dimers does not change.” (In another place Seeman has said methylspiperone possibly binds with dimers) With this difference in measurement technique in mind, the above-mentioned meta-analysis uses results from 10 different ligands. Exaggerated ligand binding results such as SDZ GLC 756 (as used in the figure) were explained by reference to this monomer-dimer equilibrium.

According to Seeman, “…Numerous postmortem studies have consistently revealed D2 receptors to be elevated in the striata of patients with schizophrenia”. However, the authors were concerned the effect of medication may not have been fully accounted for. The study introduced an experiment by Anissa Abi-Dargham et al. (2000) in which it was shown medication-free live people with schizophrenia had more D2 receptors involved in the schizophrenic process and more dopamine. Since then another study has shown such elevated percentages in D2 receptors is brain-wide (using a different ligand, which did not need dopamine depletion). In a 2009 study, Abi-Dargham et al. confirmed the findings of her previous study regarding increased baseline D2 receptors in people with schizophrenia and showing a correlation between this magnitude and the result of amphetamine stimulation experiments.

Some animal models of psychosis are similar to those for addiction – displaying increased locomotor activity. For those female animals with previous sexual experience, amphetamine stimulation happens faster than for virgins. There is no study on male equivalent because the studies are meant to explain why females experience addiction earlier than males.

Even in 1986 the effect of antipsychotics on receptor measurement was controversial. An article in Science sought to clarify whether the increase was solely due to medication by using drug-naive people with schizophrenia: “The finding that D2 dopamine receptors are substantially increased in schizophrenic patients who have never been treated with neuroleptic drugs raises the possibility that dopamine receptors are involved in the schizophrenic disease process itself. Alternatively, the increased D2 receptor number may reflect presynaptic factors such as increased endogenous dopamine levels (16). In either case, our findings support the hypothesis that dopamine receptor abnormalities are present in untreated schizophrenic patients.” (The experiment used 3-N-[11C]methylspiperone – the same as mentioned by Seeman detects D2 monomers and binding was double that of controls.)

It is still thought that dopamine mesolimbic pathways may be hyperactive, resulting in hyperstimulation of D2 receptors and positive symptoms. There is also growing evidence that, conversely, mesocortical pathway dopamine projections to the prefrontal cortex might be hypoactive (underactive), resulting in hypostimulation of D1 receptors, which may be related to negative symptoms and cognitive impairment. The overactivity and underactivity in these different regions may be linked, and may not be due to a primary dysfunction of dopamine systems but to more general neurodevelopmental issues that precede them. Increased dopamine sensitivity may be a common final pathway. Gründer and Cumming assert that of those living with schizophrenia and other dopaminergic related illnesses, up to 25% of these patients may appear to have dopaminergic markers within the normal range.

Another finding is a six-fold excess of binding sites insensitive to the testing agent, raclopride; Seeman said this increase was probably due to the increase in D2 monomers. Such an increase in monomers may occur via the cooperativity mechanism which is responsible for D2High and D2Low, the supersensitive and lowsensitivity states of the D2 dopamine receptor. More specifically, “an increase in monomers, may be one basis for dopamine supersensitivity”.

Genetic and Other Biopsychosocial Risk Factors

Genetic evidence has suggested that there may be genes, or specific variants of genes, that code for mechanisms involved in dopamine function, which may be more prevalent in people experiencing psychosis or diagnosed with schizophrenia. Advanced technology has led to the possibility of performing Genome-Wide Association (GWA) studies. These studies identify frequently seen single nucleotide polymorphisms (SNP) that are associated with common, yet complex disorders. Genetic variants found due to GWA studies may offer insight concerning impairments in dopaminergic function. Dopamine-related genes linked to psychosis in this way include COMT, DRD4, and AKT1.

While genetics play an important role in the occurrence of schizophrenia, other biopsychosocial factors must also be taken into consideration. While focusing on the risk of schizophrenia in second generation migrants, Hennsler and colleagues relay that the dopamine hypothesis of schizophrenia may be an explanation. Some migrants who have had adverse experiences in their host country, such as racism, xenophobia, and poor living conditions, were found to have high stress levels, which increased dopaminergic neurotransmission. This increase in dopaminergic neurotransmission can be seen in the striatum and amygdala, both of which are areas in the brain that process aversive stimuli.

Evidence Against the Dopamine Hypothesis

Further experiments, conducted as new methods were developed (particularly the ability to use PET scanning to examine drug action in the brain of living patients) challenged the view that the amount of dopamine blocking was correlated with clinical benefit. These studies showed that some patients had over 90% of their D2 receptors blocked by antipsychotic drugs, but showed little reduction in their psychoses. This primarily occurs in patients who have had the psychosis for ten to thirty years. At least 90-95% of first-episode patients, however, respond to antipsychotics at low doses and do so with D2 occupancy of 60-70%. The antipsychotic aripiprazole occupies over 90% of D2 receptors, but this drug is both an agonist and an antagonist at D2 receptors.

Furthermore, although dopamine-inhibiting medications modify dopamine levels within minutes, the associated improvement in patient symptoms is usually not visible for at least several days, suggesting that dopamine may be indirectly responsible for the illness.

Similarly, the second generation of antipsychotic drugs – the atypical antipsychotics – were found to be just as effective as older typical antipsychotics in controlling psychosis, but more effective in controlling the negative symptoms, despite the fact that they have lower affinity for dopamine receptors than for various other neurotransmitter receptors. More recent work, however, has shown that atypical antipsychotic drugs such as clozapine and quetiapine bind and unbind rapidly and repeatedly to the dopamine D2 receptor. All of these drugs exhibit inverse agonistic effects at the 5-HT2A/2C receptors, meaning serotonin abnormalities are also involved in the complex constellation of neurologic factors predisposing one to the self reinforcing language-based psychological deficits found in all forms of psychosis.

The excitatory neurotransmitter glutamate is now also thought to be associated with schizophrenia. Phencyclidine (also known as PCP or “Angel Dust”) and ketamine, both of which block glutamate (NMDA) receptors, are known to cause psychosis at least somewhat resembling schizophrenia, further suggesting that psychosis and perhaps schizophrenia cannot fully be explained in terms of dopamine function, but may also involve other neurotransmitters.

Similarly, there is now evidence to suggest there may be a number of functional and structural anomalies in the brains of some people diagnosed with schizophrenia, such as changes in grey matter density in the frontal and temporal lobes. It appears, therefore, that there are multiple causes for psychosis and schizophrenia, including gene mutations and anatomical lesions. Many argue that other theories concerning the cause of schizophrenia may be more reliable in some cases, such as the glutamate hypothesis, GABA hypothesis, dysconnection hypothesis, and Bayesian inference hypothesis.

Psychiatrist David Healy has argued that drug companies have inappropriately promoted the dopamine hypothesis of schizophrenia as a deliberate and calculated simplification for the benefit of drug marketing.

Relationship with Glutamate

Research has shown the importance of glutamate receptors, specifically N-methyl-D-aspartate receptors (NMDARs), in addition to dopamine in the aetiology of schizophrenia. Abnormal NMDAR transmission may alter communication between cortical regions and the striatum. Mice with only 5% of the normal levels of NMDAR’s expressed schizophrenic-like behaviours seen in animal models of schizophrenia while mice with 100% of NMDAR’s behaved normally. Schizophrenic behaviour in low NMDAR mice has been effectively treated with antipsychotics that lower dopamine. NMDAR’s and dopamine receptors in the prefrontal cortex are associated with the cognitive impairments and working memory deficits commonly seen in schizophrenia. Rats that have been given a NMDAR antagonist exhibit a significant decrease in performance on cognitive tasks. Rats given a dopamine antagonist (antipsychotic) experience a reversal of the negative effects of the NMDAR antagonist. Glutamate imbalances appear to cause abnormal functioning in dopamine. When levels of glutamate are low dopamine is overactive and results in the expression schizophrenic symptoms.

Combined Networks of Dopamine, Serotonin, and Glutamate

Psychopharmacologist Stephen M. Stahl suggested in a review of 2018 that in many cases of psychosis, including schizophrenia, three interconnected networks based on dopamine, serotonin, and glutamate – each on its own or in various combinations – contributed to an overexcitation of dopamine D2 receptors in the ventral striatum.

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An Overview of the National Psychosis Unit

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Introduction

The National Psychosis Unit is a national treatment centre for patients with schizophrenia and other psychotic disorders, in the United Kingdom. The unit is a tertiary referral centre in the National Health Service. It is located at the Bethlem Royal Hospital, part of the South London and Maudsley NHS Foundation Trust. It is closely affiliated to the Institute of Psychiatry, King’s College London, and forms part of the Psychosis Clinical Academic Group of King’s Health Partners.

Brief History

The Unit was set up in the early 1990s. It was one of the first units in the UK to offer the antipsychotic drug clozapine, following its reintroduction in the UK in 1990.

Staff

The service has a multidisciplinary team of doctors, nurses, pharmacists and psychologists, many of whom work part of their time as clinical scientists and researchers, investigating the causes of psychotic disorders, and the effectiveness of both existing and new treatments.

Sir Robin Murray, Professor of Psychiatric Research at the Institute of Psychiatry at King’s College London, is a prominent member of staff at National Psychosis Unit.

Treatment

The National Psychosis Unit specialises in evidence-based treatment for people with schizophrenia, bipolar disorder and other similar disorders, particularly where local treatment has been unsuccessful or only partially successful in relieving symptoms. Anyone receiving NHS treatment can access the service free of charge following a referral by the person’s psychiatrist or general practitioner

The service provides second opinions on medication, diagnosis or any other aspect of care. The service has an outpatient clinic and 24-bedded inpatient facility. As well as pharmaceutical treatments, there is a strong focus on psychological treatments, rehabilitation and recovery, and reducing the risk of readmission through exploring what has led to breakdowns in the past and how to avoid this happening in future. The Unit also hosts research into the treatment of psychosis, including clinical trials of new treatments for psychosis. The National Psychosis Carers’ Group, which meets monthly, supports the carers and families of people with psychosis and allows them a forum for discussion.

Links with Other Organisations

The National Psychosis Unit has strong links with the Department of Psychosis Studies at the Institute of Psychiatry, King’s College London. The Unit also has longstanding links with mental health charities, including Rethink and SANE.

Awards

The Unit won the Hospital Doctor Psychiatric Team of the Year Award in 1997.

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What is Paraphrenia?

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Introduction

Paraphrenia is a mental disorder characterised by an organised system of paranoid delusions with or without hallucinations (the positive symptoms of schizophrenia) and without deterioration of intellect or personality (its negative symptom).

This disorder is also distinguished from schizophrenia by a lower hereditary occurrence, less premorbid maladjustment, and a slower rate of progression. Onset of symptoms generally occurs later in life, near the age of 60. The prevalence of the disorder among the elderly is between 0.1% and 4%.

Paraphrenia is not included in the DSM-5; psychiatrists often diagnose patients presenting with paraphrenia as having atypical psychosis, delusional disorder, psychosis not otherwise specified, schizoaffective disorders, and persistent persecutory states of older adults. Recently, mental health professionals have also been classifying paraphrenia as very late-onset schizophrenia-like psychosis.

In the Russian psychiatric manuals, paraphrenia (or paraphrenic syndrome) is the last stage of development of paranoid schizophrenia. “Systematised paraphrenia” (with systematised delusions i. e. delusions with complex logical structure) and “expansive-paranoid paraphrenia” (with expansive/grandiose delusions and persecutory delusions) are the variants of paranoid schizophrenia (F20.0). Sometimes systematised paraphrenia can be seen with delusional disorder (F22.0). The word is from Ancient Greek: παρά – beside, near + φρήν – intellect, mind.

Brief History

The term paraphrenia was originally popularised by Karl Ludwig Kahlbaum in 1863 to describe the tendency of certain psychiatric disorders to occur during certain transitional periods in life (describing paraphrenia hebetica as the insanity of the adolescence and paraphrenia senilis as the insanity of the elders.

The term was also used by Sigmund Freud for a short time starting in 1911 as an alternative to the terms schizophrenia and dementia praecox, which in his estimation did not correctly identify the underlying condition, and by Emil Kraepelin in 1912/1913, who changed its meaning to describe paraphrenia as it is understood today, as a small group of individuals that have many of the symptoms of schizophrenia with a lack of deterioration and thought disorder. Kraepelin’s study was discredited by Wilhelm Mayer in 1921 when he conducted a follow-up study using Kraepelin’s data. His study suggested that there was little to no discrimination between schizophrenia and paraphrenia; given enough time, patients presenting with paraphrenia will merge into the schizophrenic pool. However, Meyer’s data are open to various interpretations. In 1952, Roth and Morrissey conducted a large study in which they surveyed the mental hospital admissions of older patients. They characterised patients as having:

“paraphrenic delusions which… occurred in each case in the setting of a well-preserved intellect and personality, were often ‘primary’ in character, and were usually associated with the passivity failings or other volitional disturbances and hallucinations in clear consciousness pathognomonic of schizophrenia”.

In recent medicine, the term paraphrenia has been replaced by the diagnosis of “very late-onset schizophrenia-like psychosis” and has also been called “atypical psychoses, delusional disorder, psychoses not otherwise specified, schizoaffective disorders, and persistent persecutory states of older adults” by psychotherapists.[4] Current studies, however, recognize the condition as “a viable diagnostic entity that is distinct from schizophrenia, with organic factors playing a role in a significant portion of patients.”[4]

Signs and Symptoms

The main symptoms of paraphrenia are paranoid delusions and hallucinations. The delusions often involve the individual being the subject of persecution, although they can also be erotic, hypochondriacal, or grandiose in nature. The majority of hallucinations associated with paraphrenia are auditory, with 75% of patients reporting such an experience; however, visual, tactile, and olfactory hallucinations have also been reported. The paranoia and hallucinations can combine in the form of “threatening or accusatory voices coming from neighbouring houses [and] are frequently reported by the patients as disturbing and undeserved”. Patients also present with a lack of symptoms commonly found in other mental disorders similar to paraphrenia. There is no significant deterioration of intellect, personality, or habits and patients often remain clean and mostly self-sufficient. Patients also remain oriented well in time and space.

Paraphrenia is different from schizophrenia because, while both disorders result in delusions and hallucinations, individuals with schizophrenia exhibit changes and deterioration of personality whereas individuals with paraphrenia maintain a well-preserved personality and affective response.

Causes

Neurological

Paraphrenia is often associated with a physical change in the brain, such as a tumour, stroke, ventricular enlargement, or neurodegenerative process. Research that reviewed the relationship between organic brain lesions and the development of delusions suggested that “brain lesions which lead to subcortical dysfunction could produce delusions when elaborated by an intact cortex”.

Predisposing Factors

Many patients who present with paraphrenia have significant auditory or visual loss, are socially isolated with a lack of social contact, do not have a permanent home, are unmarried and without children, and have maladaptive personality traits. While these factors do not cause paraphrenia, they do make individuals more likely to develop the disorder later in life.

Diagnosis

While the diagnosis of paraphrenia is absent from recent revisions of the DSM and the ICD, many studies have recognised the condition as “a viable diagnostic entity that is distinct from schizophrenia, with organic factors playing a role in a significant portion of patients.” As such, paraphrenia is seen as being distinct from both schizophrenia and progressive dementia in old age. Ravindran (1999) developed a list of criteria for the diagnosis of paraphrenia, which agrees with much of the research done up to the time it was published.

  1. A delusional disorder of at least six months duration characterized by the following:
    1. Preoccupation with one or more semi-systematised delusions, often accompanied by auditory hallucinations.
    2. Affect notably well-preserved and appropriate. Ability to maintain rapport with others.
    3. None of:
      1. Intellectual deterioration.
      2. Visual hallucinations.
      3. Incoherence.
      4. Flat or grossly inappropriate affect.
      5. Grossly disorganised behaviour at times other than during the acute episode.
    4. Disturbance of behaviour understandable in relation to the content of the delusions and hallucinations.
    5. Only partly meets criterion A for schizophrenia. No significant organic brain disorder.

Management

Research suggests that paraphrenics respond well to antipsychotic drug therapy if doctors can successfully achieve sufficient compliance. Herbert found that Stelazine combined with Disipal was an effective treatment. It promoted the discharging of patients and kept discharged patients from being readmitted later. While behaviour therapy may help patients reduce their preoccupation with delusions, psychotherapy is not currently of primary value.

Prognosis

Individuals who develop paraphrenia have a life expectancy similar to the normal population. Recovery from the psychotic symptoms seems to be rare, and in most cases paraphrenia results in in-patient status for the remainder of the life of the patient. Patients experience a slow deterioration of cognitive functions and the disorder can lead to dementia in some cases, but this development is no greater than the normal population.

Epidemiology

Studies suggest that the prevalence of paraphrenia in the elderly population is around 2-4%.

Sex Differences

While paraphrenia can occur in both men and women, it is more common in women, even after the difference has been adjusted for life expectancies. The ratio of women with paraphrenia to men with paraphrenia is anywhere from 3:1 to 45:2.

Age

It is seen mainly in patients over the age of 60, but has been known to occur in patients in their 40s and 50s.

Personality Type and Living Situation

It is suggested that individuals who develop paraphrenia later in life have premorbid personalities, and can be described as “quarrelsome, religious, suspicious or sensitive, unsociable and cold-hearted.” Many patients were also described as being solitary, eccentric, isolated and difficult individuals; these characteristics were also long-standing rather than introduced by the disorder. Most of the traits recognised prior to the onset of paraphrenia in individuals can be grouped as either paranoid or schizoid. Patients presenting with paraphrenia were most often found to be living by themselves (either single, widowed, or divorced). There have also been reports of low marriage rate among paraphrenics and these individuals also have few or no children (possibly because of this premorbid personality).

Physical Factors

The development of paranoia and hallucinations in old age have been related to both auditory and visual impairment, and individuals with paraphrenia often present with one or both of these impairments. Hearing loss in paraphrenics is associated with early age of onset, long duration, and profound auditory loss.

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What is Folie à Deux?

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Introduction

Folie à deux (‘folly of two’, or ‘madness [shared] by two’), also known as shared psychosis or shared delusional disorder (SDD), is a psychiatric syndrome in which symptoms of a delusional belief, and sometimes hallucinations, are transmitted from one individual to another.

The same syndrome shared by more than two people may be called folie à… trois (‘three’) or quatre (‘four’); and further, folie en famille (‘family madness’) or even folie à plusieurs (‘madness of several’).

The disorder was first conceptualised in 19th-century French psychiatry by Charles Lasègue and Jules Falret and is also known as Lasègue-Falret syndrome.

Recent psychiatric classifications refer to the syndrome as shared psychotic disorder (DSM-4 – 297.3) and induced delusional disorder (ICD-10 – F24), although the research literature largely uses the original name.

This disorder is not in the current DSM (DSM-5), which considers the criteria to be insufficient or inadequate. DSM-5 does not consider Shared Psychotic Disorder (Folie à Deux) as a separate entity, but rather, the physician should classify it as “Delusional Disorder” or in the “Other Specified Schizophrenia Spectrum and Other Psychotic Disorder”.

Signs and Symptoms

This syndrome is most commonly diagnosed when the two or more individuals of concern live in proximity, may be socially or physically isolated, and have little interaction with other people.

Various sub-classifications of folie à deux have been proposed to describe how the delusional belief comes to be held by more than one person:

  • Folie imposée:
    • Where a dominant person (known as the ‘primary’, ‘inducer’ or ‘principal’) initially forms a delusional belief during a psychotic episode and imposes it on another person or persons (the ‘secondary’, ‘acceptor’, or ‘associate’), with the assumption that the secondary person might not have become deluded if left to his or her own devices.
    • If the parties are admitted to hospital separately, then the delusions in the person with the induced beliefs usually resolve without the need of medication.
  • Folie simultanée:
    • Either the situation where two people considered to suffer independently from psychosis influence the content of each other’s delusions so they become identical or strikingly similar, or one in which two people “morbidly predisposed” to delusional psychosis mutually trigger symptoms in each other.

Folie à deux and its more populous derivatives are in many ways a psychiatric curiosity. The current Diagnostic and Statistical Manual of Mental Disorders states that a person cannot be diagnosed as being delusional if the belief in question is one “ordinarily accepted by other members of the person’s culture or subculture.” It is not clear at what point a belief considered to be delusional escapes from the folie à… diagnostic category and becomes legitimate because of the number of people holding it. When a large number of people may come to believe obviously false and potentially distressing things based purely on hearsay, these beliefs are not considered to be clinical delusions by the psychiatric profession, and are instead labelled as mass hysteria.

As with most psychological disorders, the extent and type of delusion varies, but the non-dominant person’s delusional symptoms usually resemble those of the inducer. Prior to therapeutic interventions, the inducer typically does not realise that they are causing harm, but instead believe they are helping the second person to become aware of vital or otherwise notable information.

Types of Delusion

Psychology Today magazine defines delusions as “fixed beliefs that do not change, even when a person is presented with conflicting evidence.” Types of delusion include:

TypeDescription
Bizarre DelusionsThose which are clearly implausible and not understood by peers within the same culture, even those with psychological disorders; for example, if one thought that all of their organs had been taken out and replaced by someone else’s while they were asleep without leaving any scar and without their waking up. It would be impossible to survive such a procedure, and even surgery involving transplantation of multiple organs would leave the person with severe pain, visible scars, etc.
Non-Bizarre DelusionsCommon among those with personality disorders and are understood by people within the same culture. For example, unsubstantiated or unverifiable claims of being followed by the FBI in unmarked cars and watched via security cameras would be classified as a non-bizarre delusion; while it would be unlikely for the average person to experience such a predicament, it is possible, and therefore understood by those around them.
Mood-Congruent DelusionsThese correspond to a person’s emotions within a given timeframe, especially during an episode of mania or depression. For example, someone with this type of delusion may believe with certainty that they will win $1 million at the casino on a specific night, despite lacking any way to see the future or influence the probability of such an event. Similarly, someone in a depressive state may feel certain that their mother will get hit by lightning the next day, again in spite of having no means of predicting or controlling future events.
Mood-Neutral DelusionsThese are unaffected by mood, and can be bizarre or non-bizarre; the formal definition provided by Mental Health Daily is “a false belief that isn’t directly related to the person’s emotional state.” An example would be a person who is convinced that somebody has switched bodies with their neighbour, the belief persisting irrespective of changes in emotional status.


Biopsychosocial Effects

As with many psychiatric disorders, shared delusional disorder can negatively impact the psychological and social aspects of a person’s wellbeing. Unresolved stress resulting from a delusional disorder will eventually contribute to or increase the risk of other negative health outcomes, such as cardiovascular disease, diabetes, obesity, immunological problems, and others. These health risks increase with the severity of the disease, especially if an affected person does not receive or comply with adequate treatment.

Persons with a delusional disorder have a significantly high risk of developing psychiatric comorbidities such as depression and anxiety. This may be attributable to a genetic pattern shared by 55% of SDD patients.

Shared delusional disorder can have a profoundly negative impact on a person’s quality of life. Persons diagnosed with a mental health disorder commonly experience social isolation, which is detrimental to psychological health. This is especially problematic with SDD, as social isolation contributes to the onset of the disorder; in particular, relapse is likely if returning to an isolated living situation, in which shared delusions can be reinstated.

Causes

While the exact causes of SDD are unknown, the main two contributors are stress and social isolation.

People who are socially isolated together tend to become dependent on those they are with, leading to an inducers influence on those around them. Additionally, people developing shared delusional disorder do not have others reminding them that their delusions are either impossible or unlikely. As a result, treatment for shared delusional disorder includes those affected be removed from the inducer.

Stress is also a factor, as it is a common factor in mental illness developing or worsening. The majority of people that develop shared delusional disorder are genetically predisposed to mental illness, but this predisposition is not enough to develop a mental disorder. However, stress can increase the risk of this disorder. When stressed, an individual’s adrenal gland releases the “stress hormone” cortisol into the body, increasing the brain’s level of dopamine; this change can be linked to the development of a mental illness, such as a shared delusional disorder.

Diagnosis

SDD is often difficult to diagnose. Usually, the person with the condition does not seek out treatment, as they do not realise that their delusion is abnormal, as it comes from someone in a dominant position who they trust. Furthermore, since their delusion comes on gradually and grows in strength over time, their doubt is slowly weakened during this time. SDD is diagnosed using the DSM-5, and according to this, the patient must meet three criteria:

  • They must have a delusion that develops in the context of a close relationship with an individual with an already established delusion.
  • The delusion must be very similar or even identical to the one already established one that the primary case has.
  • The delusion cannot be better explained by any other psychological disorder, mood disorder with psychological features, a direct result of physiological effects of substance abuse or any general medical condition.

Related phenomena

Reports have stated that a phenomenon similar to folie à deux was induced by the military incapacitating agent BZ in the late 1960s.

Prevalence

SDD is most commonly found in women with slightly above-average IQs, who are isolated from their family, and who are in relationships with a dominant person who has delusions. The majority of secondary cases (people who develop the shared delusion) also meet the criteria for Dependent Personality Disorder, which is characterised by a pervasive fear that leads them to need constant reassurance, support, and guidance. Additionally, 55% of secondary cases had a relative with a psychological disorder that included delusions and, as a result, the secondary cases are usually susceptible to mental illness.

Treatment

After a person has been diagnosed, the next step is to determine the proper course of treatment. The first step is to separate the formerly healthy person from the inducer, and see if the delusion goes away or lessens over time. If this is not enough to stop the delusions, there are two possible courses of action: Medication or therapy, which is then broken down into personal therapy and/or family therapy.

With treatment, the delusions, and therefore the disease, will eventually lessen so much so, that it will practically disappear in most cases. However, if left untreated, it can become chronic and lead to anxiety, depression, aggressive behaviour, and further social isolation. Unfortunately, there are not many statistics about the prognosis of shared delusional disorder, as it is a rare disease, and it is expected that the majority of cases go unreported; however, with treatment, the prognosis is very good.

Medication

If the separation alone is not working, antipsychotics are often prescribed for a short time to prevent the delusions. Antipsychotics are medications that reduce or relieve symptoms of psychosis such as delusions or hallucinations (seeing or hearing something that is not there). Other uses of antipsychotics include stabilising moods for people with mood swings and mood disorders (i.e. in bipolar patients), reducing anxiety in anxiety disorders, and lessening tics in people with Tourettes. Antipsychotics do not cure psychosis, but they do help reduce symptoms; when paired with therapy, the person with the condition has the best chance of recovering. While antipsychotics are powerful, and often effective, they do have side effects, such as inducing involuntary movements. They should only be taken if absolutely required, and under the supervision of a psychiatrist.

Therapy

The two most common forms of therapy for people with shared delusional disorder are personal and family therapy.

  • Personal therapy:
    • Is one-on-one counselling that focuses on building a relationship between the counsellor and the patient, and aims to create a positive environment where the patient feels that they can speak freely and truthfully.
    • This is advantageous, as the counsellor can usually get more information out of the patient to get a better idea of how to help them.
    • Additionally, if the patient trusts what the counsellor says, disproving the delusion will be easier.
  • Family therapy:
    • Is a technique in which the entire family comes into therapy together to work on their relationships, and to find ways to eliminate the delusion within the family dynamic.
    • For example, if someone’s sister is the inducer, the family will have to get involved to ensure the two stay apart, and to sort out how the family dynamic will work around that.
    • The more support a patient has, the more likely they are to recover, especially since SDD usually occurs due to social isolation.

Notable Cases

  • In May 2008, in the case of twin sisters Ursula and Sabina Eriksson, Ursula ran into the path of an oncoming articulated lorry, sustaining severe injuries.
    • Sabina then immediately duplicated her twin’s actions by stepping into the path of an oncoming car; both sisters survived the incident with severe but non-life-threatening injuries.
    • It was later claimed that Sabina Eriksson was a ‘secondary’ sufferer of folie à deux, influenced by the presence or perceived presence of her twin sister, Ursula – the ‘primary’. Sabina later told an officer at the police station, “We say in Sweden that an accident rarely comes alone. Usually at least one more follows—maybe two.”
    • However, upon her release from hospital, Sabina behaved erratically before stabbing a man to death.
  • Another case involved a married couple by the name of Margaret and Michael, both aged 34 years, who were discovered to have folie à deux when they were both found to be sharing similar persecutory delusions.
    • They believed that certain persons were entering their house, spreading dust and fluff, and “wearing down their shoes.”
    • Both had, in addition, other symptoms supporting a diagnosis of emotional contagion, which could be made independently in either case.
  • Psychiatrist Reginald Medlicott published an article about the Parker-Hulme murder case, called “Paranoia of the Exalted Type in a Setting of Folie a Deux – A Study of Two Adolescent Homicides”, arguing that the intense relationship and shared fantasy world of the two teenaged friends reinforced and exacerbated the mental illness that led to the murder: “each acted on the other as a resonator, increasing the pitch of their narcissism.”
  • In 2016, a case involving a family of five from Melbourne, Australia made headlines when they abruptly fled their home and travelled more than 1,600 km (1,000 mi) across the state of Victoria, because some of the family had become convinced someone was out to kill and rob them.
    • No such evidence was found by the police, and the symptoms of those involved resolved on their own once the family returned to their home.
  • The book Bad Blood: Secrets and Lies in a Silicon Valley Startup suggests that this ailment plagued the founder of Theranos, Elizabeth Holmes, and her boyfriend and business partner, Ramesh Balwani.
  • It was suspected a family of eleven members from Burari, India had this condition.
    • On 30 June 2018, the family died by mass suicide due to the shared belief of one of its members.
  • Psychologists H. O’Connell and P.G. Doyle believe folie à plusieurs to have been at least a partial factor in the murder of Bridget Cleary.
    • In 1895, Michael Cleary convinced several friends and relatives that his wife, Bridget Cleary, was a changeling who had been replaced by a fairy.
    • They assisted him in physically abusing her to “cast the fairies” out, before he ultimately burned her to death shortly afterwards.
  • Christine and Léa Papin were two French sisters who, as live-in maids, were convicted of murdering their employer’s wife and daughter in Le Mans, France on 02 February 1933.

In Popular Culture

  • “Folie à Deux” is the title of the nineteenth episode in the fifth season of The X-Files (1998). The episode details a story of a man who believes his boss is an insect monster, a delusion that Fox Mulder begins to share after investigation.
  • Bug (2006) is a film that depicts a couple with a shared delusion that aphids are living under their skin.
  • In Season 2, Episode 3 of Criminal Minds, “The Perfect Storm” (2006), Dr. Reid mentions that the rapists had this condition.
  • In 2008, American rock band Fall Out Boy released their fourth album, Folie à Deux.
  • The independent film Apart (2011) depicts two lovers affected and diagnosed with induced delusional disorder, trying to uncover a mysterious and tragic past they share. In a 2011 interview, director Aaron Rottinghaus stated the film was based on research from actual case studies.
  • In 2011, in CSI: Miami (Season 9, Episode 15 “Blood Lust”), it was revealed the killer couple had this condition.
  • The 2011 horror film Intruders contains characters who suffer from folie à deux.
  • In 2012, in Criminal Minds (Season 7, Episode 19 “Heathridge Manor”), it was revealed the killer family had this condition.
  • 2013’s horror game “Slender: The Arrival” centres around the shared hallucination by the main character Lauren, and her friend Kate, of the monster known as “Slender Man”.
  • In 2017, in Chance (Season 2, Episode 9 “A Madness of Two”), it was revealed the villains are having this condition.
  • The Vanished (2020) shows a couple who lost a child continuing to hold on to the delusional thought of their existence.
  • Nine Perfect Strangers (miniseries) shows a couple who lost one of their two children. The couple and the surviving child have shared hallucinations of the dead child.[36]

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What is Dissociation (Psychology)?

Published on by Andrew Marshall1 Comment

Introduction

Dissociation, as a concept that has been developed over time, is any of a wide array of experiences, ranging from a mild emotional detachment from the immediate surroundings, to a more severe disconnection from physical and emotional experiences. The major characteristic of all dissociative phenomena involves a detachment from reality, rather than a loss of reality as in psychosis.

The phenomena are diagnosable under the DSM-5 as a group of disorders as well as a symptom of other disorders through various diagnostic tools. Its cause is believed to be related to neurobiological mechanisms, trauma, anxiety, and psychoactive drugs. Research has further related it to suggestibility and hypnosis, and it is inversely related to mindfulness, which is a potential treatment.

Brief History

French philosopher and psychologist Pierre Janet (1859-1947) is considered to be the author of the concept of dissociation. Contrary to some conceptions of dissociation, Janet did not believe that dissociation was a psychological defence.

Psychological defence mechanisms belong to Sigmund Freud‘s theory of psychoanalysis, not to Janetian psychology. Janet claimed that dissociation occurred only in persons who had a constitutional weakness of mental functioning that led to hysteria when they were stressed. Although it is true that many of Janet’s case histories described traumatic experiences, he never considered dissociation to be a defence against those experiences. Quite the opposite: Janet insisted that dissociation was a mental or cognitive deficit. Accordingly, he considered trauma to be one of many stressors that could worsen the already-impaired “mental deficiency” of a hysteric, thereby generating a cascade of hysterical (in today’s language, “dissociative”) symptoms.

Although there was great interest in dissociation during the last two decades of the nineteenth century (especially in France and England), this interest rapidly waned with the coming of the new century. Even Janet largely turned his attention to other matters.

There was a sharp peak in interest in dissociation in America from 1890 to 1910, especially in Boston as reflected in the work of William James, Boris Sidis, Morton Prince, and William McDougall. Nevertheless, even in America, interest in dissociation rapidly succumbed to the surging academic interest in psychoanalysis and behaviourism.

For most of the twentieth century, there was little interest in dissociation. Despite this, a review of 76 previously published cases from the 1790s to 1942 was published in 1944, describing clinical phenomena consistent with that seen by Janet and by therapists today. In 1971, Bowers and her colleagues presented a detailed, and still quite valid, treatment article. The authors of this article included leading thinkers of their time – John G. Watkins (who developed ego-state therapy) and Zygmunt A. Piotrowski (famed for his work on the Rorschach test). Further interest in dissociation was evoked when Ernest Hilgard (1977) published his neodissociation theory in the 1970s. During the 1970s and 1980s an increasing number of clinicians and researchers wrote about dissociation, particularly multiple personality disorder.

Carl Jung described pathological manifestations of dissociation as special or extreme cases of the normal operation of the psyche. This structural dissociation, opposing tension, and hierarchy of basic attitudes and functions in normal individual consciousness is the basis of Jung’s Psychological Types. He theorised that dissociation is a natural necessity for consciousness to operate in one faculty unhampered by the demands of its opposite.

Attention to dissociation as a clinical feature has been growing in recent years as knowledge of post-traumatic stress disorder (PTSD) increased, due to interest in dissociative identity disorder (DID), and as neuroimaging research and population studies show its relevance.

Historically the psychopathological concept of dissociation has also another different root: the conceptualization of Eugen Bleuler that looks into dissociation related to schizophrenia.

Diagnosis

Refer to Dissociative disorder.

Dissociation is commonly displayed on a continuum. In mild cases, dissociation can be regarded as a coping mechanism or defence mechanism in seeking to master, minimise or tolerate stress – including boredom or conflict. At the non-pathological end of the continuum, dissociation describes common events such as daydreaming. Further along the continuum are non-pathological altered states of consciousness.

More pathological dissociation involves dissociative disorders, including dissociative fugue and depersonalisation disorder with or without alterations in personal identity or sense of self. These alterations can include: a sense that self or the world is unreal (depersonalisation and derealisation), a loss of memory (amnesia), forgetting identity or assuming a new self (fugue), and separate streams of consciousness, identity and self (dissociative identity disorder, formerly termed multiple personality disorder) and complex post-traumatic stress disorder (CPTSD). Although some dissociative disruptions involve amnesia, other dissociative events do not. Dissociative disorders are typically experienced as startling, autonomous intrusions into the person’s usual ways of responding or functioning. Due to their unexpected and largely inexplicable nature, they tend to be quite unsettling.

Dissociative disorders are sometimes triggered by trauma, but may be preceded only by stress, psychoactive substances, or no identifiable trigger at all. The ICD-10 classifies conversion disorder as a dissociative disorder. The DSM groups all dissociative disorders into a single category and recognises dissociation as a symptom of acute stress disorder, posttraumatic stress disorder (PTSD), and borderline personality disorder.

Misdiagnosis is common among people who display symptoms of dissociative disorders, with an average of seven years to receive proper diagnosis and treatment. Research is ongoing into aetiologies, symptomology, and valid and reliable diagnostic tools. In the general population, dissociative experiences that are not clinically significant are highly prevalent with 60% to 65% of the respondents indicating that they have had some dissociative experiences.

Diagnostic and Statistical Manual of Mental Disorders

Diagnoses listed under the DSM-5 are dissociative identity disorder, dissociative amnesia, depersonalisation/derealisation disorder, other specified dissociative disorder and unspecified dissociative disorder. The list of available dissociative disorders listed in the DSM-5 changed from the DSM-IV-TR, as the authors removed the diagnosis of dissociative fugue, classifying it instead as a subtype of dissociative amnesia. Furthermore, the authors recognised derealisation on the same diagnostic level of depersonalisation with the opportunity of differentiating between the two.

The DSM-IV-TR considers symptoms such as depersonalisation, derealisation and psychogenic amnesia to be core features of dissociative disorders. The DSM-5 carried these symptoms over and described symptoms as positive and negative. Positive symptoms include unwanted intrusions that alter continuity of subjective experiences, which account for the first two symptoms listed earlier with the addition of fragmentation of identity. Negative symptoms include loss of access to information and mental functions that are normally readily accessible, which describes amnesia.

Peritraumatic Dissociation

Peritraumatic dissociation is considered to be dissociation that is experienced during and immediately following a traumatic event. Research is on-going related to its development, its importance, and its relationship to trauma, dissociative disorders, and predicting the development of PTSD.

Measurements

Two of the most commonly used screening tools in the community are the Dissociative Experiences Scale and the Multiscale Dissociation Inventory. Meanwhile, the Structured Clinical Interview for DSM-IV – Dissociative Disorders (SCID-D) and its second iteration, the SCID-D-R, are both semi-structured interviews and are considered psychometrically strong diagnostic tools.

Other tools include the Office Mental Status Examination (OMSE), which is used clinically due to inherent subjectivity and lack of quantitative use. There is also the Dissociative Disorders Interview Schedule (DDSI), which lacks substantive clarity for differential diagnostics.

Peritraumatic dissociation is measured through the Peritraumatic Dissociative Scale.

Aetiology

Neurobiological Mechanism

Preliminary research suggests that dissociation-inducing events, drugs like ketamine, and seizures generate slow rhythmic activity (1-3 Hz) in layer 5 neurons of the posteromedial cortex in humans (retrosplenial cortex in mice). These slow oscillations disconnect other brain regions from interacting with the posteromedial cortex, which may explain the overall experience of dissociation.

Trauma

Dissociation has been described as one of a constellation of symptoms experienced by some victims of multiple forms of childhood trauma, including physical, psychological, and sexual abuse. This is supported by studies which suggest that dissociation is correlated with a history of trauma.

Dissociation appears to have a high specificity and a low sensitivity to having a self-reported history of trauma, which means that dissociation is much more common among those who are traumatised, yet at the same time there are many people who have suffered from trauma but who do not show dissociative symptoms.

Adult dissociation when combined with a history of child abuse and otherwise interpersonal violence-related PTSD has been shown to contribute to disturbances in parenting behaviour, such as exposure of young children to violent media. Such behaviour may contribute to cycles of familial violence and trauma.

Symptoms of dissociation resulting from trauma may include depersonalisation, psychological numbing, disengagement, or amnesia regarding the events of the abuse. It has been hypothesized that dissociation may provide a temporarily effective defence mechanism in cases of severe trauma; however, in the long term, dissociation is associated with decreased psychological functioning and adjustment.

Other symptoms sometimes found along with dissociation in victims of traumatic abuse (often referred to as “sequelae to abuse”) include anxiety, PTSD, low self-esteem, somatisation, depression, chronic pain, interpersonal dysfunction, substance abuse, self-harm and suicidal ideation or actions. These symptoms may lead the victim to present the symptoms as the source of the problem.

Child abuse, especially chronic abuse starting at early ages, has been related to high levels of dissociative symptoms in a clinical sample, including amnesia for abuse memories. It has also been seen that girls who suffered abuse during their childhood had higher reported dissociation scores than did boys who reported dissociation during their childhood. A non-clinical sample of adult women linked increased levels of dissociation to sexual abuse by a significantly older person prior to age 15, and dissociation has also been correlated with a history of childhood physical and sexual abuse. When sexual abuse is examined, the levels of dissociation were found to increase along with the severity of the abuse.

A 2012 review article supports the hypothesis that current or recent trauma may affect an individual’s assessment of the more distant past, changing the experience of the past and resulting in dissociative states.

Psychoactive substances

Refer to Dissociative Drug.

Psychoactive drugs can often induce a state of temporary dissociation. Substances with dissociative properties include ketamine, nitrous oxide, alcohol, tiletamine, amphetamine, dextromethorphan, MK-801, PCP, methoxetamine, salvia, muscimol, atropine, ibogaine, and minocycline.

Correlations

Hypnosis and Suggestibility

There is evidence to suggest that dissociation is correlated with hypnotic suggestibility, specifically with dissociative symptoms related to trauma. However, the relationship between dissociation and hypnotic suggestibility appears to be complex and indicates further research is necessary.

Aspects of hypnosis include absorption, dissociation, suggestibility, and willingness to receive behavioural instruction from others. Both hypnotic suggestibility and dissociation tend to be less mindful, and hypnosis is used as a treatment modality for dissociation, anxiety, chronic pain, trauma, and more. Difference between hypnosis and dissociation: one is suggested, imposed by self or other, meaning dissociation is generally more spontaneous altering of awareness.

Mindfulness and Meditation

Mindfulness and meditation have shown an inverse relationship specifically with dissociation related to re-experiencing trauma due to the lack of present awareness inherent with dissociation. The re-experiencing episodes can include anything between illusions, distortions in perceived reality, and disconnectedness from the present moment. It is believed that the nature of dissociation as an avoidance coping or defence mechanism related to trauma inhibits resolution and integration.

Mindfulness and meditation also can alter the state of awareness to the present moment; however, unlike dissociation, it is clinically used to bring greater awareness to an individual’s present state of being. It achieves this through increased abilities to self-regulate attention, emotion, and physiological arousal, maintain continuity of consciousness, and adopt an approach to the present experience that is open and curious. In practice, non-judgmental awareness has displayed a positive relationship with lower symptoms of PTSD avoidance, which can relate to greater opportunities for success with exposure therapy and lowering PTSD symptoms of hypervigilance, re-experiencing, and overgeneralization of fears.

When using mindfulness and meditation with people expressing trauma symptoms, it is crucial to be aware of potential trauma triggers, such as the focus on the breath. Often, a meditation session will begin with focused attention and move into open monitoring. With severe trauma symptoms, it may be important to start the meditation training and an individual session at the peripheral awareness, such as the limbs. Moreover, trauma survivors often report feeling numb as a protection against trauma triggers and reminders, which are often painful, making it good practice to start all trainings at the limbs as a gradual exposure to body sensations. Doing so will also increase physical attachment to the present moment and the sense of grounding, thereby increasing tolerance to trauma reminders and decreasing the need and use of dissociation.

Treatment

When receiving treatment, patients are assessed to discover their level of functioning. Some patients might be higher functioning than others. This is taken into account when creating a patient’s potential treatment targets. To start off treatment, time is dedicated to increasing a patient’s mental level and adaptive actions in order to gain a balance in both their mental and behavioural action. Once this is achieved, the next goal is to work on removing or minimising the phobia made by traumatic memories, which is causing the patient to dissociate. The final step of treatment includes helping patients work through their grief in order to move forward and be able to engage in their own lives. This is done with the use of new coping skills attained through treatment. One coping skill that can improve dissociation is mindfulness due to the introduction of staying in present awareness while observing non-judgmentally and increasing the ability to regulate emotions. Specifically in adolescents, mindfulness has been shown to reduce dissociation after practicing mindfulness for three weeks.

This page is based on the copyrighted Wikipedia article <https://en.wikipedia.org/wiki/Dissociation_(psychology) >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is Amisulpride?

Published on by Andrew Marshall3 Comments

Introduction

Amisulpride is an antiemetic and antipsychotic medication used at lower doses intravenously to prevent and treat postoperative nausea and vomiting; and at higher doses by mouth to treat schizophrenia and acute psychotic episodes.

It is sold under the brand names Barhemsys (as an antiemetic) and Solian, Socian, Deniban and others (as an antipsychotic). It is also used to treat dysthymia.

It is usually classed with the atypical antipsychotics. Chemically it is a benzamide and like other benzamide antipsychotics, such as sulpiride, it is associated with a high risk of elevating blood levels of the lactation hormone, prolactin (thereby potentially causing the absence of the menstrual cycle, breast enlargement, even in males, breast milk secretion not related to breastfeeding, impaired fertility, impotence, breast pain, etc.), and a low risk, relative to the typical antipsychotics, of causing movement disorders.

Amisulpride is indicated for use in the US in adults for the prevention of postoperative nausea and vomiting (PONV), either alone or in combination with an antiemetic of a different class; and to treat PONV in those who have received antiemetic prophylaxis with an agent of a different class or have not received prophylaxis.

Amisulpride is believed to work by blocking, or antagonising, the dopamine D2 receptor, reducing its signalling. The effectiveness of amisulpride in treating dysthymia and the negative symptoms of schizophrenia is believed to stem from its blockade of the presynaptic dopamine D2 receptors. These presynaptic receptors regulate the release of dopamine into the synapse, so by blocking them amisulpride increases dopamine concentrations in the synapse. This increased dopamine concentration is theorised to act on dopamine D1 receptors to relieve depressive symptoms (in dysthymia) and the negative symptoms of schizophrenia.

It was introduced by Sanofi-Aventis in the 1990s. Its patent expired by 2008, and generic formulations became available. It is marketed in all English-speaking countries except for Canada. A New York City based company, LB Pharmaceuticals, has announced the ongoing development of LB-102, also known as N-methyl amisulpride, an antipsychotic specifically targeting the United States. A poster presentation at European Neuropsychopharmacology seems to suggest that this version of amisulpride, known as LB-102 displays the same binding to D2, D3 and 5HT7 that amisulpride does.

Brief History

The US Food and Drug Administration (FDA) approved amisulpride based on evidence from four clinical trials of 2323 subjects undergoing surgery or experiencing nausea and vomiting after the surgery. The trials were conducted at 80 sites in the United States, Canada and Europe.

Two trials (Trials 1 and 2) enrolled subjects scheduled to have surgery. Subjects were randomly assigned to receive either amisulpride or a placebo drug at the beginning of general anaesthesia. In Trial 1, subjects received amisulpride or placebo alone, and in Trial 2, they received amisulpride or placebo in combination with one medication approved for prevention of nausea and vomiting. Neither the subjects nor the health care providers knew which treatment was being given until after the trial was complete.

The trials counted the number of subjects who had no vomiting and did not use additional medications for nausea or vomiting in the first day (24 hours) after the surgery. The results then compared amisulpride to placebo.

The other two trials (Trials 3 and 4) enrolled subjects who were experiencing nausea and vomiting after surgery. In Trial 3, subjects did not receive any medication to prevent nausea and vomiting before surgery and in Trial 4 they received the medication, but the treatment did not work. In both trials, subjects were randomly assigned to receive either amisulpride or placebo. Neither the subjects nor the health care providers knew which treatment was being given until after the trial was complete.

The trials counted the number of subjects who had no vomiting and did not use additional medications for nausea or vomiting in the first day (24 hours) after the treatment. The trial compared amisulpride to placebo.

Medical Uses

Schizophrenia

Although according to other studies it appears to have comparable efficacy to olanzapine in the treatment of schizophrenia. Amisulpride augmentation, similarly to sulpiride augmentation, has been considered a viable treatment option (although this is based on low-quality evidence) in clozapine-resistant cases of schizophrenia. Another recent study concluded that amisulpride is an appropriate first-line treatment for the management of acute psychosis.

Postoperative Nausea and Vomiting

Amisulpride is indicated for use in the United States in adults for the prevention of postoperative nausea and vomiting (PONV), either alone or in combination with an antiemetic of a different class; and to treat PONV in those who have received antiemetic prophylaxis with an agent of a different class or have not received prophylaxis.

Contraindications

Amisulpride’s use is contraindicated in the following disease states:

  • Pheochromocytoma.
  • Concomitant prolactin-dependent tumours e.g. prolactinoma, breast cancer.
  • Movement disorders (e.g. Parkinson’s disease and dementia with Lewy bodies).
  • Lactation.
  • Children before the onset of puberty.

Neither is it recommended to use amisulpride in patients with hypersensitivities to amisulpride or the excipients found in its dosage form.

Adverse Effects

  • Very Common (≥10% incidence):
    • Extrapyramidal side effects (EPS; including dystonia, tremor, akathisia, parkinsonism).
  • Common (≥1%, <10% incidence):
    • Insomnia.
    • Hypersalivation.
    • Nausea.
    • Headache.
    • Hyperactivity.
    • Vomiting.
    • Hyperprolactinaemia (which can lead to galactorrhoea, breast enlargement and tenderness, sexual dysfunction, etc.).
    • Weight gain (produces less weight gain than chlorpromazine, clozapine, iloperidone, olanzapine, paliperidone, quetiapine, risperidone, sertindole, zotepine and more (although not statistically significantly) weight gain than haloperidol, lurasidone, ziprasidone and approximately as much weight gain as aripiprazole and asenapine).
    • Anticholinergic side effects (although it does not bind to the muscarinic acetylcholine receptors and hence these side effects are usually quite mild) such as
      • Constipation.
      • Dry mouth.
      • Disorder of accommodation.
      • Blurred vision.
  • Rare (<1% incidence):
    • Hyponatraemia.
    • Bradycardia.
    • Hypotension.
    • Palpitations.
    • Urticaria.
    • Seizures.
    • Mania.
    • Oculogyric crisis.
    • Tardive dyskinesia.
    • Blood dyscrasias such as leucopenia, neutropenia and agranulocytosis.
    • QT interval prolongation (in a recent meta-analysis of the safety and efficacy of 15 antipsychotic drugs amisulpride was found to have the 2nd highest effect size for causing QT interval prolongation).
    • Somnolence.

Hyperprolactinaemia results from antagonism of the D2 receptors located on the lactotrophic cells found in the anterior pituitary gland. Amisulpride has a high propensity for elevating plasma prolactin levels as a result of its poor blood-brain barrier penetrability and hence the resulting greater ratio of peripheral D2 occupancy to central D2 occupancy. This means that to achieve the sufficient occupancy (~60–80%) of the central D2 receptors in order to elicit its therapeutic effects a dose must be given that is enough to saturate peripheral D2 receptors including those in the anterior pituitary.

Discontinuation

The British National Formulary recommends a gradual withdrawal when discontinuing antipsychotics to avoid acute withdrawal syndrome or rapid relapse. Symptoms of withdrawal commonly include nausea, vomiting, and loss of appetite. Other symptoms may include restlessness, increased sweating, and trouble sleeping. Less commonly there may be a feeling of the world spinning, numbness, or muscle pains. Symptoms generally resolve after a short period of time.

There is tentative evidence that discontinuation of antipsychotics can result in psychosis. It may also result in reoccurrence of the condition that is being treated. Rarely tardive dyskinesia can occur when the medication is stopped.

Overdose

Torsades de pointes is common in overdose. Amisulpride is moderately dangerous in overdose (with the TCAs being very dangerous and the SSRIs being modestly dangerous).

Interactions

Amisulpride should not be used in conjunction with drugs that prolong the QT interval (such as citalopram, bupropion, clozapine, tricyclic antidepressants, sertindole, ziprasidone, etc.), reduce heart rate and those that can induce hypokalaemia. Likewise it is imprudent to combine antipsychotics due to the additive risk for tardive dyskinesia and neuroleptic malignant syndrome.

Pharmacology

Pharmacodynamics

Amisulpride functions primarily as a dopamine D2 and D3 receptor antagonist. It has high affinity for these receptors with dissociation constants of 3.0 and 3.5 nM, respectively. Although standard doses used to treat psychosis inhibit dopaminergic neurotransmission, low doses preferentially block inhibitory presynaptic autoreceptors. This results in a facilitation of dopamine activity, and for this reason, low-dose amisulpride has also been used to treat dysthymia.

Amisulpride and its relatives sulpiride, levosulpiride, and sultopride have been shown to bind to the high-affinity GHB receptor at concentrations that are therapeutically relevant (IC50 = 50 nM for amisulpride).

Amisulpride, sultopride and sulpiride respectively present decreasing in vitro affinities for the D2 receptor (IC50 = 27, 120 and 181 nM) and the D3 receptor (IC50 = 3.6, 4.8 and 17.5 nM).

Though it was long widely assumed that dopaminergic modulation is solely responsible for the respective antidepressant and antipsychotic properties of amisulpride, it was subsequently found that the drug also acts as a potent antagonist of the serotonin 5-HT7 receptor (Ki = 11.5 nM). Several of the other atypical antipsychotics such as risperidone and ziprasidone are potent antagonists at the 5-HT7 receptor as well, and selective antagonists of the receptor show antidepressant properties themselves. To characterise the role of the 5-HT7 receptor in the antidepressant effects of amisulpride, a study prepared 5-HT7 receptor knockout mice. The study found that in two widely used rodent models of depression, the tail suspension test, and the forced swim test, those mice did not exhibit an antidepressant response upon treatment with amisulpride. These results suggest that 5-HT7 receptor antagonism mediates the antidepressant effects of amisulpride.

Amisulpride also appears to bind with high affinity to the serotonin 5-HT2B receptor (Ki = 13 nM), where it acts as an antagonist. The clinical implications of this, if any, are unclear. In any case, there is no evidence that this action mediates any of the therapeutic effects of amisulpride.

Amisulpride shows stereoselectivity in its actions. Aramisulpride ((R)-amisulpride) has higher affinity for the 5-HT7 receptor (Ki = 47 nM vs. 1,900 nM) while esamisulpride ((S)-amisulpride) has higher affinity for the D2 receptor (4.0 nM vs. 140 nM). An 85:15 ratio of aramisulpride to esamisulpride (SEP-4199) which provides more balanced 5-HT7 and D2 receptor antagonism than racemic amisulpride (50:50 ratio of enantiomers) is under development for the treatment of bipolar depression.

Society and Culture

Brand Names

Brand names include: Amazeo, Amipride (AU), Amival, Solian (AU, IE, RU, UK, ZA), Soltus, Sulpitac (IN), Sulprix (AU), Midora (RO) and Socian (BR).

Availability

Amisulpride was not approved by the Food and Drug Administration for use in the United States until February 2020, but it is used in Europe, Israel, Mexico, India, New Zealand and Australia to treat psychosis and schizophrenia.

An IV formulation of Amisulpride was approved for the treatment of postoperative nausea and vomiting (“PONV”) in the United States in February 2020.

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What is Tangential Speech?

Published on by Andrew Marshall1 Comment

Introduction

Tangential speech or tangentiality is a communication disorder in which the train of thought of the speaker wanders and shows a lack of focus, never returning to the initial topic of the conversation.

It tends to occur in situations where a person is experiencing high anxiety, as a manifestation of the psychosis known as schizophrenia, in dementia or in states of delirium. It is less severe than logorrhoea and may be associated with the middle stage in dementia. It is, however, more severe than circumstantial speech in which the speaker wanders, but eventually returns to the topic.

Some adults with right hemisphere brain damage may exhibit behaviour that includes tangential speech. Those who exhibit these behaviours may also have related symptoms such as seemingly inappropriate or self-centred social responses, and a deterioration in pragmatic abilities (including appropriate eye contact as well as topic maintenance).

Brief History

The earlier phenomenological description allowed for further definition on the basis of formal characteristic rather than content, producing later practice relying upon clinical assessment. The term has undergone a re-definition to refer only to a persons speech in response to a question, and to provide the definition separation from the similar symptoms loosening of association and derailment.

Definition

The term refers simplistically to a thought disorder shown from speech with a lack of observance to the main subject of discourse, such that a person whilst speaking on a topic deviates from the topic. Further definition is of speech that deviates from an answer to a question that is relevant in the first instance but deviates from the relevancy to related subjects not involved in a direct answering of the question. In the context of a conversation or discussion the communication is a response that is ineffective in that the form is inappropriate for adequate understanding. The person’s speech seems to indicate that their attention to their own speech has perhaps in some way been overcome during the occurrence of cognition whilst speaking, causing the vocalised content to follow thought that is apparently without reference to the original idea or question; or the person’s speech is considered evasive in that the person has decided to provide an answer to a question that is an avoidance of a direct answer.

Other

According to the St. Louis system for the diagnosis of schizophrenia, tangentiality is significantly associated with a low IQ prior to diagnosis.

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What is Schizophrenics Anonymous?

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Introduction

Schizophrenics Anonymous is a peer support group to help people who are affected by schizophrenia and related disorders including bipolar disorder, schizoaffective disorder, psychotic depression and psychosis.

Brief History

The programme was established in Detroit in 1985. The founder was Joanne Verbanic, who was diagnosed with schizophrenia in 1970. Shortly before forming SA, Verbanic publicly disclosed her diagnosis and discussed her illness on national television in an effort to challenge the stigma associated with the condition. She was a 2006 recipient of a Lilly Reintegration Award in recognition of her lifetime contributions to the mental health community, and she continued to be active as a spokesperson for persons with schizophrenia and other mental illness until her death on 07 May 2015.

By 2007, more than 150 local SA groups operated in 31 of the 50 United States, and in Australia, Brazil, Canada, Mexico, France, India and Venezuela.

Technical support for Schizophrenics Anonymous was provided by the National Schizophrenia Foundation (NSF) until 2007 when NSF ceased operations. In response to the loss of a national sponsor, a group of consumers, family members, and mental health providers came together to form a not-for-profit organisation, Schizophrenia and Related Disorders Alliance of America (SARDAA).

SARDAA promotes recovery for persons with schizophrenia and related brain disorders including bipolar disorder, schizoaffective disorder, depression with psychosis, and experience with psychosis. They envision a future in which every person with a schizophrenia-related brain disorder has the opportunity to recover from their disorders. The name Schizophrenics Anonymous was changed to Schizophrenia Alliance in 2015 and added Psychosis Support and Acceptance in 2018. They provide an online directory of SA groups, sponsor five weekly SA conference calls, and one Family and Friends conference call. At their annual conference, the group trains individuals and groups who have started or would like to start an SA group.

Although some SA groups are organised by mental health professionals, research has suggested that peer-led SA groups are more sustainable and longer lasting. Some groups are organised in psychiatric hospitals or jails and are not open to the public.

Programme Principles

The SA programme is based on the twelve-step model, but includes just six steps. The organisation describes the programme’s purpose of helping participants to learn about schizophrenia, “restore dignity and sense of purpose,” obtain “fellowship, positive support, and companionship,” improve their attitudes about their lives and their illnesses, and take “positive steps towards recovery.”

Joanne Verbanic wrote the original “Schizophrenics Anonymous” book, better known as “The Blue Book,” which describes the six steps to recovery. The steps require members to admit they need help, take responsibility for their choices and consequences, believe they have the inner strength to help themselves and others, forgive themselves and others, understand that false beliefs contribute to their problems and change those beliefs, and decide to turn their lives over to a higher power.

Research

One study about the risks of professional partnerships centres on the partnership between Schizophrenics Anonymous (SA) and the Mental Health Association of Michigan (MHAM) over a 14-year period. The study shows that the professional partnership resulted in increased access to SA Groups across Michigan and organisation expansion and development within SA. The professional influence also lead more SA Groups to be held in more traditional mental health treatment settings and led to more professional-led SA groups.

Self-help groups are more available to people who live independently. Researchers at Michigan State University studied whether SA would be successful in group homes. The results were positive: the groups had high attendance and participation and were well liked. However, staff members controlled who could lead and who could attend the meetings, and how the meetings should be run. The programs fell apart. The same obstacle occurred in SA groups started in prisons and monitored by employees.

This page is based on the copyrighted Wikipedia article <https://en.wikipedia.org/wiki/Schizophrenics_Anonymous&gt;; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is Foreclosure (Psychoanalysis)?

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Introduction

Foreclosure (also known as “foreclusion”; French: forclusion) is the English translation of a term that the French psychoanalyst Jacques Lacan introduced into psychoanalysis to identify a specific psychical cause for psychosis.

Brief History

According to Élisabeth Roudinesco, the term was originally introduced into psychology ‘in 1928, when Édouard Pichon published, in Pierre Janet’s review, his article on “The Psychological Significance of Negation in French”: “…[and] borrowed the legal term forclusif to indicate facts that the speaker no longer sees as part of reality’.

According to Christophe Laudou, the term was introduced by Damourette and Pichon.

Freud vs Laforgue

The publication took part against the background of the Twenties dispute between Freud and René Laforgue over scotomisation. ‘If I am not mistaken’, Freud wrote in 1927, ‘Laforgue would say in this case that the boy “scotomises” his perception of the woman’s lack of a penis. A new technical term is justified when it describes a new fact or emphasizes it. This is not the case here’. Freud went on to suggest that if one wanted to ‘reserve the word “Verdrängung” [“repression”] for the affect, then the correct German word for the vicissitude of the idea would be “Verleugnung” [“disavowal”]’.

Lacan’s Introduction of Foreclosure

In 1938 Lacan relates the origin of psychosis to an exclusion of the father from the family structure thereby reducing this structure to a mother-child relationship. Later on, when working on the distinctions between the real, imaginary and symbolic father, he specifies that it is the absence of the symbolic father which is linked to psychosis.

Lacan uses the Freudian term, Verwerfung, which the “Standard Edition” translates as “repudiation”, as a specific defence mechanism different from repression, “Verdrängung”, in which “the ego rejects the incompatible idea together with its affect and behaves as if the idea has never occurred to the ego at all.” In 1954 basing himself on a reading of the “Wolf Man” Lacan identifies Verwerfung as the specific mechanism of psychosis where an element is rejected outside the symbolic order as if it has never existed. In 1956 in his Seminar on Psychoses he translates Verwerfung as forclusion, that is foreclosure. “Let us extract from several of Freud’s texts a term that is sufficiently articulated in them to designate in them a function of the unconscious that is distinct from the repressed. Let us take as demonstrated the essence of my Seminar on the Psychoses, namely, that this term refers to psychosis: this term is Verwerfung (foreclosure)”.

Lacan and Psychosis

The problem Lacan sought to address with the twin tools of foreclosure and the signifier was that of the difference between psychosis and neurosis, as manifested in and indicated by language usage. It was common analytic ground that “when psychotics speak they always have some meanings that are too fixed, and some that are far too loose, they have a different relation to language, and a different way of speaking from neurotics.” Freud, following Bleuler and Jung had pointed to ‘a number of changes in speech…in schizophrenics…words are subjected to the same process as that which makes the dream’. Lacan used foreclosure to explain why.

When Lacan first uses the Freudian concept of Verwerfung (repudiation) in his search for a specific mechanism for psychosis, it is not clear what is repudiated (castration, speech). It is in 1957 in his article “On a question preliminary to any possible treatment of psychosis” that he advances the notion that it is the Name-of-the-Father (a fundamental signifier) that is the object of foreclosure. In this way Lacan combines two of his main themes on the causality of psychosis: the absence of the father and the concept of Verwerfung. This ideas remains central to Lacan’s thinking on psychosis throughout the rest of his work.

Lacan considered the father to play a vital role in breaking the initial mother/child duality and introducing the child to the wider world of culture, language, institutions and social reality – the Symbolic world – the father being “the human being who stands for the law and order that the mother plants in the life of the child…widens the child’s view of the world.” The result in normal development is “proper separation from the mother, as marked out by the Names-of-the-father.” Thus Lacan postulates the existence of a paternal function (the “Name of the Father” or “primordial signifier”) which allows the realm of the Symbolic to be bound to the realms of the Imaginary and the Real. This function prevents the developing child from being engulfed by its mother and allows him/her to emerge as a separate entity in his/her own right. It is a symbol of parental authority (a general symbol that represents the power of father of the Oedipus complex) that brings the child into the realm of the Symbolic by forcing him/her to act and to verbalise as an adult. As a result, the three realms are integrated in a way that is conducive to the creation of meaning and successful communication by means of what Lacan calls a Borromean knot.

When the Name-of-the-Father is foreclosed for a particular subject, it leaves a hole in the Symbolic order which can never be filled. The subject can then be said to have a psychotic structure, even if he shows none of the classical signs of psychosis. When the foreclosed Name-of-the-Father re-appears in the Real, the subject is unable to assimilate it and the result of this collision between the subject and the inassimilable signifier of the Name-of-the-father is the entry into psychosis proper characterized by the onset of hallucinations and/or delusions. In other words, when the paternal function is “foreclosed” from the Symbolic order, the realm of the Symbolic is insufficiently bound to the realm of the Imaginary and failures in meaning may occur (the Borromean knot becomes undone and the three realms completely disconnected), with “a disorder caused at the most personal juncture between the subject and his sense of being alive.” Psychosis is experienced after some environmental sign in the form of a signifier which the individual cannot assimilate is triggered, and this entails that “the Name-of-the-Father, is foreclosed, verworfen, is called into symbolic opposition to the subject.” The fabric of the individual’s reality is ripped apart and no meaningful Symbolic sense can be made of experience. “Absence of transcendence of the Oedipus places the subject under the regime of foreclosure or non-distinction between the symbolic and the real’; and psychotic delusions or hallucinations are the consequent result of the individual’s striving to account for what he/she experiences.