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==Treatment==
==Treatment==
The treatment of psychosis depends on the specific diagnosis (such as schizophrenia, bipolar disorder or substance intoxication). The [[first line treatment]] for many psychotic disorders is [[antipsychotic]] medication (oral or intramuscular injection), and sometimes [[Inpatient care|hospitalization]] is needed. However, there are significant problems associated with this class of drugs. There is evidence that they can cause brain damage including prefrontal cortex atrophy, long-lasting parkinsonian symtoms ([[tardive dyskinesia]]), and personality change.<ref>{{cite news|last=James|first=Adam|title=Myth of the Antipsychotic|url=http://www.guardian.co.uk/commentisfree/2008/mar/02/mythoftheantipsychotic|newspaper=Guardian|date=2 March 2008}}</ref> Nancy Andreasen has argued for an association between antipsychotic drugs and smaller grey matter volumes independent of illness severety.<ref>{{cite news|last=Whitaker|first=Robert|title=Andreasen Drops A Bombshell: Antipsychotics Shrink the Brain|url=http://www.psychologytoday.com/blog/mad-in-america/201102/andreasen-drops-bombshell-antipsychotics-shrink-the-brain|newspaper=Psychology Today|date=8 Feb 2011}}</ref>. Furthermore, antipsychotic drugs can themselves induce psychotic symptoms if they are administered for a long time and then discontinued.<ref>{{cite journal |author=Remington G, Kapur S |title=Antipsychotic dosing: how much but also how often? |journal=Schizophr Bull |volume=36 |issue=5 |pages=900–3 |year=2010 |month=September |pmid=20650931 |pmc=2930338 |doi=10.1093/schbul/sbq083 |url=}}</ref>.
The treatment of psychosis depends on the specific diagnosis (such as schizophrenia, bipolar disorder or substance intoxication). The [[first line treatment]] for many psychotic disorders is [[antipsychotic]] medication (oral or intramuscular injection), and sometimes [[Inpatient care|hospitalization]] is needed. However, there are significant problems associated with this class of drugs. There is evidence that they can cause brain damage including prefrontal cortex atrophy, long-lasting parkinsonian symtoms ([[tardive dyskinesia]]), and personality change.<ref>{{cite news|last=James|first=Adam|title=Myth of the Antipsychotic|url=http://www.guardian.co.uk/commentisfree/2008/mar/02/mythoftheantipsychotic|newspaper=Guardian|date=2 March 2008}}</ref> Nancy Andreasen, editor in chief of the American Journal of Psychiatry, admitted antipsychotic drugs were associated with decrease in grey matter volumes and cognitive deficit, independent of illness severety.<ref>{{cite news|last=Whitaker|first=Robert|title=Andreasen Drops A Bombshell: Antipsychotics Shrink the Brain|url=http://www.psychologytoday.com/blog/mad-in-america/201102/andreasen-drops-bombshell-antipsychotics-shrink-the-brain|newspaper=Psychology Today|date=8 Feb 2011}}</ref>. Furthermore, antipsychotic drugs can themselves induce psychotic symptoms, independent of duration of treatment.<ref>{{cite journal |author=Remington G, Kapur S |title=Antipsychotic dosing: how much but also how often? |journal=Schizophr Bull |volume=36 |issue=5 |pages=900–3 |year=2010 |month=September |pmid=20650931 |pmc=2930338 |doi=10.1093/schbul/sbq083 |url=}}</ref>.


There is growing evidence that [[cognitive behavior therapy]],<ref>{{cite journal|last=Birchwood |first=M |authorlink= |coauthors=Trower P |title=The future of cognitive-behavioural therapy for psychosis: not a quasi-neuroleptic |journal=[[British Journal of Psychiatry]] |volume=188 |issue= 2|pages=108–108 |publisher= |year=2006 | pmid = 16449695|doi=10.1192/bjp.bp.105.014985 }}</ref> [[acceptance and commitment therapy]]<ref>{{cite web |title=APA website on empirical treatments |url=http://www.div12.org/PsychologicalTreatments/treatments.html |accessdate=2009-09-01}}</ref><ref>{{cite journal |last=Ruiz |first=F. J. |year=2010 |title=A review of Acceptance and Commitment Therapy (ACT) empirical evidence: Correlational, experimental psychopathology, component and outcome studies |journal=International Journal of Psychology and Psychological Therapy |volume=10 |issue=1 |pages=125–62 |url=http://www.ijpsy.com/volumen10/num1/256.html}}</ref> and [[family therapy]]<ref>{{cite journal|last=Haddock |first=G |authorlink= |coauthors=Lewis S |title=Psychological interventions in early psychosis |journal=Schizophrenia Bulletin |volume=31 |issue=3 |pages=697–704 |publisher= |year=2005 | pmid = 16006594|doi=10.1093/schbul/sbi029 }}</ref> can be effective in managing psychotic symptoms. When other treatments for psychosis are ineffective, [[electroconvulsive therapy]] or ECT (also known as shock treatment) is sometimes applied to relieve the underlying symptoms of psychosis due to depression. There is also increasing research suggesting that [[animal-assisted therapy]] can contribute to the improvement in general well-being of people with schizophrenia.<ref name=Nathans-Barel_et_al_2005>{{cite journal |last=Nathans-Barel |first=I. |coauthors=P. Feldman, B. Berger, I. Modai and H. Silver |year=2005 |title=Animal-assisted therapy ameliorates anhedonia in schizophrenia patients |journal=Psychotherapy and Psychosomatics |volume=74 |issue=1 |pages=31–35 |doi=10.1159/000082024 |pmid=15627854}}</ref>
There is growing evidence that [[cognitive behavior therapy]],<ref>{{cite journal|last=Birchwood |first=M |authorlink= |coauthors=Trower P |title=The future of cognitive-behavioural therapy for psychosis: not a quasi-neuroleptic |journal=[[British Journal of Psychiatry]] |volume=188 |issue= 2|pages=108–108 |publisher= |year=2006 | pmid = 16449695|doi=10.1192/bjp.bp.105.014985 }}</ref> [[acceptance and commitment therapy]]<ref>{{cite web |title=APA website on empirical treatments |url=http://www.div12.org/PsychologicalTreatments/treatments.html |accessdate=2009-09-01}}</ref><ref>{{cite journal |last=Ruiz |first=F. J. |year=2010 |title=A review of Acceptance and Commitment Therapy (ACT) empirical evidence: Correlational, experimental psychopathology, component and outcome studies |journal=International Journal of Psychology and Psychological Therapy |volume=10 |issue=1 |pages=125–62 |url=http://www.ijpsy.com/volumen10/num1/256.html}}</ref> and [[family therapy]]<ref>{{cite journal|last=Haddock |first=G |authorlink= |coauthors=Lewis S |title=Psychological interventions in early psychosis |journal=Schizophrenia Bulletin |volume=31 |issue=3 |pages=697–704 |publisher= |year=2005 | pmid = 16006594|doi=10.1093/schbul/sbi029 }}</ref> can be effective in managing psychotic symptoms. When other treatments for psychosis are ineffective, [[electroconvulsive therapy]] or ECT (also known as shock treatment) is sometimes applied to relieve the underlying symptoms of psychosis due to depression. There is also increasing research suggesting that [[animal-assisted therapy]] can contribute to the improvement in general well-being of people with schizophrenia.<ref name=Nathans-Barel_et_al_2005>{{cite journal |last=Nathans-Barel |first=I. |coauthors=P. Feldman, B. Berger, I. Modai and H. Silver |year=2005 |title=Animal-assisted therapy ameliorates anhedonia in schizophrenia patients |journal=Psychotherapy and Psychosomatics |volume=74 |issue=1 |pages=31–35 |doi=10.1159/000082024 |pmid=15627854}}</ref>

Revision as of 19:47, 8 May 2013

Not to be confused with Psychopathy.
For other uses, see Psychosis (disambiguation).
Psychosis
SpecialtyPsychiatry, clinical psychology Edit this on Wikidata

Psychosis (from the Greek ψυχή "psyche", for mind/soul, and -ωσις "-osis", for abnormal condition or derangement) refers to an abnormal condition of the mind, and is a generic psychiatric term for a mental state often described as involving a "loss of contact with reality". People suffering from psychosis are described as psychotic. Psychosis is given to the more severe forms of psychiatric disorder, during which hallucinations and delusions, gross excitement or stupor and impaired insight may occur.[2]

The term "psychosis" is very broad and can mean anything from relatively normal aberrant experiences through to the complex and catatonic expressions of schizophrenia and bipolar type 1 disorder.[3][4][5] Moreover a wide variety of central nervous system diseases, from both external substances and internal physiologic illness, can produce symptoms of psychosis. This led many professionals to say that psychosis is not specific enough as a diagnostic term. Despite this, "psychosis" is generally given to noticeable deficits in normal behavior (negative signs) and more commonly to diverse types of hallucinations or delusional beliefs (e.g. grandiosity, delusions of persecution). Someone exhibiting very obvious signs may be described as "frankly psychotic", whereas one exhibiting very subtle signs could be classified in the category of an "attenuated psychotic risk syndrome".

Psychiatrists attribute an excess in dopaminergic signalling is traditionally to be linked to the positive symptoms of psychosis, especially those of schizophrenia. However this has never been proved. This is thought to occur through a mechanism of aberrant salience of environmental stimuli.[6] Many antipsychotic drugs accordingly target the dopamine system; meta-analyses of placebo-controlled trials of these drugs, however, show either no significant difference between drug and placebo, or a very small effect size, suggesting that the pathophysiology of psychosis is much more complex than an overactive dopamine system.[7][8]

People experiencing psychosis may exhibit some personality changes and thought disorder. Depending on its severity, this may be accompanied by unusual or bizarre behavior, as well as difficulty with social interaction and impairment in carrying out daily life activities.

Signs and symptoms

People with psychosis may have one or more of the following: hallucinations, delusions, catatonia, or a thought disorder, as described below. Impairments in social cognition also occur.[9][10]

Hallucinations

A hallucination is defined as sensory perception in the absence of external stimuli. Hallucinations are different from illusions, or perceptual distortions, which are the misperception of external stimuli.[11] Hallucinations may occur in any of the five senses and take on almost any form, which may include simple sensations (such as lights, colors, tastes, and smells) to experiences such as seeing and interacting with fully formed animals and people, hearing voices, and having complex tactile sensations.

Auditory hallucinations, particularly experiences of hearing voices, are a common and often prominent feature of psychosis. Hallucinated voices may talk about, or to, the person, and may involve several speakers with distinct personas. Auditory hallucinations tend to be particularly distressing when they are derogatory, commanding or preoccupying. However, the experience of hearing voices need not always be a negative one. One research study has shown that the majority of people who hear voices are not in need of psychiatric help.[12] The Hearing Voices Movement has subsequently been created to support voice hearers, regardless of whether they are considered to have a mental illness or not.

Delusions

Psychosis may involve delusional beliefs, some of which are paranoid in nature. Put simply, delusions are false beliefs which a person holds on to, without adequate evidence. It may be difficult to change the belief even with evidence to the contrary. Common themes of delusions are persecutory (person believes that others are out to harm him), grandiose (person believing that he or she has special powers or skills) etc. Depressed persons may have delusions consistent with their low mood e.g: delusions that they have sinned, or have contracted serious illness etc. Karl Jaspers has classified psychotic delusions into primary and secondary types. Primary delusions are defined as arising suddenly and not being comprehensible in terms of normal mental processes, whereas secondary delusions may be understood as being influenced by the person's background or current situation (e.g., ethnicity, religious beliefs, superstitious belief).[13]

Catatonia

Catatonia describes a profoundly agitated state in which the experience of reality is generally considered to be impaired. There are two primary manifestations of catatonic behavior. The classic presentation is a person who does not move or interact with the world in any way while awake. This type of catatonia presents with waxy flexibility. Waxy flexibility is when someone physically moves part of a catatonic person's body and the person stays in the position even if it is bizarre and otherwise nonfunctional (such as moving a person's arm straight up in the air and the arm stays there).

The other type of catatonia is more of an outward presentation of the profoundly agitated state described above. It involves excessive and purposeless motor behavior as well as extreme mental preoccupation which prevents intact experience of reality. An example would be someone walking very fast in circles to the exclusion of anything else with a level of mental preoccupation (meaning not focused on anything relevant to the situation) that was not typical of the person prior to the symptom onset. In both types of catatonia there is generally no reaction to anything that happens outside of them. It is important to distinguish catatonic agitation from severe bipolar mania although someone could have both.

Thought disorder

Thought disorder describes an underlying disturbance to conscious thought and is classified largely by its effects on speech and writing. Affected persons show loosening of associations, that is, a disconnection and disorganization of the semantic content of speech and writing. In the severe form speech becomes incomprehensible and it is known as "word salad".

Psychiatric disorders

From a diagnostic standpoint, organic disorders were those held to be caused by physical illness affecting the brain (that is, psychiatric disorders secondary to other conditions), while functional disorders were considered to be disorders of the functioning of the mind in the absence of physical disorders (that is, primary psychological or psychiatric disorders). The materialistic view of the mind–body problem holds that mental disorders arise from physical processes; in this view, the distinction between brain and mind, and therefore between organic and functional disease, is an artificial one. Subtle physical abnormalities have been found in illnesses traditionally considered functional, such as schizophrenia. The DSM-IV-TR avoids the functional/organic distinction, and instead lists traditional psychotic illnesses, psychosis due to general medical conditions, and substance-induced psychosis.

Primary psychiatric causes of psychosis include the following:[14][15][16]

Psychotic symptoms may also be seen in[16]

Stress is known to contribute to and trigger psychotic states. A history of psychologically traumatic events, and the recent experience of a stressful event, can both contribute to the development of psychosis. Short-lived psychosis triggered by stress is known as brief reactive psychosis, and patients may spontaneously recover normal functioning within two weeks.[17] In some rare cases, individuals may remain in a state of full-blown psychosis for many years, or perhaps have attenuated psychotic symptoms (such as low intensity hallucinations) present at most times.

B12 deficiency can also cause characteristics of psychosis and mania. Most hospitals and mental facilities do not check for B12 deficiencies.[citation needed]

Normal states

Brief hallucinations are not uncommon in those without any psychiatric disease. Causes or triggers include[16]

Medical conditions

A very large number of medical conditions can cause psychosis, sometimes called secondary psychosis.[16] Examples include:

Psychosis can even be caused by familiar ailments such as flu[54][55] or mumps.[56]

Psychoactive drugs

Main article: Substance-induced psychosis

Various psychoactive substances (both legal and illegal) have been implicated in causing, exacerbating, and/or precipitating psychotic states and/or disorders in users. This may be upon intoxication, for a more prolonged period after use, or upon withdrawal.[16] Individuals who have a substance induced psychosis tend to have a greater awareness of their psychosis and tend to have higher levels of suicidal thinking compared to individuals who have a primary psychotic illness.[57] Drugs that can induce psychotic symptoms include cannabis, cocaine, amphetamines, cathinones, psychedelic drugs (such as LSD and psilocybin), κ-opioid receptor agonists (such as enadoline and salvinorin A) and NMDA receptor antagonists (such as phencyclidine and ketamine).[16]

Alcohol

Approximately 3 percent of people who are suffering from alcoholism experience psychosis during acute intoxication or withdrawal. Alcohol related psychosis may manifest itself through a kindling mechanism. The mechanism of alcohol-related psychosis is due to the long-term effects of alcohol resulting in distortions to neuronal membranes, gene expression, as well as thiamin deficiency. It is possible in some cases that alcohol abuse via a kindling mechanism can cause the development of a chronic substance induced psychotic disorder, i.e. schizophrenia. The effects of an alcohol-related psychosis include an increased risk of depression and suicide as well as causing psychosocial impairments.[58]

Cannabis

The more often cannabis is abused the more likely a person is to develop a psychotic illness,[59] with frequent use being correlated with twice the risk of psychosis and schizophrenia.[60][61] While cannabis use is accepted as a contributory cause of schizophrenia by many,[62] it remains controversial.[63][64] Some studies indicate that the effects of the two active compounds in cannabis, Tetrahydrocannabinol (THC) and Cannabidiol (CBD), are separable with respect to psychosis. While THC by itself tends to induce psychotic symptoms, CBD tends to reduce them, particularly in people who already exhibit these symptoms.[65] Cannabis use has increased dramatically over the past few decades but declined in the last decade, whereas the rate of psychosis has not increased. Together, these findings suggest that cannabis only hastens the onset of psychosis in those who would otherwise become psychotic at a later date.[66]

Methamphetamine

Methamphetamine induces a psychosis in 26-46 percent of heavy users. Some of these people develop a long-lasting psychosis that can persist for longer than 6 months. Those who have had a short-lived psychosis from methamphetamine can have a relapse of the methamphetamine psychosis years later after a stress event such as severe insomnia or a period of heavy alcohol abuse despite not relapsing back to methamphetamine. Individuals who have long history of methamphetamine abuse and who have experienced psychosis in the past from methamphetamine abuse are highly likely to rapidly relapse back into a methamphetamine psychosis within a week or so of going back onto methamphetamine. Violence is common during a methamphetamine psychosis.[57]

Medication

Administration, or sometimes withdrawal, of a large number of medications may provoke psychotic symptoms.[16] Drugs that can induce psychosis experimentally and/or in a significant proportion of patients include amphetamine and other sympathomimetics, dopamine agonists, ketamine, corticosteroids (often with mood changes in addition), and some anticonvulsants such as vigabatrin.[16][67]

Pathophysiology

The first brain image of an individual with psychosis was completed as far back as 1935 using a technique called pneumoencephalography[68] (a painful and now obsolete procedure where cerebrospinal fluid is drained from around the brain and replaced with air to allow the structure of the brain to show up more clearly on an X-ray picture).

The purpose of the brain is to collect information from the body (pain, hunger, etc.), and from the outside world, interpret it to a coherent world view, and produce a meaningful response. The information from the senses enter the brain in the primary sensory areas. They process the information and send it to the secondary areas where the information is interpreted. Spontaneous activity in the primary sensory areas may produce hallucinations which are misinterpreted by the secondary areas as information from the real world.

For example, a PET or fMRI scan of a person who claims to be hearing voices may show activation in the primary auditory cortex, or parts of the brain involved in the perception and understanding of speech.[69]

Tertiary brain cortex collects the interpretations from the secondary cortexes and creates a coherent world view of it. A study investigating structural changes in the brains of people with psychosis showed there was significant grey matter reduction in the right medial temporal, lateral temporal, and inferior frontal gyrus, and in the cingulate cortex bilaterally of people before and after they became psychotic.[70] Findings such as these have led to debate about whether psychosis itself causes excitotoxic brain damage and whether potentially damaging changes to the brain are related to the length of psychotic episode. Recent research has suggested that this is not the case[71] although further investigation is still ongoing.

Studies with sensory deprivation have shown that the brain is dependent on signals from the outer world to function properly. If the spontaneous activity in the brain is not counterbalanced with information from the senses, loss from reality and psychosis may occur after some hours. A similar phenomenon is paranoia in the elderly when poor eyesight, hearing and memory causes the person to be abnormally suspicious of the environment.

On the other hand, loss from reality may also occur if the spontaneous cortical activity is increased so that it is no longer counterbalanced with information from the senses. The 5-HT2A receptor seems to be important for this, since psychedelic drugs which activate them produce hallucinations.

However, the main feature of psychosis is not hallucinations, but the inability to distinguish between internal and external stimuli. Close relatives to psychotic patients may hear voices, but since they are aware that they are unreal they can ignore them, so that the hallucinations do not affect their reality perception. Hence they are not considered to be psychotic.

Psychosis has been traditionally linked to the neurotransmitter dopamine. In particular, the dopamine hypothesis of psychosis has been influential and states that psychosis results from an overactivity of dopamine function in the brain, particularly in the mesolimbic pathway. The two major sources of evidence given to support this theory are that dopamine receptor D2 blocking drugs (i.e., antipsychotics) tend to reduce the intensity of psychotic symptoms, and that drugs which boost dopamine activity (such as amphetamines and cocaine) can trigger psychosis in some people (see amphetamine psychosis).[6] However, increasing evidence in recent times has pointed to a possible dysfunction of the excitory neurotransmitter glutamate, in particular, with the activity of the NMDA receptor.

This theory is reinforced by the fact that dissociative NMDA receptor antagonists such as ketamine, PCP and dextromethorphan (at large overdoses) induce a psychotic state more readily than dopaminergic stimulants, even at "normal" recreational doses. The symptoms of dissociative intoxication are also considered to mirror the symptoms of schizophrenia, including negative psychotic symptoms, more closely than amphetamine psychosis. Dissociative induced psychosis happens on a more reliable and predictable basis than amphetamine psychosis, which usually only occurs in cases of overdose, prolonged use or with sleep deprivation, which can independently produce psychosis. New antipsychotic drugs which act on glutamate and its receptors are currently undergoing clinical trials.

The connection between dopamine and psychosis is generally believed to be complex. While dopamine receptor D2 suppresses adenylate cyclase activity, the D1 receptor increases it. If D2-blocking drugs are administered the blocked dopamine spills over to the D1 receptors. The increased adenylate cyclase activity affects genetic expression in the nerve cell, a process which takes time. Hence antipsychotic drugs take a week or two to reduce the symptoms of psychosis. Moreover, newer and equally effective antipsychotic drugs actually block slightly less dopamine in the brain than older drugs whilst also blocking 5-HT2A receptors, suggesting the 'dopamine hypothesis' may be oversimplified.[72] Soyka and colleagues found no evidence of dopaminergic dysfunction in people with alcohol-induced psychosis[73] and Zoldan et al. reported moderately successful use of ondansetron, a 5-HT3 receptor antagonist, in the treatment of levodopa psychosis in Parkinson's disease patients.[74]

Psychiatrist David Healy has criticised pharmaceutical companies for promoting simplified biological theories of mental illness that seem to imply the primacy of pharmaceutical treatments while ignoring social and developmental factors which are known to be important influences in the aetiology of psychosis.[75]

Some theories regard many psychotic symptoms to be a problem with the perception of ownership of internally generated thoughts and experiences.[76] For example, the hallucination of hearing voices may arise from internally generated speech that is mislabeled by the psychotic person as coming from an external source.

It has been suggested that persons with bipolar disorder may have increased activity of the left hemisphere compared to the right hemisphere of the brain, while persons with schizophrenia have increased activity in the right hemisphere.[77]

Increased level of right hemisphere activation has also been found in people who have high levels of paranormal beliefs[78] and in people who report mystical experiences.[79] It also seems to be the case that people who are more creative are also more likely to show a similar pattern of brain activation.[80] Some researchers have been quick to point out that this in no way suggests that paranormal, mystical or creative experiences are in any way by themselves a symptom of mental illness, as it is still not clear what makes some such experiences beneficial and others distressing.

Neurobiology

In otherwise normal individuals, exogenous ligands can produce psychotic symptoms. NMDA receptor antagonists, such as ketamine, can produce a similar psychosis to that experienced in schizophrenia.[81]

Prolonged or high dose use of psychostimulants can alter normal functioning to be similar to the manic phase of bipolar disorder.[82] NMDA antagonists replicate some of the so-called "negative" symptoms like thought disorder in subanesthetic doses (doses insufficient to induce anesthesia), and catatonia in high doses. Psychostimulants, especially in one already prone to psychotic thinking, can cause some "positive" symptoms, such as delusional beliefs, particularly those persecutory in nature.

Diagnosis

Diagnosing the presence and/or extent of psychosis may be distinguished from diagnosing the cause of psychosis.[16]

The presence of psychosis is typically diagnosed by clinical interview, incorporating mental state examination.[14][15] Its extent may be established by formal rating scales. The Brief Psychiatric Rating Scale (BPRS)[83] assesses the level of 18 symptom constructs of psychosis such as hostility, suspicion, hallucination, and grandiosity. It is based on the clinician's interview with the patient and observations of the patient's behavior over the previous 2–3 days. The patient's family can also provide the behavior report. During the initial assessment and the follow-up, both positive and negative symptoms of psychosis can be assessed using the 30 item Positive and Negative Symptom Scale (PANSS).[84]

Establishing the cause of psychosis requires clinical examination, and sometimes special investigations, to diagnose or exclude secondary causes of psychosis; if these are excluded, a primary psychiatric diagnosis can be established.[16]

Treatment

The treatment of psychosis depends on the specific diagnosis (such as schizophrenia, bipolar disorder or substance intoxication). The first line treatment for many psychotic disorders is antipsychotic medication (oral or intramuscular injection), and sometimes hospitalization is needed. However, there are significant problems associated with this class of drugs. There is evidence that they can cause brain damage including prefrontal cortex atrophy, long-lasting parkinsonian symtoms (tardive dyskinesia), and personality change.[85] Nancy Andreasen, editor in chief of the American Journal of Psychiatry, admitted antipsychotic drugs were associated with decrease in grey matter volumes and cognitive deficit, independent of illness severety.[86]. Furthermore, antipsychotic drugs can themselves induce psychotic symptoms, independent of duration of treatment.[87].

There is growing evidence that cognitive behavior therapy,[88] acceptance and commitment therapy[89][90] and family therapy[91] can be effective in managing psychotic symptoms. When other treatments for psychosis are ineffective, electroconvulsive therapy or ECT (also known as shock treatment) is sometimes applied to relieve the underlying symptoms of psychosis due to depression. There is also increasing research suggesting that animal-assisted therapy can contribute to the improvement in general well-being of people with schizophrenia.[92]

Early intervention

Main article: Early intervention in psychosis

Early intervention in psychosis is a relatively new concept based on the observation that identifying and treating someone in the early stages of a psychosis can significantly improve their longer term outcome.[93] This approach advocates the use of an intensive multi-disciplinary approach during what is known as the critical period, where intervention is the most effective, and prevents the long term morbidity associated with chronic psychotic illness.

Newer research into the effectiveness of cognitive behavioural therapy during the early pre-cursory stages of psychosis (also known as the "prodrome" or "at risk mental state") suggests that such input can prevent or delay the onset of psychosis.[94]

Prevention

Previously the evidence for the effectiveness of early interventions to prevent psychosis appeared inconclusive.[95] Whilst early intervention in those with a psychotic episode might improve short term outcomes, little benefit was seen from these measures after five years.[96] However more recently there has been some evidence that cognitive behavioral therapy (CBT) may reduce the risk of becoming psychotic in those at high risk.[97][98]

History

The word psychosis was introduced to the psychiatric literature in 1841 by Karl Friedrich Canstatt in his work Handbuch der Medizinischen Klinik. He used it as a shorthand for 'psychic neurosis'. At that time neurosis meant any disease of the nervous system, and Canstatt was thus referring to what was thought to be a psychological manifestation of brain disease.[99] Ernst von Feuchtersleben is also widely credited as introducing the term in 1845,[100] as an alternative to insanity and mania.

The term stems from the Greek ψύχωσις (psychosis), "a giving soul or life to, animating, quickening" and that from ψυχή (psyche), "soul" and the suffix -ωσις (-osis), in this case "abnormal condition".[101][102]

The word was also used to distinguish disorders which were thought to be disorders of the mind, as opposed to "neurosis", which was thought to be a disorder of the nervous system.[103] The psychoses thus became the modern equivalent of the old notion of madness, and hence there was much debate on whether there was only one (unitary) or many forms of the new disease.[104] One type of broad usage would later be narrowed down by Koch in 1891 to the 'psychopathic inferiorities' - later renamed abnormal personalities by Schneider.[99]

The division of the major psychoses into manic depressive illness (now called bipolar disorder) and dementia praecox (now called schizophrenia) was made by Emil Kraepelin, who attempted to create a synthesis of the various mental disorders identified by 19th century psychiatrists, by grouping diseases together based on classification of common symptoms. Kraepelin used the term 'manic depressive insanity' to describe the whole spectrum of mood disorders, in a far wider sense than it is usually used today.

In Kraepelin's classification this would include 'unipolar' clinical depression, as well as bipolar disorder and other mood disorders such as cyclothymia. These are characterised by problems with mood control and the psychotic episodes appear associated with disturbances in mood, and patients will often have periods of normal functioning between psychotic episodes even without medication. Schizophrenia is characterized by psychotic episodes which appear to be unrelated to disturbances in mood, and most non-medicated patients will show signs of disturbance between psychotic episodes.

During the 1960s and 1970s, psychosis was of particular interest to counterculture critics of mainstream psychiatric practice, who argued that it may simply be another way of constructing reality and is not necessarily a sign of illness. For example, R. D. Laing argued that psychosis is a symbolic way of expressing concerns in situations where such views may be unwelcome or uncomfortable to the recipients. He went on to say that psychosis could be also seen as a transcendental experience with healing and spiritual aspects.

Arthur J. Deikman suggested use of the term "mystical psychosis" to characterize first-person accounts of psychotic experiences that are similar to reports of mystical experiences. Thomas Szasz focused on the social implications of labeling people as psychotics, a label he argues unjustly medicalises different views of reality so such unorthodox people can be controlled by society. Psychoanalysis has a detailed account of psychosis which differs markedly from that of psychiatry. Freud and Lacan outlined their perspective on the structure of psychosis in a number of works.

Since the 1970s, the introduction of a recovery approach to mental health, which has been driven mainly by people who have experienced psychosis (or whatever name is used to describe their experiences), has led to a greater awareness that mental illness is not a lifelong disability, and that there is an expectation that recovery is possible, and probable with effective support.

Other views

A 2012 paper suggested that psychiatric conditions associated with psychotic spectrum symptoms may be possible explanations for revelatory driven experiences and activities such as those of Abraham, Moses, Jesus and Saint Paul.[105]

Subtypes

Subtypes of psychosis include:

Cycloid psychosis

Cycloid psychosis is psychosis that progresses from normal to full-blown usually within a few hours, not related to drug intake or brain injury.[106] In addition, diagnostic criteria include at least four of the following symptoms:[106]

  • Confusion
  • Mood-incongruent delusions
  • Hallucinations
  • Pan-anxiety, a severe anxiety not bound to particular situations or circumstances
  • Happiness or ecstasy of high degree
  • Motility disturbances of akinetic or hyperkinetic type
  • Concern with death
  • Mood swings to some degree, but less than what is needed for diagnosis of an affective disorders

Cycloid psychosis occurs in people of generally 15–50 years of age.[106]

See also

2

References

  1. ^ http://apps.who.int/classifications/apps/icd/icd10online/
  2. ^ Gelder, Michael (2005). "Psychiatry", P. 12. Oxford University Press Inc., New York. ISBN 978-0-19-852863-0.
  3. ^ American Psychological Association (APA), 1994 The Diagnostic and Statistical Manual Revision IV (DSM-IV)
  4. ^ Gelder, Mayou & Geddes 2005
  5. ^ Yuhas, Daisy. "Throughout History, Defining Schizophrenia Has Remained a Challenge (Timeline)". Scientific American Mind (March 2013). Retrieved 2 March 2013.
  6. ^ a b Kapur S, Mizrahi R, Li M (2005). "From dopamine to salience to psychosis--linking biology, pharmacology and phenomenology of psychosis". Schizophr. Res. 79 (1): 59–68. doi:10.1016/j.schres.2005.01.003. PMID 16005191. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  7. ^ Leucht, S (2009). "How effective are second-generation antipsychotic drugs? A meta-analysis of placebo-controlled trials" (PDF). Molecular Psychiatry. 14 (4): 429–447. doi:10.1038/sj.mp.4002136. PMID 18180760. Retrieved 24 March 2013. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  8. ^ Rattehalli, R. D. (5 April 2010). "Risperidone Versus Placebo for Schizophrenia". Schizophrenia Bulletin. 36 (3): 448–449. doi:10.1093/schbul/sbq030. PMC 2879694. PMID 20368309. Retrieved 24 March 2013. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  9. ^ Fusar-Poli, P.; Deste, G.; Smieskova, R.; Barlati, S.; Yung, AR.; Howes, O.; Stieglitz, RD.; Vita, A.; McGuire, P. (2012). "Cognitive functioning in prodromal psychosis: a meta-analysis". Arch Gen Psychiatry. 69 (6): 562–71. doi:10.1001/archgenpsychiatry.2011.1592. PMID 22664547. {{cite journal}}: Unknown parameter |month= ignored (help)
  10. ^ Brown, EC.; Tas, C.; Brüne, M. (2012). "Potential therapeutic avenues to tackle social cognition problems in schizophrenia". Expert Rev Neurother. 12 (1): 71–81. doi:10.1586/ern.11.183. PMID 22149657. {{cite journal}}: Unknown parameter |month= ignored (help)
  11. ^ Harper, Douglas (2001). "hallucinate". Online Etymology Dictionary. Retrieved October 15, 2006. {{cite web}}: Unknown parameter |month= ignored (help)
  12. ^ Honig A, Romme MA, Ensink BJ, Escher SD, Pennings MH, deVries MW (1998). "Auditory hallucinations: a comparison between patients and nonpatients". J. Nerv. Ment. Dis. 186 (10): 646–51. doi:10.1097/00005053-199810000-00009. PMID 9788642. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  13. ^ Jaspers, Karl (1997-11-27) [1963]. Allgemeine Psychopathologie (General Psychopathology). Translated by J. Hoenig & M.W. Hamilton from German (Reprint ed.). Baltimore, Maryland: Johns Hopkins University Press. ISBN 0-8018-5775-9.
  14. ^ a b World Health Organization, The ICD-10 Classification of Mental and Behavioural Disorders: Clinical descriptions and diagnostic guidelines (CDDG), 1992.
  15. ^ a b American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision (DSM-IV-TR), American Psychiatric Association, 2000.
  16. ^ a b c d e f g h i j k l m Cardinal, R.N. & Bullmore, E.T., The Diagnosis of Psychosis, Cambridge University Press, 2011, ISBN 978-0-521-16484-9
  17. ^ Jauch, D. A. (1988). "Reactive psychosis. I. Does the pre-DSM-III concept define a third psychosis?". Journal of Nervous and Mental Disease. 176 (2): 72–81. doi:10.1097/00005053-198802000-00002. PMID 3276813. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  18. ^ Ohayon, M. M. (1996). "Hypnagogic and hypnopompic hallucinations: pathological phenomena?". British Journal of Psychiatry. 169 (4): 459–67. doi:10.1192/bjp.169.4.459. PMID 8894197. Retrieved 2006-10-21. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  19. ^ Sharma, Verinder (2003). "Sleep loss and postpartum psychosis". Bipolar Disorders. 5 (2): 98–105. doi:10.1034/j.1399-5618.2003.00015.x. PMID 12680898. Retrieved 2006-09-27. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  20. ^ Chan-Ob, T. (1999). "Meditation in association with psychosis". Journal of the Medical Association of Thailand. 82 (9): 925–930. PMID 10561951. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  21. ^ Devillieres, P. (1996). "[Delusion and sleep deprivation]". L'Encéphale. 22 (3): 229–31. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  22. ^ Lesser JM, Hughes S (2006). "Psychosis-related disturbances. Psychosis, agitation, and disinhibition in Alzheimer's disease: definitions and treatment options". Geriatrics. 61 (12): 14–20. PMID 17184138. {{cite journal}}: Unknown parameter |month= ignored (help)
  23. ^ McKeith, Ian G. (2002). "Dementia with Lewy bodies". British Journal of Psychiatry. 180 (2): 144–7. doi:10.1192/bjp.180.2.144. PMID 11823325. {{cite journal}}: Unknown parameter |month= ignored (help)
  24. ^ Wedekind S (2005). "[Depressive syndrome, psychoses, dementia: frequent manifestations in Parkinson disease]". MMW Fortschr Med (in German). 147 (22): 11. PMID 15977623. {{cite journal}}: Unknown parameter |month= ignored (help)
  25. ^ Lisanby, S. H. (1998). "Psychosis Secondary to Brain Tumor". Seminars in clinical neuropsychiatry. 3 (1): 12–22. PMID 10085187. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  26. ^ Template:Es icon Rodriguez Gomez, Diego (August 16–31, 2005). "Psicosis aguda como inicio de esclerosis multiple / Acute psychosis as the presenting symptom of multiple sclerosis / Psicose aguda como inicio de esclerose multipla". Revista de Neurología. 41 (4): 255–6. PMID 16075405. Retrieved 2006-09-27. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  27. ^ Evans, Dwight L. (2002-02-01). "Chapter 90: Neuropsychiatric Manifestations of HIV-1 Infection and AIDS". In Kenneth L Davis, Dennis Charney, Joseph T Coyle, Charles Nemeroff (ed.). Neuropsychopharmacology: The Fifth Generation of Progress (5th ed.). Philadelphia: Lippincott Williams & Wilkins. pp. 1281–1301. ISBN 0-7817-2837-1. Retrieved 2006-10-16. {{cite book}}: External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: multiple names: editors list (link)
  28. ^ Tilluckdharry, C. C. (1996). "A case of vivax malaria presenting with psychosis". West Indian Medical Journal. 45 (1): 39–40. PMID 8693739. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  29. ^ Fallon BA, Nields JA (1994). "Lyme disease: a neuropsychiatric illness". Am J Psychiatry. 151 (11): 1571–83. PMID 7943444. {{cite journal}}: Unknown parameter |month= ignored (help)
  30. ^ Hess A, Buchmann J, Zettl UK; et al. (1999). "Borrelia burgdorferi central nervous system infection presenting as an organic schizophrenialike disorder". Biol. Psychiatry. 45 (6): 795. doi:10.1016/S0006-3223(98)00277-7. PMID 10188012. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  31. ^ van den Bergen HA, Smith JP, van der Zwan A (1993). "[Lyme psychosis]". Ned Tijdschr Geneeskd (in Dutch; Flemish). 137 (41): 2098–100. PMID 8413733. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link) CS1 maint: unrecognized language (link)
  32. ^ Kararizou E, Mitsonis C, Dimopoulos N, Gkiatas K, Markou I, Kalfakis N (May–Jun 2006). "Psychosis or simply a new manifestation of neurosyphilis?". J. Int. Med. Res. 34 (3): 335–7. PMID 16866029.{{cite journal}}: CS1 maint: date format (link) CS1 maint: multiple names: authors list (link)
  33. ^ Brooke D, Jamie P, Slack R, Sulaiman M, Tyrer P (1987). "Neurosyphilis—a treatable psychosis". Br J Psychiatry. 151 (4): 556. doi:10.1192/bjp.151.4.556. PMID 3447677. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  34. ^ Hermle L, Becker FW, Egan PJ, Kolb G, Wesiack B, Spitzer M (1997). "[Metachromatic leukodystrophy simulating schizophrenia-like psychosis]". Der Nervenarzt (in German). 68 (9): 754–8. doi:10.1007/s001150050191. PMID 9411279.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  35. ^ Black DN, Taber KH, Hurley RA (2003). "Metachromatic leukodystrophy: a model for the study of psychosis". The Journal of neuropsychiatry and clinical neurosciences. 15 (3): 289–93. doi:10.1176/appi.neuropsych.15.3.289. PMID 12928504.{{cite journal}}: CS1 maint: multiple names: authors list (link)free full text
  36. ^ Kumperscak HG, Paschke E, Gradisnik P, Vidmar J, Bradac SU (2005). "Adult metachromatic leukodystrophy: disorganized schizophrenia-like symptoms and postpartum depression in 2 sisters". Journal of psychiatry & neuroscience : JPN. 30 (1): 33–6. PMC 543838. PMID 15644995.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  37. ^ Sethi NK, Robilotti E, Sadan Y (2005). "Neurological Manifestations Of Vitamin B-12 Deficiency". The Internet Journal of Nutrition and Wellness. 2 (1).{{cite journal}}: CS1 maint: multiple names: authors list (link)
  38. ^ Masalha R, Chudakov B, Muhamad M, Rudoy I, Volkov I, Wirguin I (2001). "Cobalamin-responsive psychosis as the sole manifestation of vitamin B12 deficiency". Isr. Med. Assoc. J. 3 (9): 701–3. PMID 11574992. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  39. ^ Rossman, Phillip L. (1956). "Postpartum Tetany and Psychosis Due to Hypocalcemia". California Medicine. 85 (3): 190–3. PMC 1531921. PMID 13356186. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  40. ^ Jana, D. K. (1973). "Hypernatremic psychosis in the elderly: case reports". Journal of the American Geriatrics Society. 21 (10): 473–7. PMID 4729012. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  41. ^ Haensch, C. A. (1996). "[Reversible exogenous psychosis in thiazide-induced hyponatremia of 97 mmol/l]". Der Nervenarzt. 67 (4): 319–22. PMID 8684511. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  42. ^ Hafez, H. (1984). "Hypokalemia-induced psychosis in a chronic schizophrenic patient". Journal of Clinical Psychiatry. 45 (6): 277–9. PMID 6725222. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  43. ^ Konstantakos, Anastasios K. (May 25, 2006). "Hypomagnesemia". eMedicine. WebMD. Retrieved October 16, 2006. {{cite web}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  44. ^ Velasco, P. Joel (1 December 1999). "Psychiatric Aspects of Parathyroid Disease". Psychosomatics. 40 (6): 486–90. doi:10.1016/S0033-3182(99)71186-2. PMID 10581976. Retrieved 2006-10-17. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  45. ^ Rosenthal, M. (1997). "Primary hyperparathyroidism: neuropsychiatric manifestations and case report". Israel Journal of Psychiatry and Related Sciences. 34 (2): 122–125. PMID 9231574. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  46. ^ Nanji, A. A. (1984). "The psychiatric aspect of hypophosphatemia". Canadian Journal of Psychiatry. 29 (7): 599–600. PMID 6391648. {{cite journal}}: Unknown parameter |month= ignored (help)
  47. ^ Padder, Tanveer (2005). "Acute Hypoglycemia Presenting as Acute Psychosis". Psychiatry online. Retrieved 2006-09-27. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  48. ^ Robert, M. (1 March 2006). "Neuropsychiatric manifestations systemic lupus erythematosus: A study from South India". Neurology India. 54 (1): 75–7. doi:10.4103/0028-3886.24713. PMID 16679649. Retrieved 2006-09-29. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: unflagged free DOI (link)
  49. ^ Bona, Joseph R. (1 August 1998). "Neurosarcoidosis as a Cause of Refractory Psychosis: A Complicated Case Report". American Journal of Psychiatry. 155 (8): 1106–8. PMID 9699702. Retrieved 2006-09-29. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  50. ^ Wilcox RA, To T, Koukourou A, Frasca J (2008). "Hashimoto's encephalopathy masquerading as acute psychosis". J Clin Neurosci. 15 (11): 1301–4. doi:10.1016/j.jocn.2006.10.019. PMID 18313925. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  51. ^ Gómez-Bernal GJ, Reboreda A, Romero F, Bernal MM, Gómez F (2007). "A Case of Hashimoto's Encephalopathy Manifesting as Psychosis". Prim Care Companion J Clin Psychiatry. 9 (4): 318–9. doi:10.4088/PCC.v09n0411f. PMC 2018852. PMID 17934563.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  52. ^ Ray M, Kothur K, Padhy SK, Saran P (2007). "Hashimoto's encephalopathy in an adolescent boy". Indian J Pediatr. 74 (5): 492–4. doi:10.1007/s12098-007-0084-0. PMID 17526963. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  53. ^ Nasky KM, Knittel DR, Manos GH (2008). "Psychosis associated with anti-N-methyl-D-aspartate receptor antibodies". CNS Spectr. 13 (8): 699–703. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  54. ^ Steinberg, D. (1972). "Influenza infection causing manic psychosis". British Journal of Psychiatry. 120 (558): 531–535. doi:10.1192/bjp.120.558.531. PMID 5041533. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  55. ^ Maurizi, C. P. (1985). "Influenza and mania: a possible connection with the locus ceruleus". Southern Medical Journal. 78 (2): 207–209. doi:10.1097/00007611-198502000-00025. PMID 3975719. {{cite journal}}: Unknown parameter |month= ignored (help)
  56. ^ Keddie, K. M. (1965). "Toxic psychosis following mumps". British Journal of Psychiatry. 111 (477): 691–696. doi:10.1192/bjp.111.477.691. PMID 14337417. {{cite journal}}: Unknown parameter |month= ignored (help)
  57. ^ a b Grant KM, LeVan TD, Wells SM; et al. (2012). "Methamphetamine-associated psychosis". J Neuroimmune Pharmacol. 7 (1): 113–39. doi:10.1007/s11481-011-9288-1. PMC 3280383. PMID 21728034. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  58. ^ Alcohol-Related Psychosis at eMedicine
  59. ^ Moore THM, Zammit S, Lingford-Hughes A et al.. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet. 2007;370(9584):319–328. doi:10.1016/S0140-6736(07)61162-3. PMID 17662880.
  60. ^ Leweke FM, Koethe D. Cannabis and psychiatric disorders: it is not only addiction. Addict Biol. 2008;13(2):264–75. doi:10.1111/j.1369-1600.2008.00106.x. PMID 18482435.
  61. ^ Sewell RA, Ranganathan M, D'Souza DC. Cannabinoids and psychosis. International review of psychiatry (Abingdon, England). 2009 Apr;21(2):152–62. doi:10.1080/09540260902782802. PMID 19367509.
  62. ^ Henquet C, Di Forti M, Morrison P, Kuepper R, Murray RM. Gene-environment interplay between cannabis and psychosis. Schizophr Bull. 2008;34(6):1111–21. doi:10.1093/schbul/sbn108. PMID 18723841.
  63. ^ McLaren JA, Silins E, Hutchinson D, Mattick RP, Hall W. Assessing evidence for a causal link between cannabis and psychosis: a review of cohort studies. Int. J. Drug Policy. 2010;21(1):10–9. doi:10.1016/j.drugpo.2009.09.001. PMID 19783132.
  64. ^ Ben Amar M, Potvin S. Cannabis and psychosis: what is the link?. Journal of Psychoactive Drugs. 2007 Jun;39(2):131–42. doi:10.1080/02791072.2007.10399871. PMID 17703707.
  65. ^ Bhattacharyya, S. (2010). "Opposite Effects of D-9-Tetrahydrocannabinol and Cannabidiol on Human Brain Function and Psychopathology". Neuropsychopharmacology. 35 (3): 764–774. doi:10.1038/npp.2009.184. PMC 3055598. PMID 19924114. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  66. ^ Degenhardt L, Hall W, Lynskey M (2001). "Comorbidity between cannabis use and psychosis: Modelling some possible relationships" (PDF). Technical Report No. 121. Sydney: National Drug and Alcohol Research Centre. Retrieved 2006-08-19. {{cite journal}}: Cite journal requires |journal= (help)CS1 maint: multiple names: authors list (link)
  67. ^ Sander JW, Hart YM, Trimble MR, Shorvon SD (1991). "Vigabatrin and psychosis". Journal of Neurology, Neurosurgery, and Psychiatry. 54 (5): 435–9. doi:10.1136/jnnp.54.5.435. PMC 488544. PMID 1865207.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  68. ^ Moore, M T (1935). "Encephalographic studies in mental disease". American Journal of Psychiatry. 92 (1): 43–67. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  69. ^ Copolov DL, Seal ML, Maruff P; et al. (2003). "Cortical activation associated with the experience of auditory hallucinations and perception of human speech in schizophrenia: a PET correlation study". Psychiatry Res. 122 (3): 139–52. doi:10.1016/S0925-4927(02)00121-X. PMID 12694889. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  70. ^ Pantelis, C (2003). "Neuroanatomical abnormalities before and after onset of psychosis: a cross-sectional and longitudinal MRI comparison". Lancet. 25 (361 (9354)): 281–8. doi:10.1016/S0140-6736(03)12323-9. PMID 12559861. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  71. ^ Ho, BC (2003). "Untreated initial psychosis: relation to cognitive deficits and brain morphology in first-episode schizophrenia". American Journal of Psychiatry. 160 (1): 142–8. doi:10.1176/appi.ajp.160.1.142. PMID 12505813. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  72. ^ Jones HM, Pilowsky LS (2002). "Dopamine and antipsychotic drug action revisited". Br J Psychiatry. 181 (4): 271–5. doi:10.1192/bjp.181.4.271. PMID 12356650. {{cite journal}}: Unknown parameter |month= ignored (help)
  73. ^ Soyka, Michael (2000). "FDG-PET and IBZM-SPECT Suggest Reduced Thalamic Activity but No Dopaminergic Dysfunction in Chronic Alcohol Hallucinosis". Journal of Neuropsychiatry & Clinical Neurosciences. 12 (2): 287–288. doi:10.1176/appi.neuropsych.12.2.287. PMID 11001615. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  74. ^ Zoldan, J. (1995). "Psychosis in advanced Parkinson's disease: treatment with ondansetron, a 5-HT3 receptor antagonist". Neurology. 45 (7): 1305–1308. doi:10.1212/WNL.45.7.1305. PMID 7617188. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  75. ^ Healy, David (2002). The Creation of Psychopharmacology. Cambridge: Harvard University Press. ISBN 0-674-00619-4. {{cite book}}: Cite has empty unknown parameter: |coauthors= (help)
  76. ^ Blakemore, SJ (2000). "The perception of self-produced sensory stimuli in patients with auditory hallucinations and passivity experiences: evidence for a breakdown in self-monitoring". Psychological Medicine. 30 (5): 1131–9. doi:10.1017/S0033291799002676. PMID 12027049. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  77. ^ Lohr, JB (1997). "Lateralized hemispheric dysfunction in the major psychotic disorders: historical perspectives and findings from a study of motor asymmetry in older patients". Schizophrophrenia Research. 30 (27 (2–3)): 191–8. doi:10.1016/S0920-9964(97)00062-5. PMID 9416648. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  78. ^ Pizaagalli, D (2000). "Brain electric correlates of strong belief in paranormal phenomena: intracerebral EEG source and regional Omega complexity analyses". Psychiatry Research. 100 (3): 139–154. doi:10.1016/S0925-4927(00)00070-6. PMID 11120441. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  79. ^ Makarec, K (1985). "Temporal lobe signs: electroencephalographic validity and enhanced scores in special populations". Perceptual and Motor Skills. 60 (3): 831–42. doi:10.2466/pms.1985.60.3.831. PMID 3927256. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  80. ^ Weinstein, S (2002). "Are creativity and schizotypy products of a right hemisphere bias?". Brain and Cognition. 49 (1): 138–51. doi:10.1006/brcg.2001.1493. PMID 12027399. Retrieved 2006-08-19. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  81. ^ (Krystal,J Subanesthetic Effects of the Noncompetitive NMDA Antagonist, Ketamine, in Humans,Arch Gen Psychiatry, 1994)
  82. ^ (Curran, C, Stimulant psychosis: systematic review, British Journal of Psychiatry, 2004)
  83. ^ Overall JE, Gorham DR. The Brief Psychiatric Rating Scale. Psychol Rep. 1962;10:799-812
  84. ^ Kay, S.R., Fiszbien, A., & Opler, L.A. 1987. The Positive and Negative Symptom Scale (PANNS) for schizophrenia. Schizophrenia Bulletin, 13, pp261-276
  85. ^ James, Adam (2 March 2008). "Myth of the Antipsychotic". Guardian.
  86. ^ Whitaker, Robert (8 Feb 2011). "Andreasen Drops A Bombshell: Antipsychotics Shrink the Brain". Psychology Today.
  87. ^ Remington G, Kapur S (2010). "Antipsychotic dosing: how much but also how often?". Schizophr Bull. 36 (5): 900–3. doi:10.1093/schbul/sbq083. PMC 2930338. PMID 20650931. {{cite journal}}: Unknown parameter |month= ignored (help)
  88. ^ Birchwood, M (2006). "The future of cognitive-behavioural therapy for psychosis: not a quasi-neuroleptic". British Journal of Psychiatry. 188 (2): 108–108. doi:10.1192/bjp.bp.105.014985. PMID 16449695. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  89. ^ "APA website on empirical treatments". Retrieved 2009-09-01.
  90. ^ Ruiz, F. J. (2010). "A review of Acceptance and Commitment Therapy (ACT) empirical evidence: Correlational, experimental psychopathology, component and outcome studies". International Journal of Psychology and Psychological Therapy. 10 (1): 125–62.
  91. ^ Haddock, G (2005). "Psychological interventions in early psychosis". Schizophrenia Bulletin. 31 (3): 697–704. doi:10.1093/schbul/sbi029. PMID 16006594. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  92. ^ Nathans-Barel, I. (2005). "Animal-assisted therapy ameliorates anhedonia in schizophrenia patients". Psychotherapy and Psychosomatics. 74 (1): 31–35. doi:10.1159/000082024. PMID 15627854. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  93. ^ Birchwood, M (1998). "Early Intervention in Psychosis: The Critical Period Hypothesis". British Journal of Psychiatry. 172 (33): 53–59. PMID 9764127. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  94. ^ French, Paul (2004). Early Detection and cognitive therapy for people at high risk of developing psychosis. Chichester: John Wiley and Sons. ISBN 0-470-86314-5. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |unused_data= ignored (help)
  95. ^ Marshall M, Rathbone J. Early intervention for psychosis. Cochrane Database Syst Rev. 2006;(4):CD004718. doi:10.1002/14651858.CD004718.pub2. PMID 17054213.
  96. ^ van Os J, Kapur S. Schizophrenia. Lancet. 2009;374(9690):635–45. doi:10.1016/S0140-6736(09)60995-8. PMID 19700006.
  97. ^ Stafford, MR (2013 Jan 18). "Early interventions to prevent psychosis: systematic review and meta-analysis". BMJ (Clinical research ed.). 346: f185. PMID 23335473. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  98. ^ USA (2013-03-25). "Randomized controlled trial of interventio... [J Clin Psychiatry. 2012] - PubMed - NCBI". Ncbi.nlm.nih.gov. Retrieved 2013-04-23.
  99. ^ a b Burgy, M. (20 August 2008). "The Concept of Psychosis: Historical and Phenomenological Aspects" (PDF). Schizophrenia Bulletin. 34 (6): 1200–1210. doi:10.1093/schbul/sbm136. PMC 2632489. PMID 18174608.
  100. ^ Beer, M D (1995). "Psychosis: from mental disorder to disease concept". Hist Psychiatry. 6 (22(II)): 177–200. doi:10.1177/0957154X9500602204. PMID 11639691. {{cite journal}}: Cite has empty unknown parameter: |coauthors= (help)
  101. ^ "Psychosis, Henry George Liddell, Robert Scott, A Greek-English Lexicon, at Perseus". Perseus.tufts.edu. Retrieved 2011-06-11.
  102. ^ "Online Etymology Dictionary". Douglas Harper. 2001. Retrieved 2006-08-19. {{cite web}}: Cite has empty unknown parameter: |coauthors= (help)
  103. ^ Berrios G E (1987). "Historical Aspects of Psychoses: 19th Century Issues". British Medical Bulletin. 43 (3): 484–498. PMID 3322481.
  104. ^ Berrios G E, Beer D (1994). "The notion of Unitary Psychosis: a conceptual history". History of Psychiatry. 5 (17 Pt 1): 13–36. doi:10.1177/0957154X9400501702. PMID 11639278.
  105. ^ Murray, ED.; Cunningham MG, Price BH. (1). "The role of psychotic disorders in religious history considered". J Neuropsychiatry Clin Neuroscience 24 (4): 410–26. doi:10.1176/appi.neuropsych.11090214. PMID 23224447
  106. ^ a b c Page 188 in: Frank Pillmann; Andreas Marneros (2004). Acute and transient psychoses. Cambridge, UK: Cambridge University Press. ISBN 0-521-83518-6.{{cite book}}: CS1 maint: multiple names: authors list (link)

Further reading

  • Sims, A. (2002) Symptoms in the mind: An introduction to descriptive psychopathology (3rd edition). Edinburgh: Elsevier Science Ltd. ISBN 0-7020-2627-1

Personal accounts

  • Dick, P.K. (1981) VALIS. London: Gollancz. [Semi-autobiographical] ISBN 0-679-73446-5
  • Hinshaw, S.P. (2002) The Years of Silence are Past: My Father's Life with Bipolar Disorder. Cambridge: Cambridge University Press.
  • Jamison, K.R. (1995) An Unquiet Mind: A Memoir of Moods and Madness. London: Picador.
    ISBN 0-679-76330-9
  • Schreber, Daniel Paul (2000) Memoirs of My Nervous Illness. New York: New York Review of Books. ISBN 0-940322-20-X
  • McLean, R (2003) Recovered Not Cured: A Journey Through Schizophrenia. Allen & Unwin. Australia. ISBN 1-86508-974-5
  • The Eden Express by Mark Vonnegut
  • James Tilly Matthews
  • Saks, Elyn R. (2007) The Center Cannot Hold—My Journey Through Madness. New York: Hyperion. ISBN 978-1-4013-0138-5
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