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Psychosis
ICD-10
ICD-9 290-299
OMIM {{{OMIM}}}
DiseasesDB {{{DiseasesDB}}}
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eMedicine {{{eMedicineSubj}}}/{{{eMedicineTopic}}}
MeSH {{{MeshNumber}}}

Psychosis is a generic psychiatric term for a mental state in which thought and perception are severely impaired. Persons experiencing a psychotic episode may experience hallucinations, hold delusional beliefs (e.g., grandiose or paranoid delusions), demonstrate personality changes and exhibit disorganized thinking (see thought disorder). This is often accompanied by lack of insight into the unusual or bizarre nature of such behavior, difficulties with social interaction and impairments in carrying out the activities of daily living. A psychotic episode is often described as involving a "loss of contact with reality".

Psychosis is sometimes divided into a number of subtypes:

Overview[]

Psychosis is considered by mainstream psychiatry to be a symptom of severe mental illness, but is not a diagnosis in itself. Although it is not exclusively linked to any particular psychological or physical state, it is particularly associated with schizophrenia, bipolar disorder (manic depression) and severe clinical depression and possible paranoia. There are also detectable physical pathologies that can induce a psychotic state, including brain injury or other neurological disorder, drug intoxication and withdrawal (especially alcohol, barbiturates, and sometimes benzodiazepines), lupus, electrolyte disorder in the elderly (such as urinary tract infections) and pain syndromes.

The term psychosis should be distinguished from the concept of insanity, which is a legal term denoting that a person should not be criminally responsible for his actions. Similarly, it should be distinguished from psychopathy, a personality disorder often associated with violence, lack of empathy and socially manipulative behavior. Despite the fact that both are colloquially abbreviated to "psycho", psychosis bears little similarity to psychopathy's core features, particularly with regard to violence, which rarely occurs in psychosis, and the distortion of perceived reality, which rarely occurs in psychopathy.

Psychosis should also be distinguished from the state of delirium, in that a psychotic individual may be able to perform actions that require a high level of intellectual effort in clear consciousness. Finally, it should be distinguished from mental illness. Psychosis may be regarded as a symptom of other mental illnesses, but as a descriptive concept it is not considered an illness in its own right. For example, persons with schizophrenia can have long periods without psychosis, and persons with bipolar disorder and depression can have mood symptoms without psychosis. Conversely, psychosis can occur in persons without chronic mental illness, as a result of an adverse drug reaction or extreme stress.

Psychotic states occurring after drug use may be particularly linked to drug overdose, chronic use and drug withdrawal. Certain compounds may be more likely to induce psychosis and some individuals may show greater sensitivity than others. Certain "street" drugs, such as cocaine, amphetamines, PCP and hallucinogens are particularly linked to the development of psychosis. Anticholinergic drugs (atropine, scopolamine, Jimson weed), and many antihistamines can also induce psychosis in some people.

Intoxication with drugs that have general depressant effects on the central nervous system (especially alcohol and barbiturates) tend not to cause psychosis during use, and can actually decrease or lessen the impact of symptoms in some people. Withdrawal from barbiturates and alcohol can be particularly dangerous, however, leading to psychosis or delirium and other, potentially lethal, withdrawal effects.

Psychological stress is also known to contribute to and trigger psychotic states. Both a history of traumatic incidents experienced throughout the life-span, and the recent experience of a stressful event, is thought to contribute to the development of psychosis. Short-lived psychosis triggered by stress is known as brief reactive psychosis.

Sleep deprivation has been linked to psychosis, although there is little evidence to suggest that it is a major risk factor in the majority of people. Some people experience hypnagogic or hypnopompic hallucinations, where unusual sensory experiences or thoughts appear during waking or drifting off to sleep. These are normal sleep phenomena, however, and are not considered signs of psychosis.

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. Thomas Szasz focused on the social implications of labelling people as psychotic; a label he argues unjustly medicalises different views of reality so such unorthodox people can be controlled by society.

Generally, however, advances in both diagnosis and the scientific study of psychosis have led to theories drawing on biology, cognitive psychology and neuropsychology being accepted as mainstream explanations. In the United States and Europe, few reputable practitioners since the 1990s have approached psychosis outside this scientific frame of reference.

Antipsychotic medication is usually the first line treatment for psychosis and can potentially minimize or eliminate the symptoms within a relatively rapid amount of time. Cognitive behavioral therapy is now recommended by many clinical standards organizations as an effective psychological treatment for psychosis.

Etymology: The word psychosis was first used by Ernst von Feuchtersleben in 1845 as an alternative to insanity and mania and stems from the Greek psyche (mind) and -osis (diseased or abnormal condition). The word was used to distinguish disorders which were thought to be disorders of the mind, as opposed to neurosis, which was thought to stem from a disorder of the nervous system.

Psychotic experience[]

A psychotic episode can be significantly colored by mood. For example, people experiencing a psychotic episode in the context of depression may experience persecutory or self-blaming delusions or hallucinations, while people experiencing a psychotic episode in the context of mania may form grandiose delusions or have an experience of deep religious significance.

Although usually distressing and regarded as an illness process, some people who experience psychosis find beneficial aspects and value the experience or revelations that stem from it.

Hallucinations[]

Hallucinations are defined as sensory perception in the absence of external stimuli. They are different from illusions, which are the misperception of external stimuli. 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, smells) to more meaningful experiences such as seeing and interacting with fully formed animals and people, hearing voices and complex tactile sensations.

Auditory hallucinations, particularly the experience 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, as outlined by the Hearing Voices Movement informed by the research of Prof. Marius Romme.

Delusions and paranoia[]

Psychosis may involve delusional or paranoid beliefs. Karl Jaspers classified psychotic delusions into primary and secondary types. Primary delusions are defined as arising out-of-the-blue 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.

Thought disorder[]

Formal thought disorder describes an underlying disturbance to conscious thought and is classified largely by its effects on speech and writing. Affected persons may show pressure of speech (speaking incessantly and quickly), derailment or flight of ideas (switching topic mid-sentence or inappropriately), thought blocking, and rhyming or punning.

Lack of insight[]

One important and puzzling feature of psychosis is usually an accompanying lack of insight into the unusual, strange or bizarre nature of the person's experience or behaviour. Even in the case of an acute psychosis, sufferers may seem completely unaware that their vivid hallucinations and impossible delusions are in any way unrealistic. This is not an absolute; however, insight can vary between individuals and throughout the duration of the psychotic episode.

In some cases, particularly with auditory and visual hallucinations, the patient has good insight and this makes the psychotic experience even more terrifying in that the patient realizes that he or she should not be hearing voices, but does.

Classification[]

In medical practice today, a descriptive approach to psychosis (and to all mental illness) is used, based on behavioral and clinical observations. This approach is adopted in the standard guide to psychiatric diagnoses employed in the United States, the Diagnostic and Statistical Manual of Mental Disorders (DSM). Since the DSM provides a widely-used standard of reference, the description presented here will largely reflect that point of view.

According to the DSM-IV-TR, the term psychosis has had many definitions in the past, both broad and narrow. The broadest was not being able to meet the demands of everyday life. The narrowest was delusions or hallucinations without insight. A middle ground may be delusions, hallucinations with or without insight, as well as disorganized behavior or speech. Thus, psychosis can be a symptom of mental illness, but it is not a mental illness in its own right. For example, people with schizophrenia often experience psychosis, but so can people with bipolar disorder (manic depression), unipolar depression, delirium, or drug withdrawal.[1][2] People diagnosed with these conditions can also have long periods without psychosis, and some may never experience them again. Conversely, psychosis can occur in people who do not have chronic mental illness (e.g. due to an adverse drug reaction or extreme stress).[3]

Psychosis should be distinguished from:

  • insanity, which is a legal term denoting that a person is not criminally responsible for his or her actions.[4] "Insanity is no longer considered a medical diagnosis..." [5]
  • psychopathy, a general term for a range of personality disorders characterized by lack of empathy, socially manipulative behavior, and occasionally criminality or violence.[6] Despite both being abbreviated to the slang word "psycho", psychosis bears little similarity to the core features of psychopathy, particularly with regard to violence, which rarely occurs in psychosis,[7][8] and distorted perception of reality, which rarely occurs in psychopathy.[9]
  • delirium: a psychotic individual may be able to perform actions that require a high level of intellectual effort in clear consciousness, whereas a delirious individual will have impaired memory and cognitive function.

The DSM-IV-TR lists 9 formal psychotic disorders, but many other disorders may have psychotic symptoms. The formal psychotic disorders are:

  1. Schizophrenia
  2. Schizoaffective disorder
  3. Schizophreniform disorder
  4. Brief psychotic disorder
  5. Delusional disorder
  6. Shared psychotic disorder (Folie à deux)
  7. Substance induced psychosis
  8. Psychosis due to a general medical condition
  9. Psychosis - Not otherwise specified

Medical understanding of psychosis[]

There are a number of possible causes for psychosis. Psychosis may be the result of an underlying mental illness such as bipolar disorder (also known as manic depression) or schizophrenia. Psychosis may also be triggered or exacerbated by severe mental stress and high doses or chronic use of drugs such as amphetamines, LSD, PCP, cocaine or scopolamine. However, incidence of psychosis resulting from a single administration of any drug is rare, although cases have been reported in the medical literature suggesting a person's sensitivities to new compounds can be unpredictable. Sudden withdrawal from CNS depressant drugs, such as alcohol and benzodiazepines, may also trigger psychotic episodes. As can be seen from the wide variety of illnesses and conditions in which psychosis has been reported to arise (including, for example, AIDS, leprosy, malaria and even mumps) there is no singular cause of a psychotic episode.

The division of the major psychoses into manic depressive insanity (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.

Psychotic episodes may vary in duration between individuals. In brief reactive psychosis, the psychotic episode is related directly to a specific stressful life event, so patients may spontaneously recover normal functioning within two weeks. 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.

Patients who are undergoing a brief psychotic episode may have many of the same symptoms as a person who is psychotic as a result of (for example) schizophrenia, and this fact has been used to support the notion that psychosis is primarily a breakdown in some specific biological system in the brain. The dopamine hypothesis of psychosis was an early, and still popular, example of a theory based on this assumption. However, it is controversial how much weight should be given to such exclusively biological theories as it has become clearer that a wide range of influences (including environmental, social and childhood development factors) may contribute to the final experience of psychosis.

It has also been argued that psychosis exists on a continuum as everybody may have some unusual and potentially reality-distorting experiences in their life. This has been backed up by research showing that experiences such as hallucinations have been experienced by large numbers of the population who may never be impaired or even distressed by their experiences10. In this view, people who are diagnosed with a psychotic illness may simply be one end of a spectrum where the experiences become particularly intense or distressing (see schizotypy).

Psychosis and brain function[]

The first brain image of a person with psychosis was completed as far back as 1935 using a technique called pneumoencephalography1 (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).

Modern brain imaging studies, investigating both changes in brain structure and changes in brain function of people undergoing psychotic episodes, have shown mixed results.

A 2003 study investigating structural changes in the brains of people with psychosis showed there was significant grey matter reduction in the cortex of people before and after they became psychotic2. Findings such as these have led to debate about whether psychosis is itself neurotoxic 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 case3 although further investigation is still ongoing.

Functional brain scans have revealed that the areas of the brain that react to sensory perceptions are active during psychosis. For example, a PET or fMRI scan of a person who claims to be hearing voices may show activation in the auditory cortex, or parts of the brain involved in the perception and understanding of speech.

On the other hand, there is not a clear enough psychological definition of belief to make a comparison between different people particularly valid. Brain imaging studies on delusions have typically relied on correlations of brain activation patterns with the presence of delusional beliefs.

One clear finding is that persons with a tendency to have psychotic experiences seem to show increased activation in the right hemisphere of the brain4. This increased level of right hemisphere activation has also been found in healthy people who have high levels of paranormal beliefs5 and in people who report mystical experiences6. It also seems to be the case that people who are more creative are also more likely to show a similar pattern of brain activation7. 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 whilst others lead to the impairment or distress of diagnosable mental pathology. However, people who have profoundly different experiences of reality or hold unusual views or opinions have traditionally held a complex role in society, with some being viewed as kooks, whilst others are lauded as prophets or visionaries.

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-blocking drugs (i.e. antipsychotics) tend to reduce the intensity of psychotic symptoms, and that drugs which boost dopamine activity (such as amphetamine and cocaine) can trigger psychosis in some people (see amphetamine psychosis).

The connection between dopamine and psychosis is generally believed to be complex. First of all, while antipsychotic drugs immediately block dopamine receptors, they usually 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 affecting serotonin function, suggesting the 'dopamine hypothesis' is vastly oversimplified.

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 psychosis8.

Some theories regard many psychotic symptoms to be a problem with the perception of ownership of internally generated thoughts and experiences9. For example, the experience of hearing voices may arise from internally generated speech that is mislabeled by the psychotic person as coming from an external source.

Cannabis and psychosis[]

There is now growing evidence for a small but significant link between cannabis use and vulnerability to psychosis11. Some studies indicate that cannabis use correlates with a slight increase in psychotic experience, which may trigger full-blown psychosis in some people. Early studies have been criticized for failing to consider other drugs (such as LSD) that the participants may also have used before or during the study, as well as other factors such as possible pre-existing mental health issues. However, more recent studies with better controls have still found a small increase in risk for psychosis in cannabis users. It is still not clear whether this is a causal link, and it may be that cannabis use only increases the chance of psychosis in people already predisposed to it. The fact that cannabis use has increased over the past few decades, whereas the reported rate of psychosis has not13, possibly suggests that a direct causal link is unlikely for all users.

Non-psychiatric conditions and psychosis[]

Psychosis can be a feature of several diseases, often when the brain or nervous system is directly affected. However, the fact that psychosis can occasionally arise in parallel with a number of ailments (including diseases such as flu or mumps for example) suggests that a variety of nervous system stressors can lead to a psychotic reaction. Psychosis arising from non-psychiatric conditions is sometimes known as 'secondary psychosis'. The mechanisms by which this happens are still not clear, but the non-specificity of psychosis has led Tsuang and colleagues to argue that "psychosis is the 'fever' of mental illness—a serious but nonspecific indicator"12.

There are some non-psychiatric conditions which are particularly linked to psychosis, which may include:

Pathophysiology[]

Brain imaging studies of psychosis, investigating both changes in brain structure and changes in brain function of people undergoing psychotic episodes, have shown mixed results.

The first brain image of an individual with psychosis was completed as far back as 1935 using a technique called pneumoencephalography[10] (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).

More recently, a 2003 study investigating structural changes in the brains of people with psychosis showed there was significant grey matter reduction in the cortex of people before and after they became psychotic.[11] Findings such as these have led to debate about whether psychosis is itself neurotoxic 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[12] although further investigation is still ongoing.

Functional brain scans have revealed that the areas of the brain that react to sensory perceptions are active during psychosis. For example, a PET or fMRI scan of a person who claims to be hearing voices may show activation in the auditory cortex, or parts of the brain involved in the perception and understanding of speech.[13]

On the other hand, there is not a clear enough psychological definition of belief to make a comparison between different people particularly valid. Brain imaging studies on delusions have typically relied on correlations of brain activation patterns with the presence of delusional beliefs.[14]

One clear finding is that persons with a tendency to have psychotic experiences seem to show increased activation in the right hemisphere of the brain.[15] This increased level of right hemisphere activation has also been found in healthy people who have high levels of paranormal beliefs[16] and in people who report mystical experiences.[17] 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.[18] 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 whilst others lead to the impairment or distress of diagnosable mental pathology. However, people who have profoundly different experiences of reality or hold unusual views or opinions have traditionally held a complex role in society, with some being viewed as kooks, whilst others are lauded as prophets or visionaries.

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-blocking drugs (i.e. antipsychotics) tend to reduce the intensity of psychotic symptoms, and that drugs which boost dopamine activity (such as amphetamine and cocaine) can trigger psychosis in some people (see amphetamine psychosis).[19] 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/detrorphan (at large overdoses) induce a psychotic state more readily than dopinergic stimulants, even at "normal" recreational doses. The symptoms of dissociative intoxication are also considered to mirror the symptoms of schizophrenia more closely, including negative psychotic symptoms 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. (See glutamate hypothesis of psychosis)

The connection between dopamine and psychosis is generally believed to be complex. While antipsychotic drugs immediately block dopamine receptors, they usually 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 affecting serotonin function, suggesting the 'dopamine hypothesis' may be oversimplified.[20] Soyka and colleagues found no evidence of dopaminergic dysfunction in people with alcohol-induced psychosis[21] 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.[22]

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.[23]

Some theories regard many psychotic symptoms to be a problem with the perception of ownership of internally generated thoughts and experiences.[24] For example, the experience of hearing voices may arise from internally generated speech that is mislabeled by the psychotic person as coming from an external source.


Treatment[]

The treatment of psychosis depends on the cause or diagnosis or diagnoses (such as schizophrenia, bipolar disorder and/ or substance intoxication). The first line treatment for many psychotic disorders is antipsychotic medication (oral or intramuscular injection), and sometimes hospitalisation is needed. There is growing evidence that cognitive behavior therapy[25] and family therapy[26] can be effective in managing psychotic symptoms. When other treatments for psychosis are ineffective, electroconvulsive therapy (ECT) (aka shock treatment) is sometimes utilized 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.[27]

See also[]

Further reading[]

Books[]

  • Chadwick,P; Birchwood,M; Trower,P. (1996) Cognitive Therapy for Delusions, Voices and Paranoia. John Wiley and Sons
  • Coleman, R., Smith, M. and Good, J. (2003). Psychiatric First Aid in Psychosis: A Handbook for Nurses, Carers and People Distressed by Psychotic Experience (2nd Edition). Fife: P&P Press Ltd.
  • Fowler, D; Garety, P; Kuipers. E.. (1995) Cognitive Behavioural Therapy for Psychosis. Wiley and Sons,West Sussex
  • Haddock, G; Slade, P. D. (1996) Cognitive-Behavioural Interventions with Psychotic Disorders. Routledge, London
  • Morrison, AP (2002)(Ed.) A Casebook of Cognitive Therapy for Psychosis. Brunner-Routledge, Hove, UK:. ISBN 1-58391-205-3
  • Morrison, A.P., Renton, J.C., French, P. & Bentall, R.P.(2009) Think you are crazy? Think again: Aresource book for cognitive therapy for psychosis.
  • Firestone, R. W., & Catlett, J. (1986). Psychosis. New York, NY: Human Sciences Press.
  • Sims, A. (2002) Symptoms in the mind: An introduction to descriptive psychopathology (3rd edition). Edinburgh: Elsevier Science Ltd. ISBN 0702026271

Schafer, I. and Dorahy, M.J. (2008). Psychosis, Trauma and Dissociation: Emerging Perspectives on Severe Psychopathology. Oxford: Wiley-Blackwell.

Personal accounts[]

References[]

1Moore, MT, Nathan, D, Elliot, AR & Laubach, C. (1935) Encephalographic studies in mental disease. American Journal of Psychiatry, 92 (1), 43-67.
2Pantelis C, Velakoulis D, McGorry PD, Wood SJ, Suckling J, Phillips LJ, Yung AR, Bullmore ET, Brewer W, Soulsby B, Desmond P, McGuire PK. (2003) Neuroanatomical abnormalities before and after onset of psychosis: a cross-sectional and longitudinal MRI comparison. Lancet, 25, 361 (9354), 281-8.
3Ho, B. C., Alicata, D., Ward, J., Moser, D. J., O'Leary, D. S., Arndt, S., et al. (2003) Untreated initial psychosis: relation to cognitive deficits and brain morphology in first-episode schizophrenia. American Journal of Psychiatry, 160(1), 142-148.
4Lohr JB, Caligiuri MP (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.
5Pizzagalli, D., Lehmann, D., Gianotti, L., Koenig, T., Tanaka, H., Wackermann, J., et al. (2000) Brain electric correlates of strong belief in paranormal phenomena: intracerebral EEG source and regional Omega complexity analyses. Psychiatry Research, 100(3), 139-154.
6Makarec, K., & Persinger, M. A. (1985) Temporal lobe signs: electroencephalographic validity and enhanced scores in special populations. Perceptual and Motor Skills, 60(3), 831-842.
7Weinstein, S., & Graves, R. E. (2002) Are creativity and schizotypy products of a right hemisphere bias? Brain and Cognition, 49(1), 138-151.
8Healy, D. (2002) The Creation of Psychopharmacology. Cambridge, MA: Harvard University Press. ISBN 0674006194
9Blakemore SJ, Smith J, Steel R, Johnstone CE, Frith CD. (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.
10Johns LC, van Os J. (2001) The continuity of psychotic experiences in the general population. Clinical Psychology Review, 21 (8), 1125-41.
11Degenhardt, L. (2003) Editorial: The link between cannabis use and psychosis: furthering the debate. Psychological Medicine, 33, 3-6.
12Tsuang, M. T., Stone, W. S., & Faraone, S. V. (2000) Toward reformulating the diagnosis of schizophrenia. American Journal of Psychiatry, 157(7), 1041-1050.
13Degenhardt, L., Hall, W., & Lynskey, M. (2001) Comorbidity between cannabis use and psychosis: Modelling some possible relationships. NDARC Technical Report No. 121. Sydney: National Drug and Alcohol Research Centre. pdf.

External links[]

  • BPS Report - Recent Advances in Understanding Mental Illness and Psychotic Experiences
This page uses Creative Commons Licensed content from Wikipedia (view authors).
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  2. Tsuang, Ming T., William S. Stone, Stephen V. Faraone (July 2000). Toward Reformulating the Diagnosis of Schizophrenia. American Journal of Psychiatry 157 (7): 1041–1050.
  3. Jauch, D. A., William T. Carpenter, Jr. (February 1988). Reactive psychosis. I. Does the pre-DSM-III concept define a third psychosis?. Journal of Nervous and Mental Disease 176 (2): 72–81.
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  8. Foley, Sharon R., Brendan D. Kelly, Mary Clarke, Orfhlaith McTigue, Maurice Gervin, Moyyad Kamali, Conall Larkin, Eadbhard O'Callaghan, and Stephen Browne (January 1, 2005). Incidence and clinical correlates of aggression and violence at presentation in patients with first episode psychosis. Schizophrenia Research 72 (2-3): 161–168.
  9. Nestor, Paul G., Matthew Kimble, Ileana Berman, and Joel Haycock (January 2002). Psychosis, Psychopathy, and Homicide: A Preliminary Neuropsychological Inquiry. American Journal of Psychiatry 159 (1): 138–140.
  10. Moore, M T, Nathan D, Elliot AR, Laubach C (1935). Encephalographic studies in mental disease. American Journal of Psychiatry 92 (1): 43–67.
  11. Pantelis, C, Velakoulis D, McGorry PD, Wood SJ, Suckling J, Phillips, LJ, Yung AR, Bullmore ET, Brewer W, Soulsby B, Desmond, P, McGuire PK (2003). Neuroanatomical abnormalities before and after onset of psychosis: a cross-sectional and longitudinal MRI comparison. Lancet 25 (361 (9354)): 281–8.
  12. Ho, BC, Alicata D, Ward J, Moser DJ, O'Leary DS, Arndt S, Andreasen NC (2003). Untreated initial psychosis: relation to cognitive deficits and brain morphology in first-episode schizophrenia. American Journal of Psychiatry 160 (1): 142–148.
  13. Copolov DL, Seal ML, Maruff P, Ulusoy R, Wong MT, Tochon-Danguy HJ, Egan GF. (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. PMID 12694889.
  14. Bell, V., Halligan, P.W. & Ellis, H.D. (2006) A Cognitive Neuroscience of Belief. In P.W. Halligan & M. Aylward (eds) The Power of Belief. Oxford: Oxford University Press.
  15. Lohr, JB, Caligiuri MP (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.
  16. Pizaagalli, D, Lehmann D, Gianotti L, Koenig T, Tanaka H, Wackermann J, Brugger P. (2000). Brain electric correlates of strong belief in paranormal phenomena: intracerebral EEG source and regional Omega complexity analyses. Psychiatry Research 100 (3): 139–154.
  17. Makarec, K, Persinger, MA (1985). Temporal lobe signs: electroencephalographic validity and enhanced scores in special populations. Perceptual and Motor Skills 60 (3): 831–842.
  18. Weinstein, S, Graves RE (2002). Are creativity and schizotypy products of a right hemisphere bias?. Brain and Cognition 49 (1): 138–151.
  19. 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. PMID 16005191
  20. Jones, H. M., & Pilowsky, L. S. (2002) Dopamine and antipsychotic drug action revisited. British Journal of Psychiatry, 181, 271-275. PMID 12356650
  21. Soyka, Michael, Thomas Zetzsche, Stefan Dresel, and Klaus Tatsch (May 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.
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