The disease is an acute, usually self-limiting, functionally psychotic state, with a very diverse clinical picture that almost consistently is characterized by the existence of some degree of confusion or distressing perplexity, but above all, of the multifaceted and diverse expressions the disease takes. The main features of the disease is thus that the onset is acute, the multifaceted picture of symptoms and typically reverses to a normal state and that the long-term prognosis is good.
In addition, diagnostic criteria include at least four of the following symptoms: . Cycloid psychosis occurs in people of generally 15—50 years of age.
A very large number of medical conditions can cause psychosis, sometimes called secondary psychosis. Various psychoactive substances both legal and illegal have been implicated in causing, exacerbating, or precipitating psychotic states or disorders in users, with varying levels of evidence. This may be upon intoxication for a more prolonged period after use, or upon withdrawal. Approximately three 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.
The effects of an alcohol-related psychosis include an increased risk of depression and suicide as well as causing psychosocial impairments. According to some studies, the more often cannabis is used the more likely a person is to develop a psychotic illness,  with frequent use being correlated with twice the risk of psychosis and schizophrenia.
Cannabis use has increased dramatically over the past few decades whereas the rate of psychosis has not increased.
Together, these findings suggest that cannabis use may hasten the onset of psychosis in those who may already be predisposed to psychosis. 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 six 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. Administration, or sometimes withdrawal, of a large number of medications may provoke psychotic symptoms.
Meditation may induce psychological side effects, including depersonalization , derealization and psychotic symptoms like hallucinations as well as mood disturbances. The first brain image of an individual with psychosis was completed as far back as using a technique called pneumoencephalography  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.
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Both first episode psychosis, and high risk status is associated with reductions in grey matter volume. First episode psychotic and high risk populations are associated with similar but distinct abnormalities in GMV. Reductions in the right middle temporal gyrus , right superior temporal gyrus , right parahippocampus , right hippocampus , right middle frontal gyrus , and left anterior cingulate cortex are observed in high risk populations.
Reductions in first episode psychosis span a region from the right STG to the right insula, left insula, and cerebellum, and are more severe in the right ACC, right STG, insula and cerebellum. During attentional tasks, first episode psychosis is associated with hypoactivation in the right middle frontal gyrus, a region generally described as encompassing the dorsolateral prefrontal cortex dlPFC. In congruence with studies on grey matter volume, hypoactivity in the right insula, and right inferior parietal lobe is also reported. Decreased grey matter volume and hyperactivity is reported in the ventral ACC i.
Studies during acute experience of hallucinations demonstrate increased activity in primary or secondary sensory cortices. As auditory hallucinations are most common in psychosis, most robust evidence exists for increased activity in the left middle temporal gyrus , left superior temporal gyrus , and left inferior frontal gyrus i. Broca's area. Activity in the ventral striatum , hippocampus , and ACC are related to the lucidity of hallucinations, and indicate that activation or involvement of emotional circuitry are key to the impact of abnormal activity in sensory cortices.
Together, these findings indicate abnormal processing of internally generated sensory experiences, coupled with abnormal emotional processing, results in hallucinations. One proposed model involves a failure of feedforward networks from sensory cortices to the inferior frontal cortex, which normally cancel out sensory cortex activity during internally generated speech. The resulting disruption in expected and perceived speech is thought to produce lucid hallucinatory experiences. The two-factor model of delusions posits that dysfunction in both belief formation systems and belief evaluation systems are necessary for delusions.
Dysfunction in evaluations systems localized to the right lateral prefrontal cortex, regardless of delusion content, is supported by neuroimaging studies and is congruent with its role in conflict monitoring in healthy persons. Abnormal activation and reduced volume is seen in people with delusions, as well as in disorders associated with delusions such as frontotemporal dementia , psychosis and Lewy body dementia.
Furthermore, lesions to this region are associated with "jumping to conclusions", damage to this region is associated with post-stroke delusions, and hypometabolism this region associated with caudate strokes presenting with delusions. The aberrant salience model suggests that delusions are a result of people assigning excessive importance to irrelevant stimuli. In support of this hypothesis, regions normally associated with the salience network demonstrate reduced grey matter in people with delusions, and the neurotransmitter dopamine , which is widely implicated in salience processing, is also widely implicated in psychotic disorders.
Specific regions have been associated with specific types of delusions.
The volume of the hippocampus and parahippocampus is related to paranoid delusions in Alzheimer's disease , and has been reported to be abnormal post mortem in one person with delusions. Capgras delusions have been associated with occipito-temporal damage, and may be related to failure to elicit normal emotions or memories in response to faces.
Psychosis is associated with ventral striatal hypoactivity during reward anticipation and feedback. Hypoactivity in the left ventral striatum is correlated with the severity of negative symptoms. The impairment that may present itself as anhedonia probably actually lies in the inability to identify goals, and to identify and engage in the behaviors necessary to achieve goals.
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. NMDA receptor dysfunction has been proposed as a mechanism in psychosis.
The symptoms of dissociative intoxication are also considered to mirror the symptoms of schizophrenia, including negative psychotic symptoms.
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The connection between dopamine and psychosis is generally believed 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, 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.
A review found an association between a first-episode of psychosis and prediabetes. Prolonged or high dose use of psychostimulants can alter normal functioning, making it similar to the manic phase of bipolar disorder. Psychostimulants, especially in one already prone to psychotic thinking, can cause some "positive" symptoms, such as delusional beliefs, particularly those persecutory in nature.
To make a diagnosis of a mental illness in someone with psychosis other potential causes must be excluded.
Tests may be done to exclude substance use, medication, toxins, surgical complications, or other medical illnesses. A person with psychosis is referred to as psychotic. Delirium should be ruled out, which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness, indicating other underlying factors, including medical illnesses.
Because psychosis may be precipitated or exacerbated by common classes of medications, medication-induced psychosis should be ruled out , particularly for first-episode psychosis. Both substance- and medication-induced psychosis can be excluded to a high level of certainty, using toxicology screening.
Because some dietary supplements may also induce psychosis or mania, but cannot be ruled out with laboratory tests, a psychotic individual's family, partner, or friends should be asked whether the patient is currently taking any dietary supplements. Common mistakes made when diagnosing people who are psychotic include: . Only after relevant and known causes of psychosis are excluded, a mental health clinician may make a psychiatric differential diagnosis using a person's family history, incorporating information from the person with psychosis, and information from family, friends, or significant others.
Types of psychosis in psychiatric disorders may be established by formal rating scales. The Brief Psychiatric Rating Scale BPRS  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 answer questions on 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.
The DSM-5 characterizes disorders as psychotic or on the schizophrenia spectrum if they involve hallucinations, delusions, disorganized thinking, grossly disorganized motor behavior, or negative symptoms. The ICD has no specific definition of psychosis. Factor analysis of symptoms generally regarded as psychosis frequently yields a five factor solution, albeit five factors that are distinct from the five domains defined by the DSM-5 to encompass psychotic or schizophrenia spectrum disorders. The five factors are frequently labeled as hallucinations, delusions, disorganization, excitement, and emotional distress.
The evidence for the effectiveness of early interventions to prevent psychosis appeared inconclusive. 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,  which can reduce the positive symptoms of psychosis in about 7 to 14 days.