Psychosis is not well-understood at theneurological level, butdopamine (along with otherneurotransmitters) is known to play an important role.[13][14][15] In the United States about 3% of people develop psychosis at some point in their lives.[1] Psychosis has been described as early as the 4th century BC byHippocrates and possibly as early as 1500 BC in theEbers Papyrus.[16][17]
Ahallucination is defined as a sensory perception in the absence of external stimuli.[18] Hallucinations are different fromillusions and perceptual distortions, which are the misperception of external stimuli.[19][20] Hallucinations may occur in any of the senses and take on almost any form. They may consist of simple sensations (such as lights, colors, sounds, tastes, or smells) or more detailed experiences (such as seeing and interacting with animals and people,hearing voices, and having complex tactile sensations). Hallucinations are generally characterized as being vivid and uncontrollable.[18][21]Auditory hallucinations, particularly experiences of hearing voices, are the most common and often prominent feature of psychosis.
Up to 15% of the general population may experience auditory hallucinations (though not all are due to psychosis).[22] The prevalence of auditory hallucinations in patients with schizophrenia is generally put around 70%.[23] Reported prevalence in bipolar disorder ranges between 11% and 68%.[24] During the early 20th century, auditory hallucinations were second tovisual hallucinations in frequency, but they are now the most common manifestation of schizophrenia, although rates vary between cultures and regions. Auditory hallucinations are most commonly intelligible voices. When voices are present, the average number has been estimated at three. Content, like frequency, differs significantly, especially across cultures and demographics. People who experience auditory hallucinations can frequently identify the loudness, location of origin, and may settle on identities for voices. Western cultures are associated with auditory experiences concerning religious content, frequently related to sin. Hallucinations may command a person to do something potentially dangerous when combined with delusions.[25]
So-called "minor hallucinations", such as extracampine hallucinations, or false perceptions of people or movement occurring outside of one's visual field, frequently occur in neurocognitive disorders, such as Parkinson's disease.[26]
Visual hallucinations occur in roughly a third of people with schizophrenia, although certain studies show rates higher than 60%, suggesting that the prevelance of visual hallucinatinations may be higher in certain samples than traditionally thought.[27] The reported prevalence in bipolar disorder is around 15%.[28] Content commonly involves animate objects, although perceptual abnormalities such as changes in lighting, shading, streaks, or lines may be seen. Visual abnormalities may conflict withproprioceptive information, and visions may include experiences such as the ground tilting.Lilliputian hallucinations are less common in schizophrenia, and are more common in various types ofencephalopathy, such aspeduncular hallucinosis.[25][29]
A visceral hallucination, also called a cenesthetic hallucination, is characterized by visceral sensations in the absence of stimuli. Cenesthetic hallucinations may include sensations of burning, or re-arrangement of internal organs.[25]
Adelusion is a fixed, false,idiosyncratic belief, which does not change even when presented with incontrovertible evidence to the contrary.[30][31][32] Delusions are context- and culture-dependent: a belief that inhibits critical functioning and is widely considered delusional in one population may be common (and even adaptive) in another, or in the same population at a later time.[32][33] Sincenormative views may contradict available evidence, a belief need not contravene cultural standards in order to be considered delusional. However, theDSM-5 considers a belief delusional only if it is not widely accepted within a cultural or subcultural context.[34]
Prevalence in schizophrenia is generally considered at least 90%, and around 50% in bipolar disorder.[citation needed]
The DSM-5 characterizes certain delusions as "bizarre" if they are clearly implausible, or are incompatible with the surrounding cultural context.[31] The concept of bizarre delusions has many criticisms, the most prominent being that judging their presence is not highly reliable even among trained individuals.[25]
A delusion may involve diverse thematic content. The most common type is apersecutory delusion, in which a person believes that an entity seeks to harm them.[31][32] Others includedelusions of reference (the belief that some element of one's experience represents a deliberate and specific act by or message from some other entity),delusions of grandeur (the belief that one possesses special power or influence beyond one's actual limits),thought broadcasting (the belief that one's thoughts are audible) andthought insertion (the belief that one's thoughts are not one's own).[32] A delusion may also involvemisidentification of objects, persons, or environs that the afflicted should reasonably be able to recognize; such examples includeCotard's syndrome (the belief that oneself is partly or whollydead) andclinical lycanthropy (the belief that oneself is or has transformed into an animal).[citation needed]
The subject matter of delusions seems to reflect the current culture in a particular time and location. For example, in the early 1900s in the United States,syphilis was a common theme in delusions. During the Second World War, it was Germany. In theCold War era, communists became a frequent focus. Now, in recent years, technology is a common subject matter of delusions.[35] Some psychologists, such as those who practice theOpen Dialogue method, believe that the content of psychosis represents an underlying thought process, that may in part, be responsible for psychosis,[36] though the accepted medical position is that psychosis is due to a brain disorder.[37]
Historically,Karl Jaspers classified psychotic delusions intoprimary andsecondary types. Primary delusions are defined as arising suddenly and not being comprehensible in terms of normal mental processes, whereas secondary delusions are typically understood as being influenced by the person's background or current situation (e.g., ethnicity, religious, superstitious, or political beliefs).[38]
Disorganized speech/thought and disorganized behavior
Disorganization is categorized into either disorganized speech (disorganized speech stemming from disorganized thought), and grossly disorganized motor behavior. Disorganized speech or thought, also formally calledthought disorder, is disorganization of thinking that isinferred from speech. Characteristics of disorganized speech include rapidly switching topics which is calledderailment or looseassociation, switching to topics that are unrelated which is calledtangential thinking, incomprehensible speech which is called incoherence and referred to as aword salad. Disorganized motor behavior includes repetitive, odd, or sometimes purposeless movement. Disorganized motor behavior rarely includescatatonia, and although it was a prominent symptom historically, it is rarely seen today. Whether this may be due to the use of historical treatments or the lack thereof is unknown.[25][21]
Catatonia describes a profoundly agitated state in which the experience of reality is generally considered 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 withwaxy 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 staying there).[39]
The other type of catatonia is more of an outward presentation of the profoundly agitated state described above. It involves excessive and purposeless motor behaviour, as well as an extreme mental preoccupation that prevents an intact experience of reality. An example is 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.[citation needed]
Psychosis is relatively rare in adolescents but not uncommon.[42] Young people who have psychosis may have trouble connecting with the world around them and may experience hallucinations or delusions.[43] Adolescents with psychosis may also have cognitive deficits that may make it harder for the youth to socialize and work.[43] Potential impairments include a reduced speed of mental processing, the lack of ability to focus without getting distracted (limitedattention span), and deficits inverbal memory.[43] If an adolescent is experiencing psychosis, they most likely have comorbidity, meaning that they could have multiple mental illnesses.[44] Because of this, it may be difficult to determine whether it is psychosis orautism,social orgeneralized anxiety disorder, orobsessive-compulsive disorder.[44]
Traumatic life events have been linked with an elevated risk of developing psychotic symptoms.[59]Childhood trauma has specifically been shown to be a predictor of adolescent and adult psychosis.[60] Individuals with psychotic symptoms are three times more likely to have experienced childhood trauma (e.g.,physical orsexual abuse, physical or emotionalneglect) than those in the general population.[60] Increased individual vulnerability toward psychosis may interact with traumatic experiences promoting an onset of future psychotic symptoms, particularly during sensitive developmental periods.[60] Importantly, the relationship between traumatic life events and psychotic symptoms appears to be dose-dependent in which multiple traumatic life events accumulate, compounding symptom expression and severity.[59][60] However, acute, stressful events can also trigger brief psychotic episodes.[61] Trauma prevention and early intervention may be an important target for decreasing the incidence of psychotic disorders and ameliorating its effects.[59] A healthy person could become psychotic when inside an empty room with no light and sound. After about 15 minutes, psychosis can occur, this is a phenomenon known assensory deprivation.[8]
Neuroticism, a personality trait associated with vulnerability to stressors, is an independent predictor of the development of psychosis.[62]
Traditionally psychotic disorders have been believed to have one of two roots: organic (physiological) or functional (mental). Organic disorders being those caused by physical conditions directly affecting the brain with psychosis as a secondary feature, and functional disorders being primary psychological or psychiatric disorders (disorders of the functioning of the mind) in the absence of physiological causes. Subtle physical abnormalities have been found in illnesses traditionally considered functional, such asschizophrenia. TheDSM-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:[63][64][45]
Cycloid psychosis is typically an acute, self-limiting form of psychosis with psychotic and mood symptoms that progress from normal to full-blown, usually between a few hours to days, and not related to drug intake orbrain injury.[65] While proposed as a distinct entity, clinically separate from schizophrenia and affective disorders, cycloid psychosis is not formally acknowledged by current ICD or DSM criteria.[65] Its unclear place in psychiatric nosology has likely contributed to the limited scientific investigation and literature on the topic.
Postpartum psychosis is a rare yet serious and debilitating form of psychosis.[66] Symptoms range from fluctuating moods and insomnia to mood-incongruent delusions related to the individual or the infant.[66] Women experiencing postpartum psychosis are at increased risk for suicide or infanticide. Many women who experience first-time psychosis from postpartum often have bipolar disorder, meaning they could experience an increase of psychotic episodes even after postpartum.[66]
Variouspsychoactive substances (both legal and illegal) have been implicated in causing, exacerbating, or precipitating psychotic states or disorders in users, with varying levels of evidence.[76] This may be upon intoxication for a more prolonged period after use, or uponwithdrawal.[45] Individuals who experience substance-induced psychosis tend to have a greater awareness of their psychosis and tend to have higher levels ofsuicidal thinking compared to those who have a primary psychotic illness.[77] Drugs commonly alleged to induce psychotic symptoms includealcohol,cannabis,cocaine,amphetamines,cathinones,psychedelic drugs (such asLSD andpsilocybin),κ-opioid receptoragonists (such asenadoline andsalvinorin A) andNMDA receptor antagonists (such asphencyclidine andketamine).[45][78]Caffeine may worsen symptoms in those with schizophrenia and cause psychosis at very high doses in people without the condition.[79][80] Cannabis and other illicit recreational drugs are often associated with psychosis in adolescents and cannabis use before 15 years old may increase the risk of psychosis in adulthood.[43]
Approximately 3% of people withalcoholism experience psychosis during acute intoxication or withdrawal. Alcohol related psychosis may manifest itself through akindling mechanism. The mechanism of alcohol-related psychosis is due to thelong-term effects of alcohol consumption resulting in distortions to neuronal membranes,gene expression, as well asthiamine deficiency. It is possible that hazardous alcohol use 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.[81]Delirium tremens, a symptom of chronic alcoholism that can appear in the acute withdrawal phase, shares many symptoms with alcohol-related psychosis suggesting a common mechanism.[82]
According to current studies, cannabis use is associated with increased risk of psychotic disorders, and the more often cannabis is used the more likely a person is to develop a psychotic illness.[83] Furthermore, people with a history of cannabis use develop psychotic symptoms earlier than those who have never used cannabis.[83] Some debate exists regarding the causal relationship between cannabis use and psychosis with some studies suggesting that cannabis use hastens the onset of psychosis primarily in those with pre-existing vulnerability.[83][84][85] Indeed, cannabis use plays an important role in the development of psychosis in vulnerable individuals, and cannabis use in adolescence should be discouraged.[86] Some studies indicate that the effects of two active compounds in cannabis,tetrahydrocannabinol (THC) andcannabidiol (CBD), have opposite effects with respect to psychosis. While THC can induce psychotic symptoms in healthy individuals, limited evidence suggests that CBD may have antipsychotic effects.[87]
Methamphetamine induces a psychosis in 26%–46% 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 stressful event such as severe insomnia or a period of hazardous alcohol use despite not relapsing back to methamphetamine.[88] Individuals who have a long history of methamphetamine use and who have experienced psychosis in the past from methamphetamine use are highly likely to re-experience methamphetamine psychosis if drug use is recommenced.[citation needed] Methamphetamine-induced psychosis is likely gated by genetic vulnerability, which can produce long-term changes in brain neurochemistry following repetitive use.[89] Methamphetamine users with more ADHD-related behaviours in childhood experience methamphetamine-related psychosis more frequently.[90]
A 2024 meta-analysis found an incidence of psychedelic-induced psychosis at 0.002% in population studies, 0.2% in uncontrolled clinical trials, and 0.6% in randomised controlled trials.[91] This meta-analysis found that in uncontrolled clinical trials involving only patients with schizophrenia, 3.8% developed prolonged psychotic reactions. A 2024 study found thatpsychedelic use was not generally associated with a change in the number of psychotic symptoms.[92] This study found that psychedelic use interacted with a family history of bipolar disorder, such that in those with a family history of bipolar disorder, psychedelic use was associated with an increase in the number of psychotic symptoms, while in those with a personal history of psychosis but no family history of psychotic disorders, psychedelic use was associated with a decrease in the number of psychotic symptoms. A 2023 study found an interaction between lifetime psychedelic use and family history of psychosis or bipolar disorder on psychotic symptoms over the past two weeks. Psychotic symptoms were highest among those with both a family history of psychosis or bipolar disorder and life-time psychedelic use, while they were lowest among those with life-time psychedelic use but no family history of these disorders.[93]
Administration, or sometimes withdrawal, of a large number of medications may provoke psychotic symptoms.[45] Drugs that can induce psychosis experimentally or in a significant proportion of people include:
The first brain image of an individual with psychosis was completed as far back as 1935 using a technique calledpneumoencephalography[97] (a painful and now obsolete procedure wherecerebrospinal fluid is drained from around the brain and replaced with air to allow the structure of the brain to show up more clearly on anX-ray picture).
Bothfirst episode psychosis, and high risk status is associated with reductions in grey matter volume (GMV). First episode psychotic and high risk populations are associated with similar but distinct abnormalities in GMV. Reductions in the rightmiddle temporal gyrus, rightsuperior temporal gyrus (STG), rightparahippocampus, righthippocampus, rightmiddle frontal gyrus, and leftanterior cingulate cortex (ACC) 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.[98][99]
Another meta analysis reported bilateral reductions in insula, operculum, STG, medial frontal cortex, and ACC, but also reported increased GMV in the rightlingual gyrus and leftprecentral gyrus.[100] TheKraepelinian dichotomy is made questionable[clarification needed] by grey matter abnormalities in bipolar and schizophrenia; schizophrenia is distinguishable from bipolar in that regions of grey matter reduction are generally larger in magnitude, although adjusting for gender differences reduces the difference to the leftdorsomedial prefrontal cortex, and rightdorsolateral prefrontal cortex.[101]
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).Altered Behavioral Inhibition System functioning could possibly cause reduced sustained attention in psychosis and overall contribute to more negative reactions.[102] In congruence with studies on grey matter volume, hypoactivity in the right insula, and right inferior parietal lobe is also reported.[103] During cognitive tasks, hypoactivities in the right insula, dACC, and the left precuneus, as well as reduced deactivations in the rightbasal ganglia, rightthalamus, rightinferior frontal and left precentral gyri are observed. These results are highly consistent and replicable possibly except the abnormalities of the right inferior frontal gyrus.[104] Decreased grey matter volume in conjunction with bilateral hypoactivity is observed in anterior insula, dorsal medial frontal cortex, and dorsal ACC. Decreased grey matter volume and bilateral hyperactivity is reported in posterior insula, ventral medial frontal cortex, and ventral ACC.[105]
Studies during acute experiences 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 leftmiddle temporal gyrus, leftsuperior temporal gyrus, and leftinferior frontal gyrus (i.e.Broca's area). Activity in theventral striatum,hippocampus,[106] 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.[107]
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 asfrontotemporal dementia, psychosis andLewy 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.
Theaberrant 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 thesalience network demonstrate reduced grey matter in people with delusions, and the neurotransmitterdopamine, 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 inAlzheimer'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.[108]
Psychosis is associated with theventral striatum (VS), which is the part of the brain that is involved with the desire to naturally satisfy the body's needs.[109] When high reports ofnegative symptoms were recorded, there were significant irregularities in the left VS. Anhedonia, defined as the inability to feel joy or pleasure,[110] is a commonly reported symptom in psychosis; experiences with the condition are present in most people with schizophrenia.[111] Previous research has indicated that a deficiency in theneural representation in regards to goals and the motivation to achieve them, has demonstrated that when a reward is not present, a strong reaction is noted in the ventral striatum; reinforcement learning is intact when contingencies about stimulus-reward are implicit, but not when they require explicit neural processing; reward prediction errors are what the actual reward is versus what the reward was predicted to be.[112] In most cases positive prediction errors are considered an abnormal occurrence. A positive prediction error response occurs when there is an increased activation in a brain region, typically thestriatum, in response to unexpected rewards. A negative prediction error response occurs when there is a decreased activation in a region when predicted rewards do not occur.Anterior Cingulate Cortex (ACC) response, taken as an indicator of effort allocation, does not increase with reward or reward probability increase, and is associated with negative symptoms; deficits inDorsolateral Prefrontal Cortex (dlPFC) activity and failure to improve performance on cognitive tasks when offered monetary incentives are present; and dopamine mediated functions are abnormal.
Psychosis has been traditionally linked to the overactivity of theneurotransmitterdopamine, in particular to its effect in themesolimbic pathway, spanning from theventral tegmental area to the ventralstriatum. Additionally, recent evidence suggests a crucial involvement of the pathway spanning from thesubstantia nigra to the dorsalstriatum.[113] The two major sources of evidence given to support this theory are thatdopamine receptor D2 blocking drugs (i.e.,antipsychotics) tend to reduce the intensity of psychotic symptoms, and that drugs that accentuate dopamine release, or inhibit its reuptake (such asamphetamines andcocaine) can trigger psychosis in some people (seestimulant psychosis).[114] However, there is substantial evidence that dopaminergic overactivity does not fully explain psychosis, and that neurodegerative pathophysiology plays a significant role. This is evidenced by the fact that psychosis commonly occurs in neurodegenerative diseases of the dopaminergic nervous system, such as Parkinson's disease, which involved reduced, rather than increased, dopaminergic activity.[115]
Theendocannabinoid system is also implicated in psychosis. This is evidenced by the propensity ofCB1 receptor agonists such asTHC to induce psychotic symptoms,[116] and the efficacy ofCB1 receptor antagonists such asCBD in ameliorating psychosis.[117]
NMDA receptor dysfunction has been proposed as a mechanism in psychosis.[118] This theory is reinforced by the fact thatdissociativeNMDA receptor antagonists such asketamine,PCP anddextromethorphan (at large overdoses) induce a psychotic state. The symptoms of dissociativeintoxication are also considered to mirror the symptoms of schizophrenia, includingnegative symptoms.[119] NMDA receptor antagonism, in addition to producing symptoms reminiscent of psychosis, mimics the neurophysiological aspects, such as reduction in the amplitude ofP50,P300, andMMNevoked potentials.[120] Hierarchical Bayesian neurocomputational models of sensory feedback, in agreement with neuroimaging literature, link NMDA receptor hypofunction to delusional or hallucinatory symptoms via proposing a failure of NMDA mediated top down predictions to adequately cancel out enhanced bottom up AMPA mediated predictions errors.[121] Excessive prediction errors in response to stimuli that would normally not produce such a response is thought to root from conferring excessive salience to otherwise mundane events.[122] Dysfunction higher up in the hierarchy, where representation is more abstract, could result in delusions.[123] The common finding of reducedGAD67 expression in psychotic disorders may explain enhanced AMPA mediated signaling, caused by reduced GABAergic inhibition.[124][125]
The connection between dopamine and psychosis is generally believed to be complex. While dopamine receptor D2 suppressesadenylate cyclase activity, theD1 receptor increases it. If D2-blocking drugs are administered, the blocked dopamine spills over to the D1 receptors. The increased adenylate cyclase activity affectsgenetic 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.[126] Soyka and colleagues found no evidence of dopaminergic dysfunction in people with alcohol-induced psychosis[127] and Zoldan et al. reported moderately successful use ofondansetron, a 5-HT3 receptor antagonist, in the treatment oflevodopa psychosis inParkinson's disease patients.[128]
A review found an association between a first-episode of psychosis and prediabetes.[129]
Prolonged or high dose use ofpsychostimulants can alter normal functioning, making it similar to the manic phase of bipolar disorder.[130] NMDA antagonists replicate some of the so-called "negative" symptoms likethought disorder in subanesthetic doses (doses insufficient to induceanesthesia), andcatatonia 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.
Cross-cultural studies into schizophrenia have found that individual experiences of psychosis and 'hearing voices' vary across cultures.[131][132] In countries such as theUnited States where there exists a predominantly biomedical understanding of the body, the mind and in turn, mental health, subjects were found to report their hallucinations as having 'violent content' and self-describing as 'crazy'.[131] This experience is at odds with the experiences of subjects inAccra, Ghana, who describe the voices they hear as having 'spiritual meaning' and are often reported as positive in nature; or subjects inChennai, India, who describe their hallucinations as kin, family members or close friends, and offering guidance.[131]
These differences are attributed to 'social kindling' or how one's social context shapes the way they interpret and experience sensations such as hallucinations. This concept aligns with preexisting cognitive theory such as reality modelling and is supported by recent research that demonstrates that individuals with psychosis can be taught to attend to their hallucinations differently, which in turn alters the hallucinations themselves.[133] Such research creates pathways for social or community-based treatment, such as reality monitoring, for individuals with schizophrenia and other psychotic disorders, providing alternatives to, or supplementing traditional pharmacologic management.
Cross-cultural studies explore the way in which psychosis varies in different cultures, countries and religions. The cultural differences are based on the individual or shared illness narratives surrounding cultural meanings of illness experience.[134] In countries such asIndia,Cambodia andMuslim majority countries, they each share alternative epistemologies. These are known as knowledge systems that focus on the connections between mind, body, culture, nature and society.[135] Cultural perceptions of mental disorders such as psychosis or schizophrenia are believed to be caused byjinn (spirits) in Muslim majority countries.[136] Furthermore, those inArab-Muslim societies perceive those who act differently than the social norm as "crazy" or as abnormal behaviour.[136] This differs from the experiences of individuals in India and how they attain their perspectives on mental health issues through a variety of spiritual and healing traditions.[137] In Cambodia, hallucinations are linked with spirit visitation, a term they call "cultural kindling".[138] These examples of differences are attributed to culture and the way it shapes conceptions of mental disorders.[136] These cultural differences can be useful in bridging the gap of cultural understanding and psychiatric signs and symptoms.[134]
To make a diagnosis of a mental illness in someone with psychosisother potential causes must be excluded.[139] An initial assessment includes a comprehensive history and physical examination by a health care provider. 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.[140] Excluding medical illnesses associated with psychosis is performed by using blood tests to measure:
MRI orCT scan of the head to exclude brain lesions.
Because psychosis may be precipitated or exacerbated by common classes of medications, medication-induced psychosis should beruled out, particularly for first-episode psychosis. Both substance- and medication-induced psychosis can beexcluded to a high level of certainty, using toxicology screening.
Because somedietary 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.[141]
Common mistakes made when diagnosing people who are psychotic include:[139]
Not appreciating medical abnormalities (e.g., vital signs),
Not obtaining a medical history and family history,
Indiscriminate screening without an organizing framework,
Missing a toxic psychosis by not screening for substancesand medications,
Not asking their families or others about dietary supplements,
Premature diagnostic closure, and
Not revisiting or questioning the initial diagnostic impression of primary psychiatric disorder.
Only after relevant and known causes of psychosis are excluded, a mental health clinician may make a psychiatricdifferential diagnosis using a person's family history, incorporating information from the person with psychosis, and information from family, friends or romantic partners.
Types of psychosis in psychiatric disorders may be established by formal rating scales. TheBrief Psychiatric Rating Scale (BPRS)[142] assesses the level of 18 symptom constructs of psychosis such ashostility,suspicion,hallucination, andgrandiosity. 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).[143]
TheDSM-5 characterizes disorders as psychotic or on the schizophrenia spectrum if they involve hallucinations, delusions, disorganized thinking, grossly disorganized motor behavior, or negative symptoms.[21] The DSM-5 does not include psychosis as a definition in the glossary, although it defines "psychotic features", as well as "psychoticism" with respect to personality disorder. TheICD-10 has no specific definition of psychosis.[144]
The PSQ (Psychosis Screening Questionnaire) is the most common tool in detecting psychotic symptoms and it includes five root questions that assess the presence of PLE (mania, thought insertion, paranoia, strange experiences and perceptual disturbances)[145] The different tools used to assess symptom severity include the Revised Behavior and Symptom Identification Scale (BASIS-R), a 24-item self-report instrument with six scales: psychosis, depression/functioning, interpersonal problems, alcohol/drug use, self-harm, and emotional lability. The Symptom Checklist-90-Revised (SCL-90-R), a 90-item self assessment tool that measures psychoticism and paranoid ideation in addition to seven other symptom scales. Finally, the Brief Symptom Inventory (BSI), a 53-item self-administered scale developed from the SCL-90-R. The BSI has good psychometric properties and is an acceptable brief alternative to the SCL-90-R.[146] These seem to be the most accurate tools at the moment,[when?] but a research in 2007 that focused on quantifying self-reports of auditory verbal hallucinations (AVH) in persons with psychosis, suggest that The Hamilton Program for Schizophrenia Voices Questionnaire (HPSVQ) is also potentially a reliable and useful measure for specifically quantifying AVHs in relation to psychosis.[147]
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 encompasspsychotic or schizophrenia spectrum disorders. The five factors are frequently labeled as hallucinations, delusions, disorganization, excitement, and emotional distress.[144] The DSM-5 emphasizes apsychotic spectrum, wherein the low end is characterized by schizoid personality disorder, and the high end is characterized by schizophrenia.[3]
Gouzoulis-Mayfrank et al. said that the pleasant or emotionally positive experiences that are common in psychosis, particularly in the early stages, are more easily overlooked in clinical practice than the negative experiences.[148] Nev Jones and Mona Shattel wrote that there is less curiosity towards the complications, or towards the richness of the good things as well as the bad things.[148]
The evidence for the effectiveness of early interventions toprevent psychosis appeared inconclusive.[149] But psychosis caused by drugs can be prevented.[150] Whilst early intervention in those with a psychotic episode might improve short-term outcomes, little benefit was seen from these measures after five years.[151] However, there is evidence thatcognitive behavioral therapy (C.B.T.) may reduce the risk of becoming psychotic in those at high risk,[152] and in 2014 the U.K.National Institute for Health and Care Excellence (N.I.C.E.) recommended preventive C.B.T. for people at risk of psychosis.[153][154]
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,[155] which can reduce the positive symptoms of psychosis in about 7 to 14 days. For youth or adolescents, treatment options include medications, psychological interventions, and social interventions.[43]
The choice of whichantipsychotic to use is based on benefits, risks, and costs.[151] It is debatable whether, as a class,typical oratypical antipsychotics are better.[156][157] Tentative evidence supports thatamisulpride,olanzapine,risperidone andclozapine may be more effective for positive symptoms but result in more side effects.[158] Typical antipsychotics have equal drop-out and symptom relapse rates to atypicals when used at low to moderate dosages.[159] There is a good response in 40–50%, a partial response in 30–40%, and treatment resistance (failure of symptoms to respond satisfactorily after six weeks to two or three different antipsychotics) in 20% of people.[160] Clozapine is an effective treatment for those who respond poorly to other drugs ("treatment-resistant" or "refractory" schizophrenia),[161] but it has the potentially serious side effect ofagranulocytosis (loweredwhite blood cell count) in less than 4% of people.[151][162][163]
Most people on antipsychotics get side effects. People on typical antipsychotics tend to have a higher rate ofextrapyramidal side effects while some atypicals are associated with considerable weight gain, diabetes and risk ofmetabolic syndrome; this is most pronounced with olanzapine, while risperidone andquetiapine are also associated with weight gain.[158] Risperidone has a similar rate of extrapyramidal symptoms to haloperidol.[158]
There are many psychosocial interventions that seek to treat the symptoms of psychosis:need adapted treatment,Open Dialogue, psychoanalysis/psychodynamic psychotherapy,major role therapy,soteria, psychosocial outpatient and inpatient treatment,milieu therapy, and cognitive behavioral therapy (C.B.T.). In relation to the success of C.B.T. for psychosis, a randomized controlled trial for a web-based C.B.T.P. (Cognitive Behavioral Therapy for Psychosis) skills program named Coping With Voices (C.W.V.) suggest that the program has promise for increasing access to C.B.T.P. It also associated benefits in the management of distressing psychotic symptoms and improved social functioning. When C.B.T. and the other psychosocial interventions[166] these are used without antipsychotic medications, they may be somewhat effective for some people, especially for C.B.T., need-adapted treatment, and soteria.[167]
Early intervention in psychosis is based on the observation that identifying and treating someone in the early stages of a psychosis can improve his or her longer-term outcome.[168] This approach advocates the use of an intensive multi-disciplinary approach during what is known as thecritical period, where intervention is the most effective, and prevents the long-term morbidity associated with chronic psychotic illness.
Addressing systematic reform is essential to creating effective prevention as well as supporting treatments and recovery for those with psychosis.
Waghorn et al.[169] suggest that education interventions can be a building block to support those with psychosis to successfully participate in society. In their study they analyse the relationship between successful education attainment and psychosis. Findings suggest proportionately more school-aged persons with psychosis discontinued their education compared to those without psychosis.[169]
Waghorn et al.[169] finds that specialised supported education for those with psychotic disorders can help lead to successful education attainment. Additionally, future employment outcomes are relative to such education attainment. Established approaches to supported education in the U.S. include three basic models, self-contained classrooms, onsite support model and the mobile support model. Each model includes the participation of mental health service staff or educational facility staff in the student's education arrangements.[169]
Potential benefits of specialised supported education found from this study include coordination with other service providers (e.g. income support, housing, etc.) to prevent disrupting education, providing specialised career counselling, development of coping skills in the academic environment.[169] These examples provide beneficial ways for people with psychosis to finish studies successfully as well as counter future experiences of psychosis.[169]
The wordpsychosis was introduced to the psychiatric literature in 1841 byKarl Friedrich Canstatt in his workHandbuch der Medizinischen Klinik. He used it as a shorthand for 'psychic neurosis'. At that time neurosis meant any disease of thenervous system, and Canstatt was thus referring to what was considered a psychological manifestation of brain disease.[170]Ernst von Feuchtersleben is also widely credited as introducing the term in 1845,[171] as an alternative toinsanity andmania.
The term stems fromModern Latinpsychosis, "a giving soul or life to, animating, quickening" and that fromAncient Greek ψυχή (psyche), "soul" and the suffix -ωσις (-osis), in this case "abnormal condition".[172][173]
In its adjective form "psychotic", references to psychosis can be found in both clinical and non-clinical discussions. However, in anon-clinical context, "psychotic" is a nonspecific colloquialism used to mean "insane".
The word was also used to distinguish a condition considered a disorder of the mind, as opposed toneurosis, which was considered a disorder of the nervous system.[174] The psychoses thus became the modern equivalent of the old notion ofmadness, and hence there was much debate on whether there was only one(unitary) or many forms of the new disease.[175] One type of broad usage would later be narrowed down byKoch in 1891 to the 'psychopathic inferiorities'—later renamed abnormal personalities bySchneider.[170]
The division of the major psychoses into manic depressive illness (now calledbipolar disorder) and dementia praecox (now calledschizophrenia) was made byEmil Kraepelin, who attempted to create a synthesis of the various mental disorders identified by 19th-centurypsychiatrists, by grouping diseases together based on classification of common symptoms. Kraepelin used the term 'manic depressive insanity' to describe the whole spectrum ofmood 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 ascyclothymia. These are characterised by problems with mood control and the psychotic episodes appear associated with disturbances in mood, and patients often have periods of normal functioning between psychotic episodes even without medication.Schizophrenia is characterized by psychotic episodes that appear unrelated to disturbances in mood, and most non-medicated patients show signs of disturbance between psychotic episodes.
Written record of supernatural causes and resultant treatments can be traced back to theNew Testament.Mark 5:8–13 describes a man displaying what would today be described as psychotic symptoms.Christ cured this "demonic madness" by casting out the demons and hurling them into a herd of swine. Exorcism is still utilized in some religious circles as a treatment for psychosis presumed to be demonic possession.[176] A research study of out-patients in psychiatric clinics found that 30% of religious patients attributed the cause of their psychotic symptoms to evil spirits. Many of these patients underwent exorcistic healing rituals that, though largely regarded as positive experiences by the patients, had no effect on symptomology. Results did however show a significant worsening of psychotic symptoms associated with exclusion of medical treatment for coercive forms of exorcism.[177]
Bust of Hippocrates
The medical teachings of the fourth-century philosopher and physicianHippocrates of Cos proposed a natural, rather than supernatural, cause of human illness. In Hippocrates' work, theHippocratic corpus, a holistic explanation for health and disease was developed to include madness and other "diseases of the mind". Hippocrates writes:
Men ought to know that from the brain, and from the brain only, arise our pleasures, joys, laughter, and jests, as well as our sorrows, pains, griefs and tears. Through it, in particular, we think, see, hear, and distinguish the ugly from the beautiful, the bad from the good, the pleasant from the unpleasant.... It is the same thing which makes us mad or delirious, inspires us with dread and fear, whether by night or by day, brings sleeplessness, inopportune mistakes, aimless anxieties, absentmindedness, and acts that are contrary to habit.[178]
Hippocrates espoused a theory ofhumoralism wherein disease is resultant of a shifting balance in bodily fluids includingblood,phlegm,black bile, andyellow bile.[179] According to humoralism, each fluid or "humour" has temperamental or behavioral correlates. In the case of psychosis, symptoms are thought to be caused by an excess of both blood and yellow bile. Thus, the proposed surgical intervention for psychotic or manic behavior wasbloodletting.[180]
18th-century physician, educator, and widely considered "founder of American psychiatry",Benjamin Rush, also prescribed bloodletting as a first-line treatment for psychosis. Although not a proponent of humoralism, Rush believed that active purging and bloodletting were efficacious corrections for disruptions in the circulatory system, a complication he believed was the primary cause of "insanity".[181] Although Rush's treatment modalities are now considered antiquated and brutish, his contributions to psychiatry, namely the biological underpinnings of psychiatric phenomenon including psychosis, have been invaluable to the field. In honor of such contributions, Benjamin Rush's image is in the official seal of theAmerican Psychiatric Association.
Early 20th-century treatments for severe and persisting psychosis were characterized by an emphasis on shocking the nervous system. Such therapies includeinsulin shock therapy,cardiazol shock therapy, andelectroconvulsive therapy.[182] Despite considerable risk, shock therapy was considered highly efficacious in the treatment of psychosis includingschizophrenia. The acceptance of high-risk treatments led to more invasive medical interventions includingpsychosurgery.[183]
Gottlieb Burckhardt (1836–1907)
In 1888, Swiss psychiatristGottlieb Burckhardt performed the first medically sanctioned psychosurgery in which thecerebral cortex was excised. Although some patients showed improvement of symptoms and became more subdued, one patient died and several developedaphasia or seizure disorders. Burckhardt would go on to publish his clinical outcomes in a scholarly paper. This procedure was met with criticism from the medical community and his academic and surgical endeavors were largely ignored.[184] In the late 1930s,Egas Moniz conceived theleucotomy (AKAprefrontal lobotomy) in which the fibers connecting thefrontal lobes to the rest of the brain were severed. Moniz's primary inspiration stemmed from a demonstration by neuroscientists John Fulton and Carlyle's 1935 experiment in which two chimpanzees were given leucotomies and pre- and post-surgical behavior was compared. Prior to the leucotomy, the chimps engaged in typical behavior including throwing feces and fighting. After the procedure, both chimps were pacified and less violent. During the Q&A, Moniz asked if such a procedure could be extended to human subjects, a question that Fulton admitted was quite startling.[185] Moniz would go on to extend the controversial practice to humans with various psychotic disorders, an endeavor for which he received aNobel Prize in 1949.[186] Between the late 1930s and early 1970s, the leucotomy was a widely accepted practice, often performed in non-sterile environments such as smalloutpatient clinics and patient homes.[185] Psychosurgery remained standard practice until the discovery of antipsychotic pharmacology in the 1950s.[187]
The first clinical trial ofantipsychotics (also commonly known as neuroleptics) for the treatment of psychosis took place in 1952.Chlorpromazine (brand name: Thorazine) passed clinical trials and became the first antipsychotic medication approved for the treatment of both acute and chronic psychosis. Although the mechanism of action was not discovered until 1963, the administration of chlorpromazine marked the advent of thedopamine antagonist, or first generation antipsychotic.[188] While clinical trials showed a high response rate for both acute psychosis and disorders with psychotic features, theside effects were particularly harsh, which included high rates of often irreversible Parkinsonian symptoms such astardive dyskinesia. With the advent ofatypical antipsychotics (also known as second generation antipsychotics) came a dopamine antagonist with a comparable response rate but a far different, though still extensive, side-effect profile that included a lower risk of Parkinsonian symptoms but a higher risk of cardiovascular disease.[189] Atypical antipsychotics remain the first-line treatment for psychosis associated with various psychiatric andneurological disorders including schizophrenia,bipolar disorder,major depressive disorder,anxiety disorders,dementia, and someautism spectrum disorders.[190]
Dopamine is now one of the primary neurotransmitters implicated in psychotic symptomology. Blocking dopamine receptors (namely, the dopamine D2 receptors) and decreasing dopaminergic activity continues to be an effective but highly unrefined effect of antipsychotics, which are commonly used to treat psychosis. Recent pharmacological research suggests that the decrease in dopaminergic activity does not eradicate psychoticdelusions orhallucinations, but rather attenuates the reward mechanisms involved in the development of delusional thinking; that is, connecting or finding meaningful relationships between unrelated stimuli or ideas.[114] The author of this research paper acknowledges the importance of future investigation:
The model presented here is based on incomplete knowledge related to dopamine, schizophrenia, and antipsychotics—and as such will need to evolve as more is known about these.
— Shitij Kapur, From dopamine to salience to psychosis—linking biology, pharmacology and phenomenology of psychosis
Freud's former student Wilhelm Reich explored independent insights into the physical effects of neurotic and traumatic upbringing, and published his holistic psychoanalytic treatment with a schizophrenic. With his incorporation of breathwork and insight with the patient, a young woman, she achieved sufficient self-management skills to end the therapy.[191]
Lacan extended Freud's ideas to create a psychoanalytic model of psychosis based upon the concept of "foreclosure", the rejection of the symbolic concept of the father.
PsychiatristDavid 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 that are known important influences in the etiology of psychosis.[192]
Symptoms of psychosis can also include visions or quasi-visual experiences, felt presences, alterations of time, alterations of space, or alterations of spatiotemporal qualities of objects and things.[148] While there are many overwhelmingly negative experiences of psychosis, some experiences of psychosis can be overwhelmingly positive and can be experienced as uplifting or as healing or as difficult but meaningful.[148] Jones and Shattell said that mutual dialogue in clinical practice would in theory allow the meaning and complexity of psychotic experiences to emerge.[148]
The classification of psychosis as asocial disability is a common occurrence.
Psychosis is considered to be among the top ten causes of social disability among adults in developed countries.[193] The traditional, negative narrative around disability has been shown to adversely influence employment and education for people experiencing psychosis.[194]
Social disability by way of social disconnection is a significant public health concern and is associated with a broad range of negative outcomes, including premature mortality. Social disconnection refers to the ongoing absence of family or social relationships with marginal participation in social activities.
Research on psychosis found that reduced participation in social networks, not only negatively effects the individual on a physical and mental level, it has been shown that failure to be included in social networks influences the individual's ability to participate in the wider community through employment and education opportunities.[195][196][197]
Equal opportunity to participate in meaningful relationships with friends, family and romantic partners, as well as engaging in social constructs such as employment, can provide significant physical and mental value to people's lives.[195] And how breaking the disability mind-set around people experiencing psychosis is imperative for their overall, long-term health and well-being as well as the contributions they are able to make to their immediate social connections and the wider community.[196]
Further research in the form of randomized controlled trials is needed to determine the effectiveness of treatment approaches for helpingadolescents with psychosis.[43] Through 10 randomized clinical trials, studies showed that Early Intervention Services (EIS) for patients with early-phase schizophrenia spectrum disorders have generated promising outcomes.[198] EIS are specifically intended to fulfill the needs of patients with early-phase psychosis.[198] In addition, one meta-analysis that consisted of four randomized clinical trials has examined and discovered the efficacy of EIS to Therapy as Usual (TAU) for early-phase psychosis, revealing that EIS techniques are superior to TAU.[198]
A study suggests that combining cognitive behavioral therapy (C.B.T.) with SlowMo, an application that helps notice their "unhelpful quick-thinking", might be more effective for treating paranoia in people with psychosis than C.B.T. alone.[199][200]
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