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Christian89/Sandkasse2
Klassifikation
Tøj broderet af en person lidende af skizofreni.
Information
NavnChristian89/Sandkasse2
SKSDF20
ICD-10F20
ICD-9295

Skizofreni er en psykisk lidelse karakteriseret ved forstyrrelser i tankeprocesserne og hæmning af typisk følelsesmæssig reaktion.[1] Hyppigt sete symptomer inkluderer hørelseshallucinationer, paranoide og bizarre vrangforestillinger samt tanke og taleforstyrrelser, som oftest er associeret med nedsat social interaktion. Symptomerne på skizofreni debuterer oftest i teenageårene eller ung voksenalder med global livstidsprævalens på 0.3–0.7%.[2] Diagnosen er baseret på observationer af patientens opførsel og vedkommenes beskrivelse af sine oplevelser.

Skizofreni er afledt af græsk skhizein (σχίζειν, "spaltet") og phren (φρήν, φρεν-; sind), men der er ikke tale om personlighedsspaltning, som det oftest forveksles med i folkemunde.[3] Derimod henviser ordet til en spaltning af tanker og følelser.[4]

Nogle af de vigtigste faktorer der antages at være afgørende i udviklingen af skizofreni involverer genetik, tidlige miljømæssige påvirkninger, neurobiologi, psykosociale og sociale interaktioner. Nuværende forskning fokuserer især på neurobiologiske mekanismer, men der er endnu ikke blevet fundet nogen selvstændig organisk årsag. De mange forskellige symptomer har givet anledning til overvejelser om diagnosen repræsenterer en enkel lidelse eller flere forskellige syndromer.

Den primære behandling af skizofreni involverer antipsykotisk medicin, som hæmmer dopaminerg (og nogle gange serotonerg) receptoraktivitet. Psykoterapi og social genetablering er ligeledes vigtige led i behandlingen. I mere alvorlige tilfælde hvor vedkommende kan være til fare for sig selv eller sine omgivelser, kan tvangsindlæggelse være nødvendig. Disse tvunge hospitalsophold er dog af kortere varighed og mindre anvendte i dag.[5]

Personer med skizofreni lider oftest også af andre tilstande (co-morbiditet), som inkluderer depression og angst samt misbrugsproblemer.[6] Sociale problemer som langtidsarbejdsløshed, fattigdom og hjemløshed er oftest sete. Middellevetiden for mennesker med denne lidelse er 12 til 15 år mindre end dem uden, hvilket er et resultat af fysiske sundhedsproblemer og høj selvmordsrate (omkring 5%)[2][7]

Symptomer

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Skizofreni er karakteriseret ved problemer med tankeprocesserne, der kan lede til forstyrret tankeindhold (vrangforestillinger) og/eller tankeform (sproglige tankeforstyrrelser). Sidstnævnte symptom indebærer forstyrrelser i tankerne, som kommer til udtryk i sproget.[8] Eksempelvis kan disse vise sig som dannelse af nye ord (neolgismer), opløsning af sætningsstrukturen (inkohærens), associationsforstyrrelser hvor patientens tankegang følger et mønster, der er svært at sætte sig ind i for en udestående.[9] Ligeledes ses forstyrrelser af sanseoplevelserne i form af hallucinationer, (hvor hørelseshallucintaioner er den hyppigst sete form).[8]

De forstyrrede tankeprocesser kan også give andre kognitive symptomer, der omfatter problemer med arbejds- og langtidshukommelse, koncentrationsevne, hastigheden af informationsbearbejdning og eksekutivfunktioner (f.eks begrebsdannelse, ordmobilisering, evnen til at danne, fastholde og skifte kognitive strategier).[2]

Social kognition er også fundet nedsat, og menes at bidrage til adfærdsmæssige symptomer som social tilbagetrækning[10]. Udover social isolation[11] er hygiejneforsømmelse, tab af motivation og dømmekraft,[12] samt hæmmet emotionel reaktion[13] også ofte sete adfærdsmæssige symptomer. Mellem 30 og 50% lidende af skizofreni har ingen sygdomsindsigt.[14]

I visse tilfælde kan der også forekomme bevægelsesmæssige forstyrrelser i form af katatone symptomer, hvor patienten fastfryses i forvredne stillinger i længere tid.[15]

Schneideriansk klassifikation

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I begyndelsen af det 20. århundrede opstillede den tyske psykiater Kurt Schneider en række psykotiske symptomer, som han mente adskilte sig fra andre psykotiske lidelser. Disse kaldes førsterangssymptomer, og inkluderer styringsoplevelse (følelsen af at blive kontrolleret af en udefrakommende kraft), tankepåvirkningsoplevelse (følelsen af at ens tanker stjæles, påføres, kan høres eller overføres til omgivelserne), tredjepersons hørehallucinationer (høre kommenterende stemmer eller diskuterende stemmer)[16].

Selvom førsterangssymptomerne har været definerende for de diagnostiske kriterier for skizofreni, er disses specifitet omdiskuteret: I en oversigtsartikel baseret på diagnostiske studier indsamlet mellem 1970 og 2005 blev der hverken fundet be- eller afkræftelse på Schneiders opstilling, hvilket har ledt til forslaget om at førsterangssymptomer burde have mindre vægt i de kommende diagnose klassifikationssystemer. [17]

Positive og negative symptomer

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I klinikken skelnes der oftest mellem positive og negative symptomer.[18] De positive symptomer dækker over vrangforestillinger (ofte forfølgelses eller bizarrre forestillinger), tanke- og taleforstyrrelser samt hallucinationer som både kan påvirke føle-, hørelse-, syns-, lugte- og smagssanserne, som er typiske træk ved psykoser.[19] Hallucinationerne er ofte associeret med vrangforestillingernes indhold.[20] Den antipsykotiske medicin har meget gunstig effekt på de positive symptomer.[20]

Negative symptomer dækker over fravær af en række normale psykologiske og sociale funktioner, som den antipsykotiske medicin er mindre gavnlig overfor.[12] Disse indebærer typisk sløvhed, affektafladning, sprogfattigdom, manglende interesser, social tilbagetrækning og indsynken i sig selv.[21] Undersøgelser peger på at negative symptomer medfører dårligere livskvalitet, ringere fremdrift og større byrde for omgivelserne end de positive symptomer.[22] Individer med fremtrædende negative symptomer har hyppigt i forvejen dårlig tilpasningsevne inden sygdomsdebut og responderer også dårligere på medicinen.[12][23]

Sygdomsdebut

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De sene teenageår samt tidlig voksenalder er en afgørende periode for udvikling af sociale og faglige kompentencer,[24] og er også den typiske periode for udvikling af skizofreni.[2] 40% af mændene og 23% af kvinderne diagnosticeret med skizofreni havde sygdomsdebut før 19 års alderen.[25] For at reducere udviklingsforstyrelserne associeret med skizofreni, er der blevet iværksat store undersøgelser med henblik på at identificere og behandle den prodrome (før-debut) fase af sygdommen, som er blevet observeret helt op til 30 måneder før det endelige sygdomsdebut.[24]

Individer i den prodrome fase kan opleve korte forbigående psykotiske symptomer[26] og ikke-specifikke symptomer som social tilbagetrækning, irritabilitet, kortvarig forstemt tristehed (dysfori)[27] og klodsethed[28]

Årsager

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En kombination af genetiske og miljømæssige faktorer spiller en rolle for udviklingen af skizofreni.[2][3] Individer beslægtet med personer diagnosticeret med skizofreni som oplever en forbigående psykoser har 20-40% sandsynlighed for at få diagnosen er år senere.[29]

Genetik

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Der er stor variation i den estimerede familiære arvelighed af skizofreni, hvilket skyldes forskelle i diagnostik, statistiske forhold[30] samt vanskeligheder med at adskille genetiske og miljømæssige faktorer.[31] Til trods for den store variation i estimaterne er der dog blevet påvist en signifikant forhøjet risiko for udvikling af skizofreni i familier med sygdommen sammenlignet med raske kontrolgrupper.[30] Den største risiko for at udvikle skizofreni er at have førstegenerationsslægtninge med sygdommen (risiko på 6,5%). Ved forældre begge lidende af skizofreni stiger risikoen for at få et afkom med lidelsen til 46%.[32]

Tvillingestudier har anslået at mere end 40% af fuldkommen genetisk identiske enæggede tvillinger, med forældre lidende af skizofreni, får symptomer på lidelsen.[33] Den resterende procentdel angiver tilfælde, hvor kun en af tvillingerne eller ingen af tvillingerne har arvet sygdommen, hvilket indikerer også ikke-genetiske faktorer (som f.eks. miljø) er involveret.[32]

Molekylærgenetiske studier har ikke fundet noget specifik gen knyttet til skizofreni, men identificeret en række risikogener som menes at være involveret i udviklingen. Viden om hvor meget disse øger risikoen er dog begrænset,[34] og det menes at generne hver bidrager med en mindre effekt, som i kombination med miljømæssige faktorer kan overstige en hvis tærskelværdi, som leder til udtryk af symptomerne.[32] Riskogentiske kandidater involverer bla. ændringer i generne kodende for proteinerne neuregulin 1, dysbindin og catechol-O-methyltransferase, som menes at kunne lede til ændret funktion af disse og derved forstyrrelser i den synaptiske transmission mellem nervecellerne (som er en forstyrrelse karakteristisk for skizofreni).[35] Yderligere synes der at være et signifikant overlap mellem gener for skizofreni og bipolær affektiv sindslidelse.[36]

Fra evolutionspsykologisk perspektiv er der dog blevet fokuseret på hvorfor gener der øger tendensen til psykose er blevet nedarvet, da disse lidelser er uhensigtmæssige fra et evolutionært synspunkt. En påstand er at de samme gener som øger risikoen for psykose også er involveret i sprog og menneskelig adfærd, men disse påstande er til dato kun hypotetiske.[37][38]

Miljø

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Miljømæssige faktorer associeret med udviklingen af skizofreni inkluderer opvækstmiljøet, brug af visse euforiserende stoffer og graviditetskomplikationer som f.eks. lav fødselsvægt.[39] Opdragelse virker ikke til at have nogen betydelig indvirkning på udvikling af skizofreni, men det lader til at individer med støttende forældre bedre håndterer deres skizofreni end personer med bearbejdende og fjendtlige forældre.[3] Opvækst som barn og bopæl som voksen i storbyen er konsekvent blevet fundet at øge risikoen for udviklingen af skizofreni med en faktor to,[2][3] selv efter at have medregnet brug af euforiserende stoffer, etnicitet og størrelsen af ens sociale omgangskreds. Andre faktorer som spiller en vigtig rolle inkluderer social isolation, immigration associeret med social udstødelse, racistisk diskrimmination, dårligt fungerende familier, arbejdsløshed og dårlige boligtilstande.[3][40]

Brug af stoffer

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Amfetamin, kokain og til en mindre grad alkohol kan resultere i skizofrenilignende psykoser.[3][41] Der ses ligeledes et højere forbrug af nikotin blandt individer lidende af skizofreni sammenlignet med den generelle befolkning. Nikotin menes dog ikke at bidrage til udviklingen af lidelsen.[42] Misbrug blandt skizofrene er udbredt, og det anslås at over halvdelen indtager større mængder alkohol eller andre euforiserende stoffer.[43] Epidemiologiske studier har i de senere år belyst en relation mellem cannabismisbrug og tidligere debut af skizofreni - en association som ikke blev fundet ved alkoholmisbrug.[44] Brugen af stoffer menes ligeledes at fungerer som et værktøj til at håndtere andre omstændigheder blandt skizofrene som depression, angst, kedsomhed og ensomhed.[43][45]

Der er beviser på at alkoholmisbrug via en kindling mekanisme kan medføre udvikling af kronisk psykotiske tilstande som f.eks. skizofreni.[46] Epidemilogiske studier peger på, at jo oftere cannabis bruges jo større risiko er der for at udvikle en psykotisk tilstand.[47] For det enkelte individ menes hyppigt brug, at fordoble risikoen for udvikling af psykoser og skizofreni.[48] Der er dog stadig stor uenighed om det er cannabismisbrug som leder til udviklingen af skizofreni, eller cannabismisbrug er en adfærd knyttet til lidelsen.[49][50]

Fosterskader

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Omstændigheder som iltmangel, infektioner, stress og underernæring hos den gravide kan medføre udvikling af skizofreni ved afkommet senere i livet.[2] Individer diagnosticeret med lidelsen er ofte født om vinteren eller foråret, hvor der er størst risiko for virale infektioner af fosteret.[3] Mistanken om sammenhængen mellem underernæring og udvikling af skizofreni er bla. baseret på en periode under 2. verdenskrig, hvor vestlige dele af Holland var blokeret af tyskerene og der var udbredt sult, mens den østlige del ikke var så hårdt ramt. Sammenligning mellem de to grupper viste at fostre i vinteren 1944-1945 havde en øget risiko for senere at udvikle skizofreni som følge af den dårligere ernæring.[51]

Psykopatologi

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Flere neuropsykiatriske studier har forsøgt at forklare sammenhængen mellem ændret hjernefunktion og skizofreni, hvilket har ledt til en række fund og teorier.[52] En af de mest kendte er dopaminhypotesen, som antager at skizofreni skyldes øget dopaminerg signalering i hjernens pandelapper.[2]

Psykologisk

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Hos et flertal af patienterne er der fundet ændringer i de kognitive funktioner.[53] Blandt individer diagnosticeret med skizofreni (eller med risiko for udvikling af lidelsen) er der blevet observeret kognitive biasser, især når disse er under stress eller i forvirrende situationer.[54] Andre kognitive ændringer involverer områder som hukommelse, opmærksomhed og eksekutivfunktioner, men kan også relateres til specifikke situationer eller oplevelser.[55][56] Mange af de kognitive forstyrrelse afspejles i de negative symptomer.[53]

Til trods for den ofte hæmmet følelsesmæssige reaktion viser nyere studier, at individer diagnosticeret med skizofreni er i stand til at reagere emotionelt, især på stressende eller negative stimuli, og at denne form for overfølsomhed kan give øget sårbarhed for symptomerne og lidelsen.[57][58] Visse fund tyder på at vrangforestillingernes indhold i en psykotisk episode kan afspejle emotionelle årsager, og hvordan en person tolker disse oplevelser kan have indflydelse på symptompatologien.[59][60][61] Tendensen til sikkerhedsadfærd overfor vrangforestillingernes indhold kan bidrage til varigheden af disse.[62] Yderligere beviser på de psykologiske mekanismers rolle kommer fra effekten af psykoterapi på symptomerne ved skizofreni.[63]

Neurological

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Functional magnetic resonance imaging (fMRI) and other brain imaging technologies allow for the study of differences in brain activity in people diagnosed with schizophrenia. The image shows two levels of the brain, with areas that were more active in healthy controls than in schizophrenia patients shown in orange, during an fMRI study of working memory.

Schizophrenia is associated with subtle differences in brain structures, found in 40 to 50% of cases, and in brain chemistry during acute psychotic states.[2] Studies using neuropsychological tests and brain imaging technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to most commonly occur in the frontal lobes, hippocampus and temporal lobes.[64] Reductions in brain volume, smaller than those found in Alzheimer's disease, have been reported in areas of the frontal cortex and temporal lobes. It is uncertain whether these volumetric changes are progressive or preexist prior to the onset of the disease.[65] These differences have been linked to the neurocognitive deficits often associated with schizophrenia.[66] Because neural circuits are altered, it has alternatively been suggested that schizophrenia should be thought of as a collection of neurodevelopmental disorders.[67]

Particular attention has been paid to the function of dopamine in the mesolimbic pathway of the brain. This focus largely resulted from the accidental finding that phenothiazine drugs, which block dopamine function, could reduce psychotic symptoms. It is also supported by the fact that amphetamines, which trigger the release of dopamine, may exacerbate the psychotic symptoms in schizophrenia.[68] The influential dopamine hypothesis of schizophrenia proposed that excessive activation of D2 receptors was the cause of (the positive symptoms of) schizophrenia. Although postulated for about 20 years based on the D2 blockade effect common to all antipsychotics, it was not until the mid-1990s that PET and SPET imaging studies provided supporting evidence. The dopamine hypothesis is now thought to be simplistic, partly because newer antipsychotic medication (atypical antipsychotic medication) can be just as effective as older medication (typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect.[69]

Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in schizophrenia, largely because of the abnormally low levels of glutamate receptors found in the postmortem brains of those diagnosed with schizophrenia,[70] and the discovery that glutamate-blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.[71] Reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function, and glutamate can affect dopamine function, both of which have been implicated in schizophrenia, have suggested an important mediating (and possibly causal) role of glutamate pathways in the condition.[72] But positive symptoms fail to respond to glutamatergic medication.[73]

Diagnosis

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Hovedartikel: Diagnosis of schizophrenia.
John Nash, a U.S. mathematician and joint winner of the 1994 Nobel Prize for Economics, who had schizophrenia. His life was the subject of the 2001 Academy Award-winning film A Beautiful Mind.

Schizophrenia is diagnosed based on criteria in either the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, version DSM-IV-TR, or the World Health Organization's International Statistical Classification of Diseases and Related Health Problems, the ICD-10.[2] These criteria use the self-reported experiences of the person and reported abnormalities in behavior, followed by a clinical assessment by a mental health professional. Symptoms associated with schizophrenia occur along a continuum in the population and must reach a certain severity before a diagnosis is made.[3] As of 2009 there is no objective test.[2]

Criteria

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The ICD-10 criteria are typically used in European countries, while the DSM-IV-TR criteria are used in the United States and to varying degrees around the world, and are prevailing in research studies. The ICD-10 criteria put more emphasis on Schneiderian first-rank symptoms. In practice, agreement between the two systems is high.[74]

According to the revised fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), to be diagnosed with schizophrenia, three diagnostic criteria must be met:[75]

  1. Characteristic symptoms: Two or more of the following, each present for much of the time during a one-month period (or less, if symptoms remitted with treatment).
    • Delusions
    • Hallucinations
    • Disorganized speech, which is a manifestation of formal thought disorder
    • Grossly disorganized behavior (e.g. dressing inappropriately, crying frequently) or catatonic behavior
    • Negative symptoms: Blunted affect (lack or decline in emotional response), alogia (lack or decline in speech), or avolition (lack or decline in motivation)
    If the delusions are judged to be bizarre, or hallucinations consist of hearing one voice participating in a running commentary of the patient's actions or of hearing two or more voices conversing with each other, only that symptom is required above. The speech disorganization criterion is only met if it is severe enough to substantially impair communication.
  2. Social or occupational dysfunction: For a significant portion of the time since the onset of the disturbance, one or more major areas of functioning such as work, interpersonal relations, or self-care, are markedly below the level achieved prior to the onset.
  3. Significant duration: Continuous signs of the disturbance persist for at least six months. This six-month period must include at least one month of symptoms (or less, if symptoms remitted with treatment).

If signs of disturbance are present for more than a month but less than six months, the diagnosis of schizophreniform disorder is applied.[75] Psychotic symptoms lasting less than a month may be diagnosed as brief psychotic disorder, and various conditions may be classed as psychotic disorder not otherwise specified. Schizophrenia cannot be diagnosed if symptoms of mood disorder are substantially present (although schizoaffective disorder could be diagnosed), or if symptoms of pervasive developmental disorder are present unless prominent delusions or hallucinations are also present, or if the symptoms are the direct physiological result of a general medical condition or a substance, such as abuse of a drug or medication.

Subtypes

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The DSM-IV-TR contains five sub-classifications of schizophrenia, although the developers of DSM-5 are recommending they be dropped from the new classification:[76][77]

  • Paranoid type: Delusions or auditory hallucinations are present, but thought disorder, disorganized behavior, or affective flattening are not. Delusions are persecutory and/or grandiose, but in addition to these, other themes such as jealousy, religiosity, or somatization may also be present. (DSM code 295.3/ICD code F20.0)
  • Disorganized type: Named hebephrenic schizophrenia in the ICD. Where thought disorder and flat affect are present together. (DSM code 295.1/ICD code F20.1)
  • Catatonic type: The subject may be almost immobile or exhibit agitated, purposeless movement. Symptoms can include catatonic stupor and waxy flexibility. (DSM code 295.2/ICD code F20.2)
  • Undifferentiated type: Psychotic symptoms are present but the criteria for paranoid, disorganized, or catatonic types have not been met. (DSM code 295.9/ICD code F20.3)
  • Residual type: Where positive symptoms are present at a low intensity only. (DSM code 295.6/ICD code F20.5)

The ICD-10 defines two additional subtypes:[77]

  • Post-schizophrenic depression: A depressive episode arising in the aftermath of a schizophrenic illness where some low-level schizophrenic symptoms may still be present. (ICD code F20.4)
  • Simple schizophrenia: Insidious and progressive development of prominent negative symptoms with no history of psychotic episodes. (ICD code F20.6)

Differential

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Se også Se også: Dual diagnosis.

Psychotic symptoms may be present in several other mental disorders, including bipolar disorder,[78] borderline personality disorder,[79] drug intoxication and drug-induced psychosis. Delusions ("non-bizarre") are also present in delusional disorder, and social withdrawal in social anxiety disorder, avoidant personality disorder and schizotypal personality disorder. Schizophrenia is comorbid with obsessive-compulsive disorder (OCD) considerably more often than could be explained by pure chance, although it can be difficult to distinguish obsessions that occur in OCD from the delusions of schizophrenia.[80] A small number of people withdrawing from benzodiazepines experience a severe protracted withdrawal syndrome which can resemble schizophrenia and be misdiagnosed as such.[81]

A more general medical and neurological examination may be needed to rule out medical illnesses which may rarely produce psychotic schizophrenia-like symptoms,[75] such as metabolic disturbance, systemic infection, syphilis, HIV infection, epilepsy, and brain lesions. Stroke, multiple sclerosis, hyperthyroidism, hypothyroidism and dementias such as Alzheimer's disease, Huntington's disease, frontotemporal dementia and Lewy Body dementia may also be associated with schizophrenia-like psychotic symptoms.[82] It may be necessary to rule out a delirium, which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness, and indicates an underlying medical illness. Investigations are not generally repeated for relapse unless there is a specific medical indication or possible adverse effects from antipsychotic medication.

Prevention

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Prevention of schizophrenia is difficult as there are no reliable markers for the later development of the disease.[83] The evidence for the effectiveness of early interventions to prevent schizophrenia is inconclusive.[84] While there is some evidence that early intervention in those with a psychotic episode may improve short term outcomes, there is little benefit from these measures after five years.[2] Attempting to prevent schizophrenia in the prodrome phase is of uncertain benefit and therefore as of 2009 is not recommended.[85] Cognitive behavioral therapy may reduce the risk of psychosis in those at high risk after a year.[86] Another preventative measure is to avoid drugs that have been associated with development of the disorder, including cannabis, cocaine, and amphetamines.[3]

Management

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Hovedartikel: Management of schizophrenia.

The primary treatment of schizophrenia is antipsychotic medications, often in combination with psychological and social supports.[2] Hospitalization may occur for severe episodes either voluntarily or (if mental health legislation allows it) involuntarily. Long-term hospitalization is uncommon since deinstitutionalization beginning in the 1950s, although it still occurs.[5] Community support services including drop-in centers, visits by members of a community mental health team, supported employment[87] and support groups are common. Some evidence indicates that regular exercise has a positive effect on the physical and mental health of those with schizophrenia.[88]

Medication

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Risperidone (trade name Risperdal) is a common atypical antipsychotic medication.

The first-line psychiatric treatment for schizophrenia is antipsychotic medication,[89] which can reduce the positive symptoms of psychosis in about 7–14 days. Antipsychotics, however, fail to significantly ameliorate the negative symptoms and cognitive dysfunction.[23][90] In those on antipsychotics, continued use decreases the risk of relapse.[91][92] There is little evidence regarding consistent benefits from their use beyond two or three years.[92]

The choice of which antipsychotic to use is based on benefits, risks, and costs.[2] It is debatable whether, as a class, typical or atypical antipsychotics are better.[93][94] Both have equal drop-out and symptom relapse rates when typicals are used at low to moderate dosages.[95] 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.[23] Clozapine is an effective treatment for those who respond poorly to other drugs ("treatment-resistant" or "refractory" schizophrenia),[96] but it has the potentially serious side effect of agranulocytosis (lowered white blood cell count) in less than 4% of patients.[2][3][97]

With respect to side effects typical antipsychotics are associated with a higher rate of extrapyramidal side effects while atypicals are associated with considerable weight gain, diabetes and risk of metabolic syndrome.[95] While atypicals have fewer extrapyramidal side effects these differences are modest.[98] Some atypicals such as quetiapine and risperidone are associated with a higher risk of death compared to the typical antipsychotic perphenazine, while clozapine is associated with the lowest risk of death.[99] It remains unclear whether the newer antipsychotics reduce the chances of developing neuroleptic malignant syndrome, a rare but serious neurological disorder.[100]

For people who are unwilling or unable to take medication regularly, long-acting depot preparations of antipsychotics may be used to achieve control.[101] They reduce the risk of relapse to a greater degree than oral medications.[91] When used in combination with psychosocial interventions they may improve long-term adherence to treatment.[101] The American Psychiatric Association suggests considering stopping antipsychotics in some people if there are no symptoms for more than a year.[92]

Psychosocial

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A number of psychosocial interventions may be useful in the treatment of schizophrenia including: family therapy,[102] assertive community treatment, supported employment, cognitive remediation,[103] skills training, cognitive behavioral therapy (CBT), token economic interventions, and psychosocial interventions for substance use and weight management.[104] Family therapy or education, which addresses the whole family system of an individual, may reduce relapses and hospitalizations.[102] The evidence for CBT's effectiveness in either reducing symptoms or preventing relapse is minimal.[105][106] Art or drama therapy have not been well-researched.[107][108]

Prognosis

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Hovedartikel: Prognosis of schizophrenia.

Schizophrenia has great human and economic costs.[2] It results in a decreased life expectancy of 12–15 years, primarily because of its association with obesity, sedentary lifestyles, and smoking, with an increased rate of suicide playing a lesser role.[2] These differences in life expectancy increased between the 1970s and 1990s,[109] and between the 1990s and first decade of the 21st century did not change substantially in a health system with open access to care (Finland).[99]

Schizophrenia is a major cause of disability, with active psychosis ranked as the third-most-disabling condition after quadriplegia and dementia and ahead of paraplegia and blindness.[110] Approximately three-fourths of people with schizophrenia have ongoing disability with relapses[23] and 16.7 million people globally are deemed to have moderate or severe disability from the condition.[111] Some people do recover completely and others function well in society.[112] Most people with schizophrenia live independently with community support.[2] In people with a first episode of psychosis a good long-term outcome occurs in 42%, an intermediate outcome in 35% and a poor outcome in 27%.[113] Outcomes for schizophrenia appear better in the developing than the developed world.[114] These conclusions, however, have been questioned.[115][116]

There is a higher than average suicide rate associated with schizophrenia. This has been cited at 10%, but a more recent analysis of studies and statistics revises the estimate to 4.9%, most often occurring in the period following onset or first hospital admission.[7][117] Several times more (20 to 40%) attempt suicide at least once.[118][119] There are a variety of risk factors, including male gender, depression, and a high intelligence quotient.[118]

Schizophrenia and smoking have shown a strong association in studies world-wide.[120][121] Use of cigarettes is especially high in individuals diagnosed with schizophrenia, with estimates ranging from 80% to 90% being regular smokers, as compared to 20% of the general population.[121] Those who smoke tend to smoke heavily, and additionally smoke cigarettes with high nicotine content.[119] Some evidence suggests that paranoid schizophrenia may have a better prospect than other types of schizophrenia for independent living and occupational functioning.[122]

Epidemiology

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Disability-adjusted life year for schizophrenia per 100,000 inhabitants in 2004.
     no data      ≤ 185      185–197      197–207      207–218      218–229      229–240
     240–251      251–262      262–273      273–284      284–295      ≥ 295
Hovedartikel: Epidemiology of schizophrenia.

Schizophrenia affects around 0.3–0.7% of people at some point in their life,[2] or 24 million people worldwide as of 2011.[123] It occurs 1.4 times more frequently in males than females and typically appears earlier in men[3]—the peak ages of onset are 20–28 years for males and 26–32 years for females.[124] Onset in childhood is much rarer,[125] as is onset in middle- or old age.[126] Despite the received wisdom that schizophrenia occurs at similar rates worldwide, its prevalence varies across the world,[127] within countries,[128] and at the local and neighborhood level.[129] It causes approximately 1% of worldwide disability adjusted life years.[3] The rate of schizophrenia varies up to threefold depending on how it is defined.[2]

In 2000, the World Health Organization found the prevalence and incidence of schizophrenia to be roughly similar around the world, with age-standardized prevalence per 100,000 ranging from 343 in Africa to 544 in Japan and Oceania for men and from 378 in Africa to 527 in Southeastern Europe for women.[130]

History

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Hovedartikel: History of schizophrenia.

The history of schizophrenia is complex and does not lend itself easily to a linear narrative.[131] Accounts of a schizophrenia-like syndrome are thought to be rare in the historical record before the 19th century, although reports of irrational, unintelligible, or uncontrolled behavior were common. A detailed case report in 1797 concerning James Tilly Matthews, and accounts by Phillipe Pinel published in 1809, are often regarded as the earliest cases of the illness in the medical and psychiatric literature.[132] The Latinized term dementia praecox was first used by German alienist Heinrich Schule in 1886 and then in 1891 by Arnold Pick in a case report of a psychotic disorder (hebephrenia). In 1893 Emil Kraepelin borrowed the term from Schule and Pick and in 1899 introduced a broad new distinction in the classification of mental disorders between dementia praecox and mood disorder (termed manic depression and including both unipolar and bipolar depression).[133] Kraepelin believed that dementia praecox was probably caused by a long-term, smouldering systemic or "whole body" disease process that affected many organs and peripheral nerves in the body but which affected the brain after puberty in a final decisive cascade.[134] His use of the term dementia distinguished it from other forms of dementia such as Alzheimer's disease which typically occur later in life.[135] It is sometimes argued that the use of the term démence précoce in 1852 by the French physician Bénédict Morel constitutes the medical discovery of schizophrenia. However this account ignores the fact that there is little to connect Morel's descriptive use of the term and the independent development of the dementia praecox disease concept at the end of the nineteenth-century.[136]

Molecule of chlorpromazine (trade name Thorazine), which revolutionized treatment of schizophrenia in the 1950s

The word schizophrenia—which translates roughly as "splitting of the mind" and comes from the Greek roots schizein (σχίζειν, "to split") and phrēn, phren- (φρήν, φρεν-, "mind")[137]—was coined by Eugen Bleuler in 1908 and was intended to describe the separation of function between personality, thinking, memory, and perception. American and British interpretations of Beuler led to the claim that he described its main symptoms as 4 A's: flattened Affect, Autism, impaired Association of ideas and Ambivalence.[138][139] Bleuler realized that the illness was not a dementia, as some of his patients improved rather than deteriorated, and thus proposed the term schizophrenia instead. Treatment was revolutionized in the mid-1950s with the development and introduction of chlorpromazine.[140]

In the early 1970s, the diagnostic criteria for schizophrenia were the subject of a number of controversies which eventually led to the operational criteria used today. It became clear after the 1971 US-UK Diagnostic Study that schizophrenia was diagnosed to a far greater extent in America than in Europe.[141] This was partly due to looser diagnostic criteria in the US, which used the DSM-II manual, contrasting with Europe and its ICD-9. David Rosenhan's 1972 study, published in the journal Science under the title "On being sane in insane places", concluded that the diagnosis of schizophrenia in the US was often subjective and unreliable.[142] These were some of the factors leading to the revision not only of the diagnosis of schizophrenia, but the revision of the whole DSM manual, resulting in the publication of the DSM-III in 1980.[143] The term schizophrenia is commonly misunderstood to mean that affected persons have a "split personality". Although some people diagnosed with schizophrenia may hear voices and may experience the voices as distinct personalities, schizophrenia does not involve a person changing among distinct multiple personalities. The confusion arises in part due to the literal interpretation of Bleuler's term schizophrenia (Bleuler originally associated Schizophrenia with dissociation and included split personality in his category of Schizophrenia[144][145]). Dissociative identity disorder (having a "split personality") was also often misdiagnosed as Schizophrenia based on the loose criteria in the DSM-II.[145][146] The first known misuse of the term to mean "split personality" was in an article by the poet T. S. Eliot in 1933.[147] Other scholars have traced earlier roots.[148]

Society and culture

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Se også Se også: List of people with schizophrenia.
The term schizophrenia was coined by Eugen Bleuler.

In 2002 the term for schizophrenia in Japan was changed from Seishin-Bunretsu-Byō 精神分裂病 (mind-split-disease) to Tōgō-shitchō-shō 統合失調症 (integration disorder) to reduce stigma.[149] The new name was inspired by the biopsychosocial model; it increased the percentage of patients who were informed of the diagnosis from 37% to 70% over three years.[150]

In the United States, the cost of schizophrenia—including direct costs (outpatient, inpatient, drugs, and long-term care) and non-health care costs (law enforcement, reduced workplace productivity, and unemployment)—was estimated to be $62.7 billion in 2002.[151] The book and film A Beautiful Mind chronicles the life of John Forbes Nash, a Nobel Prize-winning mathematician who was diagnosed with schizophrenia.

Violence

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Individuals with severe mental illness including schizophrenia are at a significantly greater risk of being victims of both violent and non-violent crime.[152] On the other hand, schizophrenia has sometimes been associated with a higher rate of violent acts, although this is primarily due to higher rates of drug use.[153] Rates of homicide linked to psychosis are similar to those linked to substance misuse, and parallel the overall rate in a region.[154] What role schizophrenia has on violence independent of drug misuse is controversial, but certain aspects of individual histories or mental states may be factors.[155]

Media coverage relating to schizophrenia tends to revolve around rare but unusual acts of violence. Furthermore, in a large, representative sample from a 1999 study, 12.8% of Americans believed that individuals with schizophrenia were "very likely" to do something violent against others, and 48.1% said that they were "somewhat likely" to. Over 74% said that people with schizophrenia were either "not very able" or "not able at all" to make decisions concerning their treatment, and 70.2% said the same of money management decisions.[156] The perception of individuals with psychosis as violent has more than doubled in prevalence since the 1950s, according to one meta-analysis.[157]

See also

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Referencer

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Litteratur

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  • Cullberg, Johan (1999). Dynamisk Psykiatri. København: Hans Reitzels Forlag. ISBN 87-412-3092-2.
  • Kasper, Siegfried (2009). Schizophrenia. United Kingdom: Informa Healthcare. s. 377. ISBN 13: 978-1-4200-8004-9. {{cite book}}: |access-date= kræver at |url= også er angivet (hjælp); Tjek |isbn=: invalid character (hjælp); Tjek datoværdier i: |accessdate= (hjælp); Ukendt parameter |coauthors= ignoreret (|author= foreslået) (hjælp)

Eksterne henvisninger

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Fodnoter

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