Editing Schizophrenia (section)

==Signs and symptoms==
Schizophrenia is a [[mental disorder]] characterized by significant alterations in [[perception]], thoughts, mood, and behavior.<ref name=NICE2014/> Symptoms are described in terms of [[Signs and symptoms#Types|positive]], negative, and [[cognitive deficit|cognitive symptoms]].<ref name=NIH2022/><ref>{{cite journal |vauthors=Stępnicki P, Kondej M, Kaczor AA |title=Current Concepts and Treatments of Schizophrenia |journal= Molecules|volume=23 |issue=8 |date=20 August 2018 |pmid=30127324|doi=10.3390/molecules23082087 |pmc=6222385 |page=2087|doi-access=free }}</ref> The positive symptoms of schizophrenia are the same for any [[psychosis]] and are sometimes referred to as psychotic symptoms. These may be present in any of the different psychoses and are often transient, making early diagnosis of schizophrenia problematic. Psychosis noted for the first time in a person who is later diagnosed with schizophrenia is referred to as a first-episode psychosis (FEP).<ref name=RAISE>{{cite web |title=RAISE Questions and Answers |url=https://www.nimh.nih.gov/health/topics/schizophrenia/raise/raise-questions-and-answers.shtml#4 |publisher= US [[National Institute of Mental Health]]|access-date=29 December 2019}}</ref><ref>{{cite journal | vauthors = Marshall M | title = Association between duration of untreated psychosis and outcome in cohorts of first-episode patients: a systematic review | journal = Archives of General Psychiatry | date = September 2005 | volume = 62 | issue = 9 | pages = 975–983 | doi = 10.1001/archpsyc.62.9.975 | pmid = 16143729| s2cid = 13504781 | doi-access =  }}</ref>

===Positive symptoms===
Positive symptoms are those symptoms that are not normally experienced, but are present in people during a psychotic episode in schizophrenia, including [[delusion]]s, [[hallucination]]s, and disorganized thoughts, speech and behavior or inappropriate affect, typically regarded as manifestations of psychosis.<ref name=RAISE/> Hallucinations occur at some point in the lifetimes of 80% of those with schizophrenia<ref name=Montagnese2021>{{cite journal |vauthors=Montagnese M, Leptourgos P, Fernyhough C, et al |title=A Review of Multimodal Hallucinations: Categorization, Assessment, Theoretical Perspectives, and Clinical Recommendations |journal=Schizophr Bull |volume=47 |issue=1 |pages=237–248 |date=January 2021 |pmid=32772114 |pmc=7825001 |doi=10.1093/schbul/sbaa101 }}</ref> and most commonly involve the sense of [[hearing]] (most often [[auditory verbal hallucinations|hearing voices]]), but can sometimes involve any of the other [[sense]]s such as [[taste]], [[visual perception|sight]], [[Olfaction|smell]], and [[tactile hallucination|touch]].<ref>{{cite journal |vauthors=Császár N, Kapócs G, Bókkon I |s2cid=52813070 |title=A possible key role of vision in the development of schizophrenia |journal=Reviews in the Neurosciences |volume=30 |issue=4 |pages=359–379 |date=27 May 2019 |pmid=30244235 |doi=10.1515/revneuro-2018-0022}}</ref> The frequency of hallucinations involving multiple senses is double the rate of those involving only one sense.<ref name=Montagnese2021/> They are also typically related to the content of the delusional theme.<ref name=DSMIV>{{cite book | author = American Psychiatric Association. Task Force on DSM-IV. | year = 2000 | title = Diagnostic and statistical manual of mental disorders: DSM-IV-TR. | publisher = American Psychiatric Pub. | isbn = 978-0-89042-025-6 | pages = 299–304 }}</ref> [[Delusion]]s are [[Delusion#Types|bizarre]] or [[Persecutory delusions|persecutory]] in nature. [[Self-disorder|Distortions of self-experience]] such as feeling that [[Thought broadcasting|others can hear one's thoughts]] (thought broadcasting delusion) or that [[Thought insertion|thoughts are being inserted into one's mind]], sometimes termed passivity phenomena, are also common.<ref name=Heinz2016>{{cite journal | vauthors = Heinz A, Voss M, Lawrie SM, Mishara A, Bauer M, Gallinat J, Juckel G, Lang U, Rapp M, Falkai P, Strik W, Krystal J, Abi-Dargham A, Galderisi S | title = Shall we really say goodbye to first rank symptoms? | journal = European Psychiatry | volume = 37 | pages = 8–13 | date = September 2016 | pmid = 27429167 | doi = 10.1016/j.eurpsy.2016.04.010 | s2cid = 13761854 }}</ref><ref name=NIH2022/> Positive symptoms generally respond well to medication<ref name=Lancet2016/> and become reduced over the course of the illness, perhaps linked to the age-related decline in dopamine activity.<ref name=DSM5/>

===Negative symptoms===
Negative symptoms are deficits of normal emotional responses, or of other thought processes. The five recognized domains of negative symptoms are: [[blunted affect]] – showing flat expressions (monotone) or little emotion; [[alogia]] – a poverty of speech; [[anhedonia]] – an inability to feel pleasure; [[asociality]] – the lack of desire to form relationships, and [[avolition]] – a lack of motivation and [[apathy]].<ref name=Adida2015>{{cite journal |vauthors=Adida M, Azorin JM, Belzeaux R, Fakra E |title=[Negative Symptoms: Clinical and Psychometric Aspects] |journal=L'Encephale |volume=41 |issue=6 Suppl 1 |pages=6S15–17 |date=December 2015 |pmid=26776385 |doi=10.1016/S0013-7006(16)30004-5}}</ref><ref>{{cite journal |vauthors=Mach C, Dollfus S |title=[Scale for Assessing Negative Symptoms in Schizophrenia: A Systematic Review] |journal=L'Encephale |volume=42 |issue=2 |pages=165–171 |date=April 2016 |pmid=26923997 |doi=10.1016/j.encep.2015.12.020}}</ref> Avolition and anhedonia are seen as motivational deficits resulting from impaired reward processing.<ref>{{cite book |vauthors=Waltz JA, Gold JM |title=Behavioral Neuroscience of Motivation |chapter=Motivational Deficits in Schizophrenia and the Representation of Expected Value | series = Current Topics in Behavioral Neurosciences|volume=27 |pages=375–410 |date=2016 |pmid=26370946 |doi=10.1007/7854_2015_385 |pmc=4792780 |isbn=978-3-319-26933-7 }}</ref><ref name=Husain2018>{{cite journal |vauthors=Husain M, Roiser JP |s2cid=49428707 |title=Neuroscience of apathy and anhedonia: a transdiagnostic approach. |journal=Nature Reviews. Neuroscience|volume=19 |issue=8 |pages=470–484 |date=August 2018 |pmid=29946157 |doi=10.1038/s41583-018-0029-9|url=https://ora.ox.ac.uk/objects/uuid:3e481f87-0ede-47dd-bdd8-2db78dfd3694 }}</ref> Reward is the main driver of motivation and this is mostly mediated by dopamine.<ref name=Husain2018/> It has been suggested that negative symptoms are multidimensional and they have been categorised into two subdomains of apathy or lack of motivation, and diminished expression.<ref name=Adida2015/><ref name=Galderisi2018>{{cite journal |vauthors=Galderisi S, Mucci A, Buchanan RW, Arango C |title=Negative symptoms of schizophrenia: new developments and unanswered research questions |journal=The Lancet. Psychiatry |volume=5 |issue=8 |pages=664–677 |date=August 2018 |pmid=29602739 |doi=10.1016/S2215-0366(18)30050-6 |s2cid=4483198 }}</ref> Apathy includes avolition, anhedonia, and social withdrawal; diminished expression includes blunt affect and alogia.<ref>{{cite journal |vauthors=Klaus F, Dorsaz O, Kaiser S |title=[Negative symptoms in schizophrenia – overview and practical implications] |journal=Revue médicale suisse |volume=14 |issue=619 |pages=1660–1664 |date=19 September 2018 |doi=10.53738/REVMED.2018.14.619.1660 |pmid=30230774|s2cid=246764656 }}</ref> Sometimes diminished expression is treated as both verbal and non-verbal.<ref>{{cite journal |vauthors=Batinic B |title=Cognitive Models of Positive and Negative Symptoms of Schizophrenia and Implications for Treatment. |journal=Psychiatria Danubina |volume=31 |issue=Suppl 2 |pages=181–184 |date=June 2019 |pmid=31158119}}</ref>

Apathy accounts for around 50% of the most often found negative symptoms and affects functional outcome and subsequent quality of life. Apathy is related to disrupted cognitive processing affecting memory and planning, including goal-directed behaviour.<ref>{{cite journal |vauthors=Bortolon C, Macgregor A, Capdevielle D, Raffard S |s2cid=13411386 |title=Apathy in schizophrenia: A review of neuropsychological and neuroanatomical studies. |journal=Neuropsychologia |volume=118 |issue=Pt B |pages=22–33 |date=September 2018 |pmid=28966139 |doi=10.1016/j.neuropsychologia.2017.09.033}}</ref> The two subdomains have suggested a need for separate treatment approaches.<ref name=Marder2014>{{cite journal |vauthors=Marder SR, Kirkpatrick B |s2cid=5172022 |title=Defining and measuring negative symptoms of schizophrenia in clinical trials |journal=European Neuropsychopharmacology|volume=24 |issue=5 |pages=737–743 |date=May 2014 |pmid=24275698 |doi=10.1016/j.euroneuro.2013.10.016}}</ref> A lack of distress is another noted negative symptom.<ref name=Tatsumi2020>{{cite journal |vauthors=Tatsumi K, Kirkpatrick B, Strauss GP, Opler M |s2cid=211141678 |title=The brief negative symptom scale in translation: A review of psychometric properties and beyond |journal=European Neuropsychopharmacology |date=April 2020 |volume=33 |pages=36–44 |doi=10.1016/j.euroneuro.2020.01.018 |pmid=32081498}}</ref> A distinction is often made between those negative symptoms that are inherent to schizophrenia, termed primary; and those that result from positive symptoms, from the side effects of antipsychotics, substance use disorder, and social deprivation, termed secondary negative symptoms.<ref>{{cite journal |vauthors=Klaus F, Kaiser S, Kirschner M |title=[Negative Symptoms in Schizophrenia – an Overview]. |journal=Therapeutische Umschau |volume=75 |issue=1 |pages=51–56 |date=June 2018 |pmid=29909762 |doi=10.1024/0040-5930/a000966|s2cid=196502392 }}</ref> Negative symptoms are less responsive to medication and the most difficult to treat.<ref name=Marder2014/> However, if properly assessed, secondary negative symptoms are amenable to treatment.<ref name=Galderisi2018/> There is some evidence that the negative symptoms of schizophrenia are amenable to psychostimulant medication, although such drugs have varying degrees of risk for causing positive psychotic symptoms.<ref name="sciencedirect.com">{{Cite journal |last1=Lindenmayer |first1=Jean-Pierre |last2=Nasrallah |first2=Henry |last3=Pucci |first3=Michael |last4=James |first4=Steven |last5=Citrome |first5=Leslie |date=2013-07-01 |title=A systematic review of psychostimulant treatment of negative symptoms of schizophrenia: Challenges and therapeutic opportunities |url=https://www.sciencedirect.com/science/article/abs/pii/S0920996413001655 |journal=Schizophrenia Research |volume=147 |issue=2 |pages=241–252 |doi=10.1016/j.schres.2013.03.019 |pmid=23619055 |issn=0920-9964}}</ref>

Scales for specifically assessing the presence of negative symptoms, and for measuring their severity, and their changes have been introduced since the earlier scales such as the [[Positive and Negative Syndrome Scale|PANNS]] that deals with all types of symptoms.<ref name=Marder2014/> These scales are the ''Clinical Assessment Interview for Negative Symptoms'' (CAINS), and the ''Brief Negative Symptom Scale'' (BNSS) also known as second-generation scales.<ref name=Marder2014/><ref name=Tatsumi2020/><ref>{{cite journal |vauthors=Wójciak P, Rybakowski J |title=Clinical picture, pathogenesis and psychometric assessment of negative symptoms of schizophrenia. |journal=Psychiatria Polska |volume=52 |issue=2 |pages=185–197 |date=30 April 2018 |pmid=29975360 |doi=10.12740/PP/70610|doi-access=free }}</ref> In 2020, ten years after its introduction, a cross-cultural study of the use of BNSS found valid and reliable [[psychometric]] evidence for its five-domain structure cross-culturally. The BNSS can assess both the presence and severity of negative symptoms of the five recognized domains and an additional item of reduced normal distress. It has been used to measure changes in negative symptoms in trials of psychosocial and pharmacological interventions.<ref name=Tatsumi2020/>

===Cognitive symptoms===
{{See also |Visual processing abnormalities in schizophrenia}}
[[File:SchizophreniaBrain.jpg|thumb|Map of deficits in [[neural tissue]] throughout the human brain in a patient with schizophrenia. The most deficient areas are magenta, while the least deficient areas are blue.]]
An estimated 70% of those with schizophrenia have cognitive deficits, and these are most pronounced in early-onset and late-onset illness.<ref name=Murante2017/><ref name=Kar2016>{{cite journal |vauthors=Kar SK, Jain M |title=Current understandings about cognition and the neurobiological correlates in schizophrenia |journal=Journal of Neurosciences in Rural Practice |volume=7 |issue=3 |pages=412–418 |date=July 2016 |pmid=27365960 |doi=10.4103/0976-3147.176185 |pmc=4898111 |doi-access=free }}</ref> These are often evident long before the onset of illness in the [[Prodromal schizophrenia|prodromal stage]], and may be present in childhood or early adolescence.<ref name=Bozikas2011/><ref>{{cite journal | vauthors = Shah JN, Qureshi SU, Jawaid A, Schulz PE | s2cid = 10970088 | title = Is there evidence for late cognitive decline in chronic schizophrenia? | journal = The Psychiatric Quarterly | volume = 83 | issue = 2 | pages = 127–144 | date = June 2012 | pmid = 21863346 | doi = 10.1007/s11126-011-9189-8 }}</ref> They are a core feature but not considered to be core symptoms, as are positive and negative symptoms.<ref name=Biedermann2016>{{cite journal |vauthors = Biedermann F, Fleischhacker WW | title = Psychotic disorders in DSM-5 and ICD-11 | journal = CNS Spectrums | date = August 2016 | volume = 21 | issue = 4 | pages = 349–354 | doi = 10.1017/S1092852916000316 | pmid = 27418328| s2cid = 24728447 }}</ref><ref name=Vidailhet2013/> However, their presence and degree of dysfunction is taken as a better indicator of functionality than the presentation of core symptoms.<ref name=Bozikas2011>{{cite journal | vauthors = Bozikas VP, Andreou C | s2cid = 26135485 | title = Longitudinal studies of cognition in first episode psychosis: a systematic review of the literature | journal = The Australian and New Zealand Journal of Psychiatry | volume = 45 | issue = 2 | pages = 93–108 | date = February 2011 | pmid = 21320033 | doi = 10.3109/00048674.2010.541418 }}</ref> Cognitive deficits become worse at first episode psychosis but then return to baseline, and remain fairly stable over the course of the illness.<ref name=Hashimoto2019/><ref name=Green2019/>

The deficits in [[cognition]] are seen to drive the negative psychosocial outcome in schizophrenia, and are claimed{{By whom|date=March 2024}} to equate to a possible reduction in IQ from the norm of 100 to 70–85.<ref>{{cite journal | vauthors=Javitt DC, Sweet RA |title=Auditory dysfunction in schizophrenia: integrating clinical and basic features. |journal=Nature Reviews. Neuroscience|volume=16 |issue=9 |pages=535–550 |date=September 2015|pmid=26289573|doi=10.1038/nrn4002|pmc=4692466 }}</ref><ref name=Megreya2016>{{cite journal |vauthors=Megreya AM |s2cid=26125559 |title=Face perception in schizophrenia: a specific deficit |journal=Cognitive Neuropsychiatry |volume=21 |issue=1 |pages=60–72 |date=2016 |pmid=26816133|doi=10.1080/13546805.2015.1133407}}</ref>{{failed verification|date=January 2025}} Cognitive deficits may be of [[neurocognition]] (nonsocial) or of [[social cognition]].<ref name=Murante2017>{{cite journal |vauthors=Murante T, Cohen CI |title=Cognitive Functioning in Older Adults With Schizophrenia |journal=Focus (American Psychiatric Publishing) |volume=15 |issue=1 |pages=26–34 |date=January 2017 |pmid=31975837 |doi=10.1176/appi.focus.20160032|pmc=6519630 }}</ref> Neurocognition is the ability to receive and remember information, and includes verbal fluency, [[memory]], [[reason]]ing, [[problem solving]], [[Information processing (psychology)|speed of processing]], and [[auditory system|auditory]] and visual perception.<ref name=Green2019/> [[Verbal memory]] and attention are seen to be the most affected.<ref name=Megreya2016/><ref>{{cite journal |vauthors=Eack SM |title=Cognitive remediation: a new generation of psychosocial interventions for people with schizophrenia |journal=Social Work |volume=57 |issue=3 |pages=235–246 |date=July 2012 |pmid=23252315 |doi=10.1093/sw/sws008|pmc=3683242 }}</ref> Verbal memory impairment is associated with a decreased level of [[semantic processing]] (relating meaning to words).<ref>{{cite journal
|vauthors=Pomarol-Clotet E, Oh M, Laws KR, McKenna PJ | title=Semantic priming in schizophrenia: systematic review and meta-analysis |journal=The British Journal of Psychiatry |volume=192 |issue=2 | pages=92–97 |date=February 2008 |pmid=18245021 |doi=10.1192/bjp.bp.106.032102 | hdl=2299/2735 |doi-access=free |hdl-access=free }}</ref> Another memory impairment is that of [[episodic memory]].<ref>{{cite journal | vauthors = Goldberg TE, Keefe RS, Goldman RS, Robinson DG, Harvey PD | title = Circumstances under which practice does not make perfect: a review of the practice effect literature in schizophrenia and its relevance to clinical treatment studies | journal = Neuropsychopharmacology | volume = 35 | issue = 5 | pages = 1053–1062 | date = April 2010 | pmid = 20090669 | pmc = 3055399 | doi = 10.1038/npp.2009.211 | df = dmy-all }}</ref> An impairment in visual perception that is consistently found in schizophrenia is that of [[visual backward masking]].<ref name=Green2019/> [[Visual processing]] impairments include an inability to perceive complex [[visual illusion]]s.<ref>{{cite journal |vauthors=King DJ, Hodgekins J, Chouinard PA, Chouinard VA, Sperandio I |title=A review of abnormalities in the perception of visual illusions in schizophrenia. |journal=Psychonomic Bulletin and Review |volume=24 |issue=3 |pages=734–751 |date=June 2017 |pmid=27730532 |doi=10.3758/s13423-016-1168-5 |pmc = 5486866}}</ref> Social cognition is concerned with the mental operations needed to interpret, and understand the self and others in the social world.<ref name=Green2019>{{cite journal |vauthors=Green MF, Horan WP, Lee J |title=Nonsocial and social cognition in schizophrenia: current evidence and future directions |journal=World Psychiatry|volume=18 |issue=2 |pages=146–161 |date=June 2019 |pmid=31059632 |doi=10.1002/wps.20624|pmc=6502429 }}</ref><ref name=Murante2017/> This is also an associated impairment, and [[Face perception#Schizophrenia|facial emotion perception]] is often found to be difficult.<ref>{{cite journal | vauthors = Kohler CG, Walker JB, Martin EA, Healey KM, Moberg PJ | title = Facial emotion perception in schizophrenia: a meta-analytic review | journal = Schizophrenia Bulletin | volume = 36 | issue = 5 | pages = 1009–1019 | date = September 2010 | pmid = 19329561 | pmc = 2930336 | doi = 10.1093/schbul/sbn192 | df = dmy-all }}</ref><ref>{{cite journal | vauthors = Le Gall E, Iakimova G | title = [Social cognition in schizophrenia and autism spectrum disorder: Points of convergence and functional differences] | journal = L'Encéphale | volume = 44 | issue = 6 | pages = 523–537 | date = December 2018 | pmid = 30122298 | doi = 10.1016/j.encep.2018.03.004 | s2cid = 150099236 }}</ref> Facial perception is critical for ordinary social interaction.<ref>{{cite journal | vauthors = Grill-Spector K, Weiner KS, Kay K, Gomez J | title = The Functional Neuroanatomy of Human Face Perception | journal = Annual Review of Vision Science | volume = 3 | pages = 167–196 | date = September 2017 | pmid = 28715955 | pmc = 6345578 | doi = 10.1146/annurev-vision-102016-061214 }}</ref> Cognitive impairments do not usually respond to antipsychotics, and there are a number of [[#Psychosocial interventions|interventions]] that are used to try to improve them; [[cognitive remediation therapy]] is of particular help.<ref name=Vidailhet2013/>

[[Neurological soft signs]] of clumsiness and loss of fine motor movement are often found in schizophrenia, which may resolve with effective treatment of FEP.<ref name=Ferri2019/><ref>{{cite journal |vauthors=Fountoulakis KN, Panagiotidis P, Kimiskidis V, Nimatoudis I, Gonda X |s2cid=56476015 |title=Neurological soft signs in familial and sporadic schizophrenia |journal=Psychiatry Research |volume=272 |pages=222–229 |date=February 2019 |pmid=30590276 |doi=10.1016/j.psychres.2018.12.105 }}</ref>

===Onset===
{{Further|Basic symptoms of schizophrenia}}
{{See also|Childhood schizophrenia|Adolescence#Changes in the brain}}
Onset typically occurs between the late teens and early 30s, with the peak incidence occurring in males in the early to mid-twenties, and in females in the late twenties.<ref name=NIH2022/><ref name=DSM5/><ref name=Ferri2019/> Onset before the age of 17 is known as early-onset,<ref>{{cite journal |vauthors=Bourgou Gaha S, Halayem Dhouib S, Amado I, Bouden A |title=[Neurological soft signs in early onset schizophrenia] |journal=L'Encephale |volume=41 |issue=3 |pages=209–214 |date=June 2015 |pmid=24854724 |doi=10.1016/j.encep.2014.01.005}}</ref> and before the age of 13, as can sometimes occur, is known as [[childhood schizophrenia]] or very early-onset.<ref name=DSM5 /><ref name=DaFonseca2018>{{cite journal |vauthors=Da Fonseca D, Fourneret P |title=[Very early onset schizophrenia] |journal=L'Encephale |volume=44 |issue=6S |pages=S8–S11 |date=December 2018 |pmid=30935493 |doi=10.1016/S0013-7006(19)30071-5|s2cid=150798223 }}</ref> Onset can occur between the ages of 40 and 60, known as late-onset schizophrenia.<ref name=Murante2017/> Onset over the age of 60, which may be difficult to differentiate as schizophrenia, is known as very-late-onset schizophrenia-like psychosis.<ref name=Murante2017/> Late onset has shown that a higher rate of females are affected; they have less severe symptoms and need lower doses of antipsychotics.<ref name=Murante2017/> The tendency for earlier onset in males is later seen to be balanced by a [[post-menopausal]] increase in the development in females. [[Estrogen]] produced pre-menopause has a dampening effect on dopamine receptors but its protection can be overridden by a genetic overload.<ref>{{cite journal |vauthors=Häfner H |title=From Onset and Prodromal Stage to a Life-Long Course of Schizophrenia and Its Symptom Dimensions: How Sex, Age, and Other Risk Factors Influence Incidence and Course of Illness |journal=Psychiatry Journal |volume=2019 |page=9804836 |date=2019 |pmid=31139639 |doi=10.1155/2019/9804836 |pmc=6500669 |doi-access=free }}</ref> There has been a dramatic increase in the numbers of older adults with schizophrenia.<ref>{{cite journal | vauthors = Cohen CI, Freeman K, Ghoneim D, Vengassery A, Ghezelaiagh B, Reinhardt MM | title = Advances in the Conceptualization and Study of Schizophrenia in Later Life | journal = The Psychiatric Clinics of North America | volume = 41 | issue = 1 | pages = 39–53 | date = March 2018 | pmid = 29412847 | doi = 10.1016/j.psc.2017.10.004 }}</ref>

Onset may happen suddenly or may occur after the slow and gradual development of a number of signs and symptoms, a period known as the [[Prodromal schizophrenia|prodromal stage]].<ref name=DSM5 /> Up to 75% of those with schizophrenia go through a prodromal stage.<ref name=George2017>{{cite journal |vauthors=George M, Maheshwari S, Chandran S, Manohar JS, Sathyanarayana Rao TS |title=Understanding the schizophrenia prodrome |journal=Indian Journal of Psychiatry |volume=59 |issue=4 |pages=505–509 |date=October 2017 |pmid=29497198 |doi=10.4103/psychiatry.IndianJPsychiatry_464_17|doi-broken-date=1 November 2024 |doi-access=free|pmc=5806335 }}</ref> The negative and cognitive symptoms in the prodrome stage can precede FEP (first episode psychosis) by many months and up to five years.<ref name=Hashimoto2019>{{cite journal |vauthors=Hashimoto K |s2cid=195814019 |title=Recent Advances in the Early Intervention in Schizophrenia: Future Direction from Preclinical Findings |journal=Current Psychiatry Reports |volume=21 |issue=8 |page=75 |date=5 July 2019 |pmid=31278495 |doi=10.1007/s11920-019-1063-7}}</ref><ref name=Conroy2018>{{cite journal |vauthors=Conroy S, Francis M, Hulvershorn LA |title=Identifying and treating the prodromal phases of bipolar disorder and schizophrenia |journal=Current Treatment Options in Psychiatry |volume=5 |issue=1 |pages=113–128 |date=March 2018 |pmid=30364516 |doi=10.1007/s40501-018-0138-0|pmc=6196741 }}</ref> The period from FEP and treatment is known as the duration of untreated psychosis (DUP) which is seen to be a factor in functional outcome. The prodromal stage is the high-risk stage for the development of psychosis.<ref name=Green2019/> Since the progression to first episode psychosis is not inevitable, an alternative term is often preferred of [[at risk mental state]].<ref name=Green2019/> Cognitive dysfunction at an early age impacts a young person's usual cognitive development.<ref>{{cite journal |vauthors=Lecardeur L, Meunier-Cussac S, Dollfus S |title=[Cognitive deficits in first episode psychosis patients and people at risk for psychosis: from diagnosis to treatment] |journal=L'Encephale |volume=39 |pages=S64-71 |date=May 2013 |issue=Suppl 1 |pmid=23528322 |doi=10.1016/j.encep.2012.10.011}}</ref> Recognition and early intervention at the prodromal stage would minimize the associated disruption to educational and social development and has been the focus of many studies.<ref name=Hashimoto2019/><ref name=Conroy2018/>