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Home , Stimulant psychosis

BRITISH JOURNAL OF (2004), 185, 196^204 REVIEW ARTICLE

Stimulant : systematic review using the search terms , CRACK, , METHYL- AMPHETAMINE, METHAMPHETA- CATHERINE CURRAN, NEETHA BYRAPPA and ANDREW McBRIDE MINE, METHAMFETAMINE, DD-- AMPHETAMINE, DEXAMPHETAMINE, ,PSYCHOACTIVE , CNS DRUGS and -INDUCED PSYCHOSIS (for stimu- lants)lants) andand PSYCHOSIS, PSYCHOSES, and SCHIZO- AFFECTIVE (for psychoses). Where Medi- cal Subject Headings (MeSH) terms were Background Psychosis associated with have been used for many cen- available, they were exploded and com- stimulantuse is anincreasing problem, but turies but only latterly have there been bined. Papers were checked for references reports of associated psychosis (Guttmann to other relevant studies. there islittle research evidence aboutthe & Sargant, 1937), culminating in Connell’s nature ofofthe the problem andandits its monograph (Connell, 1958), which re- Identifying and evaluating management. viewed cases of ‘stimulant’ psychosis that the studies resolved rapidly. In Japan, where there Following the initial searches by C.C., all Aims To critically review the literature was an epidemic of injected amphetamine experimental case–control and longitudinal on stimulant psychosis and sensitisation. use, the duration of psychosis appeared to studies were independently appraised by be prolonged and chronic (Koyama et aletal,, C.C. and N.B. Any disagreements on MethodMethod Systematic review of studies 1991). The theory was proposed that re- whether a study should be included were that have investigated stimulantuse and peated low doses of a stimulant lead to resolved by reference to the criteria. Three changes in the central nervous system psychosisin humans.The main outcome methodologically distinct types of studies (CNS) (Ellingwood & Kilbey, 1980), a measures wereincreasesin psychosis with were identified, which were reviewed form of ‘kindling’, which produces a psy- separately. Studies were included if they stimulant use, and differences between chotic illness similar to schizophrenia. Ani- met the following criteria. stimulantusers and non-users. mal experiments seem to support such an effect (Post & Kopanda, 1976). Others Experimental studies ResultsResults Fifty-four studies met the dispute this theory of sensitisation (e.g. inclusion criteria. Experimental studies Brabbins & Poole, 1996). If sensitisation Studies were included if: show that a single dose of a stimulantdrug is occurring, then early treatment and re- (a)(a)participantsparticipants were given stimulants can produce a brief increase in psychosis tention of stimulant users in (cocaine, or methyl- care services would appear to be desirable phenidate); and ratings (a‘response’) in 50^70% of to prevent chronic psychoses developing. (b)(b)participantsparticipants were monitored for poss- participants with schizophrenia and pre- There is a lack of good-quality evidence ible psychotic reactions; and existing acute psychotic symptoms, as to the effectiveness of this: a recent (c)(c)circumstancescircumstances of administration were unaffected by the presence of Cochrane review found no relevant trials (Srisurapanont et aletal, 2004).,2004). controlled for dose, route and timings medication.Those with The purpose of this study is to examine (if variable doses were given, this was schizophrenia who do not have acute evidence for the theory of sensitisation. The related to dose per kilogram or dose psychotic symptoms respond, but less hypothesis is that stimulant psychoses can according to physiological response or blood level); and frequently (30 %).There has been little be divided into a ‘toxic’ type of response researchintoresearch into the longer-term effects of and a chronic persisting response resulting (d)(d)psychosispsychosis or changes in psychosis were from longer-term use of stimulants. measured in a standardised fashion. use. Longitudinal studies Conclusions Compliance with METHOD antipsychotic medicationbysomeonewith Studies were included if: (a)(a)aa cohort of substance users with or schizophrenia will not prevent a relapse or We searched for experimental and obser- without psychosis, defined by opera- worsening of psychotic symptoms if vational studies in humans taking stimu- tional criteria, was followed up for a lants that investigated or described the stimulants are used.Low-dose defined period; and development of psychotic symptoms. We antipsychotic treatment may be beneficial did not include case series or cross-sectional (b)(b)stimulantstimulant users were identified and in stimulantusers,stimulant users, to prevent sensitisation. studies, as these give little information as to differentiated from other substance the direction of effect or changes over time. users in the report. Declaration of interest None. We performed electronic searches on Medline, PsycLIT and EMBASE psychiatry Case^control studies from the earliest dates available to 2001, Studies were included if:

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(a)(a)individualsindividuals using stimulants with stimulants. In the control group there was Longitudinal studies psychosis were compared with those a greater response to the second dose of Seven longitudinal studies met the inclusion using stimulants with no psychosis; or dexamfetamine than to the first. Partici- criteria (Table 2). Studies of this type were (b)(b)individualsindividuals with psychosis using stimu- pants with pre-existing psychosis showed most commonly excluded because of the lants were compared with control no such enhanced response to a second difficulty of separating stimulants from individuals with psychosis but with no dose.dose. the other substances used. Two studies history of drug use; or The study by Casey et aletal (1961)(1961) examined individuals prescribed stimulants: examined additional drug therapy in (c)(c)individualsindividuals using stimulants were adults with narcolepsy (Pawluck et aletal,, compared with individuals using non- patients with schizophrenia, all of whom 1995) and children with attention-deficit stimulant substances; and were taking antipsychotic medication hyperactivity disorder (Cherland & Fitz- regularly and had not responded to 200– patrick, 1999). Two of the 11 adults in (d)(d)StimulantStimulant users are identified and 600 mg of chlorpromazine taken daily for the first study developed acute psychotic differentiated from other substance at least 2 months. One arm of the study symptoms, as did 9 of the 192 children in users in the report. examined the addition of dexamfetamine the latter study. Two follow-up studies of as an adjunctive treatment for schizo- cocaine users (Gawin & Kleber, 1986; phrenia. There was no benefit from the RESULTSRESULTS CarrollCarroll et aletal, 1993) reported no case of addition of dexamfetamine 60 mg daily chronic psychosis. Sato et aletal (1983) studied compared with placebo, with worsen- A total of 84 experimental or observational ampheamphetaminetamine users who had previously ing of ‘hostile belligerency, paranoid studies were identified by the search and hadhadlong-lastinglong-lasting psychotic episodes who re- belligerency and thinking disturbance’. cross-referencing strategies. Initial agree- used a stimulant after long periods of absti- For 26 studies it was possible to ment on studies meeting the criteria in the nence. These individuals were found to perform a statistical analysis of differences review was present for 89% of the experi- relapse after using a lower dose of amphe- in psychotic response between controls, mental studies, 82% of the longitudinal tamine than they had used before first be- those with schizophrenia in remission studies and 75% of the case–control coming psychotic. In one case the person’s and those with positive symptoms, using studies. After discussion between the relapse seemingly was due to stress, with- the definitions provided by the studies to raters, it was agreed that 43 studies met out drug use. The researchers also con- determine the presence or absence of the criteriathecriteriaand were thus included in the ducted a small, uncontrolled trial of positive symptoms. There was a method- review.review. haloperidol 3 mg daily in eight of these ological difference between participants individuals, none of whom then relapsed given i.v. dexamfetamine and those Experimental studies following subsequent amphetamine use. given oral dexamfetamine or i.v. meth- IwanamiIwanami et aletal (1994) studied individuals A total of 32 experimental studies were amphetamine (see Table 6): the doses of who presented with a psychotic illness in included (Table 1). Twenty-eight of these dexamfetamine used intravenously were the presence of amphetamine use; they involved single doses of oral or intravenous lower and fixed, as opposed to being identified a small group whose psychotic (i.v.) dexamfetamine or methylphenidate variedaccording to body weight (dexamfet- symptoms persisted for several months given to individuals with schizophrenia, amine 20 mg as opposed to 0.5 mg/kg after ceasing amphetamine use who were and 9 of these 28 studies included a control methylphenidate). being prescribed antipsychotic treatment. group. One of the remaining 4 studies Across the 26 studies, 51.4% of those This group did not meet criteria for included a heterogeneous group of indivi- with schizophrenia who had positive symp- DSM–III schizophrenia (American Psychi- duals with psychosis and controls given toms (toms(nn¼149), 28.3% of those with schizo- atric Association, 1980) but had definite two doses of dexamfetamine orally 48 h phrenia in remission (nn¼69) and 10.2% of psychotic symptoms. apart (Strakowski et aletal, 1997). Two studies controls (controls(nn¼9) had a temporary increase in Kwapil (1996) reported a 10-year involved substance users (Cami et aletal, 2000;,2000; positive symptoms, usually lasting for only follow-up study of substance-using FarrenFarren et aletal, 2000). The final study (Casey a matter of hours. An analysis of the effects individuals and controls who scored highly et aletal, 1961) was a randomised controlled of the presence of positive symptoms v.v. ab-ab- on the Chapman Questionnaire ‘psychosis trial of 520 individuals with schizophrenia sence of positive symptoms in participants proneness’ section. This self-report ques- in which one group received dexamfeta- with schizophrenia found a significant tionnaire is designed to measure symptoms 22 mine orally for 20 weeks. All studies used difference (ww ¼46.3, d.f.46.3,d.f.¼1,1, PP550.0001).0.0001). and traits reported to be characteristic of some form of standardised rating scale – We also examined modulating effects of proneness to schizophrenia or psychosis. most commonly the Brief Psychiatric antipsychotic drugs on the psychotic re- The study showed that psychosis was not Rating Scale (BPRS) – to measure changes sponse. We did not detect a significant predicted by earlier substance use, but the resulting from stimulant use. A ‘response’ effect of antipsychotic medication in the small number of stimulant users meant that was considered to have occurred when response of participants with schizophrenia the power of the study was insufficient for a 22 changes were measured in the psychosis to a single dose of stimulant (ww ¼0.06,0.06, meaningful analysis of any link between component of the various scales. The d.f.d.f.¼1,1, PP¼0.80); this was true whether psychosis and stimulants. response to a single dose of stimulant, when the participants were defined as having present, was brief, seldom lasting more positive symptoms or as being in remission than a few hours. ((ww22¼0.16, d.f.0.16,d.f.¼1,1, PP¼0.68 for those with CaseCase^control ^ control studies The Strakowski et aletal (1997) study positive symptoms; ww22¼0.36, d.f.0.36,d.f.¼1,1, Most case–control studies identified by the looked for a response to repeated doses of PP¼0.55 for those in remission). search strategy were excluded because it

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Downloaded from https://www.cambridge.org/core. 24 Sep 2021 at 03:14:37, subject to the Cambridge Core terms of use. CURRCURRAN AN ET AL )) continued continued (( ]IBZM binding potential (increased ]IBZM binding potential (increased 123 123 dopamine transmission) Psychosis group did not show enhanced responsesecond with dose; controls did. No recordings forpatients individual Negative symptom measures reduced in both groups Comments All participants were in-patients High initial positive symptom score predictedafter high amphetamine score Mean negative symptom score significantly decreasedamphetamine; after positive symptom score showed a non- significant increase Lithium attenuated activation but not positive symptoms with reduced negative symptoms on pimozide Effects no different in people with or withouthistory lifetime of substance use Pre-infusion psychosis ratings did not correlate with dexamfetamine-induced changes reduction in [ 11showedanincreaseinextrapyramidalsymptoms including 3 who developed tardive dyskinesia Worsening positive symptoms correlated with lack of enlargement of VBR and better responseOnly to 1 treatment patient who showed no responseresponded in in first second trial Trend to lower negative symptoms in thosenegative symptoms with score. higher No recordings for individual patients Pimozide-treated patients who worsened had higher psychosis ratings dopamine transmission) Psychosis group did not show enhanced response with second dose; controls did. No recordings for individual patients Negative symptom measures reduced in both groups Comments All participants were in-patients High initial positive symptom score predictedafter high amphetamine score Mean negative symptom score significantly decreased after amphetamine; positive symptom score showed a non- significant increase Lithium attenuated activation but not positive symptoms Reduced negative symptoms on dexamfetamine correlated with reduced negative symptoms on pimozide Effects no different in people with or withouthistory lifetime of substance use r-nuinpsychosisPre-infusion ratings did not correlate with changes dexamfetamine-induced Worsening of positive symptoms associated with larger reduction in [ 11 showed an increase in extrapyramidalincluding symptoms 3 who developed tardive dyskinesia Worsening positive symptoms correlated with lackenlargement of of VBR and better responseOnly to 1 patient treatment who showed no response inresponded first in trial second Trend to lower negative symptoms in thosenegative with symptoms score. higher No recordings for individual patients Pimozide-treated patients who worsened had higher psychosis ratings ) ) Reduced negative symptoms on dexamfetamine correlated cc (1982 (1982 et aletal NR Yes (all) Decreased/no positive symptoms NR Yes Yes No 1. Yes 2. Yes2.Yes Yes Yes Yes YesYes NR Yes (all others) 1. Yes 2. Yes2.Yes YesYes 1. Yes 2. Yes2.Yes Yes (all) Yes (all) NR Decreased/no positive symptoms NR Yes Yes No 1. Yes Yes Yes Yes NR Yes (all others) Worsening of positive symptoms associated with larger 1. Yes 1. Yes Increased/new No 1. Yes (drug-free) positive symptoms Yes Yes Yes Yes Yes 2. Yes (on lithium) Results as for Van Kammen Yes Yes Yes Yes (schizophrenia) No (controls) 1. Yes (drug-free) 2. Yes (post-pimozide) 1. Yes (drug-free) 2. Yes No No Yes (all) Yes Increased/new positive symptoms Yes Yes Yes Yes 1. Yes (drug-free) 2. Yes (on lithium) Results as for Van Kammen Yes Yes Yes Yes Yes Yes (schizophrenia) No (controls) 1. Yes (drug-free) 2. Yes (post-pimozide) Yes 1. Yes (drug-free) 2. Yes 2, 48 h apart 2, 48 h apart Yes 66 2priortoand 2priortoand 2priortoand 2priortoand 2priortoand 2priortoand 66 66 66 Dexamfetamine 60 mg orally, daily for 20 weeks Dexamfetamine 30 mg orally Substance and dosage Dexamfetamine 0.25 mg/kg orally eaftmn 0.5Dexamfetamine mg/kg orally stat Dexamfetamine 0.5 mg/kg orally eaftmn 0.5Dexamfetamine mg/kg orally stat Dexamfetamine 20 mg infusion eaftmn 0.5Dexamfetamine mg/kg orally Dexamfetamine 30 mg orally stat Dexamfetamine 20 mg infusion Dexamfetamine 20 mg infusion/placebo infusion eaftmn 0.5Dexamfetamine mg/kg orally stat following pimozide treatment for 6 weeks eaftmn 0.3Dexamfetamine mg/kg i.v. eaftmn 20Dexamfetamine mg infusion Dexamfetamine 20 mg infusion following pimozide treatment for 6 weeks following pimozide treatment for 6 weeks Dexamfetamine 20 mg infusion Dexamfetamine 20 mg infusion Dexamfetamine 40 mg orally No Dexamfetamine 30 mg orally Substance and dosage Dexamfetamine 0.25 mg/kg orally Dexamfetamine 60 mg orally, daily for 20 weeks Yes 0.5Dexamfetamine mg/kg orally stat eaftmn 0.5Dexamfetamine mg/kg orally stat Dexamfetamine 20 mg infusion 0.5Dexamfetamine mg/kg orally Dexamfetamine 20 mg infusion eaftmn 0.5Dexamfetamine mg/kg orally stat following pimozide treatment for 6 weeks eaftmn 0.5Dexamfetamine mg/kg orally 0.3Dexamfetamine mg/kg i.v. Dexamfetamine 30 mg orally stat Dexamfetamine 20 mg infusion Dexamfetamine 20 mg infusion/placebo infusion Yes Dexamfetamine 20 mg infusion Dexamfetamine 20 mg infusion following pimozide treatment for 6 weeks Dexamfetamine 20 mg infusion following pimozide treatment for 6 weeks ) ) nn disorder (12) Other psychotic disorder (13) Controls (11) Study sample ( Schizophrenia (30) Schizophrenia (12) Schizophrenia (45) Schizophrenia (15) Controls (15) ciohei (22) Schizophrenia Schizophrenia (30) Schizophrenia (13) Substance users: ecstasy (14) Dexamfetamine 40 mg orally Studysample( Schizophrenia (520 ) Schizophrenia spectrum disorder (12) Other psychotic disorder (13) Psychosis (13) Controls (11) ciohei (21) Schizophrenia ciohei (26) Schizophrenia Schizophrenia (17) Schizophrenia (30) (17) Schizophrenia Schizophrenia (37) ciohei (25) Schizophrenia Schizophrenia (19) Schizophrenia (12) Schizophrenia (45) Schizophrenia (15) Controls (15) ciohei (22) Schizophrenia Schizophrenia (30) Schizophrenia (13) (1985) (1985) Schizophrenia (17) (1997) 18)18)Shzprna(19) Schizophrenia (1989)(1989) (1997) Psychosis (13) et aletal et aletal et aletal et aletal et aletal et aletal et aletal (1996)(1996) (37) Schizophrenia (2000)(2000) spectrum Schizophrenia (1980) (1982) (1985) (1980) Schizophrenia (21) (1982) (26) Schizophrenia (1985) (25) Schizophrenia (1994) (1994) Schizophrenia (17) et aletal et aletal (1961) (1961) Schizophrenia (520 ) (2000)(2000) Substance users: ecstasy (14) xeietlstudies Experimental xeietlstudies Experimental et aletal et aletal et aletal et aletal et aletal et aletal )) )) )) )) et aletal et aletal aa dd cc bb Cami able 1a l e 1 Ta b l e 1Tab Study Angrist Kirrane Casey Strakowski Angrist Angrist Van Kammen & Boronow (1988)(1988) Wolkin SanfilipoSanfilipo Van Kammen (1998)(1998) PandurangiPandurangi Van Kammen (1980)(1980) Van Kammen (1982 Abi-Dargham Van Kammen (1982 Van Kammen (1982 Van Kammen (1982 Cami Study Angrist Kirrane Casey Strakowski Angrist Angrist Van Kammen & Boronow Wolkin Van Kammen Van Kammen Van Kammen (1982 Abi-Dargham Van Kammen (1982 Van Kammen (1982 Van Kammen (1982

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Downloaded from https://www.cambridge.org/core. 24 Sep 2021 at 03:14:37, subject to the Cambridge Core terms of use. STIMULANT PSYCHOSIS Clozapine reduced mean expected high; no attenuation of paranoid or craving scores. Cocaineclozapineclozapine levels increased by No recordings for individual patients Group with psychosis showed an increase in positivenegative and symptoms in controls. No recordings for individual patients One patient withdrew owing to hypertension. No change in symptoms Mean change in BPRS ratings greater ingroup; schizophrenia there was response in both schizophrenianon-schizophrenia and groups but also individuals in both groups who did not respond No significant difference in psychotic activation on ormedication. off More euphoric activation on neuroleptics All participants were out-patients Comment alter the response in acutely ill patients Clozapine reduced mean expected high; noof attenuation paranoid or craving scores. Cocaine levels increased by No recordings for individual patients No recordings for individual patients Group with psychosis showed an increase innegative positive symptoms and greater in schizophrenia groupin but controls. not No recordings for individual patients One patient withdrew owing to hypertension. Nosymptoms change in Mean change in BPRS ratings greater ingroup; schizophrenia there was response in both schizophrenianon-schizophrenia groups and but also individuals in both groups who did not respond No significant difference in psychotic activation on ormedication. off More euphoric activation on neuroleptics All participants were out-patients Comment 17 patients evaluated off antipsychotics. No evidenceantipsychotics alter that the response in acutely ill patients nously. NR (schizophrenia) No (controls) 1. Yes (23/33) 2. Yes (21/27) Yes (others) Yes (controls) Yes Schizophrenia: Yes Non-schizophrenia: YesYes 1. Yes (15/25) 2. Yes (21/29) YesYes Yes YesYes Decreased/no positive symptoms Yes (all others) NR NR (schizophrenia) No (controls) No (stabilised phase) No recordings for individual patients 1. Yes (23/33) 2. Yes (21/27) Yes (others) Yes (controls) Thought disorder greater in schizophrenia group but not Yes Schizophrenia: Yes Non-schizophrenia: 1. Yes (15/25) 2. Yes (21/29) Yes Decreased/no positive symptoms Yes (all others) 17 patients evaluated off antipsychotics. No evidence that Yes (both groups) 1. Yes (10/33) off Yes (paranoid symptoms) Schizophrenia: Yes No (mCPP) Yes (methylphenidate) Yes (acute phase) neuroleptics 2. Yes (6/27) on neuroleptics Yes (results presented Yes (both groups) Yes (59% schizophrenia) No (controls) as mean difference) Non-schizophrenia: Yes Yes 1. Yes (10/25) off neuroleptics 2. Yes (8/29) on neuroleptics Yes Yes Increased/new positive symptoms schizophrenia group, group) Yes (paranoid symptoms) NR No (mCPP) Yes (methylphenidate) Yes (acute phase) No (stabilised phase) 1. Yes (10/33) off neuroleptics 2. Yes (6/27) on neuroleptics Yes (59% schizophrenia) No (controls) Yes(resultspresented as mean difference) No Schizophrenia: Yes Non-schizophrenia: Yes 1. Yes (10/25) off neuroleptics 2. Yes (8/29) on neuroleptics Yes Yes Yes Increased/new positive symptoms Yes (all acutely ill schizophrenia group, mania group) Yes (both groups) Yes (both groups) clrpprzn;NR, not-chloropiperazine; VBR, recorded; stat, to ventricle brain immediately; ratio; intrave i.v., clrpprzn;NR, not-chloropiperazine; VBR, recorded; stat, to ventricle brain immediately; ratio; intravenously. i.v., mm Cocaine intranasally 2 mg/kg 2 hor after clozapine placebo Methylphenidate 0.5 mg/kg i.v. or mCPP 0.1mg/kg Methylphenidate 0.5 mg/kg i.v. Methylphenidate 0.3 mg/kg orally daily for 5 days Methylphenidate 0.5 mg/kg i.v. Methylphenidate 0.5 mg/kg i.v. Methylphenidate 0.5 mg/kg i.v. Methylphenidate 0.5 mg/kg i.v. over 2 h Substance and dosage Methylphenidate 0.5 mg/kg i.v. over 30 s Methylphenidate 0.5 mg/kg i.v. Methylphenidate 0.5 mg/kg i.v. Cocaine 2 intranasally mg/kg 2 h after placebo or clozapine Methylphenidate 0.5 mg/kg i.v. Methylphenidate 0.5 mg/kg i.v. Methylphenidate 0.5 mg/kg i.v. or mCPP 0.1mg/kg Methylphenidate 0.5 mg/kg i.v. ehlhndt 0.5 mg/kgMethylphenidate i.v. Methylphenidate 0.3 mg/kg orally daily for 5 days No Methylphenidate 0.5 mg/kg i.v. Methylphenidate 0.5 mg/kg i.v. ehlhndt 0.5 mg/kgMethylphenidate i.v. Methylphenidate 0.5 mg/kg i.v. over 2 h Methylphenidate 0.5 mg/kg i.v. Methylphenidate 0.5 mg/kg i.v. over 2 h Substance and dosage Methylphenidate 0.5 mg/kg i.v. over 30 s Yes (all acutely ill Methylphenidate 0.5 mg/kg i.v. Methylphenidate 0.5 mg/kg i.v. over 2 h Methylphenidate 0.5 mg/kg i.v. ) ) nn Controls (8) Controls (50) Study sample ( history of hyperactivity (8) Controls (9) (2)(2) Affective disorder (9) remission (29) Schizoaffective (5) l 2)l (22) ill (22)ill Schizophrenia remitted (3) Mania (10) Depression (4) Controls (12) Non-psychotic in-patients (18) Cocaine users (8) Schizophrenia (11) Schizophrenia (32) Controls (8) Schizophrenia (41) Schizophrenia (70) Controls (50) Schizophrenia with history of (8) hyperactivity Schizophrenia (13) Controls (9) Schizophrenia (9) Schizoaffective disorder Affective disorder (9) Schizophrenia in remission (29) Schizophrenia (38) Schizophrenia (34) Schizophrenia (6) Schizoaffective (5) Schizophrenia, acutely Schizophrenia remitted (3) Mania (10) Depression (4) Controls (12) Schizophrenia (16) Non-psychotic in-patients (18) Studysample( )) (1994) 19)19)Shzprna(70) Schizophrenia (1993)(1993) (1987) 18)18)Shzprna(6) Schizophrenia (1984)(1984) (1994) (41) Schizophrenia (1987) (34) Schizophrenia (1992) (1992) Schizophrenia with (1991) (1973) (16) Schizophrenia (1977)(1977) (1991) Schizophrenia in (1973) Schizophrenia, acutely (1997) (1991) (1997) Schizophrenia (32) (1991) Schizophrenia (9) (2000)(2000) Cocaine users (8) (1999) (1999) Schizophrenia (11) et aletal et aletal et aletal et aletal et aletal continuedcontinued (1993)(1993) (13) Schizophrenia (( et aletal et aletal et aletal (1990)(1990) (38) Schizophrenia et aletal et aletal et aletal et aletal et aletal et aletal Szesko FarrenFarren Koreen Lieberman Lieberman Levy Carpenter Sharma Jody RobinsonRobinson Janowsky Janowsky Lieberman Ta b l e 1 BPRS, Rating Brief Scale; Psychiatric mCPP, iodobenzamide; IBZM, Lieberman Study Szesko Koreen Lieberman Lieberman Levy Carpenter Sharma Jody BPRS, Rating Brief Scale; Psychiatric mCPP, iodobenzamide; IBZM, Janowsky Janowsky Lieberman Ta b l e 1 Lieberman Study

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Ta b l e 2 Longitudinal studies

Study Study sample Follow-upFindings Comments

Pawluck et aletal (1995)(1995)Adults with narcolepsy on 55years years 2/11 psychotic symptoms Both premorbid difficulties, former had methylphenidate (44100 mg/day)mg/day)100 1 and persecutory paranoid ideas, latter family history of psychosis and head injury 1 hypnogogic hallucinations with no insight Cherland &&Cherland ChildrenwithADHDonmethyl- 55years years 9/192 developed mood-incongruent Notes three symptom clusters: Fitzpatrick (1999) phenidate, pemoline or psychotic symptoms MPH toxic hallucinations (first doses) dextroamfetamine 11/192 developed mood-congruent slower-developing psychotic symptoms mood-congruent psychotic symptoms Gawin & Kleber Cocaine users in treatment 4^6 weeksScreened with DIS, no reported case of Looking for withdrawal symptoms (1986) programme psychosispsychosis Carroll et aletal (1993)(1993)Treatment-seeking cocaine users1 year No evidence of any chronic psychotic Most abstinent or markedly decreased use disorder SatoSato et aletal (1983) users with 441month(variable1 month (variable 16 patients reused MAP after long-term 8 patients treated with haloperidol 3 mg chronic psychosis within group) abstinence (up to 5 years) and relapsed daily did not relapse with MAP use after with less MAP than previously, 4 with abstinenceabstinence only one injection, 1 with none Iwanami et aletal (1994)(1994)Methamphetamine users with 441month(variable1 month (variable Two groups, symptoms lasting for: Excluded if met DSM^III criteria for psychosis within group) 1 week after abstinence (transient schizophrenia group, nn¼54)54) All given antipsychotics 3 months after abstinence (persistent Abstinence ensured group, nn¼17) PersistentPersistentgroupmorelikelytohavenon- group more likely to have non- auditory non-visual hallucinations Kwapil (1996)High scores on Chapman 10 years Psychosis-prone group used more Of 8000 screened, 193 were ‘psychosis- Questionnaire (‘psychosis-prone’) stimulants than controls prone’; 182 followed up: using substances at initial DSM^III^R cocaine use disorder 12 interview not predictive of later DSM^III^R amphetamine use disorder 11 psychosispsychosis power therefore small to detect link between psychosis and stimulants (controls nn¼153)153)

ADHD, attention-deficit hyperactivity disorder; DIS, Diagnostic Interview Schedule; MAP, methamphetamine; MPH, methylphenidate.

Ta b l e 3 Case ^ control studies of stimulant users: with v. without psychosis

Study Cases (nn)C) Controlsontrols (nn)) Significant differences (cases v.v. controls)Comments

Brady et aletal (1991)Cocaine users with Cocaine users, no Greater duration and amount of use prior 72% reported psychosis occurring psychosis (29) psychosis (26) to admission in psychosis group; greater with increased frequency, greater proportion of males in psychosis group speedofonsetandwithsmallerspeed of onset and with smaller amounts of cocaine over time SatelSatel&Edell(1991) & Edell (1991)Cocaine users with Cocaine users without ‘Psychosis proneness’ score on the Perceptual Unable to determine direction or paranoia (10) paranoia (10) Aberration Scale and Magic Ideation Scale causality of relationship positivelypositivelycorrelatedwithparanoia correlated with paranoia BartlettBartlett et aletal (1997)Cocaine users with Non-paranoid users Greater duration of cocaine use in sensitised Sensitisation linked to other paranoia (22) (18) group psychotic features of cocaine Sensitised users11 (11) Non-sensitised users ReduceddoseescalationinsensitisedgroupReduced dose escalation in sensitised group (7)(7) Increased referentiality and unease in sensitised group Manschreck et aletal Psychosis 4424 h, cocaine users Cocaine users, non- Past psychiatric history, violence and total Freebase cocaine used; psychosis (1988) (31)(31) psychotic (28) drug use all greater in cases present in 29% of cocaine-using patients hospitalised in 1 year

1. Users whose paranoia had worsened over time.

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Ta b l e 44Tab Case^control studies of people with psychosis: stimulant users v. non-usersnon-users

Study Cases (nn) Controls (nn) Significant differences (cases v.v. controls)Comments

Seibyl et aletal (1993)Schizophrenia, cocaine Schizophrenia, non- Age at onset of schizophrenia lower in In the cases group, 5 used cocaine users (16) users (20)(20)users cocaine users prior to disease onset and 8 after onset (3 undefined) Lysaker et aletal (1994)(1994)Schizophrenia, cocaine Schizophrenia, non- Negative symptoms reduced and age at first Cocaine users more likely to be users (25)(25)users users (18) admission lower in cocaine users paranoid Rosse et aletal (1994)(1994)Cocaine users with Schizophrenia, non- Number and intensity of first-rank No reported psychosis (29) users (16) symptoms less in cases, but paranoid themes more common Dermatis et aletal (1998)(1998)Schizophrenia, cocaine Schizophrenia, non- Lower educational level and more users (43)(43)users users (27)(27)users prior hospitalisation in cocaine users Serper et aletal (1995)Schizophrenia, cocaine Schizophrenia, non- Hallucinatory experiences more common Cocaine users with schizophrenia users (32)(32)users users (54)(54)users in cocaine users with schizophrenia than similar to users without psychosis Cocaine users, no in the other two groups on negative symptoms and psychosis (30) moods, and similar to non-users with schizophrenia on most positive symptoms Negative symptoms in schizophrenia groups less among cocaine users

Ta b l e 55Tab Case ^ control studies of stimulant users v. other drug users

Study Cases ((Cases nn)C) Controlsontrols (nn)) Significant differences (cases v. controls)Comments

Graf et aletal (1977)Stimulant users (15) ^ users (14) Psychotic profile on MMPI at discharge users (17) greater in stimulant user group vv..allothers all others Multi-drug users (20) DalmauDalmau et aletal (1999)(1999)Amphetamine users (461) Opiate users (371) Psychosis greater in amphetamine and Users recruited from users (425) cannabis users v.v. opiate users (30% v. 6%)6%) in-patient drugs unit

MMPI, Minnesota Multiphasic Personality Inventory.

Ta b l e 66Tab Change in psychotic ratings per substance used and pre-existing psychosis among participants with psychosis com- pared with controls in three studies Dexamfetamine MethylphenidateTotal nn (%) (Manschreck et aletal, 1988; Brady et aletal,, i.v.i.v. nn (%)(%) 1991; Bartlett et aletal, 1997). In two studies Oral nn (%)i.v. nn (%) it was reported that the psychotic episodes worsened over time (Brady et aletal, 1991;,1991; RemissionRemission BartlettBartlett et aletal, 1997). Five studies compared Increased 13 (27.7) 55(27.8) (27.8) 51 (28.5)(28.5)51 69 (28.3)(28.3)69 individuals with schizophrenia or another No increase 34 (72.3) 13 (72.2)(72.2)13 128 (71.5)(71.5)128 175 (71.7)(71.7)175 psychotic illness who had been using stimu- Active psychosis lants with matched groups who had not Increased 28 (73.7)28(73.7) 79 (39.9)79(39.9) 42 (77.8) 149 (51.4) been using stimulants (Table 4). These No increase 10 (26.3)(26.3)10 119 (60.1)(60.1)119 12 (22.2)(22.2)12 141 (48.6) studies showed a lower age of onset of Control psychosis in the stimulant-user group, Increased 0(0.0) 0(0.0)0(0.0) 9 (26.5)9(26.5) 9 (10.2)9(10.2) fewer negative symptoms and more para- No increase 39 (100.0) 15 (100.0)15(100.0) 25 (73.5) 79 (89.8)79(89.8) noid themes. First-rank symptoms were noted to be fewer and hallucinatory experi- Total ences more common. Seibyl et aletal (1993)(1993) Increased 41 (33.1) 84 (36.4)84(36.4) 102 (38.2)(38.2)102 227 (36.5)227(36.5) showed that most of the people misusing No increase 83 (66.9)(66.9)83 147 (63.6)(63.6)147 165 (61.8)(61.8)165 395 (63.5)(63.5)395 drugs in their study had begun their cocaine use after psychosis had developed. i.v., intravenous. Two studies compared people misusing was impossible to separate stimulant use Four studies compared cocaine users stimulants with those misusing other drugs from other drug use known to be associated with psychosis with users with no psychosis (Table 5). Graf et aletal (1977) showed an with psychotic states, such as cannabis. (Table 3). Heavier cocaine use was shown increase in the psychotic profile on the

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Minnesota Multiphasic Personality Inven- more frequently for in-patient detoxifica- antipsychotic drugs, whereas the psychotic tory at discharge in people using stimulants tion, whereas stimulant users (in whom reaction in the expression phase is not rather than other drugs, and Dalmau et aletal the withdrawal syndrome is less severe) always blocked (Lieberman et aletal, 1990).,1990). (1999) showed a significant difference in might have been given out-patient treat- Castner & Goldman-Rakic (1999) investi- the rates of psychosis between patients for- ment. The proportion presenting with psy- gated rhesus monkeys, which were given merly using amphetamines and those using chosis as in-patients would therefore be intermittent, escalating low doses of opiates in a study of residents of a drug greater for those using stimulants rather amphetamine over a 12-week period, rehabilitation unit. than opiates. followed by an acute challenge with low- The difficulties of researching the longer- dose amphetamine (0.4–0.46 mg/kg). term effects of stimulants are seen in the Enhanced responses (hallucinatory-like DISCUSSION two Japanese studies (Sato et aletal, 1983;,1983; behaviours, static posturing and motor IwamaniIwamani et aletal, 1994). The widespread use ) were noted in response to a The studies reviewed here provide useful of high-dose injected methamphetamine low-dose amphetamine challenge 5 days evidence about the effect of stimulant use led to hospital admissions of individuals after withdrawal and up to 28 months later. on people with pre-existing psychotic ill- with chronic psychosis that persisted after The monkeys also showed an increase in ness, but more limited evidence about the substance use had ceased. Many patients responses ‘independent of stimuli’, possibly phenomenon of sensitisation. in these studies could have been given a indicating hallucinations, in the absence of The expectation that antipsychotic DSM–IV diagnosis of schizophrenia or additional drug challenges. Antipsychotic medication might block the action of stimu- other psychotic illness (American Psychi- drugs were not used. lants and prevent deterioration in psychotic atric Association, 1994) but were classed MengMeng et aletal (1998) performed a similar illnesses on exposure is not borne out by as having methamphetamine psychosis. experiment on rats, but also pre-treated these studies. The presence of positive The small open-label trial of haloperi- one group of rats with high-dose halo- symptoms of schizophrenia (as distinct dol (Satodol(Sato et aletal, 1983) merits attention, if peridol (0.5 mg/kg) or clozapine (20 mg/ from being in remission) appears to make only because of the paucity of other evi- kg), withholding the ‘sensitising’ phase of an individual more likely to experience a dence and the relationship of its results to amphetamines. This group showed an worsening of psychotic symptoms in animal studies. Eight of the cohort of enhanced response to amphetamine chal- response to a single dose of a stimulant drug. stimulant users with chronic psychoses lenge in a similar way to those sensitised There is clear evidence from these who had relapsed following stimulant use with amphetamines. Rats that had been studies that, irrespective of the individual’s were prescribed small doses of haloperidol given low-dose antipsychotic treatment mental state, a large enough dose of a (3 mg daily) following recovery and were (haloperidol 0.1 mg/kg or clozapine 4 mg/ stimulant drug can produce a brief psy- observed for further relapse. These partici- kg) alongside regular amphetamine admin- chotic reaction, usually lasting only hours pants did not relapse, even if they returned istration did not show an enhanced effect, and being self-limiting in the majority of to stimulant use; however, participants who suggesting that they were not sensitised, in individuals. The differences between i.v. were not given haloperidol relapsed into a a similar way to the humans in the study dexamfetamine, oral dexamfetamine and psychotic state lasting days to weeks after by SatobySato et aletal (1983). The sensitisation i.v. methamphetamine in participants with using stimulants. The results could lead us following high-dose antipsychotic treat- active symptoms are probably due to the to postulate that where people are unable ment is presumably related to dopamine lower doses used in the i.v. dexamfetamine to abstain from stimulant use despite re- receptor upregulation, which occurs in condition – usually a maximum of 20 mg. peated psychotic episodes, small doses of these circumstances, increasing the vulner- Evidence for sensitisation is found in only regular antipsychotic medication adminis- ability of the brain to stimulants once the two studies. Strakowski et aletal (1997)(1997) tered once the episode has settled might antipsychotic treatment is stopped. showed that when two doses of a stimulant reduce or prevent sensitisation in the future. Evidence against sensitisation occurring were given to volunteers free from psycho- Human experimental studies investigat- can be found. Seibyl et aletal (1993) noted that sis, the second dose produced a greater ing sensitisation are unlikely because of for the majority of participants stimulant psychotic response as measured by the ethical considerations, but a number of an- use began after the onset of psychotic ill- BPRS – a ‘sensitised’ response. Stimulant imal experiments have been carried out. ness, again weakening the case for a causa- users in the study by Brady et aletal (1991)(1991) Stimulant-induced stereotyped behaviour tive role for stimulants. We identified only reported psychotic symptoms occurring in small mammals and possible hallucina- two studies that looked specifically at the with lower doses over time. tory experiences in primates have been used therapeutic use of methylphenidate and The difference between patients who as a model for schizophrenia in humans. In psychosis (Pawluck et aletal, 1995; Cherland were substance users in the study by animals, the response to chronic ampheta- & Fitzpatrick, 1999), but many studies DalmauDalmau et aletal (1999), where psychosis rates mine use has been divided into two phases. have established the safety of this agent, were noted to be greater among in-patients In the ‘initiation’ phase of these experi- although not specifically reporting or ex- who used cannabis or stimulants rather ments animals are ‘sensitised’ by small amining for psychosis (e.g. Efron et aletal,, than opiates, is interesting. Sensitisation is regular doses of stimulants, insufficient to 1997). Illicit use of methylphenidate, how- a possible contributing factor, but not the cause a ‘psychotic’ reaction on their own. ever, tends to follow a different pattern, only one. The results might have been con- The ‘expression’ phase occurs if the animals with binges and escalation of dose founded by differences in rates of admission are either stressed or given a single dose of occurring.occurring. to the unit. It is possible, for example, that a stimulant. In the first phase, sensitisa- The lack of evidence in this area of psy- those with opiate problems were admitted tion has been shown to be blocked by chiatry causes problems for clinicians who

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must plan management without a solid evi- Brabbins, C. & Poole, R.(19 (1996) 9 6) Psychiatrists’ Janowsky, D. S., Huey, L., Storms, L., et aletal (19 7 7) dence base for a group of patients whose knowledge of drug induced psychosis. Psychiatric Bulletin,, Methylphenidate hydrochloride effects on psychological 2020, 410^412. tests in acute schizophrenia and non psychotic patients. management is challenging. Using the data Archives of General Psychiatry,, 3434,189^194.,189^194. Brady, K. T., Lydiard, R. B., Malcolm, R., et aletal (19 91) from these studies, we can say clearly that Cocaine induced psychosis. Journal of Clinical Psychiatry,, Jody, D., Lieberman, J. A., Geisler, S., et al (19 9 0)0)(19 use of stimulants leads to a brief psychotic 5252,509^512. Behavioral response to methylphenidate and treatment outcomes in first episode schizophrenia. reaction, usually only hours in length, that Cami, J., Farre, M., Mas, M., et aletal (2000)(2000) Human Psychopharmacology Bulletin,, 2626, 224^230. is more pronounced in people who already pharmacology of 3,4-MDMA (Ecstasy): psychomotor have active symptoms of psychosis and is performance and subjective effects. Journal of Clinical Kirrane, R. M., Mitropoulou,V.,Nunn, M., et aletal (2000)(2000) Psychopharmacology,, 2020,455^466., 455^466. seemingly unaffected by antipsychotic Effects of amphetamine on visuospatial working memory performance in schizophrenia spectrum personality Carpenter, M. D.,Winsberg, B. G. & Camus, L. A. medication. With regard to the hypothesis disorder. Neuropsychopharmacology,, 22,14^18. (19 92) Methylphenidate augmentation therapy in that stimulant use can produce chronic schizophrenia. Journal of Clinical Psychopharmacology,, 12,, Koreen, A. R., Lieberman, J. A., Alvir, J., et aletal (19 9 7) psychosis, supportive evidence is present 273^275. The behavioural effect of m-chloropiperazine (mCPP) and methylphenidate in first episode schizophrenia and in studies of humans but is of lower quality, Carroll, K. M., Power, M.-E. D., Bryant, K., et aletal normal controls. Neuropsychopharmacology,, 1616, 61^68.,61^68. although supported by experimental animal (19 93) One year follow up status of treatment seeking studies.studies. cocaine abusers: and dependence Koyama,T.,Koyama, T., Muraki, A., Nakayama, M., et aletal (19 91)91)(19 severity as predictors of outcome. Journal of Nervous and CNS stimulant abuse; long lasting symptoms of In the absence of better evidence, treat- Mental Disease,, 181181, 71^79.,71^79. amphetamine psychosis. Biological Psychiatry,, 22, 63^65. ment of stimulant-induced psychosis should Casey, J. F., Hollister, L. E., Klett, C. J., et aletal (19 61)61)(19 Kwapil, T. R .(19 9 6) A longitudinal study of drug and probably involve efforts to encourage Combined drug therapy of chronic schizophrenics. use by psychosis-prone and impulsive- abstinence from stimulants and medication American Journal of Psychiatry,, 117117,997^1003.,997^1003. non-comforming individuals. Journal of Abnormal with antipsychotic drugs until the acute Castner, S. A. & Goldman-Rakic, P.(1999) LongLong PsychologyPsychology,, 105105,114^123.,114^123. symptoms settle. This should be followed lasting psychomimetic consequences of repeated low Levy,Levy,D.L.,Smith,M.,Robinson,D., D. L., Smith, M., Robinson, D., et aletal (19 93) by regular low doses of antipsychotics in dose amphetamine exposure in rhesus monkeys. Methylphenidate increases thought disorder in recent Neuropsychopharmacology,, 20,10^28.,10^28. onset schizophrenics but not in normal controls. those who have experienced more than Cherland, E. & Fitzpatrick, R.(1999) Psychotic side Biological Psychiatry,, 3434, 507^514.,507^514. one episode of psychosis. Given that the effects of psychostimulants: a five year review. Canadian Lieberman, J. A., Kane, J. M., Gadaleta, D., et aletal evidence (however poor) points to sensitisa- Journal of Psychiatry,, 4444,,811^813. 811^813. (19 8 4) Methylphenidate challenge as a predictor of tion occurring, it is important that people Connell, P.H.(195 (1958) 8) Amphetamine Psychosis. Maudsley relapse in schizophrenia. American Journal of Psychiatry,, using stimulants should be assertively Monograph No. 5. London: Chapman & Hall. 141141, 633^638. managed in an attempt to prevent long- Dalmau, A., Bergman, B. & Brismar, B.(1999) Lieberman, J. A., Kane, J. M., Sarantakos, S., et aletal term chronic psychosis. Psychotic disorders among in-patients with abuse of (19 87) Prediction of relapse in schizophrenia. Archives ofofArchives cannabis, amphetamines and opiates. Do dopaminergic General Psychiatry,, 4444, 597^603. stimulants facilitate psychiatric illness? European Lieberman, J. A., Kinon, B. J. & Loebal, A. D.(19 (1990) 9 0) ACKNOWLEDGEMENT PsychiatryPsychiatry,, 1414, 366^371. Dopamine mechanisms in idiopathic and drug induced Dermatis, H., Galanter, M., Egelko, S., et aletal (19 9 8) psychosis.psychosis. Schizophrenia Bulletin,, 66,97^110.,97^110. We thank Dr Janice Morgan for her advice. Schizophrenic patients and cocaine use: antecedents to Lieberman, J. A., Jody, D., Alvir, J. M. J., et aletal (19 93)93)(19 hospitalisation and course of treatment. SubstanceSubstance Brain morphology, dopamine and eye-tracking Abuse,, 19, 169^177.,169^177. REFERENCES abnormalities in first episode schizophrenia. 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