Summary
Abstract
Amisulpride, a substituted benzamide derivative, is a second-generation (atypical) antipsychotic. At low doses, it enhances dopaminergic neurotransmission by preferentially blocking presynaptic dopamine D2/D3 autoreceptors. At higher doses, amisulpride antagonises postsynaptic dopamine D2 and D3 receptors, preferentially in the limbic system rather than the striatum, thereby reducing dopaminergic transmission.
In patients with acute exacerbations of schizophrenia, the recommended dosage of amisulpride is 400 to 800 mg/day, although dosages ≤1200 mg/day may be administered. In comparative trials, amisulpride administered within this range (400 to 1200 mg/day) was as effective as haloperidol 5 to 40 mg/day, flupenthixol 25 mg/day and risperidone 8 mg/day in patients with acute exacerbations of schizophrenia with predominantly positive symptoms. Amisulpride was more effective than haloperidol but equally effective as risperidone in controlling negative symptoms. Amisulpride 400 to 800 mg/day was more effective than haloperidol, risperidone and flupenthixol in controlling affective symptoms in these patients.
In randomised, double-blind trials involving patients with predominantly negative symptoms of schizophrenia, amisulpride 50 to 300 mg/day was more effective than placebo.
Amisulpride is effective as maintenance therapy in patients with chronic schizophrenia. Long-term treatment with amisulpride was associated with improvements in quality of life and social functioning.
Amisulpride is generally well tolerated. In well-controlled trials, the neurological tolerability profile (including ratings on extrapyramidal symptom scales) of amisulpride 400 to 1200 mg/day was superior to that of the conventional antipsychotics (haloperidol or flupenthixol), but was similar to that of the atypical antipsychotic risperidone. At low dosages of amisulpride (≤300 mg/day), the incidence of adverse events (including extrapyramidal symptoms) reported with amisulpride was similar to that with placebo.
Conclusion: In comparative trials, amisulpride 400 to 1200 mg/day showed efficacy in reducing overall symptomatology and positive symptoms similar to that of conventional antipsychotics and newer atypical antipsychotics in patients with acute exacerbations of schizophrenia. Moreover, its effective alleviation of negative and affective symptoms, its lower association with extrapyramidal symptoms and loss of cognitive function than conventional antipsychotics and its long-term efficacy justifies consideration of the use of higher dosages of amisulpride in this group of patients. Consequently, the dosage of amisulpride that is recommended in patients with acute exacerbations of schizophrenia is 400 to 800 mg/day, although dosages ≤1200 mg/day may be administered. Lower dosages of amisulpride (50 to 300 mg/day) should be considered for the management of patients with negative symptoms of schizophrenia. Amisulpride is a first-line treatment option in the management of schizophrenia in the acute phase and for the maintenance of treatment response.
Pharmacodynamic Properties
Amisulpride binds selectively and with high affinity to dopamine D2 and D3 receptor subtypes with preferential binding to limbic structures rather than the striatum. Amisulpride has little affinity for other dopamine receptor subtypes (D1, D4 or D5) or other neurotransmitter receptors (serotonin, histamine, muscarinic, adrenergic). In animals, low doses of amisulpride facilitate presynaptic dopamine receptor-mediated behaviours, whereas higher doses decrease behaviours associated with postsynaptic receptor activation.
Single oral doses of amisulpride of up to 400mg and multiple doses of amisulpride (50 mg/day for 4 days) were devoid of detrimental effects on psychometric and/or cognitive performance in healthy volunteers. Amisulpride increased prolactin levels in volunteers. Consistent with its lack of effects on the α-adrenergic and cholinergic system, amisulpride produced minor or no neurocardiac effects.
Pharmacokinetic Properties
After single oral doses of amisulpride 50mg, the peak plasma amisulpride con-centration was approximately 56 μg/L at 4 hours. An earlier lower peak (42 μg/L) was detected 1 hour earlier. Amisulpride distributes widely and rapidly to tissues (volume of distribution 5.8 L/kg) and is minimally bound to plasma protein (17%). Absolute bioavailability of amisulpride is ≈50%. Metabolism of amisulpride is limited and the two main metabolites are inactive. Amisulpride is primarily excreted in the urine. Elimination is biphasic, with a terminal elimination half-life of approximately 12 hours. Renal clearance is approximately 20 L/h in healthy volunteers.
Therapeutic Efficacy
In patients with acute exacerbations of schizophrenia with predominantly positive symptoms, amisulpride 400 to 1200 mg/day reduced overall symptomatology [assessed by the Brief Psychiatric Rating Scale (BPRS) total scores] by 42 to 59% and positive symptom scores [assessed by the Positive and Negative Syndrome Scale (PANSS) positive subscore or Scale for the Assessment of Positive Symptoms (SAPS)] by 48 to 75%, a response rate not significantly different from that produced by haloperidol 5 to 40 mg/day, flupenthixol 25 mg/day and risperidone 8 mg/day in long-term and short-term randomised, double-blind trials. Amisulpride 400 to 1200 mg/day reduced negative symptom scores [assessed by negative PANSS subscore or Scale for Assessment of Negative Symptoms (SANS)] by 35 to 47% in these patients, a response rate that was significantly higher than that of haloperidol but not significantly different from that of risperidone. Amisulpride 400 to 800 mg/day reduced affective symptoms to a greater extent than haloperidol, risperidone and flupenthixol. Amisulpride 400 to 800 mg/day was associated with an earlier onset of action than haloperidol.
In patients with predominantly negative symptoms, low dosages of amisulpride 50 to 300 mg/day significantly reduced negative symptom scores (assessed by SANS) by 32 to 46% compared with 8 to 23% in placebo recipients in randomised, double-blind trials.
In long-term studies, amisulpride 200 to 1200 mg/day was effective as maintenance therapy in patients with chronic schizophrenia with mixed symptoms. In a randomised, double-blind trial, low dosages of amisulpride (≤300 mg/day) prevented an increase in both negative and positive symptom scores when administered as maintenance therapy to patients with predominantly negative symptoms. Long-term amisulpride administration was associated with improvements in measures of quality of life and social functioning.
Tolerability
Amisulpride at low and high dosages is well tolerated. At low dosages (≤300 mg/day), the incidence of adverse events was similar in amisulpride-and placebo-treated patients. At higher dosages (400 to 1200 mg/day), the overall incidence of adverse events in amisulpride recipients was similar to that in recipients of haloperidol, flupenthixol and risperidone. The most commonly reported adverse events associated with higher dosages of amisulpride were extrapyramidal symptoms, insomnia, hyperkinesia, anxiety, bodyweight increase and agitation.
The incidence of extrapyramidal symptoms was dose related. The neurological tolerability profile [assessed according to the Simpson-Angus Scale (SAS; an extrapyramidal symptom scale), the Barnes Akathisia Scale (BAS) or the Abnormal Involuntary Movement Scale (AIMS)] of amisulpride 400 to 1200 mg/day was superior to that of the conventional antipsychotics (haloperidol or flupenthixol), but was similar to that of the atypical antipsychotic risperidone. Ratings on extrapyramidal symptom scales were similar in recipients of low-dosage amisulpride and placebo. The increase in bodyweight associated with amisulpride (200 to 1200 mg/day) was slightly greater than that associated with haloperidol 5 to 30 mg/day in two long-term studies but lower than that associated with risperidone 8 mg/day in an 8-week study.
Plasma prolactin levels were increased 3-fold after 12 months’ therapy with amisulpride in patients with schizophrenia. However, the incidence of endocrine disorders was low in patients treated with higher dosages of amisulpride and similar to that observed in haloperidol and risperidone recipients. Pooled results from comparative trials showed that amisulpride had a satisfactory cardiovascular profile and was not associated with any clinical abnormalities in laboratory parameters including haematological and hepatological tests.
Pharmacoeconomic and Quality-of-Life Studies
Data from a retrospective study showed that amisulpride was more cost effective than haloperidol in patients with schizophrenia in ambulatory care. This was mainly the result of lower hospitalisation costs. In addition, amisulpride was more effective than haloperidol in improving measures of quality of life in medium-and long-term studies.
Dosage and Administration
An oral amisulpride dosage of 400 to 800 mg/day is recommended for acute psychotic episodes in patients with schizophrenia. The dosage may be increased up to 1200 mg/day; however, tolerability data for dosages >1200 mg/day are not available. It is recommended that maintenance therapy should be established individually with the minimally effective dosage. For patients with predominantly negative symptoms of schizophrenia, oral dosages of 50 to 300 mg/day are recommended. Dosages above 400 mg/day should be administered twice daily. Dosage reductions are recommended in patients with creatinine clearance below 60 ml/min.
Similar content being viewed by others
References
Coukell AJ, Spencer CM, Benfield P. Amisulpride: a review of its pharmacodynamic and pharmacokinetic properties and therapeutic efficacy in the management of schizophrenia. CNS Drugs 1996; 6(3): 237–56
Scatton B, Claustre Y, Cudennec A, et al. Amisulpride: from animal pharmacology to therapeutic action. Int Clin Psychopharmacol 1997 May; 12 Suppl. 2: S29–36
Perrault GH, Depoortere R, Morel E, et al. Psychopharmacological profile of amisulpride: an antipsychotic drug with presynaptic D2/D3 dopamine receptor antagonist activity and limbic selectivity. J Pharmacol Exp Ther 1997 Jan; 280: 73–82
Schoemaker H, Claustre Y, Fage D, et al. Neurochemical characteristics of amisulpride, an atypical dopamine D2/D3 receptor antagonist with both presynaptic and limbic selectivity. J Pharmacol Exp Ther 1997 Jan; 280: 83–97
Kerwin R. From pharmacological profiles to clinical outcomes. Int Clin Psychopharmacol 2000; 15 Suppl. 4: S1–4
Schotte A, Janssen PFM, Gommeren W, et al. Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding. Psychopharmacology 1996; 124: 57–73
Nordström AL, Farde L, Nyberg S, et al. D1, D2, and 5-HT2 receptor occupancy in relation to clozapine serum concentration; a PET study of schizophrenic patients. Am J Psychiatry 1995; 152: 1444–9
Cudennec A, Fage D, Benavides J, et al. Effects of amisulpride, an atypical antipsychotic which blocks preferentially presynaptic dopamine autoreceptors, on integrated functional cerebral activity in the rat. Brain Res 1997 Sep 12; 768: 257–65
Guyon A, Assouly-Besse F, Biala G, et al. Potentiation by low doses of selected neuroleptics of food-induced conditioned place preference in rats. Psychopharmacology 1993 Mar; 110: 460–6
Di Giovanni G, Di Mascio M, Di Matteo V, et al. Effects of acute and repeated administration of amisulpride, a dopamine D2/D3 receptor antagonist on the electrical activity of mid-brain dopaminergic neurons. J Pharmacol Exp Ther 1998; 287: 51–7
Martinot JL, Paillère-Martinot ML, Poirier MF, et al. In vivo characteristics of dopamine D2 receptor occupancy by amisulpride in schizophrenia. Psychopharmacology 1996; 124: 154–8
Farde L, Nordström A-L, Wiesel F-A, et al. Positron emission tomographic analysis of central D1 and D2 dopamine receptor occupancy in patients treated with classical neuroleptics and clozapine: relation to extrapyramidal side effects. Arch Gen Psychiatry 1992 Jul; 49: 538–44
Farde L, Nordström A-L, Karlsson P, et al. Positron emission tomography studies on dopamine receptors in schizophrenia. Clin Neuropharmacol 1995; 18 Suppl. 1: S121–9
Xiberas X, Martinot J-L, Mallet L, et al. In. vivo extrastriatal and striatal D2 dopamine receptor blockade by amisulpride in schizophrenia. J Clin Psychopharmacol 2001; 21(2): 207–14
Trichard C, Paillère-Martinot M-L, Attar-Levy D, et al. Binding of antipsychotic drugs to cortical 5-HT2A receptors: a PET study of chlorpromazine, clozapine, and amisulpride in schizophrenic patients. Am J Psychiatry 1998 Apr; 155: 505–8
Liddle PF. Cognitive impairment in schizophrenia: its impact on social functioning. Acta Psychiatr Scand 2000; 101: 11–6
King D. The effect of neuroleptics on cognitive and psychomotor function. Br J Psychiatry 1990; 157: 799–811
Medalia A, Gold J, Merriam A. The effects of neuroleptics on neuropsychological test results of schizophrenics. Arch Clin Neuropsychol 1988; 3: 249–71
King DJ. Guidelines for the use of antipsychotic drugs in healthy volunteers. J Psychopharmacol 1997; 11(3): 201–9
Perault MC, Bergougnan L, Paillat A, et al. Lack of interaction between amisulpride and lorazepam on psychomotor performance and memory in healthy volunteers. Human Psychopharmacol 1998; 13(7): 493–500
Ramaekers JG, Louwerens JW, Muntjewerff ND, et al. Psychomotor, cognitive, extrapyramidal, and affective functions of healthy volunteers during treatment with an atypical (amisulpride) and a classic (haloperidol) antipsychotic. J Clin Psychopharmacol 1999 Jun; 19: 209–21
Mattila MJ, Patat A, Seppälä T, et al. Single oral doses of amisulpride do not enhance the effects of alcohol on the performance and memory of healthy subjects. Eur J Clin Pharmacol 1996; 51: 161–6
Peretti CS, Danion JM, Kauffmann-Muller F, et al. Effects of haloperidol and amisulpride on motor and cognitive skill learning in healthy volunteers. Psychopharmacology Berl 1997 Jun; 131: 329–38
Legangneux E, McEwen J, Wesnes KA, et al. The acute effects of amisulpride (50 mg and 200 mg) and haloperidol (2 mg) on cognitive function in healthy elderly volunteers. J Psychopharmacol 2000 Jun; 14: 164–71
Sanofi-Synthelabo. Amisulpride prescribing information (UK). 1999
Patat A, Rosenzweig P, Miget N, et al. Effects of 50mg amisulpride on EEG, psychomotor and cognitive functions in healthy sleep-deprived subjects. Fundam Clin Pharmacol 1999; 13: 582–94
Adler G, Weber D, Grieshaber A, et al. Atypical antipsychotics and memory function in patients with chronic schizophrenia [abstract]. Int J Neuropsychopharmacol 2000; 3 Suppl. 1: S165
Hamon-Vilcot B, Chaufour S, Deschamps C, et al. Safety and pharmacokinetics of a single oral dose of amisulpride in healthy elderly volunteers. Eur J Clin Pharmacol 1998 Jul; 54: 405–9
Wetzel H, Wiesner J, Hiemke C, et al. Acute antagonism of dopamine D2-like receptors by amisulpride: effects on hormone secretion in healthy volunteers. J Psychiatr Res 1994 Sep–Oct; 28: 461–73
Noble S, Benfeld P. Amisulpride: a review of its clinical potential in dysthymia. CNS Drugs 1999 Dec; 12: 471–83
Dufour A, Desanti C. Pharmacokinetics and metabolism of amisulpride [in French]. Ann Psychiatry 1988; 3(3): 298–305
Rosenzweig P, Canal M, Patat L, et al. A review of the pharmacokinetics, tolerability and pharmacodynamics of amisulpride in healthy volunteers. Human Psychopharmacol 2001. In press
Canal M, Chaufour S, Lavanant C, et al. Amisulpride pharmacokinetics: no difference between young and elderly subjects [abstract]. Eur Neuropsychopharmacol 2000 Sep; 10 Suppl. 3: 331
Canal M, MacMahon M, Kwan J, et al. Amisulpride: kinetics in patients with renal failure [abstract]. Eur Neuropsychopharmacol 2000 Sep; 10 Suppl. 3: 330
Gillet G, Dormerque M, Canal M, et al. Amisulpride does not inhibit cytochrome P450 isozymes. Eur Neuropsychopharmacol 2000; 10 Suppl. 3: S331
Canal M, Chaufour S, Zieleniuk I, et al. No effect of amisulpride on lithium pharmacokinetics [abstract]. Eur Neuropsychopharmacol 2000 Sep; 10 Suppl. 3: S330–331
Expert Consensus Panels for Schizophrenia. Treatment of schizophrenia 1999. J Clin Psychiatry 1999; 60 Suppl. 11: 1–80
Miller DD. Schizophrenia: its etiology and impact. Pharmacotherapy 1996 Jan/Feb; 16 (1 Pt 2): 2S–5S
Strauss JS, Carpenter Jr WT, Bartko JJ. The diagnosis and understanding of schizophrenia. Part III. Speculations on the processes that underlie schizophrenic symptoms and signs. Schizophr Bull 1974; 11: 61–75
American Psychiatric Association. Practice guideline for the treatment of patients with schizophrenia. Am J Psychiatry 1997 April; 154(4) Suppl 4: 1–63
Carpenter WT, Heinrichs DW, Wagman AMI. Deficit and non-deficit forms of schizophrenia: the concept. Am J Psychiatry 1988; 145: 578–83
Costa-e-Silva JA. A comparative double-blind trial of amisulpride versus haloperidol in the treatment of acute psychotic disorders [in French]. Ann Psychiatry 1990; 5(1): 71–8
Pichot P, Boyer P. A double blind, controlled, multicenter trial of amisulpride versus high dose haloperidol in acute psychotic disorders [in French]. Ann Psychiatry 1988; 3(3): 326–32
Puech A, Fleurot O, Rein W. Amisulpride, an atypical antipsychotic, in the treatment of acute episodes of schizophrenia: a dose-ranging study vs haloperidol. Amisulpride Study Group. Acta Psychiatr Scand 1998 Jul; 98: 65–72
Delcker A, Schoon ML, Oczkowski B, et al. Amisulpride versus haloperidol in treatment of schizophrenic patients: results of a double-blind study. Pharmacopsychiatry 1990 May; 23: 125–30
Möller HJ, Boyer P, Fleurot O, et al. Improvement of acute exacerbations of schizophrenia with amisulpride: a comparison with haloperidol. PROD-ASLP Study Group. Psychopharmacology (Berl) 1997 Aug; 132: 396–401
Wetzel H, Gründer G, Hillert A, et al. Amisulpride versus flupentixol in schizophrenia with predominantly positive symptomatology —a double-blind controlled study comparing a selective D2-like antagonist to a mixed D1-/D2-like antagonist. Amisulpride Study Group. Psychopharmacology (Berl) 1998 Jun; 137: 223–32
Peuskens J, Bech P, Möller HJ, et al. Amisulpride vs. risperidone in the treatment of acute exacerbations of schizophrenia. Amisulpride Study Group. Psychiatry Res 1999 Nov 8; 88: 107–17
Carrière P, Bonhomme D, Lemperière T. Amisulpride has a superior benefit/risk profile to haloperidol in schizophrenia: results of a multicentre, double-blind study. The Amisulpride Study Group. Eur Psychiatry 2000 Aug; 15: 321–9
Colonna L, Saleem P, Dondey-Nouvel L, et al. Long-term safety and efficacy of amisulpride in subchronic or chronic schizophrenia. Amisulpride Study Group. Int Clin Psychopharmacol 2000 Jan; 15: 13–22
American Psychiatric Association. DSM III-R: diagnostic and statistical manual of mental disorders. 3rd revised ed. Washington DC: American Psychiatric Association, 1987
American Psychiatric Association. DSM-IV: diagnostic and statistical manual of mental disorders. 4th ed. Washington DC: American Psychiatric Association, 1994
Lader M. Rating scales in schizophrenia: a review of their use fulness for assessing atypical antipsychotics. CNS Drugs 2000; 14(1): 23–32
Peuskens J, Moller H-J, Puech A, et al. Amisulpride improves affective symptoms in acute schizophrenia. World J Biol Psychiatry 2001; 2 Suppl. 1: P021–28
Burns T, Bale R. Clinical advantages of amisulpride in the treatment of acute schizophrenia. J Int Med Res. In press
Lecrubier Y, Benkert O, Kasper S, et al. Amisulpride versus risperidone in schizophrenia: comparing clinical and functional outcome in a 6 month study [abstract no. 196]. 39th Annual Meeting of the American College of Neuropsychopharmacology; 2000 Dec 10–14; San Juan
Chabannes JP, Pelissolo A, Farah S, et al. Evaluation of efficacy and safety of amisulpride in the treatment of schizophrenia [in French]. Encephale 1998 Jul–Aug; 24: 386–92
Möller H-J, van Praag HM, Aufdembrinke B, et al. Negative symptoms in schizophrenia: considerations for clinical trials. Working group on negative symptoms in schizophrenia. Psychopharmacology 1994; 115(1–2): 221–8
Kirkpatrick B, Kopelowicz A, Buchanan RW, et al. Assessing the efficacy of treatments for the deficit syndrome of schizophrenia. Neuropsychopharmacology 2000; 22(3): 303–10
Carpenter WT. Psychopathology and common sense: where we went wrong with negative symptoms. Biol Psychiatry 1991; 29: 735–7
Committee for Proprietary Medicinal Products. Note for guidance on the clinical investigation of medicinal products in the treatment of schizophrenia. London: The European Agency for the Evaluation of Medicinal Products, 1998
Loo H, Poirier-Littre MF, Theron M, et al. Amisulpride versus placebo in the medium-term treatment of the negative symptoms of schizophrenia. Br J Psychiatry 1997 Jan; 170: 18–22
Boyer P, Lecrubier Y, Puech AJ, et al. Treatment of negative symptoms in schizophrenia with amisulpride. Br J Psychiatry 1995 Jan; 166: 68–72
Paillère-Martinot M-L, Lecrubier Y, Martinot J-L, et al. Improvement of some schizophrenic deficit symptoms with low doses of amisulpride. Am J Psychiatry 1995 Jan; 152: 130–3
Danion J-M, Rein W, Fleurot O. Improvement of schizophrenic patients with primary negative symptoms treated with amisulpride. Amisulpride Study Group. Am J Psychiatry 1999 Apr; 156: 610–6
Pichot P, Boyer P. A double blind, controlled, multicenter trial of low dose amisulpride (Solian 50) versus low dose fluphenazine in the treatment of negative symptoms in chronic schizophrenia [in French]. Ann Psychiatry 1988; 3(3): 312–20
Saletu B, Küfferle B, Grünberger J, et al. Clinical, EEG mapping and psychometric studies in negative schizophrenia: comparative trials with amisulpride and fluphenazine. Neuropsychobiology 1994; 29(3): 125–35
Speller JC, Barnes TRE, Curson DA, et al. One-year, low-dose neuroleptic study of in-patients with chronic schizophrenia characterised by persistent negative symptoms. Amisulpride v. haloperidol. Br J Psychiatry 1997 Dec; 171: 564–8
Bogetto F, Fonzo V, Maina G, et al. Adjunctive fluoxetine or amisulpride improves schizophrenic negative symptoms. Eur J Psych 1995; 9(2): 119–26
Coulouvrat C, Dondey-Nouvel L. Safety of amisulpride (Solian): a review of 11 clinical studies. Int Clin Psychopharmacol 1999 Jul; 14: 209–18
Taylor DM, McAskill R. Atypical antipsychotics and weight gain-a systematic review. Acta Psychiatr Scand 2000 Jun; 101: 416–32
Russell JM, Mackell JA. Body weight gain associated with atypical antipsychotics: epidemiological and therapeutic implications. CNS Drugs 2001; 15(7): 537–51
Stanniland C, Taylor D. Tolerability of atypical antipsychotics. Drug Saf 2000 Mar; 22: 195–214
Agelink MW, Majewski T, Wurthmann C, et al. Effects of newer atypical antipsychotics on autonomic neurocardiac function: a comparison between amisulpride, olanzapine, sertindole, and clozapine. J Clin Psychopharmacol 2001 Feb; 21: 8–13
Rupp A, Keith SJ. The costs of schizophrenia. Assessing the burden. Psychiatr Clin North Am 1993; 16: 413–23
Rouillon F, Toumi M, Dansette G-Y, et al. Some aspects of the cost of schizophrenia in France. Pharmacoeconomics 1997; 11: 578–94
Evers S, Ament AJ. Costs of schizophrenia in The Netherlands. Schizophr Bull 1995; 21: 141–53
Davies LM, Drummond MF. Economics and schizophrenia: the real cost. Br J Psychiatry 1994; 165 Suppl. 25: 18–21
De Hert M, Thys E, Boydens J, et al. Health care expenditure on schizophrenia patients in belgium. Schizophr Bull 1998; 24(4): 519–27
Rund BR, Ruud T. Costs of services for schizophrenic patients in Norway. Acta Psychiatr Scand 1999; 99: 120–5
Knapp M. Costs of schizophrenia. Br J Psychiatry 1997; 171: 509–18
Lindstrom E. The hidden costs of schizophrenia. J Drug Dev Clin Pract 1996; 7: 281–8
Souétre E, Martin P, Lecanu JP, et al. Economic assessment of neuroleptic strategies in schizophrenia. Encephale 1992; 8: 263–9
Olie JP, Levy E, Carita P, et al. Impact of amisulpride on health care resources in schizophrenia; intermediate results of OASIS study [abstract]. World J Biol Psychiatry 2001; 2 Suppl. 1: 308
Sechter D, Lenne X. A comparison of resources utilization in schizophrenia: amisulpride versus risperidone [abstract]. World J Biol Psychiatry 2001; 2 Suppl. 1: 308
Sanofi-Synthelabo. Prescribing information (Ireland). 1998
Sanofi-Synthelabo. Prescribing information (Norway). 2000
Peuskens J. Switching approach in the management of schizophrenia patients. Int Clin Psychopharmacol 2000; 15 Suppl. 4: S15–9
Chabannes JP, Giudicelli A, Farah S, et al. Switching to amisulpride: findings from a retrospective questionnaire [abstract]. Eur Psychiatry 2000; 15 Suppl. 2: 412S
Lehman AF. Managing schizophrenia: interventions and outcomes. Dis Manage Health Outcomes 1997 Jun; 1: 286–95
Patterson TL, Kaplan RM, Jeste DV. Measuring the effect of treatment on quality of life in patients with schizophrenia: focus on utility-based measures. CNS Drugs 1999 Jul; 12: 49–64
Wynn Owen PA, Castle DJ. Late-onset schizophrenia: epidemiology, diagnosis, management and outcomes. Drugs Aging 1999 Aug; 15: 81–9
Sajatovic M, Madhusoodanan S, Buckley P. Schizophrenia in the elderly: guidelines for management. CNS Drugs 2000 Feb; 13: 103–15
Dixon L, Lehman A, Levine J. Conventional antipsychotic medications for schizophrenia. Schizophr Bull 1995; 21: 567–78
Lehman AF, Carpenter Jr WT, Goldman HH, et al. Treatment outcomes in schizophrenia: implications for practice, policy, and research. Schizophr Bull 1995; 21(4): 669–75
Adams C, Wilson P, Gilbody S, et al. Drug treatments for schizophrenia. Qual Health Care 2000; 9(1): 73–9
Collaborative Working Group on Clinical Trial Evaluations. Evaluating the effects of antipsychotics on cognition in schizophrenia. J Clin Psychiatry 1998; 59 Suppl. 12: 35–40
Emsley RA. Role of newer atypical antipsychotics in the management of treatment-resistant schizophrenia. CNS Drugs 2000; 13(6): 409–20
Opler LA, Albert D, Ramirez PM. Psychopharmacologic treatment of negative schizophrenic symptoms. Compr Psychiatry 1994; 35(1): 16–28
Kane JM, Mayerhoff D. Do negative symptoms respond to pharmacological treatment? Br J Psychiatry 1989; 155 Suppl. 7: 115–8
Blin O. A comparative review of new antipsychotics. Can J Psychiatry 1999 Apr; 44: 235–44
Caccia S. Biotransformation of post-clozapine antipsychotics: pharmacological implications. Clin Pharmacokinet 2000 May; 38: 393–414
Huber G, Gross G. Conventional and newer neuroleptics in the treatment of schizophrenia spectrum disorders. Neurol Psychiatry Brain Res 1999; 7(1): 15–26
Balestrieri M, Vampini C, Bellantuono C. Efficacy and safety of novel antipsychotics: a critical review. Human Psychopharmacol 2000; 15(7): 499–512
Geddes J, Freemantle N, Harrison P, et al. Atypical antipsychotics in the treatment of schizophrenia: systematic overview and meta-regression analysis. BMJ 2000; 321(7273): 1371–6
Buckley PF. New antipsychotic agents: emerging clinical profiles. J Clin Psychiatry 1999; 60 Suppl. 1: 12–7
Marder SR. Newer antipsychotics. Curr Opin Psychiatry 2000; 13(1): 11–4
Barnes TR, McPhillips MA. Novel antipsychotics, extrapyramidal side effects and tardive dyskinesia. Int Clin Psychopharmacol 1998 Mar; 13 Suppl. 3: S49–57
Kerwin R. Atypical neuroleptics. Prescr J 1999; 39(3): 154–60
Waddington JL, Scully PJ, O’Callaghan E. The new antipsychotics, and their potential for early intervention in schizophrenia. Schizophr Res 1997; 28(2–3): 207–22
Möller H-J. Atypical neuroleptics: a new approach in the treatment of negative symptoms. Eur Arch Psychiatry Clin Neurosci 1999; 249 Suppl. 4: IV99–107
Leucht S, Pitschel-Walz G, Kissling W. Meta-analysis of amisulpride-a selective dopamine receptor antagonist with an ‘atypical’ profile [abstract]. Eur Neuropsychopharmacol 2000 Sep; 10 Suppl. 3: S326
Allison DB, Mentore LJ, Heo M, et al. Antipsychotic induced weight gain; a comprehensive research synthesis. Am J Psychiatry 1999; 156: 1686–96
Davis JM. Overview: maintenance therapy in psychiatry, I: schizophrenia. Am J Psychiatry 1975; 132: 1237–45
Kane JM. Treatment programme and long-term outcome in chronic schizophrenia. Acta Psychiatr Scand 1990; 82 Suppl. 358: 151–7
Kane JM. Schizophrenia. N Engl J Med 1996 Jan 04; 334(1): 34–41
Author information
Authors and Affiliations
Corresponding author
Additional information
Various sections of the manuscript reviewed by: M. Balestrieri, Clinica Psichiatrica, Policlinico Universitario, Udine, Italy; P. Bech, Psychiatric Research Unit, Frederiksborg General Hospital, Hillerød, Denmark; W.T. Carpenter, Maryland Psychiatric Research Center, University of Maryland, Baltimore, Maryland, USA; R. Emsley, Department of Psychiatry, University of Stellenbosch, Capetown, South Africa; F. Frankenburg, McLean Hospital, Belmont, Maryland, USA; R. Kerwin, Department of Psychological Medicine, Institute of Psychiatry, London, England; H.-J. Möller, Psychiatric Hospital of the Ludwig-Maximilians University, Munich, Germany; J. Peuskens, University Centre St. Jozef, Leuvensesteenweg, Kortenberg, Leuven, Belgium; J.L. Waddington, Department of Clinical Pharmacology, Royal College of Surgeons in Ireland, St Stephen’s Green, Dublin, Ireland.
Data Selection
Sources: Medical literature published in any language since September 1996 on Amisulpride, identified using Medline and EMBASE, supplemented by AdisBase (a proprietary database of Adis International). Additional references were identified from the reference lists of published articles. Bibliographical information, including contributory unpublished data, was also requested from the company developing the drug.
Search strategy: Medline search terms were ‘Amisulpride’. EMBASE search terms were ‘Amisulpride’. AdisBase search terms were ‘Amisulpride’. Searches were last updated 19 Oct 2001.
Selection: Studies in patients with schizophrenia who received amisulpride. Inclusion of studies was based mainly on the methods section of the trials.When available, large, well-controlled trials with appropriate statistical methodology were preferred. Abstracts or other conference proceedings were included if they were published in 2000 or later. Relevant pharmacodynamic and pharmacokinetic data were also included.
Index terms: Amisulpride, schizophrenia, pharmacodynamics, pharmacokinetics, therapeutic use.
Rights and permissions
About this article
Cite this article
Curran, M.P., Perry, C.M. Amisulpride. Drugs 61, 2123–2150 (2001). https://doi.org/10.2165/00003495-200161140-00014
Published:
Issue Date:
DOI: https://doi.org/10.2165/00003495-200161140-00014