Subject: A retrospective cross-sectional, observational survey study to analyze role of amisulpride in management of negative symptoms of schizophrenia.

Schizophrenia is a psychiatric brain disorder characterized by multiple symptom domains, including positive symptoms (e.g. hallucinations, delusions), negative symptoms (e.g. emotional apathy, lack of drive), and cognitive deficits (e.g. impaired memory). The early onset of the disease, along with its chronic course, make it a disabling disorder for many patients and their families.¹ The negative symptoms are associated with poor functional outcome and pose a substantial burden on people with schizophrenia, their families, and health-care systems.

Schizophrenia occurs worldwide, and for decades it was generally thought to have a uniform lifetime morbid risk of 1% across time, geography, and sex. In 2017, 3·5 million people had schizophrenia in India and it contributed to 9.8% to DALYs due to mental disorders in India. The prevalence of schizophrenia increased swiftly in young age groups, peaked in the 35–44 years age group.² Negative symptoms are frequently observed; two large cross-sectional retrospective studies involving more than 1000 people with schizophrenia reported that over 50% of study participants had at least one negative symptom.³

Antipsychotic medications are the cornerstone of treatment for schizophrenia alongside psychosocial interventions. The selection of medication should be based on a person’s past response to medication, the side effects that might be particularly harmful in individual circumstances, and routes of administration. No treatments have shown robust efficacy in treating primary and enduring negative symptoms. However, one meta-analysis⁴ reported that new dopamine antagonists (d=0·54) had a significant effect on negative symptoms, but old ones did not.

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.

Four randomised, double-blind, placebo-controlled trials of 6 to 24 weeks’ duration have shown that low dosages of amisulpride (≤300 mg/day) were more effective than placebo in patients with chronic schizophrenia with a high negative symptom and a low positive symptom score. Amisulpride has been compared with the conventional antipsychotics fluphenazine and haloperidol in randomised, double-blind studies in patients with negative symptoms of schizophrenia. A nonblind study also compared the effects of adding amisulpride or fluoxetine to existing haloperidol therapy in patients with negative symptoms of schizophrenia. In these trials, the effect of amisulpride on negative symptoms was similar to that of the comparator drug.⁵

Sulpitac (amisulpride 50,100,200,300,400 mg) tablets are marketed by Sun Pharmaceutical Industries Ltd. Although every product is marketed only after regulatory approval, it is important to know how it performs in day-to-day practice of individual medical practitioners. For this purpose, we have planned to conduct a survey to analyze role of amisulpride in management of negative symptoms of schizophrenia.