Emergence Of Extrapyramidal Symptoms Research Articles

TO STUDY EFFICACY OF AMISULPRIDE IN TREATMENT OF SCHIZOPHRENIA.

The study was performed at the Department of Pharmacology in collaboration with Department of Psychiatry, NSCB Medical College, Jabalpur. The maximum numbers of patients in were in reproductive age group that is in between 20 to 49 years. The mean age in Amisulpride group was 33.26(±10.23) years while in Olanzapine group it was 31.25 (±12.22) years.
 Schizophrenia was more common (80%) in younger (20-49years) age group. In our study the male /female ratio was 1.7. Our study supports the notion that Schizophrenia is more common in Married and Urban population. Only one patient from Olanzapine Group suffered Extrapyramidal symptoms of moderate severity requiring withdrawal from study.2 patients from Olanzapine group and 1 patient from Amisulpride group had Tremors and Akathesia of mild severity. There was no emergence of Extrapyramidal symptoms in rest of the patients (p>.05)
 Keywords: Efficacy, Amisulpride, Olanzapine & Schizophrenia.

Response to: A Commentary on "Antipsychotic-Induced Parkinsonism is Associated with Working Memory Deficits in Schizophrenia-Spectrum Disorders".

Response to: A Commentary on "Antipsychotic-Induced Parkinsonism is Associated with Working Memory Deficits in Schizophrenia-Spectrum Disorders".

A double-blind randomised comparative trial of amisulpride versus olanzapine for 2 months in the treatment of subjects with schizophrenia and comorbid depression

Purpose To compare the efficacy and safety of amisulpride and olanzapine in subjects with schizophrenia and comorbid depression in a randomised double-blind trial. Patients Eighty-five adult patients fulfilling DSM-IV criteria for schizophrenia and presenting a depressive episode were randomised to amisulpride (200–600 mg/day) or olanzapine (5–15 mg/day) for 8 weeks. Primary efficacy variables were change in Calgary Depression Scale (CDS) score and Clinical Global Impression (CGI) of Change. Safety was monitored by adverse event reporting and determination of extrapyramidal function and metabolic variables. Results The mean change from baseline of CDS score was –6.84 in the amisulpride group and –7.36 in the olanzapine group. 65.9% and 61.5% of subjects, respectively, were considered “much” or “very much” improved. No significant inter-group difference in effect size was observed. The frequency of adverse events was low and emergence of extrapyramidal symptoms was not seen. Four patients in the olanzapine group developed abnormal triglyceride levels. Mean weight gain was 1.45 and 0.5 kg, respectively, in the olanzapine and amisulpride groups. Conclusion Amisulpride and olanzapine are effective in patients with schizophrenia and comorbid depression. Tolerance of both drugs was acceptable, although use of olanzapine was associated with a trend toward greater metabolic side-effects [19].

Aripiprazole-Induced Acute Dystonia

Back to table of contents Previous article Next article Letters to the EditorFull AccessAripiprazole-Induced Acute DystoniaPUSHPAL DESARKAR M.D., D.P.M.ANUPAM THAKUR M.D.VINOD KUMAR SINHA M.D., D.P.M.,PUSHPAL DESARKAR M.D., D.P.M.Search for more papers by this authorANUPAM THAKUR M.D.Search for more papers by this authorVINOD KUMAR SINHA M.D., D.P.M.Search for more papers by this author,Published Online:1 Jun 2006AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Aripiprazole, the new-generation atypical antipsychotic that is a dopamine system stabilizer, is known for its low propensity to cause extrapyramidal symptoms (1) . Although several reports of dystonia associated with the use of newer atypical antipsychotics are accumulating, a thorough PubMed search through Nov. 6, 2005, did not reveal a single such case induced by aripiprazole. We report a case of acute dystonia observed during aripiprazole therapy. “Mr. A,” an 18-year-old man with no contributory family, past, or personal history was brought to our community clinic with a 4-week history suggestive of a psychotic manic episode. Treatment was initiated with tablet divalproex, which was increased to 500 mg b.i.d., along with aripiprazole, 15 mg/day. In the next follow up, his parents complained about episodes suggestive of dystonia in the form of torticollis, which started within 3 days of treatment initiation. Mr. A did not receive any other medication in between. Trihexyphenidyl, 2 mg/day, was added to the regimen, and dystonia did not recur. Exact mechanism of neuroleptic-induced acute dystonia is still unclear and possibly attributable to a higher ratio of dopamine-acetylcholine antagonism (2) or postsynaptic dopamine hypersensitivity (3) in the basal ganglia. However, preclinical studies with aripiprazole have shown that the drug’s unique partial agonism at dopamine D 2 and serotonin 5-HT 1A receptors, along with antagonism of 5-HT 2A receptors, actually protects against emergence of extrapyramidal symptoms (1) . In our case report, Mr. A had two known risk factors for dystonia, i.e., being young and male (1) . Additionally, we propose the following neurobiological mechanisms that either alone or in combinations could have resulted in acute dystonia with aripiprazole. First, aripiprazole—unlike clozapine, which does not induce acute dystonia—lacks protective anticholinergic action (1) . This was supported by the fact that, in our case, dystonia resolved with anticholinergic medicines. Second, aripiprazole’s action on the D 3 receptor and antagonism of 5-HT 6 and 5-HT 7 receptors is still unknown (1) and could play a potential role. Third, postsynaptic dopamine hypersensitivity was found in bipolar patients (4) , which may be a significant factor. Fourth, the possibility of complex drug interaction of aripiprazole with divalproex cannot be eliminated. Last, preclinical studies found inhibitory action of aripiprazole on serotonin transporter (1) , which could potentially alter dopamine balance in the basal ganglia region. In short, our case report reveals that even aripiprazole may cause rare dystonia in vulnerable individuals, despite having a favorable receptor profile. However, this side effect is amenable to conventional anticholinergic treatment.Ranchi, India Jharkhan, India

Zotepine for Behavioural and Psychological Symptoms in Dementia: An Open-Label Study

Objective: To provide initial information on the safety and efficacy of the atypical antipsychotic zotepine in the treatment of behavioural and psychological symptoms of dementia (BPSD). Methods: This was an open-label, single-centre field study. Twenty-four patients with BPSD associated with Alzheimer's disease (n = 12) or other forms of dementia (n = 12) were included. During the 8-week observation period, the patients received zotepine (Nipolept®) [12.5-150 mg/day] for the psychotic components of BPSD; no other treatment interventions for BPSD were allowed. At baseline, day 28 and day 56, patients were evaluated using the Clinical Global Impressions (CGI) scale; the Mini-Mental State Examination (MMSE), the Syndrome Brief Test (SKT) and the Age Concentration Test (AKT) to assess cognition; and the Neuropsychiatric Inventory (NPI) and the Cohen-Mansfield Agitation Inventory (CMAI) to assess BPSD. General adverse effects and, more specifically, the emergence of extrapyramidal symptoms were also assessed. Results: There was no change from baseline to day 56 in the CGI score and the caregiver burden (as indicated by the caregiver-related section of the NPI). There was also no change in cognition (as assessed by the MMSE, SKT and AKT). The neuropsychiatric symptom score according to part 1 of the NPI (especially key psychotic symptoms, aggression and disinhibition) and the CMAI scores improved by 36% and 15%, respectively, between baseline and the end of the study in a highly statistically significant fashion. No significant differences in treatment response or adverse effect profile were noted between the 12 patients with Alzheimer's disease and the 12 patients with other types of dementia. Zotepine was well tolerated, with tiredness and sedation (five and four cases, respectively) being the most frequent complaints. No clinically significant emergence of extrapyramidal symptoms was seen. Conclusions: Zotepine appears to be well tolerated and effective in treating BPSD, consistent with the performance of other atypical antipsychotic drugs in this condition. Larger, controlled studies are warranted.

A Double-blind, Randomised Comparative Trial of Amisulpride Versus Olanzapine in the Treatment of Schizophrenia: Short-term Results at Two Months

SummaryObjective: To compare the efficacy and safety of the atypical antipsychotics amisulpride and olanzapine in the treatment of acute psychotic exacerbations of schizophrenia.Design and setting: A multinational, double-blind randomised clinical trial.Patients and treatment:Three hundred and seventy-seven patients with predominantly positive symptomatology were treated for six months with either amisulpride (200-800 mg/d) or olanzapine (5-20 mg/d).Main outcome measures: Short-term results were analysed after two months of treatment. The primary efficacy measure was the change of score on the Brief Psychiatric Rating Scale (BPRS). Other measures of efficacy and safety were also evaluated.Results: Psychotic symptoms, as measured on the BPRS score, improved with both treatments, amisulpride being equivalent to olanzapine. All BPRS factor scores, as well as depressive symptoms, improved to a similar extent with both treatments. Less than five per cent of patients withdrew for adverse events, and there was no evidence for the emergence of extrapyramidal symptoms with either treatment. Statistically significant greater weight gain (2.7 ± 3.9 kg) was observed during the study in the olanzapine group, compared with the amisulpride group (0.9 ± 3.2 kg, p < 0.0001).Conclusions: Amisulpride and olanzapine show equivalent efficacy at 2 months in the treatment of acute psychotic exacerbations of schizophrenia. Amisulpride offers a significant advantage in preserving body weight.

Risperidone in the treatment of patients with Alzheimer's disease with negative symptoms.

Negative symptoms such as diminished initiative, drive, motivation, and emotional reactivity have been described in patients with Alzheimer's disease (AD). The purpose of this study was to retrospectively analyze the efficacy and tolerability of risperidone for the treatment of clinically significant positive and negative symptoms in AD. We reviewed the charts of 50 community-residing AD patients who had been treated in a specialized university-based dementia management clinic. Clinical data comparing baseline and 12 weeks of treatment were obtained by reviewing a series of rating scales that were recorded as part of a comprehensive behavioral assessment. Reviewed subjects had a mean age of 79.7 6 years and a mean of 12 +/- 3.6 years of school. Seventy percent of the subjects were female and the majority was White. The mean dose of risperidone prescribed was 1.3 +/- 0.6 mg per day (range from 0.5 mg to 3.0 mg). After 12 weeks of treatment, the severity of positive and negative symptoms was significantly reduced. Importantly, improvement in negative symptoms with the use of risperidone appeared to be independent of a positive treatment effect on positive symptoms. Risperidone had insignificant effects on both cognitive status and the emergence of extrapyramidal symptoms. This retrospective study demonstrates that risperidone appears to be efficacious in the treatment of clinically significant positive and negative symptoms in patients with AD.

The development of treatment resistance in patients with schizophrenia: a clinical and pathophysiologic perspective.

The pathophysiologic process and clinical factors that contribute to the development of treatment resistance in schizophrenia are not well defined. This article describes data indicating that treatment resistance may evolve over the course of the patients' illness and maturational development. Data from multiepisode patients suggest that early effective intervention with clozapine can prevent treatment resistance. Early identification of patients with signs of treatment resistance is vital. Treatments must be effective and prevent relapse. At the first indication that a patient may be developing resistance (e.g., the emergence of extrapyramidal symptoms or increases in negative symptomatology) or may not be complying with treatment, clozapine therapy should be considered.