A Comparative Study of Aripiprazole, Olanzapine, and L-Methylfolate Augmentation in Treatment Resistant Obsessive-Compulsive Disorder.

About half of the patients with Obsessive-compulsive disorder (OCD) do not respond to serotonin reuptake inhibitors (SRIs) or have a partial improvement in their symptoms. This study aimed to compare the efficiency and safety of aripiprazole, olanzapine, and L-methyl folate in patients with resistant OCD. The study consisted of an open-label prospective phase of 12-weeks to ascertain resistance to SRIs and a second 6-week open-label addition phase for non or, partial responders of the first phase. One-hundred-fifteen patients entered the 16-week open-label phase. Fifty patients (43.47%) responded to the SRIs monotherapy, two patients developed adverse effects and another three were lost to the follow up. Sixty patients (52.2%) were considered treatment-resistant and entered the 6-week open-label aripiprazole, olanzapine, or L-methyl folate addition phase; Patients showed a significant improvement over 6-week study period in olanzapine and aripiprazole group as measured by YBOCS total score (p < 0.001) while there was no change in the L-methyl folate group at the end as compared with baseline (p = 0.150). Clinical Global Impression-Severity decreased from 4.90 to 2.90 in olanzapine and aripiprazole group at the end of 6 weeks while there was no change in the L-methyl folate group. The CGI-I was significant in the olanzapine and aripiprazole group (p < 0.001) while it was insignificant in the L-methyl folate group (p = 0.088). Augmentation of SRIs with olanzapine or aripiprazole could be a promising option for resistant OCD. L-methyl folate though shown to be effective in resistant depression was not effective in treatment resistant OCD.

Obsessive Compulsive Disorder Presenting as Neurological Emergency.

Chronic epilepsy is leading to behavioral changes including obsessive-compulsive symptoms has been well-studied and shown to be about 22%, but the converse has not been reported. Here, we present a case discussion of a 45-year-old female, who presented with recurrent seizures with hyponatremia, which latter was ascribed to her undiagnosed obsessive compulsive disorder (OCD). This patient later did well on anti-obsessional treatment without any antiepileptic. This embarks the need for detailed psychiatric evaluation for patients in emergency care settings and gives a rare presentation of OCD.

Seasonal Affective Disorder (SAD): Role of Lamotrigine Augmentation to Anti-Depressant Medication in Winter Depression.

BACKGROUND: Many therapeutic options have been evaluated and tried for seasonal affective disorder (SAD) including bright light therapy (BLT), anti-depressants, beta-blockers and psychotherapy, but the data supporting use of mood-stabilizing agents is just handful in spite of this condition being understood most frequently to be associated with bipolar affective disorder II (BPAD II). So we planned to study role of Lamotrigine (Mood stabilizing agent) in SAD. MATERIALS AND METHODS: 30 patients of SAD who were prescribed lamotrigine in addition to antidepressant medications for a minimum of 8 weeks and were assessed for severity using HAM-D were selected retrospectively from the hospital records for this study. HAM-D scores at 2, 4 and 8 weeks were compared to baseline scores. STATISTICS ANALYSIS: Single tailed t-test was used to study the difference of means to assess the therapeutic response and pre/post analysis of change. Statistical significance was set at P < 0.05. RESULTS: Though no significant difference was seen in HAM-D Scores at 2 weeks of treatment compared to baseline, but results were statistically significant at 4 and 8 weeks of treatment with lamotrigine augmentation of antidepressant medications. CONCLUSION: We conclude that lamotrigine augmentation was found to be effective treatment strategy for managing winter depression phase of Seasonal Affective Disorder.

Role of lamotrigine augmentation in treatment-resistant obsessive compulsive disorder: a retrospective case review from South Asia.

BACKGROUND: Resistance to pharmacotherapy is one of the major challenges in the management of obsessive-compulsive disorder (OCD). OCD being a quite prevalent disorder, this resistance adds to the disability. Different strategies are being employed to counter this resistance, one of them being augmentation with glutamatergic modulators. Lamotrigine is being used for same since the recent past with mixed results. OBJECTIVE: The aim was to study the role of lamotrigine augmentation in serotonin reuptake inhibitor (SRI) resistant OCD patients. METHODOLOGY AND RESULTS: This study was carried by studying the case sheets of SRI resistant cases having already completed the treatment. A total of 22 cases sheets over 2 years met the study criteria with a mean age of mean age of 34.14 years. Over a period of 16 weeks, with a mean lamotrigine dose of 150 mg/day, 20 out of 22 patients had shown a significant response. The mean decrease in Yale-Brown Obsessive Compulsive Scale score was 67.23% with a baseline score of 28.87. There was a similar change on different domains of World Health Organization quality of life (P = 0.00564). CONCLUSION: Lamotrigine augmentation to on-going treatment with SRIs may be an effective move in case of SRI resistant OCD patients.

Effects of switching from olanzapine to aripiprazole on the metabolic profiles of patients with schizophrenia and metabolic syndrome: a double-blind, randomized, open-label study.

BACKGROUND: Patients with schizophrenia suffer high rates of metabolic derangements on some antipsychotic medications that predispose them to cardiovascular diseases. Keeping this fact in mind, we planned this open-label study to see the effect on various metabolic parameters after switching stable schizophrenia subjects, who had developed metabolic syndrome on olanzapine, to aripiprazole. METHODS: Sixty-two patients with schizophrenia who were stable on olanzapine and were fulfilling modified National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP-III) criteria for the presence of metabolic syndrome were enrolled on the study. Patients were randomly assigned either to switch to aripiprazole or to stay on olanzapine, on a 1:1 basis. Cross-tapering over a period of 1 month was done while switching patients to aripiprazole. Laboratory assessment for metabolic parameters was done at baseline, 8 weeks, and 24 weeks after enrollment; efficacy assessment was done using the Positive and Negative Syndrome Scale (PANSS) at baseline and 24 weeks, the Clinical Global Impressions severity subscale (CGI-S) at baseline, and the Clinical Global Impressions improvement subscale (CGI-I) at 24 weeks. RESULTS: All parameters of metabolic syndrome (waist circumference, blood pressure, triglyceride level, fasting blood glucose, and high-density lipoprotein cholesterol) kept deteriorating in the stay group, compared with a continuous improvement in the switch group over time. At the end of the study, 26 patients (100%) from the stay group and 15 patients (42.8%) from switch group met the modified NCEP ATP-III criteria for presence of metabolic syndrome (P<0.001). There were no statistically significant differences between groups in psychopathology changes as measured by the PANSS total score and CGI-I scores. CONCLUSION: Clinically stable patients with schizophrenia who are taking olanzapine and who have evidence of metabolic syndrome can be successfully switched to aripiprazole, with improvement in various parameters of metabolic syndrome and without any significant change in efficacy measures.

Diabetes mellitus and impaired glucose tolerance in patients with schizophrenia, before and after antipsychotic treatment.

BACKGROUND: Treatment with antipsychotics increases the risk of developing diabetes in patients of schizophrenia but this diabetogenic potential of different antipsychotics seems to be different. Moreover, there may be an independent link between schizophrenia and diabetes. So we plan to study the prevalence of glucose dysregulation in patients of schizophrenia before and after treatment with various antipsychotics. MATERIALS AND METHODS: Fifty patients (32 males and 18 females) diagnosed with schizophrenia were evaluated for glucose dysregulation using oral glucose tolerance test, initially (drug naive) and after antipsychotic treatment. Age- and sex-matched healthy volunteer group of 50 subjects (35 males and 15 females) was taken for comparison. Results were interpreted using American Diabetic Association criteria. RESULTS: Though the glycemic status of the patient group was comparable with healthy controls initially but antipsychotic treatment was associated with glucose dysregulation. For first 6 weeks the antipsychotic (olanzapine, risperidone, haloperidol and aripiprazole)-induced glucose dysregulation was comparable, which was seen to be maximum with the olanzapine-treated group at the end of this study, 14 weeks. CONCLUSION: We conclude that antipsychotic treatment of nondiabetic drug naive schizophrenia patients was associated with adverse effects on glucose regulation. For initial 6 weeks the antipsychotic-induced glucose dysregulation was comparable, which was seen to be maximum with olanzapine at the end of study, i.e. 14 weeks. Keeping this at the back of mind we can stabilize a patient initially with a more effective drug, olanzapine, and later on shift to one with less metabolic side effects.

Rapid Response of Long-Standing, Treatment-Resistant Non-Catatonic Mutism in Paranoid Schizophrenia with Single ECT session.

CONTEXT: Mutism is a common manifestation of catatonia, but mutism due to other forms of psychopathology and neurological disorders have also been described. Although not common, long-standing mutism has also been a feature of non-catatonic schizophrenia and traditionally responds less to conventional therapies. CASE REPORT: We describe a rare case of paranoid schizophrenia presenting with continuous mutism for about 4 years. This 26-year-old male had symptoms of schizophrenia without catatonia. After failed trial of adequate pharmacotherapy and psychological intervention and considering his level of dysfunction, he was started on electroconvulsive therapy (ECT). To our surprise, he improved with a single session of ECT while he was on concurrent pharmacotherapy. We also discuss the possible explanation for this rapid effect of ECT in such clinical presentation. To our knowledge, this is the first case of non-catatonic mutism of schizophrenia of this long duration responding so promptly to ECT, although there are other reports as well in literature, but multiple ECT sessions were applied in those cases. CONCLUSION: Non-catatonic mutism is perhaps presenting as a cultural variant in this part of the world and whenever encountered, ECT should be an option. Further research should be carried out to validate this idea.