No abstract

Intraoperative electrocorticography (ECoG) has been traditionally used in the surgical management of medically refractory partial epilepsies to identify the location and limits of the epileptogenic area, to guide the extent of resection, and to assess its completeness. Although in clinical use for many years, the basic questions regarding indications and limitations of this method has remained unanswered. ECoG plays a major role in tailored temporal lobectomies, whereas, it serves no practical purpose in standard resection of medial temporal lobe epilepsy (TLE) with magnetic resonance imaging (MRI) evidence of mesial temporal sclerosis (MTS). Residual hippocampal spikes, unaltered by resection, correlate with a greater proportion of seizure recurrence. Intraoperative hippocampal ECoG can allow sparing of functionally important hippocampus, thus minimising postoperative memory decline. ECoG eminently aids removal of developmental malformations of brain, and most importantly, the excision of highly epileptogenic cortical dysplasias (CDs) for deciding the extent of resection for best seizure control. The ECoG can be a valuable tool during multiple subpial transections (MST).

Fixed oral doses of clozapine produce up to 45-fold interindividual variability among its serum levels in patients with treatment-resistant schizophrenia. Although the relationship between serum clozapine level and its therapeutic response is uncertain, the presence of a therapeutic window and level-dependent adverse effects require the estimation of serum clozapine levels. As routine therapeutic drug monitoring of clozapine is not feasible in many clinical settings, identification of clinical predictors of serum clozapine levels is desirable. Hence, we aimed to evaluate the clinical variables associated with serum clozapine levels. We assessed the sociodemographic and clinical profiles, cognition, disability and psychopathology of 101 consecutive patients with treatment-resistant schizophrenia on a stable dose of clozapine, using standard assessment schedules. We determined their serum clozapine levels using high-performance liquid chromatography with ultraviolet detection. While employing multivariate robust regression models, oral clozapine dose (P<0.001), caffeine intake (P=0.04) and Valproate comedication (P=0.005) were associated with serum clozapine levels. Serum clozapine levels above 750 ng/ml increased the risk of seizures (odds ratio 5.15; P=0.03). Clinical variables are useful to model a dosing nomogram for serum clozapine levels. The importance of caffeine consumption and Valproate comedication should be considered during clozapine dose adjustments to enhance its therapeutic response and safety profile.

Public awareness, education and community-level interventions for reducing the misconceptions and stigma related to intellectual disability are needed in addition to culturally sensitive treatment methods to improve the attitude towards and management of intellectual disability.

Subjects with common mental disorders are commonly seen in primary health care settings. Illiteracy and poverty are associated with caseness. Primary health care research and policy needs to focus on common mental disorders.

Sildenafil citrate is safe and effective in the treatment of antipsychotic-induced erectile dysfunction. It is also well tolerated.

1. Serum prolactin levels were measured in large cohorts of schizophrenic patients (67 males and 42 females) and normal subjects (78 males and 42 females). 2. There was no significant differences between the serum prolactin levels of patients and controls, except in the age group 15-29 years. There were no significant differences between the serum prolactin levels of males and females, either among the patients or the control subjects. 3. The rise in serum prolactin levels after the commencement of neuroleptic medication in the patients was greater in females than in males even though the female patients received neuroleptics at lower doses. 4. These data indicate that serum prolactin levels in unmedicated males and females are similar; however, the prolactin response to neuroleptic medication is greater in females than in males.

Vascular parkinsonism (VP) accounts for 2.5-5% of all cases of parkinsonism in various population based and clinical cohort studies. VP develops as a result of ischaemic cerebrovascular disease, so aetiologically it is classified as secondary parkinsonism. It has been variably referred to in the literature as arteriosclerotic parkinsonism, vascular pseudo-parkinsonism, and lower body parkinsonism. The most important consideration while making a diagnosis of VP should be to differentiate VP from Parkinson's disease (PD) because of prognostic and therapeutic implications. The salient clinical features in VP which differentiate it from PD are presentation with postural instability and falls rather than with upper limb rest tremor or bradykinesia; short shuffling parkinsonian gait in VP is accompanied by a wider base of stance and variable stride length (parkinsonian-ataxic gait), absence of festination, frequent occurrence of pyramidal signs, and early subcortical dementia. In a patient where the clinical features are suggestive of VP the clinical diagnosis can be supported by demonstration of diffuse white matter lesions and/or strategic subcortical infarcts in the MRI of the brain. The therapeutic options in VP are limited to levodopa, and a poor or non-sustained response to levodopa is another differentiating feature between VP and PD.