Conversion of clinically isolated syndrome to multiple sclerosis: a prospective multi-center study in Eastern India.

BACKGROUND: In White populations more than 60% of clinically isolated syndrome (CIS) convert to multiple sclerosis (MS) on a long-term follow-up; several predictors for conversion have been identified. OBJECTIVE: This study aimed to determine the conversion rate and the predictors of conversion from CIS to MS (McDonald 2010) among Indians. The other objective was to evaluate the diagnostic accuracy of the new McDonald 2017 criteria in prediction of a second clinical attack. METHODS: Clinical and demographic data of CIS cohorts were collected. Baseline investigations included cerebrospinal magnetic resonance imaging (MRI) with contrast and cerebrospinal fluid (CSF) testing for oligoclonal band (OCB). Follow-up clinical and MRI examinations were performed annually for at least 24 months. RESULTS: Of the 82 subjects (age range 15-58 years), 36 (43.9%) converted to MS; 31/82 (37.8%) converted in 24 months. The predictors for conversion were earlier age of onset, CSF-OCB, cerebral MRI T2 lesion count, and periventricular and juxtacortical location of lesions. Twenty-two (26.83%) CIS fulfilled the McDonald MS 2017 criteria at baseline. CONCLUSION: In this first prospective study of CIS in India, the risk factors for conversion are similar but the conversion rate to MS is lower than that in the western nations.

Neurological complications due to Semple-type antirabies vaccine. Clinical and therapeutic aspects.

Thirty nine patients with neuroparalytic accidents due to the use of Semple-type antirabies vaccine were studied. The mean age of the patients was 25.8 +/- 13.2 years. The suspected source of infection was the bite of a dog in 36 (92.3%) cases. The mean interval between the first dose of ARV and the onset of neurological deficits was 14.4 +/- 8.7 days. The number of doses was 7 or less in 28 (71.8%) and more than 7 in 11 (28.2%) cases. With regard to neurological deficits, 5 (12.8%) had encephalopathy, 1 (2.6%) had encephalomyeloradiculopathy, 12 (30.7%) had cervical myeloradiculopathy, 4 (10.3%) had dorsolumbar myeloradiculopathy and 17 (43.6%) had polyradiculopathy. Lumbar cerebrospinal fluid analysis was done in 31 (79.5%) cases and was abnormal in 15 (48.4%), in the form of pleocytosis or raised protein or both. Electroencephalogram was done in 24 (61.5) cases and was abnormal in 7 (29.2%); in 6 (85.7%) of theme the abnormalities were subclinical. Electroneuromyography was done in 15 (38.5%) patients and was abnormal in 13 (72.2%). Visual evoked potentials were studied in 11 (28.2%) cases and were abnormal in 2 (18.2%). Thirty six (92.3%) cases received steroids and 25 (64.1%) received cyclophosphamide in addition. The therapeutic results were better in those who received cyclophosphamide. Three patients died; One died due to respiratory failure and two due to unrelated causes while on respirator. The latter two were autopsied, and findings in the brain were unremarkable.

Serum and urinary zinc in fulminant hepatic failure.

Patients with chronic hepatic encephalopathy have been shown to have low serum zinc levels. Moreover, in a controlled study, significant improvement was seen in these patients on oral zinc supplementation. Information on zinc status in fulminant hepatic failure is insufficient. Serum and urinary zinc abnormalities were studied in 22 patients with fulminant hepatic failure (FHF) and they were compared with age- and sex-matched controls. The mean serum zinc values were significantly less in patients with FHF (72.7 +/- 3.7 micrograms/100 mL versus 107.9 +/- 6.2 micrograms/mL) while the urinary zinc values were significantly higher compared with controls (603.5 +/- 9.3 micrograms/24 h versus 334.4 +/- 10 micrograms/24 h). The serum zinc levels significantly and progressively decreased, while urinary zinc significantly increased after admission in patients with FHF. The serum zinc values in the group that survived were significantly higher than those in the group of patients who died. Correspondingly, urinary zinc was lower in survivors than in the group that expired. This study indicates that serum and urinary zinc levels could be used as a prognostic indicator in FHF. A therapeutic trial with zinc supplementation is justified in this group of patients.