Risk of multiple sclerosis following clinically isolated syndrome: a 4-year prospective study.

The aim of the study was to estimate the rate of conversion from clinically isolated syndrome (CIS) to multiple sclerosis (MS) and to investigate variables predicting conversion in a cohort of patients presenting with symptoms suggestive of MS. Patients with a first symptom suggestive of MS in the preceding 6 months and exclusion of other diseases were enrolled in an observational prospective study from December 2004 through June 2007. Conversion from CIS to MS according to both McDonald and Clinically Defined Multiple Sclerosis (CDMS) criteria was prospectively recorded until March 2010. The multivariate Cox proportional hazard model was used to assess the best predictive factors of conversion from CIS to MS. Among 168 patients included in the analysis, 122 converted to MS according to McDonald criteria whereas 81 converted to MS according to CDMS criteria. The 2-year probability of conversion was 57% for McDonald Criteria and 36% for CDMS criteria. Variables at enrolment significantly associated with conversion according to McDonald criteria were age and positivity for Barkhof criteria, and according to Poser's CDMS criteria, age, positivity for Barkhof criteria and no disease modifying therapy. In this large prospective cohort study the conversion rate from CIS to MS in patients presenting with recent symptoms suggestive of MS was within the range of previous observational studies and lower than that reported in the placebo arm of randomized trials. We confirm the prognostic value of MRI in addition to the previous experimental data on the protective role of disease-modifying therapies.

Impact of treatment on the short-term prognosis of status epilepticus in two population-based cohorts.

PURPOSE: Epidemiological surveys on status epilepticus (SE) in adults in two Italian areas (Bologna and Lugo di Romagna) disclosed a major difference in 30-day case fatality (33% versus 7 %). Since suboptimal management was hypothesised in the first site, we compared the quality of treatment in the two cohorts and examined its contribution to prognosis. METHODS: The Bologna and Lugo di Romagna cohorts of adults with incident SE were included. Patients with post-anoxic encephalopathy were excluded. Quality of treatment was independently classified by two experts. Clinical and treatment features were compared in the two sites. The contribution of variables collected to the 30-day case fatality was explored through multivariate logistic analysis in the whole group of patients. RESULTS: Fifty-seven patients were included. No differences were observed between Bologna and Lugo di Romagna either in clinical features or the time of management. The quality of global drug treatment significantly differed in disfavour of Bologna (p = 0.044). Independent predictors of a worse 30-day case fatality in the whole group of patients were the onset of SE in hospital (OR 9.67, p = 0.0095) and the poor global quality of treatment (partially correct versus correct OR 3.59, p = 0.55, and incorrect versus correct OR 21.09, p = 0.0084). By subgroup analysis, the site of onset factor encompasses the aetiologic background of patients. CONCLUSION: In addition to previously known prognostic factors, epidemiological comparison of mortality rates of SE between different regions must also consider the quality of treatment.

Transient hypohidrosis induced by topiramate.

PURPOSE: Hypohidrosis during topiramate (TPM) treatment was recently reported in children. We describe an adult epilepsy patient who developed inability to sweat as well as heat intolerance while undergoing treatment with TPM. METHODS: To detect the site of the sweat block, patient underwent examination of sweat gland function, cardiovascular autonomic test, and body temperature rhythm determination. RESULTS: During TPM treatment, cardiovascular autonomic function and circadian rhythm of body core temperature were normal, whereas thermoregulatory sweat test (TST) showed anhydrosis. This adverse drug effect was quickly resolved after drug discontinuation. CONCLUSIONS: Because of normal cardiovascular autonomic function and central and peripheral thermoregulatory mechanisms, we hypothesize that hypohidrosis during TPM treatment could be due to a carbonic anhydrases (CA) block at the level of sweat gland.