The levels of uric acid (UA), a natural peroxynitrite scavenger, were measured in sera from 240 patients with multiple sclerosis (MS) and 104 sex- and age-matched control patients with other neurological diseases (OND). The mean serum UA concentration was lower in the MS than in the OND group, but the difference did not reach the level of statistical significance (P = 0.068). However, the mean serum UA level from patients with active MS (202.6 + 67.1 mumol/l) was significantly lower than that in inactive MS patients (226.5 + 78.6 mumol/l; P = 0.046) and OND controls (P = 0.007). We found a significant inverse correlation of serum UA concentration with female gender (P = 0.0001), disease activity (P = 0.012) and duration (P = 0.017), and a trend towards an inverse correlation with disability as assessed by EDSS score, which did not reach statistical significance (P = 0.067). Finally, multivariate linear regression analyses showed that UA concentration was independently correlated with gender (P = 0.0001), disease activity (P = 0.014) and duration of the disease (P = 0.043) in MS patients. These findings suggest that serum UA might serve as a possible marker of disease activity in MS. They also provide support to the potential beneficial therapeutic effect of radical-scavenging substances in MS.

Summary:Purpose: In patients with multiple sclerosis (MS), epileptic seizures occur more frequently than in the general population. The aim of this study was to analyze clinical characteristics of epilepsy in patients with MS, potential correlation between the semiology of seizures, EEG and magnetic resonance imaging (MRI) findings in these patients, as well as to examine the response to anticonvulsant therapy.Methods: In a series of 268 consecutive patients with definite MS hospitalized at the Institute of Neurology, Belgrade, we identified 20 (7.5%) patients with seizures or epilepsy. All patients with seizures or epilepsy were submitted to standard EEG and brain MRI with gadopentetate dimeglumine.Results: In four patients, epilepsy occurred 1-5 years before other clinical manifestations of MS. Eight patients had seizures only during MS relapses (provoked seizures). In two of them, seizures were the only manifestations of relapse. In 12 patients, seizures occurred regardless of the phase of MS (chronic epilepsy). In the majority of patients, seizures were partial with secondary generalization. Five patients experienced episodes of status epilepticus, and they all had dementia. Abnormal EEG pattern was found in 11 patients. Brain MRI disclosed corticalsubcortical lesions in nine patients and focal cortical atrophy in one, whereas in the remaining patients, findings were inconclusive. Probable EEG-MRI-seizure type correlation existed in 10 patients.Conclusions: Our data suggest that epilepsy may represent an initial symptom of MS and a single clinical manifestation of a relapse, and further support the assumption of the existing correlation between the presence of cortical-subcortical lesions and epileptic seizures or epilepsy in patients with MS.

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We report a 51-year-old woman with vitamin B12 deficiency who presented with slight megaloblastic anemia and severe neurologic deficits associated with multiple focal and confluent T2-weighted white matter hyperintensities on brain MRI. Forty-four months after initiation of hydroxocobalamin therapy, there was clinical improvement and striking reduction in the MRI abnormalities. B12 deficiency should be considered in the differential diagnosis of neurologic disorders associated with multiple areas of white matter hyperintensities on T2-weighted brain MRI.

Ten patients in acute exacerbation of multiple sclerosis were treated with 1000 mg of methylprednisolone for 7 days, followed by abrupt cessation of therapy. The function of hypothalamic-pituitary-adrenal (HPA) axis was assessed by the response of ACTH and cortisol to insulin tolerance test (ITT). ITT was performed 1 day before and 1, 3, 8, 13 and 23 days after the termination of the therapy (days 0, 8, 10, 15, 20 and 30 of the study, respectively). The response of these hormones to insulin-induced hypoglycemia prior to therapy was normal. There was no suppression of the ACTH response to hypoglycemia after the methylprednisolone therapy based on the 100% rise of ACTH after ITT. Cortisol response during ITT was suppressed at day 8 (1 day after ending of therapy) but recovered on day 10 (3 days after ending of therapy). In conclusion, 7 day-therapy with 1000 mg methylprednisolone does not result in the permanent suppression of the HPA axis, suggesting that no regular supplemental corticosteroid coverage is required. The observed transitory suppression of the HPA axis recovered spontaneously after the therapy.