We compared 65 anti-acetylcholine receptor (AChR)-negative myasthenia gravis (MG) patients, including 32 anti-muscle-specific tyrosine kinase (MuSK)-positive (49%) and 33 anti-MuSK-negative (seronegative) (51%) patients, with 161 anti-AChR-positive MG patients. The anti-MuSK-positive group had a higher frequency of bulbar involvement and respiratory crises. The seronegative group was in between the anti-MuSK positive and the anti-AChR positive groups, being closer to the latter, with regard to the severity of the disease. At the end of follow-up, the outcome of the anti-MuSK-positive patients was not different from that of the anti-AChR-positive patients, although their maintenance corticosteroid dose was higher. The seronegative patients had better outcome than the other two groups. NEUROLOGY 2007;68:609-611 Anti-muscle-specific tyrosine kinase (MuSK) antibodies have been found in up to 70% of antiacetylcholine receptor (AChR) antibody-negative (anti-AChR-neg) myasthenia gravis (MG) patients. [1][2][3][4][5][6] The clinical characteristics of patients with anti-MuSK antibodies have been described 2-8 and compared with anti-AChR-/anti-MuSK-negative (seronegative [SN]) patients in several series. 2,4,5,7,8 Comparison with anti-AChR antibody-positive (anti-AChR-pos) MG, however, has only been done in studies concentrating on electrophysiologic aspects. 8 There is general agreement on the severity of anti-MuSK antibody-positive (anti-MuSK-pos) patients, but there are some conflicting results regarding predominant symptomatology and outcome. [2][3][4][5] Here we compare anti-MuSK-pos patients with both SN and anti-AChR-pos patients to evaluate whether the severity, bulbar symptoms, and outcomes were indeed worse in anti-MuSK-pos patients.

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Patients with severe stroke and salvageable brain tissue at admission, who have higher glycaemic and blood pressure levels, may have a risk of iatrogenic hypoglycemia/iatrogenic hypotension. In this study, we examined the relationship between the presence of diffusion-weighted imaging (DWI)/perfusion-weighted imaging (PWI) mismatch, admission blood glucose level, and admission blood pressure level in patients who were admitted in the first 12 hours after onset. We studied 212 patients who were prospectively and consecutively registered to the stroke unit from 2006 to 2009. Correlations between mismatch and admission blood pressure level (ABPL) and admission blood glucose level (ABGL) were analyzed using multivariate logistic regression. Mismatch ( P = .064, adjusted OR = 2.297, 95% CI, 0.953–5.536) was not associated with a high ABGL in the whole group. However, after excluding patients with diabetes mellitus (DM) (n = 67, 35%), mismatch ( P = .033, adjusted OR = 3.801, 95% CI, 1.110–13.015), an impaired level of consciousness, use of anti-DM medication, glycated hemoglobin levels, and cardioembolic aetiology were independent predictors of a high ABGL. The presence of mismatch or proximal vessel occlusion was not associated with ABPL. Female sex ( P = .048) and total anterior circulation stroke ( P = .008) were independent predictors associated with a higher ABPL. We conclude that patients with hyperacute ischemic stroke with PWI/DWI mismatch are more likely to have hyperglycemia.