Neuromyelitis optica spectrum disorder mimicking stroke: A case report and literature review.

Hemiparesis is a frequently observed manifestation of stroke but exceptionally rare in the context of neuromyelitis optica spectrum disorder (NMOSD). In this case, a 68-year-old woman initially presented with acute right-sided weakness, leading to suspicion of ischemic stroke. However, her symptoms worsened despite treatment with aspirin and statins. Subsequent spinal MRI and aquaporin 4 antibody testing confirmed the diagnosis of NMOSD. The administration of methylprednisolone and immunoglobulin resulted in improved clinical outcomes. This case serves as an illustrative example of the diverse manifestations encountered in NMOSD and underscores the significance of considering this potential etiology in elderly patients to facilitate prompt diagnosis and therapeutic intervention.

[An analysis of the risk factors for the severity of paralysis in patients with hypokalemic periodic paralysis].

OBJECTIVES: To analyze the independent factors for the severity of paralysis in the patients with hypokalemic periodic paralysis (HOPP). METHODS: Eighty patients admitted with HOPP were reviewed. Using univariate analysis and multivariate analysis, the independent factors for the severity of paralysis were revealed. RESULTS: A total of 76 cases were male and 4 female with a mean age of (26.3 +/- 4.5) years. Univariate analysis showed that patients with low serum magnesium level, low serum potassium level, high serum creatine kinase level, changes of electrocardiogram, chest distress and palpitation, nausea and vomiting as well as muscular soreness had more severe paralysis, while multivariate analysis revealed that serum magnesium < 0.8 mmol/L (OR 8.3, 95%CI 1.0 - 68.4, P < 0.05), serum potassium 1.5 - 1.8 mmol/L (OR 1.3, 95% CI 1.1 - 16.0, P < 0.01) and serum creatine kinase > 200 U/L (OR 1.1, 95%CI 1.0 - 1.1, P < 0.01) were the independent factors for the severity of paralysis. CONCLUSION: Low serum magnesium level, low serum potassium level and high serum creatine kinase level are the independent risk factors for more severe paralysis in patients with HOPP.

Oncosis, the possible cell death pathway in astrocytes after focal cerebral ischemia.

Swelling of astrocytes at early stage of cerebral ischemia has been reported, however, the fate and the cell death pathway of astrocytes are still unclear. Focal cerebral ischemia was induced in Sprague-Dawley rats by permanent occlusion of middle cerebral artery for 3 to 48 h. Haematoxylin and eosin (HE) staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), glial fibrillary acidic protein (GFAP), caspase-3 immunostaining, and double-staining with TUNEL and GFAP were carried out on consecutive sections. The ultrastructure was revealed by electron microscopy. Using electron microscope, apoptotic neurons were confirmed with condensed chromatin and apoptotic bodies. In the core of the infarct, clumps of heterochromatin around the edge of nucleus, vacuolar degeneration of the nucleus and leakage of chromatin were demonstrated at 3, 6, and 12 h respectively in the swelling astrocytes, which accorded with the process of oncosis; in the peripheral zone of the infarct, reactive astrocytes with nuclear membranes preserved demonstrated increased cell size and number and coexisted with oncotic astrocytes. Scattered GFAP-positive cells and ubiquitous caspase-3-positive cells were found in the core after 12 h following cerebral ischemia, and no cells positive for double-staining with TUNEL and GFAP were found in the ischemic regions, indicating that most GFAP-positive astrocytes did not die by apoptosis. Findings from present study demonstrate that after cerebral ischemia, oncosis may be the possible cell death pathway of astrocytes in the ischemic region, and oncotic astrocytes coexist with reactive astrocytes in the peripheral zone.