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Neurology Alert – January 1, 2022

January 1, 2022

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  • Thalamic Stroke and Sleep Impairment: An Experiment of Nature

    In a detailed clinical and electrophysiological study of sleep patterns in 12 patients with thalamic stroke, comparing them with 11 patients who had extrathalamic stroke, the investigators identified a marked decrease in slow wave sleep activity in the group with thalamic stroke. The clinical significance of this finding is uncertain but may have an effect on daytime cognitive performance.

  • Neuropathological Findings in the Brains of Patients Who Died from COVID-19

    In an autopsy study of 41 patients who died from COVID-19 in a single medical center in New York City, most of the brain pathology was the result of hypoxic-ischemic injury, infarction, and hemorrhage, with microglial activation and neuronophagia caused by inflammation. Studies for the presence of viral proteins were negative, and very low levels of viral ribonucleic acid were detected.

  • Intravenous Immunoglobulin for Stable CIDP: Stop or Taper?

    First-line therapy for chronic inflammatory demyelinating polyneuropathy is intravenous immunoglobulin (IVIG), but the timing and method for withdrawal of this treatment are uncertain. In a retrospective review of stable patients on IVIG, investigators at the National Hospital in London observed that there was no significant difference in the likelihood of deterioration or response to retreatment if IVIG was stopped abruptly or tapered slowly.

  • Neuropathological Variability of NMDAR-Encephalitis

    The neuropathological features of N-methyl-D-aspartate receptor (NMDAR)-encephalitis are described in an autopsy cohort of four patients two diagnosed in life with comorbid brain disorders, and two diagnosed at autopsy and never treated. The two untreated patients had inflammatory infiltrates composed of perivascular and parenchymal T cells and B cells/plasma cells in the basal ganglia, amygdala, and hippocampus. The two treated patients had variable pathologies that reflected their underlying neurological disorders (lymphoproliferative disease and multiple sclerosis). Overall, the topographic distribution of inflammation in patients with NMDAR-encephalitis reflects the clinical symptoms of movement disorders, abnormal behavior, and memory dysfunction with inflammation predominantly observed in the basal ganglia, amygdala, and hippocampus. Loss of NMDAR-immunoreactivity correlated with disease severity.