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Neurology Alert – December 1, 2025

December 1, 2025

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  • Home Training for Cerebellar Ataxias: A Randomized Clinical Trial

    In this randomized clinical trial comparing home high-intensity aerobic training to home balance training among individuals with cerebellar ataxias, investigators found that home high-intensity aerobic training improved ataxia symptoms, fatigue, and aerobic fitness more than dose-matched home balance training.

  • Relationship Between Abnormal Amyloid-β Deposition and Regional Brain Atrophy on MRI

    In a retrospective review of patients followed in the Wisconsin Alzheimer Disease Research Center, the time course of early deposition of amyloid-β correlated with regional atrophy in temporoparietal regions of interest independent of tau positivity.

  • Progressive Encephalomyelitis with Rigidity and Myoclonus with GlyR Antibodies

    This is a retrospective observational study of patients with a clinical diagnosis of progressive encephalomyelitis with rigidity and myoclonus (PERM) and glycine receptor (GlyR) antibodies identified at a specialized neuroimmunology laboratory, as well as an accompanying systematic literature review. The goal of the study was to describe the clinical features and long-term outcome of patients with GlyR antibody-mediated PERM.

  • Vertigo and Altered Postural Perception: Overlapping Symptoms, Distinct Mechanisms

    Two distinct vestibular disorders, persistent postural-perceptual dizziness (PPPD) and vestibular migraine (VM), both involve vertigo as a primary symptom. Nearly half of chronic migraine patients also experience vertigo, especially those with aura and allodynia. Since PPPD is seen as a functional maladaptation and VM is associated with cortical hyperexcitability, treatment for vertigo in these two conditions should be tailored to their unique pathophysiological mechanisms.

  • Iatrogenic Cerebral Amyloid Angiopathy-Related Inflammation

    In this multicenter, retrospective case series, the authors sought to describe the co-occurrence of two rare variants of cerebral amyloid angiopathy: iatrogenic cerebral amyloid angiopathy, thought to be caused by prion-like spread of amyloid beta after seeding from neurosurgical procedures decades prior to symptom onset, and cerebral amyloid angiopathy-related inflammation, characterized by robust perivascular inflammatory response in amyloid-laden vessels. This series demonstrates that inflammation can complicate iatrogenic cerebral amyloid angiopathy, supporting a spectrum model of disease and urging multicenter study.