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Background and purpose: The pathogenesis of idiopathic normal pressure hydrocephalus (iNPH) remains controversial. Limited studies have indicated a high prevalence of obstructive sleep apnoea (OSA) amongst iNPH patients. The aim was to investigate the clinical correlates of OSA in iNPH patients. Methods: In this cross‐sectional observational study, consecutive iNPH patients were prospectively enrolled. Evaluations included the iNPH Rating Scale, the Movement Disorder Society Unified Parkinson's Disease Rating Scale part III, the time and number of steps to walk 10 m, the Epworth Sleepiness Scale, the Pittsburgh Sleep Quality Index, a complete neuropsychological evaluation, 3‐T brain MRI, full‐night video‐polysomnography, tap test and cerebrospinal fluid (CSF) neurodegeneration biomarkers. Results: Fifty‐one patients were screened, of whom 38 met the inclusion criteria. Amongst the recruited patients, 19/38 (50%) exhibited OSA, with 12/19 (63.2%) presenting moderate to severe disorder. OSA+ iNPH patients required more time (p = 0.02) and more steps (p = 0.04) to complete the 10‐m walking test, had lower scores on the gait subitem of the iNPH Rating Scale (p = 0.04) and demonstrated poorer performance on specific neuropsychological tests (Rey Auditory Verbal Learning Test immediate recall, p = 0.03, and Rey–Osterrieth Complex Figure, p = 0.01). Additionally, OSA+ iNPH patients had higher levels of total tau (p = 0.02) and phospho‐tau (p = 0.03) in their CSF but no statistically significant differences in beta‐amyloid (1–42) levels compared to OSA− iNPH patients. Conclusion: Obstructive sleep apnoea is highly prevalent in iNPH patients, particularly at moderate to severe levels. OSA is associated with worse motor and cognitive performance in iNPH. The CSF neurodegeneration biomarker profile observed in OSA+ iNPH patients may reflect OSA‐induced impairment of cerebral fluid dynamics. [ABSTRACT FROM AUTHOR]

The article discusses a case report of a 70-year-old male with acquired progressive ataxia and palatal tremor following a static lesion. The patient showed signs of neurodegeneration, including elevated levels of tau proteins in cerebrospinal fluid, indicating a potential degenerative process. The study suggests a secondary neurodegenerative phenomenon due to persistent hemosiderin deposition after a hemorrhagic stroke, potentially triggering neurodegeneration. The findings highlight the importance of distinguishing between different forms of acquired palatal tremor and ataxia, emphasizing the need for further research in this area. [Extracted from the article]

Background: Pseudo-orthostatic tremor is a hyperkinetic movement disorder usually associated with other neurological comorbidities, mainly Parkinson's disease. Case report: A 65-year-old male presented with unsteadiness and leg tremor while standing. Electrophysiological evaluation confirmed the presence of pseudo-orthostatic tremor. Blood test showed an undiagnosed Graves' disease. A complete remission of tremor was achieved with methimazole. Dopamine transporter scintigraphy showed a mild reduction of the striatal binding, bilaterally. Discussion: Graves' disease can be associated with pseudo-orthostatic tremor. Thyroid function should be assessed in patients complaining of unsteadiness. The causative role of hyperthyroidism in determining dopaminergic degeneration and uncovering subclinical parkinsonism warrants further investigations. [ABSTRACT FROM AUTHOR]