Background: Various neurological manifestations have been described in relation to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and coronavirus disease 2019 (COVID-19). However, the development of cerebellar ataxia after recovery from COVID-19 is rare. We present a case of cerebellar ataxia 3 weeks after recovery from COVID-19.
Case Presentation: A 70-year-old male patient from an urban area of India presented with ataxia. He was hypertensive and had been receiving treatment for post-traumatic epilepsy for the previous 3 years. He had previously had laboratory-confirmed COVID-19 infection with mild symptoms that resolved within 2 weeks. However, 3 weeks after symptom improvement, he developed severe pan-cerebellar ataxia. Investigations were suggestive of post-infectious cerebellar ataxia. Other causes of ataxia were excluded. He responded well to pulse methylprednisolone therapy and was discharged with mild tremor and ataxia.
Conclusion: Post-infectious cerebellar ataxia is an unusual presentation after COVID-19. The clinician should be aware of such complications following COVID-19 infection as early diagnosis and proper management leads to better outcomes in many patients.
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http://dx.doi.org/10.1111/cen3.12700 | DOI Listing |
Cureus
December 2024
Department of Neurology, St. Joseph Medical Center, Stockton, USA.
Cerebellar mutism syndrome (also known as posterior fossa syndrome) has been mostly seen in pediatric patients after surgery for neoplastic disease and is characterized by mutism, with variable symptoms such as emotional lability, ataxia, apraxia, and hypotonia. While the mechanism is not precisely defined, it is thought to result from disconnections between the cortical and cerebellar brain networks. Presentation in adult patients is rare, with various etiologies including posterior fossa ischemia, hemorrhage, and tumors being most reported.
View Article and Find Full Text PDFIntroduction: COQ4 mutation often leads to a fatal multi-system disease in infants. Recently, it was reported that the biallelic COQ4 variants may be a potential cause of hereditary spastic paraplegia (HSP). This study aims to describe the clinical features and genotype of the COQ4 associated hereditary spastic paraplegia (HSP).
View Article and Find Full Text PDFJ Neuroophthalmol
January 2025
Departments of Ophthalmology and Visual Sciences (HMM, AH, EM), and Radiology (DMM), University of Toronto, Toronto, Canada; Department of Ophthalmology (LD), McMaster University, Hamilton, Canada; Departments of Ophthalmology and Visual Sciences, and Neurology (JDT), University of Michigan, Ann Arbor, Michigan; Department of Neurology (JDT), University of Michigan, Ann Arbor, Michigan; Division of Neurology, Department of Medicine (EM), University of Toronto, Toronto, Canada.
Background: Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) is a rare and poorly understood inflammatory disorder of the central nervous system centered on the pons. It has a characteristic imaging appearance with enhancing and T2-hyperintense punctate and curvilinear lesions in the pons. The lesions lack restricted diffusion and have relatively little perilesional edema.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Human Molecular Genetics and Biochemistry, Faculty of Health & Medical Sciences, Tel Aviv University, Tel Aviv 69978, Israel.
Ataxia-telangiectasia (A-T) is a pleiotropic genome instability syndrome resulting from the loss of the homeostatic protein kinase ATM. The complex phenotype of A-T includes progressive cerebellar degeneration, immunodeficiency, gonadal atrophy, interstitial lung disease, cancer predisposition, endocrine abnormalities, chromosomal instability, radiosensitivity, and segmental premature aging. Cultured skin fibroblasts from A-T patients exhibit premature senescence, highlighting the association between genome instability, cellular senescence, and aging.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Anesthesiology and the Center for Shock, Trauma and Anesthesiology Research (S.T.A.R.), University of Maryland School of Medicine, 685 Baltimore St., Baltimore, MD 21201, USA.
The cerebellum, a key target of ethanol's toxic effects, is associated with ataxia following alcohol consumption. However, the impact of ethanol on Purkinje cell (PC) mitochondria remains unclear. To investigate how ethanol administration affects mitochondrial dynamics in cerebellar Purkinje cells, we employed a transgenic mouse model expressing mitochondria-targeted yellow fluorescent protein in Purkinje cells (PC-mito-eYFP).
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