Objective: To report 2 cases of transitory cerebellar ataxia related to lidocaine administered topically for endoscopy. case summaries: Two patients developed transitory cerebellar ataxia a few minutes after local anesthesia using lidocaine 10% spray and lidocaine 2% orally for a bronchoscopy and transesophageal echocardiography. This effect completely disappeared in 3-5 hours. In neither case was an alternate etiology of cerebellar ataxia identified. The second patient had previously experienced a similar reaction to lidocaine.
Discussion: Several central neurologic effects of lidocaine have been reported, but until now, only few cases of cerebellar ataxia. In these 2 cases, the Naranjo probability scale indicated that a probable and a highly probable relationship existed between lidocaine administration and the transitory cerebellar ataxia.
Conclusions: Cerebellar ataxia may occur after local anesthesia with lidocaine; therefore, care must be taken to avoid overdose, even when administered topically.
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http://dx.doi.org/10.1345/aph.1D494 | 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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