Driving is an important issue for people with epilepsy. Doctors need to understand the Road Traffic Act and give appropriate advice and guidance to patients. Driving is legally allowed for a person without seizures, impaired awareness, or motor components for more than 2 years. Although there is no specific rule about the first unprovoked seizure, observing for 6 months is recommended before starting to drive. If we notice a patient driving despite having seizures, we can report this to the National Public Safety Commission without violating confidentiality.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.11477/mf.1416202330 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Interneuron FGF13 regulates seizure susceptibility via a sodium channel-independent mechanism.
Elife
January 2025
Cardiovascular Research Institute, Weill Cornell Medicine, New York City, United States.
Developmental and epileptic encephalopathies (DEEs), a class of devastating neurological disorders characterized by recurrent seizures and exacerbated by disruptions to excitatory/inhibitory balance in the brain, are commonly caused by mutations in ion channels. Disruption of, or variants in, were implicated as causal for a set of DEEs, but the underlying mechanisms were clouded because is expressed in both excitatory and inhibitory neurons, undergoes extensive alternative splicing producing multiple isoforms with distinct functions, and the overall roles of FGF13 in neurons are incompletely cataloged. To overcome these challenges, we generated a set of novel cell-type-specific conditional knockout mice.
View Article and Find Full Text PDFInfantile Spasms in Pediatric Down Syndrome: Potential Mechanisms Driving Therapeutic Considerations.
Children (Basel)
December 2024
Division of Pediatric Neurology, Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Infantile spasms are common in Down Syndrome (DS), but the mechanisms by which DS predisposes to this devastating epilepsy syndrome are unclear. In general, neuronal excitability and therefore seizure predisposition results from an imbalance of excitation over inhibition in neurons and neural networks of the brain. Animal models provide clues to mechanisms and thereby provide potential therapeutic approaches.
View Article and Find Full Text PDFSLC35A2 loss of function variants affect glycomic signatures, neuronal fate, and network dynamics.
bioRxiv
December 2024
Division of Pharmacotherapy and Experimental Therapeutics, Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, NC, 27599, USA.
encodes a UDP-galactose transporter essential for glycosylation of proteins and galactosylation of lipids and glycosaminoglycans. Germline genetic variants have been identified in congenital disorders of glycosylation and somatic variants have been linked to intractable epilepsy associated with malformations of cortical development. However, the functional consequences of these pathogenic variants on brain development and network integrity remain elusive.
View Article and Find Full Text PDFImpact of Post-Traumatic Epilepsy on Mental Health and Multidimensional Outcome and Quality of Life: An NIDILRR TBIMS Study.
J Neurotrauma
January 2025
Department of Physical Medicine & Rehabilitation, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Traumatic brain injury (TBI) and subsequent post-traumatic epilepsy (PTE) often impair daily activities and mental health (MH), which contribute to long-term TBI-related disability. PTE also affects driving capacity, which impacts functional independence, community participation, and satisfaction with life (SWL). However, studies evaluating the collective impact of PTE on multidimensional outcomes are lacking.
View Article and Find Full Text PDFSynaptic Vesicle glycoprotein 2A knockout in parvalbumin and somatostatin interneurons drives seizures in the postnatal mouse brain.
J Neurosci
January 2025
Nervous System Disorders and Therapy, GIGA Institute, University of Liège, 4000 Liège, Belgium
Synaptic vesicle glycoprotein 2A (SV2A) is a presynaptic protein targeted by the antiseizure drug levetiracetam. One or more of the three SV2 genes is expressed in all neurons and is essential to normal neurotransmission. Loss of SV2A results in a seizure phenotype in mice and mutations in humans are also linked to congential seizures.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!