title: Ictal analgesia in temporal lobe epilepsy - The mechanism of seizure-related burns.
abstract: Seizure-related injuries have major impact in the excess mortality and morbidity of epilepsy patients. Experimental data suggest that analgesia may develop during seizures contributing to the severity of seizure-related accidents, especially burns. We aimed to identify those seizure-types that may lead to burn-injuries by seizure-related analgesia. In our tertiary epilepsy centre, we asked 100 epilepsy patients having a history of seizure-related injury, to complete our burn-and-pain questionnaire. Fifty-one patients completed the survey; their epileptology data were collected and those with a seizure-related burn were interviewed. Forty-two out of the 51 patients (82%) had partial epilepsy and 9 (18%) had idiopathic generalised epilepsy. Twenty-six persons (51%) reported decreased pain perception during or after seizures in general. Twelve patients (23%) had suffered one or more seizure-related burn. Five of them fell onto a hot surface or fire accidentally, during generalized tonic-clonic seizures. Seven out of the 12 burnt patients (58%) grasped a hot object or reached into boiling fluid during complex partial seizures; without experiencing-, or reacting in response to pain. These patients had temporal lobe epilepsy, 5 of them had left temporal seizure onset. Our hypothesis based on the circumstantial analysis of our patients' burn-injuries; is that temporal lobe seizures may cause ictal/postictal analgesia. It may be caused by the seizure-related epileptic facilitation of the periaqueductal gray matter; the central pain-inhibiting structure of the brain. Seizure-related endogenous opioid-release my have a contributory role in inhibiting pain-perception. Ictal analgesia warrants better burn-prevention in temporal lobe epilepsy patients. Understanding the mechanism of ictal analgesia and specifying those seizures-types prone to cause it; may help indentifying human pain-inhibiting pathways.
authors.affiliation: National Institute of Clinical Neurosciences, Budapest, Hungary. Electronic address: szucsan@gmail.com.
authors.forename: Anna
authors.initials: A
authors.lastname: Szűcs
authors.affiliation: National Institute of Clinical Neurosciences, Budapest, Hungary.
authors.forename: András
authors.initials: A
authors.lastname: Horváth
authors.affiliation: National Institute of Clinical Neurosciences, Budapest, Hungary.
authors.forename: György
authors.initials: G
authors.lastname: Rásonyi
authors.affiliation: National Institute of Clinical Neurosciences, Budapest, Hungary.
authors.forename: Dániel
authors.initials: D
authors.lastname: Fabó
authors.affiliation: Dr. Kenessey Albert Hospital, Balassagyarmat, Hungary.
authors.forename: Géza
authors.initials: G
authors.lastname: Szabó
authors.affiliation: National Institute of Clinical Neurosciences, Budapest, Hungary.
authors.forename: Anna
authors.initials: A
authors.lastname: Sákovics
authors.affiliation: National Institute of Clinical Neurosciences, Budapest, Hungary.
authors.forename: Anita
authors.initials: A
authors.lastname: Kamondi
mesh_terms: D000222:Adaptation, Physiological; D000328:Adult; D000368:Aged; D000698:Analgesia / Q000379:methods; D001921:Brain / Q000503:physiopathology*; D002056:Burns / Q000150:complications* / Q000503:physiopathology*; D004833:Epilepsy, Temporal Lobe / Q000209:etiology* / Q000503:physiopathology*; D019317:Evidence-Based Medicine; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008959:Models, Neurological; D010146:Pain / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control; D058748:Pain Perception; D055815:Young Adult