Epilepsy After Traumatic Brain Injury
Autor: | Jenni Kyyriäinen, Asla Pitkänen, Pedro Andrade, Lotta Pasanen, Xavier Ekolle Ndode-Ekane |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Traumatic brain injury Bioinformatics medicine.disease Epileptogenesis World health nervous system diseases 03 medical and health sciences Epilepsy Seizure susceptibility 030104 developmental biology 0302 clinical medicine nervous system Fluid percussion Anesthesia medicine Biomarker (medicine) Model development Psychology 030217 neurology & neurosurgery |
Popis: | According to the World Health Organization, 50 million people worldwide have epilepsy. Traumatic brain injury (TBI) is estimated to cause 10%–20% of all of symptomatic epilepsies, and 5% of all epilepsies. Over the past 15 years, several laboratories have reported spontaneous seizures after inducing TBI in rats and mice. The TBI models in which spontaneous seizures are detected include fluid percussion injury, and controlled cortical impact models. Increased seizure susceptibility has also been described in a weight-drop model. Recent studies identified some genotypes that predispose to post-TBI epileptogenesis or comorbidogenesis. The use of post-TBI models in antiseizure drug-discovery is rare, but they have been used in more than 10 proof-of-concept preclinical antiepileptogenesis trials in an attempt to find treatments to alleviate the development of post-TBI epilepsy and comorbidities. Despite significant progress in modeling posttraumatic epileptogenesis, the animal models still represent only a few of the injury types and pathologies of patients with TBI destined to develop epilepsy. Also, experimental studies investigating posttraumatic epileptogenesis in young or old animals, as well as in females, are lacking. Endophenotyping human epileptogenic TBI is critical for the advancement of preclinical model development. |
Databáze: | OpenAIRE |
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