Abstract
The occurrence of seizures in the first week after traumatic brain injury is a well known phenomenon and requires the physician to address several issues in the management of patients with such an injury. There is a wide range in the reported incidence of clinical seizures after brain injury. An incidence of 5 to 15% is often quoted, although the incidence can be higher (20 to 24%) if non-convulsive electroencephalographic (EEG) criteria for seizures are used. The main clinical risk factors for seizures are younger age, greater severity of brain injury and subdural haematoma and penetrating wounds.
The significance of seizures is highlighted by initially considering the patho-physiology of brain injury. Early after brain injury there is a selective increase in nonoxidative glucose metabolism, increased extracellular levels of glutamate and potassium, and a moderate reduction in cerebral blood flow. This state of cellular stress creates vulnerability in the cells to further injury. Seizures give rise to similar metabolic stress and serve to exaggerate hyperglycolysis and thereby may give rise to secondary injury.
It is important to recognise and treat post-traumatic seizures that occur in the early postinjury period. These seizures may be nonconvulsive and require EEG monitoring. We have gained considerable experience with continuous EEG monitoring of traumatic brain-injured patients and find that over 20% of patients will have seizures, 50% of which are nonconvulsive. Ongoing repeated seizures or status epilepticus, require immediate treatment with benzodiazepines, followed by long-acting anticonvulsants (e.g. phenytoin). Recalcitrant status epilepticus requires treatment with continuous intravenous infusions of anticonvulsants (e.g. barbiturates, propofol, midazolam).
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Vespa, P.M., Nuwer, M.R. Post-Traumatic Seizures. Mol Diag Ther 13, 129–138 (2000). https://doi.org/10.2165/00023210-200013020-00006
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DOI: https://doi.org/10.2165/00023210-200013020-00006