Post-traumatic seizures - Epidemiology and approaches to diagnosis, prevention and treatment

The occurrence of seizures in the first week after traumatic brain injury i s a well known phenomenon and requires the physician to address several iss ues in the management of patients with such an injury. There is a wide rang e in the reported incidence of clinical seizures after brain injury. An inc idence of 5 to 15% is often quoted, although the incidence can be higher (2 0 to 24%) if nonconvulsive electroencephalographic (EEG) criteria fur seizu res are used. The main clinical risk factors for seizures are younger age, greater severity of brain injury and subdural haematoma and penetrating wou nds. The significance of seizures is highlighted by initially considering the pa thophysiology of brain injury. Early after brain injury there is a selectiv e increase in nonoxidative glucose metabolism, increased extracellular leve ls of glutamate and potassium, and a moderate reduction in cerebral blood f low. This state of cellular stress creates vulnerability in the cells to fu rther injury. Seizures give rise to similar metabolic stress and serve to e xaggerate hyperglycolysis and thereby may give rise to secondary injury. It is important to recognise and treat post-traumatic seizures that occur i n the early postinjury period. These seizures may be nonconvulsive and requ ire EEG monitoring. We have gained considerable experience with continuous EEG monitoring of traumatic brain-injured patients and find that over 20% o f patients will have seizures, 50% of which are nonconvulsive. Ongoing repe ated seizures or status epilepticus, require immediate treatment with benzo diazepines, followed by long-acting anticonvulsants (e.g. phenytoin). Recal citrant status epilepticus requires treatment with continuous intravenous i nfusions of anticonvulsants (e.g. barbiturates. propofol, midazolam).