The potential role of genetic factors in the etiology of posttraumatic and alcohol-associated seizures was studied in 289 male patients with recurrent seizures and in 174 individuals who had never experienced a seizure. The incidence of seizures in first-degree relatives of probands was compared with that in relatives of unaffected individuals. Relatives of patients with alcohol-associated seizures had a rate ratio of 2.45 [95% confidence interval (CI) 1.41-4.25], whereas no excess incidence was noted among relatives of posttraumatic epilepsy patients (rate ratio 1.20, 0.64-2.25 CI). Relatives of probands with both antecedents showed an intermediate rate ratio of 1.72 (0.92-3.20 CI). Among probands with alcohol-associated seizures, the rate ratio of 2.05 for patients with alcohol-related seizures (i.e., spontaneously occurring seizures in association with chronic alcohol abuse) was slightly higher than that of 1.85 for probands with alcohol withdrawal seizures. Trauma severity had a slight impact on the incidence of affected relatives; patients with severe head injuries had a rate ratio of 0.73 and probands with milder trauma had a rate ratio of 0.99. The results indicate a limited, if any, role of genetic predisposition in development of posttraumatic seizures. Alcohol-related seizures, however, showed familial aggregation of unprovoked seizures, suggesting an involvement of genetic factors in the origin of such seizures.
Hyposmolar hyponatremia (serum sodium5130 mmol/l) is a common phenomenon in the spinal cord injury (SCI) patient population and in most cases, it is of relatively little consequence. However, rapid correction or over correction of hyponatremia (a change in serum sodium425 mmol/l within 48 h) has been linked to Central Pontine Myelinolysis (CPM) and Extra Pontine Myelinolysis (EPM), usually along with other recognized predisposing factors. We report the ®rst case of isolated Extra Pontine Myelinolysis in an SCI patient without any of the recognized predisposing factors, following correction of hyponatremia. The signs and symptoms of Extra Pontine Myelinolysis were not very remarkable in our patient because of prior spinal cord injury. The diagnosis was con®rmed by the typical ®nding of myelinolysis in the basal ganglion region on MRI. Hyponatremia occurs frequently in the SCI patient population, thus placing them at increased risk for Extra Pontine Myelinolysis. Therefore, we emphasize the importance of watching for this entity during the management of hyponatremia in the SCI patient population and recommend the use of MRI scans to con®rm the clinical diagnosis.
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