Post-traumatic epilepsy: clinical, neurophysiological and neuroimaging study

Post-traumatic epilepsy [PTE] is a recurrent seizure disorder due to traumatic injury of the brain. There is controversy regarding the precise mechanism by which epilepsy may results from traumatic brain injury. Mesial temporal lobe sclerosis [MTS] is reported as a major risk factor for intractability of posttraumatic epilepsy. We aimed from this work to revise patients with post-traumatic epilepsy, to define risk factors, and assess the clinical, neurophysiological and neuroradiological characteristics. The frequency of mesial temporal epilepsy in contrast to neocortical epilepsy was also assessed in these patients. Twenty- three patients with post-traumatic epilepsy were included in this study. Clinical assessment, video EEG monitoring and MRI brain results were reviewed. We found that 14 patients [60.9%] with neocortical epilepsy [NCE], 8 patients [34.8%] of them had their trauma below or equal to 10 years and 6 patients [26.1%] had their trauma above 10 years old. We found also 8 patients [34.8%] with mesial temporal epilepsy [MTE], 5 patients [21.8%] had their trauma below or equal to 10 years and 3 patients [13%] had their trauma above 10 years. There was one patient [4.3%] with mixed neocorical and mesial temporal epilepsy. Of these patients, 6 had temporal lobectomy with successful post-operative results and the diagnosis of mesial temporal sclerosis was pathologically definite in 5 patients. We concluded that MTS could occur in patients with PTE in young or old ages. Detection of MTS is mandatory for all patients with PTE as resective surgeries of these patients gave a good outcome for the control of their intractable epilepsy

Serum soluble vascular cell adhesion molecule-1 [sVCAM-1] in acute ischemic stroke

Neuroinflammatory mechanisms play an important role in ischemic injury and interruption of these processes can result in improved neurological outcomes. Firm adhesion of leukocytes to the endothelial cells as well as leukocyte activation and transmigration across the endothelium is mediated by adhesion molecules. We aimed to assess the levels of serum soluble vascular cell adhesion molecule-1 [sVCAM-1] in acute stroke and their correlation to the extent of neurological deficits and short term clinical outcome. Forty four patients with first ever acute ischemic stroke admitted within 72 hours of stroke onset were enrolled, in addition to eighteen normal controls and twelve patients with vascular risk factors matched with age and sex to the patients group. Blood samples were obtained from the patients at the third day of stroke onset and from the control groups and subjected to the measurement of the level of sVCAM-1 in the serum. There is a higher mean sVCAM-1 among patients with ischemic stroke compared to normal controls and the difference is highly significant statistically, P<0.01. There is a higher mean sVCAM among patients with large vessel disease compared to patients with small vessel disease and the difference is highly significant statistically, P<0.01. There is a highly significant positive correlation between sVCAM-1 and NIHSS score, P<0.01. Also we found a statistically significant negative correlation between Barthel Index Score and sVCAM-1, P<0.05. The results support the prior hypothesis of involvement of the adhesion molecules [VCAM-1] in the pathogenesis of acute cerebral ischemia and their impact on neuronal damage and neurological deficit. Therapeutic trials that attempt to interfere with the function of adhesion molecules could be of benefit in acute stroke management