Effect of Continuous External Ventricular Drainage on Delayed Ischemic Neurologic Deficits after Aneurysmal Clipping in Spontaneous Subarachnoid Hemorrhage

OBJECTIVE: The purpose of this reports is to describe the influence of continuous external ventricular drainage (EVD) on delayed ischemic neurologic deficit (DIND) after early surgery in ruptured aneurysmal patients. METHODS: The authors reviewed 229 patients with aneurysmal subarachnoid hemorrhage (SAH) who had been treated with clipping at a single institution between 1998 and 2004. Of these, 121 patients underwent continuous EVD (Group A) postoperatively, whereas 108 patients did not (Group B). EVD was performed at ipsilateral Kocher's point and maintained 2 to 14 days postoperatively. RESULTS: DIND occurred in 15.7% (19 cases) of patients in Group A, 25% (27 cases) from Group B (P value=0.112). Compared with Group A, Group B was more likely to suffer acute symptom of DIND and showed poor response to 3- H therapy. Major symptoms of DIND in Group A were mild confusion (36.8%) and mild deterioration of mental state (26.3%), contrary to weakness of extremities (59.2%) in Group B. At discharge, Glasgow Outcome Scales (GOS) of Group A were: good recovery (63.2%), moderately disabled (21%), severely disabled (10.5%), dead (5.3%) and Group B : good recovery (48.1%), moderately disabled (37%), severely disabled (14.8%) and dead (0%). Of 121 patients from group A, 35 patients (28.9%) suffered ventriculitis. CONCLUSION: Continuous EVD after aneurysmal clipping in patients with SAH reduced the risk of DIND and its sequelae, relieved its symptoms, and improved the outcome.

Epileptogenic Properties of Balloon Cells in Cortical Tubers of Tuberous Sclerosis: Upregulation of Drug Resistance Proteins

OBJECTIVES: Balloon cells and dysplastic neurons are histopathological hallmarks of the cortical tubers of tuberous sclerosis complex (TSC) and focal cortical dysplasia (FCD) of the Taylor type. They are believed to be the epileptogenic substrate and cause therapeutic drug resistant epilepsy in man. P-glycoprotein (P-gp) is the product of multidrug resistance gene (MDR1), and it maintains intracellular drug concentration at a relatively low level. The authors investigated expression of P-gp in balloon cells and dysplastic neurons of cortical tubers in patients with TSC. METHODS: An immunohistochemical study using the primary antibody for P-gp, as an indicative of drug resistance, was performed in the cortical tuber tissues in two patients of surgical resection for epilepsy and six autopsy cases. RESULTS: Balloon cells of each lesion showed different intensity and number in P-gp immunopositivity. P-gp immunopositivity in balloon cells were 28.2%, and dysplastic neurons were 22.7%. These immunoreactivities were more prominent in balloon cells distributed in the subpial region than deeper region of the cortical tubers. Capillary endothelial cells within the cortical tubers also showed P-gp immunopositivity. CONCLUSION: In this study, the drug resistance protein P-glycoprotein in balloon cells and dysplastic neurons might explain medically refractory epilepsy in TSC.