Human epileptogenic and nonepileptogenic surface cerebral blood flow (CBF) was studied during hyperventilation (HV) recovery. Bilateral subdural temporal lobe CBF probes were placed for long-term monitoring. Epileptic cortex became ischemic as an inverse linear function of HV duration (r = 0.923, df = 9, P < 0.05). During 5 min recovery from 13 hyperventilation periods in 8 patients, mean CBF remained significantly reduced below baseline in epileptic versus non-epileptic temporal lobe (7.5 ± 2.4 vs 1.8 ± 0.9 ml/100gm-min below baseline, respectively, P < 0.05). Epileptic CBF response to HV reversal was an inverse and direct linear function of HV duration and focus ischemia during HV, respectively (r = 0.890, df = 9, P < 0.05 and r = 0.784, df = 5, P < 0.05, respectively). During HV recovery, nonepileptic CBF increased linearly with increasing HV duration (r = 0.782, df = 9, P < 0.05). The data suggest that epileptic cortex has abnormal vasomotor response to recovery from hyperventilation. We propose that abnormal cortical vasomotor control represents a fundamental pertubation in the pathogenesis of human epilepsy. Cortical vasomotor analysis may provide a new physiologic basis for localization of the epileptic focus.
- Cerebral blood flow
- Subdural electrode
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Physiology (medical)