TY - JOUR
T1 - Abnormal vasomotor response of human epileptogenic cortex to reversal of hyperventilation a long-term surface cerebral blood flow monitoring study
AU - Weinand, Martin E.
AU - El-Saadany, Waleed F.
AU - Labiner, David M.
AU - Carter, L. Philip
AU - Oommen, Kalarickal J.
AU - Talwar, Dinesh
AU - Ahern, Geoffrey L.
PY - 1996/3
Y1 - 1996/3
N2 - 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.
AB - 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.
KW - Cerebral blood flow
KW - Epilepsy
KW - Hyperventilation
KW - Subdural electrode
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U2 - 10.1016/0928-4680(95)00050-X
DO - 10.1016/0928-4680(95)00050-X
M3 - Article
AN - SCOPUS:0029940728
SN - 0928-4680
VL - 3
SP - 41
EP - 45
JO - Pathophysiology
JF - Pathophysiology
IS - 1
ER -