Long-term subdural surface cortical cerebral blood flow (CBF) and electrocorticographic monitoring was performed in 12 patients with complex partial seizures. A total of 40 seizures were analyzed. Baseline CBF values from nonepileptic and epileptic temporal lobe (mean +/- standard error) were 60.0 +/- 1.0 and 50.2 +/- 1.8 ml/100 g per minute, respectively (P < 0.05). In general, clinical seizure onset was preceded by a 20-minute preictal CBF increase from baseline in the epileptic temporal lobe. Peak early postictal CBF values of nonepileptic and epileptic temporal lobes were 57.7 +/- 13.3 and 89.0 +/- 21.7 ml/100 g per minute (P > 0.05) at 5.2 +/- 2.2 and 2.4 +/- 1.0 minutes (P > 0.05) after clinical seizure onset, respectively. Statistically significant differences between nonepileptic and epileptic temporal lobe CBF were detected at 50 minutes (74.0 +/- 14.2 and 37.5 +/- 9.2 ml/100 g per minute, respectively; P < 0.05) and 60 minutes (75.6 +/- 13.6 and 36.1 +/- 8.5 ml/100 g per minute, respectively; P < 0.05) postictal. The data suggest that the optimal times for CBF analysis to differentiate epileptic from nonepileptic temporal lobe are 1) during the interictal period and 2) late (50 to 60 minutes) postictal. The results of this study should improve the understanding of the dynamic cerebral perfusion patterns in the epileptic human brain.
The aims of this study were to verify that tissue-type plasminogen activator given either 1 or 2 hours after experimental embolic stroke in rabbits diminishes the volume of resulting ischemic brain and to ascertain the effect of the simultaneous administration of heparin. We embolized the middle cerebral artery of rabbits by injecting performed autologous arterial ("white") thrombus into one internal carotid artery. Treatment with 2 mg/kg tissue-type plasminogen activator, alone or in combination with heparin, was commenced either 1 or 2 hours after embolization. The animals were killed 5 hours after treatment commenced, and their brains were examined for evidence of ischemia and hemorrhage. Administration of tissue-type plasminogen activator significantly diminished the size of the resulting brain ischemia. Administration of heparin, with or instead of tissue-type plasminogen activator, did not result in a significant decrease in the volume of cerebral ischemia, but it also did not lead to hemorrhagic transformation of the stroke. In the rabbit model, administration of tissue-type plasminogen activator within 2 hours diminished the volume of brain rendered acutely ischemic by embolic stroke. Since the simultaneous administration of heparin during this same period did not result in any instances of hemorrhagic transformation, tissue-type plasminogen activator may have some place for use in such circumstances to mitigate a tendency to further embolic or thrombotic events.
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