Biomedical subjects
Publications and source records attributed to E H Schakel.
A new classification system for head injury based on the findings of computerized tomography was used in a population of 809 head injured patients. The system emphasizes the status of mesencephalic cisterns, the degree of midline shift and the presence or absence of mass lesions, allowing high risk patients to be identified and outcome to be predicted.
The population analysed consisted of 268 out of 819 patients of a European nimodipine multicentre trial on severe head injury, whose first CT scan after injury showed signs of subarachnoid bleeding. The study demonstrated the importance of traumatic subarachnoid haemorrhage (tSAH) per se as a prognostic factor. The outcome of patients with tSAH is significantly worse than that of patients whose first CT does not show subarachnoid blood (noSAH). The outcome was unfavourable (dead, persistent vegetative state, severe disability) in 60% of tSAH patients compared to 30% of noSAH patients (p < 0.001). The difference in mortality was 42% vs. 14% (p < 0.001). The six month follow-up of tSAH patients complying with the study protocol and treated with intravenous nimodipine, 2 mg per hour for 7 days, showed a statistically significant reduction of unfavourable outcome from 66% to 51% (p < 0.05), compared to placebo treated patients.
Increased intracellular calcium is involved in the death of neurons associated with cerebral ischemia. After extensive experimental work, the calcium antagonist nimodipine has been investigated in several clinical trials in patients with disorders of the cerebral circulation. A short overview on trials in subarachnoid hemorrhage, head injury, ischemic stroke and cerebral resuscitation is given in this paper.
The effects of Nimodipine on the global and regional cerebral blood flow were studied in 42 patients with cerebrovascular disorders. In 25 patients with focal deficits such as transitory ischemic attack (TIA), prolonged reversible ischemic neurological deficit (PRIND), and minor stroke due to arteriosclerosis, and in eleven patients with cerebral vasospasm after subarachnoid hemorrhage, the cerebral blood flow was measured by 133Xenon inhalation technique 60 min after oral administration of 40, 60, or 80 mg Nimodipine. In 6 patients with vasospasm the effects of Nimodipine i.v. were examined. The result in twelve patients with minor stroke who were only given placebo (lactose; "test-retest") was identical regional (rCBF) and global (CBF) cerebral blood flow before and 60 min after; placebo, blood pressure, and arterial pCO2 remained constant as well. After Nimodipine, however, the CBF increases, the increase after vasospasm being significant when taking the pCO2 in the Wilcoxon test into account. The rCBF increases much more in the regions with low perfusion rates than in well-perfused areas. This is also observed in the patients with TIA, PRIND, or minor stroke, most clearly after oral administration of 60 mg, whereas regions with normal perfusion rates show little reaction. The blood pressure was lowered, depending on the initial pressure. There was no evidence of a steal phenomenon.