Posttraumatic ischemia appears to be largely responsible for the extension of lesions in acute injury of the spinal cord. In the present study, we have evaluated the putative improvement of axonal function by the calcium channel blocker nimodipine after acute trauma of the spinal cord. Three techniques were used: (1) spinal cord blood flow (SCBF) using a scanographic technique with stable xenon, (2) somatosensory evoked potentials (SEPs), and (3) magnetic resonance imaging (MRI). Thirteen baboons were used in this study. Acute trauma was achieved by compression of the spinal cord at level L1 by applying pressure for 5 sec with an inflated balloon catheter injected with Ringer's solution. Following the injury, one group (n = 5) received a saline infusion (placebo) for seven days, and a second group (n = 8) received a nimodipine infusion (0.04 mg/kg/h) during the same period of time. SCBF and SEP were first recorded prior to trauma. SCBF, SEPs, and MRI were then recorded on the day of the injury and eight days prior to histologic examination of the spinal cord. In these studies nimodipine significantly improved SCBF. The decrease in SCBF observed at day one and day eight following trauma was significantly reduced in the treated group. Two baboons in the treated group also showed improvement of axonal function as assessed by SEP. No significant difference was observed with MRI, however, histologic study revealed that the lesions were significantly smaller in the treated group. Based on these observations we conclude that a week of nimodipine treatment following spinal cord injury enhances SCBF, limits the size of the spinal cord lesion, and perhaps improves functional recovery.

In unilateral mesiotemporal epilepsy, asymmetrical interictal hippocampal perfusion was correlated with restricted unilateral ictal discharges, whereas bilateral hippocampal hypoperfusion was correlated with ictal discharges spreading to the contralateral mesiotemporal structures. The lack of correlation between the degree of hypoperfusion and the percentage of neuron cell loss indicated that the decrease in rCBF has both functional and lesional origins.

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Reported evaluations of CBF with Xe/CT were performed in 11 patients during the lucid interval following CO intoxication. Results were compared with clinical and SPECT data. Two patients developed neuropsychiatric behavior (delayed enceph alopathy) one month following the initial recovery. The symptoms persisted in one of them 15 months later. Their CBF values as well as those in most of the other patients, monitored at the basal ganglia and white matter areas, were in relation with the clinical outcome. However, further studies with a larger number of patients, are needed to confirm the predictive significance of Xe/CT measurements for the long term sequelae of CO poisoning.

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