Cavernous malformations that are associated with seizures are often treated by surgical resection consisting of lesion removal, "lesionectomy," alone. Through retrospective analysis the authors have examined some factors that may predict failure to eradicate seizures by such a procedure. A group of 51 patients were examined who had been treated for supratentorial cavernous malformations with preoperative seizures and received postoperative follow up lasting at least 1 year. There was one mortality in the group. Of the remaining 50 patients, 15 (30%) had continued postoperative seizures despite therapeutic levels of antiepileptic medications. Variables that were significantly associated with continued seizures postoperatively included increasing duration of preoperative seizure history (p = 0.03), increasing number of preoperative seizures (p < 0.003), and female sex (p < 0.04). One hundred percent of patients with only one preoperative seizure or a seizure history lasting less than 2 months were seizure free following lesionectomy: approximately 75% to 80% of all patients with two to five seizures, or a seizure history lasting 2 to 12 months, were seizure free; and only 50% to 55% of those with more than five seizures or with preoperative seizure histories lasting more than 1 year were seizure free postoperatively. This investigation indicates that patients with shorter seizure histories and fewer preoperative seizures can be effectively treated by lesionectomy alone, whereas those with longer histories and more seizures are not effectively treated by this procedure and may require more extensive resections.
During retrosigmoid and far-lateral skull base surgical approaches, the head may be positioned at the extreme limits of rotation and flexion. In rare instances, patients may develop acute sialadenitis after surgery as a result of this positioning technique. Over a 4-year period, five patients developed postoperative sialadenitis after undergoing either a retrosigmoid craniotomy in the supine position (n ¼ 4) or a far-lateral craniotomy in the park-bench position. Based on all the retrosigmoid and far-lateral approaches performed by the senior author (RFS), the incidence of sialadenitis was 0.84%. In all five patients, the acute sialadenitis was not clinically apparent at the conclusion of the operation. However, the diagnosis was evident within 4 hours of surgery. In each case, the neck swelling in the vicinity of the submandibular gland was contralateral to the craniotomy site. All patients were treated with intravenous hydration and antibiotic therapy. One patient was extubated immediately after surgery with no obvious evidence of sialadenitis. However, she required emergent reintubation due to airway compromise. The mechanism of acute sialadenitis in these patients was obstruction of the salivary duct caused by surgical positioning. This previously unreported observation in patients undergoing skull base surgery deserves consideration during perioperative and postoperative management.
The cerebroprotective effects of hypothermia in focal models of ischemia are well established, but little is known about the underlying mechanisms of this form of brain protection. Cortical cooling in global transient ischemic models suggests that hypothermia limits glutamate excitotoxicity by decreasing the release of glutamate during ischemia. Few studies have examined glutamate release in the more physiological model of permanent focal ischemia. In this study, we used a rat model of middle cerebral artery occlusion (MCAO) of permanent focal ischemia. Extracellular glutamate concentration was analyzed bilaterally by microdialysis for 30 minutes before MCAO to 120 minutes after MCAO. Normothermic animals (n = 13) had a baseline glutamate concentration of 9.23 +/- 2.5 mumol/ml (mean +/- standard error of the mean) before MCAO. Extracellular glutamate rose quickly after vessel occlusion and peaked at 33.95 +/- 6.3 mumol/ml 30 minutes after MCAO. By 60 minutes after MCAO, this level had decreased to 25.14 +/- 6.3 mumol/ml; glutamate levels decreased slightly to 21.35 +/- 6.8 mumol/ml by 120 minutes. Hypothermic animals (n = 11) had an initial extracellular glutamate concentration of 5.22 +/- 1.3 mumol/ml before MCAO. This value rose gradually to a maximum of 10.69 +/- 3.3 microns/ml at 50 minutes after MCAO and then returned to a baseline value of 2.58 +/- 1.2 mumol/ml by 120 minutes. Contralateral control glutamate dialysates in the normothermic and hypothermic groups remained near baseline throughout the experimental period. The mean percentages of right hemispheric volumes occupied by infarcts were 11.96 +/- 1.68% in the hypothermic group and 19.77 +/- 2.03% in the normothermic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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