Delayed selective cerebral hypothermia decreases infarct volume after reperfused stroke in baboons.

BACKGROUND: Hypothermia is known to provide neuroprotection from focal ischemia. However, lethal cardiovascular complications resulting from total body cooling have greatly restricted hypothermia as a therapy for stroke. This study determined whether selective cerebral cooling induced after reversible cerebral artery occlusion would decrease the infarct volume. METHODS: Under general anesthesia, 8 baboons were subjected to 1-hour simultaneous occlusion of the left internal carotid artery and anterior cerebral arteries by transorbital surgical approach. Four animals were treated with selective cerebral hypothermia to 25°C, initiated 2.5 hours after placement of cerebral artery clips. Selective cerebral hypothermia was achieved, after heparinization, by continuous withdrawal of femoral arterial blood into an extracorporeal closed-circuit pump system, cooling by water bath and perfusion into the right internal carotid artery. Pump flow was adjusted to maintain right internal carotid artery pressure near systemic blood pressure. Cerebral cortical temperature was maintained below 27°C for 12 hours, whereas systemic temperature was preserved near normal by convective air mattresses and warm water blankets. Four control animals were maintained at 36°C. Blood pressure, pH, and blood gases were maintained at normal values for both groups. Forty-eight to 72 hours after cerebral artery occlusion, magnetic resonance imaging brain scans were obtained and infarct volume measured. RESULTS: Normothermic baboons had infarction of 35.4±4.4% (mean±SD) of the left cerebral hemisphere compared with 0.5±1% for baboons treated with cerebral hypothermia (P<0.01). In brain-cooled animals, esophageal temperature was maintained greater than 34°C, despite cerebral temperature less than 27°C. CONCLUSION: Selective brain cooling initiated 2.5 hours after onset of focal ischemia resulted in marked reduction in infarct volume, without cardiovascular derangement.

Dexmedetomidine may impair cognitive testing during endovascular embolization of cerebral arteriovenous malformations: a retrospective case report series.

After the reported successful use of dexmedetomidine to sedate patients in the intensive care unit without respiratory depression, we began to use dexmedetomidine for interventional neuroradiologic procedures. We report on five patients who had dexmedetomidine administered for sedation during embolization of cerebral arteriovenous malformations. All patients were comfortably sedated and breathing spontaneously. However, although patients were awake and following simple commands 10 minutes after the discontinuation of the infusion of dexmedetomidine, they were nevertheless unable to undergo cognitive testing. They were still unable to undergo cognitive testing 45 minutes after the infusion was stopped. In contrast, 10 minutes after the discontinuation of the infusion of propofol, all patients were awake, alert, cooperative, and able to undergo cognitive testing without difficulty. In conclusion, on examination of five non-randomly selected case records, we found that dexmedetomidine significantly prevented neurologic and cognitive testing.

Modified ECT Using Succinylcholine After Remission of Neuroleptic Malignant Syndrome.

The authors report two patients with a history of neuroleptic malignant syndrome (NMS) who were treated with ECT using succinylcholine as muscle relaxant, without ensuing complications. Most, though not all, of the evidence suggests that NMS is primarily central in origin in contrast to malignant hyperthermia, which is due to a genetic defect in skeletal muscle. Regardless of the theoretical debate over the origin of the high temperatures noted in NMS, reports to date suggest that modified ECT using succinylcholine can be safely used after remission of an episode of NMS.