Intracranial dermoids are rare congenital tumors. Supratentorial dermoid cysts were more frequently reported in the last decade, and they are known to have a predilection for the cavernous sinus. Interdurally localized dermoids presenting with ophthalmoplegia is uncommon. Previously, the association of dermoid lesions with the cavernous sinus and the complexity of the operative procedure were emphasized only by a few authors. We report a case of a dermoid cyst that was embedded fully in the cavernous sinus and review the related cavernous dermoid lesions in the literature. Fronto-orbitozygomatic craniotomy was performed, and despite adherence of the tough capsule to the cranial nerves, the lesion was grossly removed in total. The patient was doing well 1 year after the operation, and there was no recurrence of signs and symptoms. Interdural growth of cavernous dermoid tumors must be considered, and careful evaluation of preoperative computed tomography and magnetic resonance images aids in making the decision concerning the operative approach. Upon review of the literature, we detected only eight similar cases concerning cavernous dermoid cysts. Although total excision of these cavernous lesions has been reported previously, we believe that total excision can sometimes be hazardous and not feasible.

Aquaporin-4 (AQP4), the principal water channel in astrocytes, is involved in brain water movement, inflammation, and neuroexcitation. In this study, there was strong neuroprotection in mice lacking AQP4 in a model of global cerebral ischemia produced by transient, bilateral carotid artery occlusion (BCAO). Survival and neurological outcome were greatly improved in the AQP4(-/-) vs. AQP4(+/+) mice after occlusion, with large and robust differences in both outbred (CD1) and inbred (C57bl/6) mouse strains without or with mechanical ventilation. Improved survival was also seen in mice lacking the scaffold protein α-syntrophin, which manifest reduced astrocyte water permeability secondary to defective AQP4 plasma membrane targeting. Intracranial pressure elevation and brain water accumulation were much reduced in the AQP4(-/-) vs. AQP4(+/+) mice after carotid artery occlusion, as were blood-brain barrier (BBB) disruption and neuronal loss. Brain slices from AQP4(-/-) mice showed significantly reduced cell swelling and cytotoxicity in response to oxygen-glucose deprivation, compared with slices from AQP4(+/+) mice. Our findings suggest that the neuroprotective effect of AQP4 deletion in global cerebral ischemia involves reduced astrocyte swelling and brain water accumulation, resulting in reduced BBB disruption, inflammation, and neuron death. AQP4 water transport inhibition may improve survival and neurological outcome after cardiac arrest and in other conditions associated with global cerebral ischemia.

Propofol has cerebral vascular and metabolic effects similar to those of barbiturates, and it is used to maintain neurosurgical anesthesia because it reduces cerebral metabolic rate, cerebral blood flow, and intracranial pressure. Although the use of propofol as a cerebral protectant during certain neurosurgical procedures has been advocated, consensus has not been reached as to a protective effect of propofol on cerebral ischemia. In this study we observed the neuroprotective effects of propofol during global cerebral ischemia-reperfusion injury by the use of four-vessel occlusion method in a rat model. We measured the levels of malondialdehyde as a marker of lipid peroxidation in ischemic tissue, and the results indicate that propofol plays a role in the inhibition of neuronal death induced by brain ischemia.

No abstract

Astrocyte water channel aquaporin-4 (AQP4) facilitates water movement across the blood–brain barrier and into injured astrocytes. We previously showed reduced cytotoxic brain edema with improved neurological outcome in AQP4 knockout mice in water intoxication, infection and cerebral ischemia. Here, we established a 4-vessel transient occlusion model to test the hypothesis that AQP4 deficiency in mice could improve neurological outcome following severe global cerebral ischemia as occurs in cardiac arrest/resuscitation. Mice were subjected to 10-min transient bilateral carotid artery occlusion at 24 h after bilateral vertebral artery cauterization. Cerebral blood flow was reduced during occlusion by >94% in both AQP4+/+ and AQP4−/− mice. The primary outcome, neurological score, was remarkably better at 3 and 5 days after occlusion in AQP4−/− than in AQP4+/+ mice, and survival was significantly improved as well. Brain water content was increased by 2.8 ± 0.4% in occluded AQP4+/+ mice, significantly greater than that of 0.3 ± 0.6% in AQP4−/− mice. Histological examination and immunofluorescence of hippocampal sections at 5 days showed significantly greater neuronal loss in the CA1 region of hippocampus in AQP4+/+ than AQP4−/− mice. The neuroprotection in mice conferred by AQP4 deletion following severe global cerebral ischemia provides proof-of-concept for therapeutic AQP4 inhibition to improve neurological outcome in cardiac arrest.