Intraoperative hypothermia during vascular neurosurgical procedures. Neurosurg Focus 26:E24

Department of Neurosurgery, Stanford University Medical Center, Stanford, California 94305-5327, USA.
Neurosurgical FOCUS (Impact Factor: 2.11). 06/2009; 26(5):E24. DOI: 10.3171/2009.3.FOCUS0927
Source: PubMed


Increasing evidence in animal models and clinical trials for stroke, hypoxic encephalopathy for children, and traumatic brain injury have shown that mild hypothermia may attenuate ischemic damage and improve neurological outcome. However, it is less clear if mild intraoperative hypothermia during vascular neurosurgical procedures results in improved outcomes for patients. This review examines the scientific evidence behind hypothermia as a treatment and discusses factors that may be important for the use of this adjuvant technique, including cooling temperature, duration of hypothermia, and rate of rewarming.

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    ABSTRACT: A small reduction of body temperature during reperfusion following cerebral ischemia has been known to ameliorate neuronal injury. However, the mechanisms underlying postischemic hypothermia-induced neuroprotection are poorly understood. The burst of reactive oxygen species (ROS) formation that occurs during reperfusion has been documented to be involved in ischemic neuronal degeneration. In this study, we investigated the effect of postischemic hypothermia on ROS production following transient forebrain ischemia using an in vivo microdialysis technique. Forebrain ischemia was induced by bilateral carotid artery occlusion combined with hemorrhagic hypotension for 20 min in male Wistar rats. The body temperature was kept at 37 degrees C during ischemia and controlled at either 32 degrees C or 37 degrees C after reperfusion. The amount of hydroxyl radical produced in striatum was evaluated by measurement of 2,3- and 2,5-dihydroxybenzoic acid (DHBA), which is generated by salicylate hydroxylation. We also measured the extracellular concentration of xanthine, while determining striatal blood flow by the hydrogen clearance technique. In animals whose postischemic body temperature was maintained at 37 degrees C, the levels of 2,3- and 2,5-DHBA significantly increased after reperfusion. The peak levels of 2,3- and 2,5- DHBA were 2.9-fold and 2.7-fold increased above the corresponding baseline values, respectively. Postischemic hypothermia completely inhibited the hydroxyl radical formation. Likewise, xanthine formation was also inhibited by postischemic hypothermia. In contrast, striatal cerebral blood flow was not altered by temperature modulation during reperfusion. These results suggest that inhibition of ROS production accompanied with suppression of xanthine formation is implicated in the neuroprotection of postischemic hypothermia.
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    ABSTRACT: Moyamoya disease (MMD) was first described in the Japanese medical literature in 1957 by Takeuchi and Shimizu [1]. The term “moyamoya” (Japanese for “puff of smoke”), was coined by Suzuki and Takaku in 1969 to describe the diagnostic appearance of angiogenesis on catheter angiogram [2]. Since its initial discovery, the features of the disease have become clearer; however, its etiology remains unknown. MMD is a chronic cerebrovascular disease characterized by stenosis or occlusion of the bilateral terminal internal carotid arteries resulting in the characteristic development of an abnormal vascular network in the areas of the arterial occlusions [3]. It is hypothesized that, in the setting of arterial stenosis or occlusion, hypoxic regions of the brain induce deep collateral flow through dilated and tortuous perforating arteries. It has been shown that this native revascularization strategy is orchestrated by the expression of various angiogenic signaling cascades [4, 5]. Despite intense research, the etiology of MMD remains unclear [6]. Familial MMD has been noted in as many as 15% of patients, indicating an autosomal dominant inheritance pattern with incomplete penetrance. Genetic analyses in familial MMD and genome-wide association studies represent promising strategies for elucidating the pathophysiology of this condition. A recent study described that carriers of a mutation in the vascular smooth muscle cell-specific isoform of alpha-actin can present with a diversity of vascular diseases, including premature onset of coronary artery disease and thoracic artery aneurysm and dissection, as well as MMD [7].
    Moyamoya Disease Update, 01/2010: pages 353-360; , ISBN: 978-4-431-99702-3
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