These findings indicate that hypothermic preconditioning induces a form of delayed tolerance to focal ischemic damage. The time course over which tolerance occurs and the ability of a protein synthesis inhibitor to block tolerance suggest that increased expression of one or more gene products is necessary to establish tissue tolerance following hypothermia. The attenuation of hypoxic injury in vitro following in vivo preconditioning indicates that tolerance is due, at least in part, to direct effects on the brain neuropil. Hypothermic preconditioning could provide a relatively low-risk approach for improving surgical outcome after invasive surgery, including high-risk neurological and cardiovascular procedures.

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Delayed resistance to ischemic injury can be induced by a variety of conditioning stimuli. This phenomenon, known as delayed ischemic tolerance, is initiated over several hours or a day, and can persist for up to a week or more. The present paper describes recent experiments in which transient hypothermia was used as a conditioning stimulus to induce ischemic tolerance. A brief period of hypothermia administered 6 to 48 hours prior to focal ischemia reduces subsequent cerebral infarction. Hypothermia-induced ischemic tolerance is reversed by 7 days postconditioning, and is blocked by the protein synthesis inhibitor anisomycin. Electrophysiological studies utilizing in vitro brain slices demonstrate that hypoxic damage to synaptic responses is reduced in slices prepared from hypothermia-preconditioned animals. Taken together, these findings indicate that transient hypothermia induces tolerance in the brain parenchyma, and that increased expression of one or more gene products contributes to this phenomenon. Inasmuch as hypothermia is already an approved clinical procedure for intraischemic and postischemic therapy, it is possible that hypothermia could provide a clinically useful conditioning stimulus for limiting injury elicited by anticipated periods of ischemia.

The results of these experiments indicate that HPC may provide an effective and safe means for limiting cellular injury resulting from predictable periods of central nervous system ischemia.

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Background:Most spinal cavernous haemangiomas occur in the vertebral body and purely extradural cavernous hemangiomas without any vertebral body involvement is rare and account for only 4% of all extradural spinal tumors. Dumbbell-shaped spinal cavernous angioma is extremely rare, only 10 cases have been reported in the literature.Case Description:A 77-year-old female presented with a one-year history of lumbago and right-sided L3 dermatomal hypoesthesia. A dumbbell mass at the L2/3 vertebral level was identified on lumbar MRI. The lesion was irregularly shaped and isointense on T1W and hyperintense on T2W and DWI images with homogenous contrast enhancement. A presumptive diagnosis was schwannoma, but other malignant neoplasms were also considered because of its irregular shape, minimally dilated neural foramen and the involvement of the non-enhanced L3 nerve root. The patient underwent surgery with a lateral extracavitary approach. A histopathological examination revealed cavernous hemangioma.Conclusion:Cavernous hemangioma should be included in the differential diagnosis of dumbbell-shaped spinal tumors when the intervertebral foramina is not highly dilated and non-enhanced nerve root is identified in the tumor.

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Idiopathic carpal tunnel syndrome (CTS) is a common complaint, reflecting entrapment neuropathy of the upper extremity. CTS produces symptoms similar to those of other conditions, such as cervical spondylosis or ischemic or neoplastic intracranial disease. Because of these overlaps, patients with CTS are often referred to a neurosurgeon. Surgical treatment of CTS was started recently in our department. Through this experience, we realized that neurosurgeons should have an increased awareness of this condition so they can knowledgeably assess patients with a differential diagnosis that includes CTS and cervical spinal and cerebral disease. We conducted a literature review to gain the information needed to summarize current knowledge on the clinical, pathogenetic, and therapeutic aspects of CTS. Because the optimal diagnostic criteria for this disease are still undetermined, its diagnosis is based on the patient’s history and physical examination, which should be confirmed by nerve conduction studies and imaging modalities such as magnetic resonance imaging and ultrasonography. Treatment methods include observation, medication, splinting, steroid injections, and surgical intervention. Understanding the clinical features and pathogenesis of CTS, as well as the therapeutic options available to treat it, is important for neurosurgeons if they are to provide the correct management of patients with this disease.