J Neurosurg Sci
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Cerebral vasospasm following aneurysmal subarachnoid hemorrhage is one of the most important causes of cerebral ischemia, and is the leading cause of death and disability after aneurysmal rupture. The optimal treatment of vasospasm awaits development of agents for blocking or inactivating spasmogenic substances, or blocking arterial smooth muscle contraction. Rheological and/or hemodynamic manipulation using triple-H (hypertensive-hypervolemic-hemodilution) therapy to prevent or reverse ischemic consequences are relatively effective, but complicated and hazardous, and should be viewed principally as interim measures awaiting development of more specific therapies for arterial narrowing.
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Recent evidence indicates that the relationship between "brain protection" and the degree of hypothermia is not linear, and even mild reduction of body temperature (i.e. 2-5 degrees C) may provide protection against cerebral ischemia. The protective effects of mild hypothermia have been demonstrated in various animal models of cerebral ischemia, and are encouraging in human studies. At the present time, although there is no randomized clinical trial assessing the benefits of mild hypothermia for intracranial aneurysm clipping, some neurosurgical centers are routinely instituting mild hypothermia before vascular occlusion.
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Review Case Reports
Spinal epidural hematoma during anticoagulant therapy. A case report and review of the literature.
The authors present a case of spinal epidural hematoma during anticoagulant therapy. Clinical presentation is characterized by classic paravertebral back pain, followed by progressive neurological deficit due to spinal cord and radicular compression, with sensory deficits and bladder disturbance. ⋯ Early surgical decompression of the spinal cord minimizes the degree of permanent neurological damage, because of the long-time compression of the spinal cord resulting in irreversible disturbance of circulation; therefore an early diagnosis is a better prognosis. The thoracic and cervical spine canal is smaller than the lumbar, therefore there is less space to reward the formation of hematomas, consequently the postoperative recovery is lower in patient with high spinal epidural hematomas with respect to lumbo-sacral spinal epidural hematomas; at this level the epidural hematoma may be insidious in its onset and tends to become chronic before definite treatment is undertaken.
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During centuries, the loss of spontaneous cardio-pulmonary function was found to predict permanent non-functioning of the "organism as a whole", therefore serving adequately as a criterion of death, but during the era of Intensive Care, there was a shift to brain-oriented definitions of death, ie, the irreversible cessation of brain functions, started to be considered as the main reason for cessation of functioning of the "organism as a whole". A concept or definition of death is related to the question: What is it "about human life, which is irreplaceable by any artifice, and that its loss is so essential, that the individual who loses it ought to be called dead?" Further work has been centered on how much of the brain needs to be dead, before a person can be declared dead on neurological grounds: "whole brain", "brainstem death" ("brain as a whole") and "higher brain" formulations of death. ⋯ I propose a concept of death that excludes those states taking in consideration the basic mechanisms of consciousness generation in human beings: "The irreversible loss of consciousness, considering both its capacity and its content". This definition of human death takes consideration as hallmarks, both components of consciousness which are essentially significant to the nature of man, to provide the functioning of the "organism as a whole".
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Fibrin and fibrinogen degradation products in the cerebrospinal fluid (CSF-FDP) were first studied in a group of 29 patients observed during the first and the second week after subarachnoid hemorrhage (SAH), then in a second group of 26 patients for a total of 55 patients. In the latter group only the first FDP value obtained as soon as possible after SAH was taken in consideration. In the whole series of 55 patients several noteworthy factors were found: 1) FDP determination should be performed as soon as possible after SAH; 2) CSF-FDP at or above 40, 80 micrograms/ml was found both in the patients with severe neurological deficits and in those with cerebral ischemia (statistically significant); 3) the significance of CSF-FDP in patients who rebled was also evaluated. In conclusion CSF-FDP could be considered useful in predicting cerebral ischemia.