Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2008
Cerebrovascular reactivity and autonomic drive following traumatic brain injury.
The autonomic nervous system exerts tonic control on cerebral vessels, which in turn determine the autoregulation of cerebral blood flow. We hypothesize that the impairment of cerebral autoregulation following traumatic brain injury might be related to the acute failure of the autonomic system. ⋯ Following traumatic brain injury, autonomic failure and cerebrovascular autoregulation impairment are both associated with fatal outcome. Impairment of cerebrovascular autoregulation and autonomic drive are interdependent phenomena. With some refinements, HRV might become a tool for screening patients at risk for cerebral autoregulation derangement following TBI.
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Acta Neurochir. Suppl. · Jan 2008
Clinical TrialHyperbaric oxygen therapy for consciousness disturbance following head injury in subacute phase.
Hyperbaric oxygen (HBO) therapy has been shown to improve outcome after brain injury, however its mechanisms are not understood. The purpose of the present study was to investigate the effect of hyperbaric oxygen (HBO) therapy on the cerebral circulation and metabolism of patients with disturbances in consciousness after head injury in the subacute phase. ⋯ The measurement of cerebral circulation and metabolism parameters, especially PI and lac-JV, is useful for estimation of effect of HBO therapy in patients with distubances in consciousness after head injury in the subacute phase.
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Acta Neurochir. Suppl. · Jan 2008
The modulation of aquaporin-4 by using PKC-activator (phorbol myristate acetate) and V1a receptor antagonist (SR49059) following middle cerebral artery occlusion/reperfusion in the rat.
We have pursued the concept that traumatic brain edema is predominantly cellular and that water entry is modulated in part by aquaporins. Aquaporin-4 (AQP4) has been shown to play a significant role in cellular edema formation. Phorbol myristate acetate (PMA) is a potent PKC activator; purportedly involved in modulation of AQP4 activity. Alternatively, AQP4 may be regulated by arginine-vasopressin. Administration of the vasopressin antagonist (SR49059) reduced brain water content and sodium shift following MCAo. To investigate if edema formation is affected by the reduction of AQP4 expression, we utilized PMA and SR49059 following middle cerebral artery occlusion model (MCAo), and measured AQP4 expression by Western-Blot (WB) techniques. ⋯ These studies support the hypotheses that PMA and SR49059 may be useful in reducing cerebral water accumulation by modulating AQP4 expression and that pharmacological manipulation of AQP4 may emerge as a viable strategy for the reduction of fulminating edema following ischemic injury.
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Acta Neurochir. Suppl. · Jan 2008
Noninvasive estimation of intracranial compliance in idiopathic NPH using MRI.
The pathophysiology of idiopathic normal pressure hydrocephalus (I-NPH) is still unclear and the diagnosis is sometimes difficult. The aim of this study was to assess the biophysics of I-NPH by measuring intracranial compliance using cine MRI. ⋯ It is possible to estimate intracranial compliance as CI non-invasively using cine MRI. CI could become a useful method for the diagnosis of I-NPH.
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Acta Neurochir. Suppl. · Jan 2008
The antioxidant effects of melatonin after intracerebral hemorrhage in rats.
Free radical mechanisms are involved in secondary brain injury after intracerebral hemorrhage (ICH). Since melatonin is a potent free radical scavenger and indirect antioxidant, the objective of this study was to evaluate whether melatonin administration would attenuate oxidative stress, brain edema, and neurological deficits in a rat model of ICH. Animals were assigned into groups consisting of sham (needle trauma), vehicle, and melatonin (15 or 150 mg/kg). ⋯ Results demonstrated dramatically increased lipid peroxidation after collagenase-induced ICH; however, melatonin treatment effectively attenuated this lipid peroxidation. Nonetheless, neurological scoring and brain water content in the right basal ganglia was without significant difference between any treatment regimens (15 or 150 mg/kg of melatonin) or time points of drug administration (15 min or 3 h post-ICH). Therefore, melatonin reduced oxidative stress but did not change extent of brain edema or neurologic deficits.