Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2006
Magnesium restores altered aquaporin-4 immunoreactivity following traumatic brain injury to a pre-injury state.
Magnesium reduces edema following traumatic brain injury (TBI), although the associated mechanisms are unknown. Recent studies suggest that edema formation after TBI may be related to alterations in aquaporin-4 (AQP4) channels. In this study, we characterize the effects of magnesium administration on AQP4 immunoreactivity following TBI. ⋯ In untreated animals, AQP4 immunoreactivity was increased in the subependymal inner glia limitans and the subpial outer glia limitans, and decreased in perivascular astrocytic processes in the cerebrum and brain stem. In contrast, animals treated with magnesium sulphate had AQP4 profiles similar to normal and sham control animals. We conclude that magnesium decreases brain edema formation after TBI, possibly by restoring the polarized state of astrocytes and by down-regulation of AQP4 channels in astrocytes.
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Acta Neurochir. Suppl. · Jan 2006
Electrical stimulation of the anterior cingulate cortex in a rat neuropathic pain model.
Electrical stimulation is currently employed to treat several neurological conditions, including pain and Parkinson's disease. It is one of several minimally invasive alternatives to drug treatments for painful conditions. A number of studies have shown that the anterior cingulate cortex (ACC) plays an important role in the processing of pain and pain modulation. The purpose of this study is to investigate these neuropathic pain-relieving effects by delivering electrical stimulation into the ACC of rat models. ⋯ The mechanical allodynia of the neuropathic pain could be modulated by ACC electrical stimulation.
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Acta Neurochir. Suppl. · Jan 2006
The effect of intravenous fluid replacement on the response to mannitol in experimental cerebral edema: an analysis of intracranial pressure, serum osmolality, serum electrolytes, and brain water content.
Albino rabbits that had undergone a cryogenic insult over the left parieto-occipital cortex were analyzed for serum osmolality, serum electrolytes, brain water content, and intracranial pressure (ICP) following either a baseline infusion of intravenous (i.v.) fluid (45 mL total) for 3 hours or above-maintenance isotonic saline (73.5 +/- 12 mL or 90.5 +/- 1.5 mL) and mannitol therapy. The subgroups were compared amongst themselves and to sham-operated controls. Serum osmolality was elevated in the higher-dose mannitol subgroup compared with maintenance i.v. fluids subgroup (1 g/kg/h vs 1 g/kg/3 h; p < 0.05), accompanied by an insignificant reduction of serum sodium. ⋯ Reduction of ICP was not found in the lower mannitol dose group. We conclude that the ability of mannitol to reduce cerebral edema is related to the total amount of i.v. fluid replacement. This implies that the amount of i.v. crystalloid fluid that is administered to patients with cerebral edema and raised ICP requiring mannitol for control needs to be carefully monitored.
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Acta Neurochir. Suppl. · Jan 2005
Randomized Controlled TrialIntravenous magnesium sulfate to improve outcome after aneurysmal subarachnoid hemorrhage: interim report from a pilot study.
Magnesium sulfate (MgSO4) may be useful in preventing neurological injury after subarachnoid haemorrhage (SAH). In this randomized, double-blind study we evaluated the safety and efficacy of MgSO4 infusion to improve clinical outcome after aneurysmal SAH. ⋯ MgSO4 infusion after aneurysmal SAH is well tolerated and may be useful in producing better outcome. A larger study is required to confirm the neuroprotective effect of MgSO4.
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Acta Neurochir. Suppl. · Jan 2005
Controlled Clinical TrialCerebral metabolism and intracranial hypertension in high grade aneurysmal subarachnoid haemorrhage patients.
We evaluated the effect of intracranial hypertension on cerebral metabolism in patients with high grade aneurysmal subarachnoid hemorrhage (SAH) using bedside cerebral microdialysis (MD). Thirty-six patients with SAH were studied and classified into two groups (intracranial pressure, ICP > 20 mmHg, n = 25) and (ICP < 20 mmHg, n = 11). ICP was monitored hourly using an intraventricular drainage (n = 36). ⋯ In patients with ICP > 20 mmHg from day 1 to 7 after SAH, extracellular concentrations of glucose were significantly lower, while the lactate/ pyruvate ratio was higher compared to SAH patients with normal ICP values. The differences between groups in glutamate levels was only significant on day 1 after SAH due to high inter-individual differences. We concluded that intracranial hypertension in associated with an anaerobic cerebral metabolism indicated cerebral ischemia in high grade SAH patients.