Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2006
Stimulation of primary motor cortex for intractable deafferentation pain.
To treat intractable deafferentation pains, we prefer stimulation of the primary motor cortex (M1). The methods of stimulation we utilize are electrical stimulation and repetitive transcranial magnetic stimulation (rTMS). In our department, we first attempt rTMS, and if this rTMS is effective, we recommend the patient to undergo procedures for motor cortex stimulation (MCS). ⋯ Only M1 stimulation was effective for pain reduction in 10 of 20 patients (50%). Twenty-nine MCS procedures were performed by subdural implantation of electrodes, and in the case of hand or face pain, electrodes were implanted within the central sulcus (11 cases), because the main part of M1 is located in the central sulcus in humans. The success rate of MCS was around 63%, and seemed to be higher in cases of pain with spinal cord and peripheral origins, while it was lower in cases of post-stroke pain.
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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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Traumatic brain injury and stroke are both characterized by an ischemic core surrounded by a penumbra of low to hyperemic flows. The underperfused ischemic core is the focus of edema development, but the source of the edema fluid is not known. We hypothesized that flow of edema fluid into the tissue is derived from cerebral venous circulation pressure, which always exceeds intracranial pressure (ICP). ⋯ In studies on 2 pigs, cerebral cortical venous, intracranial (subarachnoid), sagittal sinus, and central venous pressures were monitored with manipulation of ICP by raising and lowering a reservoir above and below the external auditory meatus zero point. The results show that cerebral venous pressure is always higher than or equal to ICP at pressures of up to 60 mmHg. On the basis of these observations, we hypothesize that increased cerebral venous pressure initiated after traumatic brain injury and stroke drives edema fluid into the tissue, which thereby increases ICP and a further increase in cerebral venous pressure in a vicious cycle of brain edema.
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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 2006
Granulocyte colony-stimulating factor does not affect contusion size, brain edema or cerebrospinal fluid glutamate concentrations in rats following controlled cortical impact.
Granulocyte colony-stimulating factor (G-CSF) is an established treatment in the neutropenic host. Usage in head-injured patients at risk for infection may aggravate brain damage. In contrast, evidence of G-CSF neuroprotective effects has been reported in rodent models of focal cerebral ischemia. We investigated effects of G-CSF in acute focal traumatic brain injury (TBI) in rats. ⋯ A single injection of G-CSF did not influence cortical contusion volume, brain edema, or glutamate concentrations in CSF determined 24 hours following CCII in rats. G-CSF, administered 30 minutes following experimental TBI, failed to exert neuroprotective effects.