Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2006
Systemic zinc protoporphyrin administration reduces intracerebral hemorrhage-induced brain injury.
Hemoglobin degradation products result in brain injury after intracerebral hemorrhage (ICH). Recent studies found that intracerebral infusion of heme oxygenase inhibitors reduces hemoglobin- and ICH-induced brain edema in rats and pigs. The present study examined whether systemic use of zinc protoporphyrin (ZnPP), a heme oxygenase inhibitor, can attenuate brain edema, behavioral deficits, and brain atrophy following ICH. ⋯ In addition, ZnPP given immediately or 6 hours after ICH improved neurological deficits (p < 0.05). In conclusion, systemic zinc protoporphyrin treatment started at 0 or 6 hours after ICH reduced brain edema, neurological deficits, and brain atrophy after ICH. These results indicate that heme oxygenase may be a new target for ICH therapeutics.
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Acta Neurochir. Suppl. · Jan 2006
Long term results from percutaneous radiofrequency neurotomy on posterior primary ramus in patients with chronic low back pain.
We report on our experience of percutaneous radiofrequency neurotomy (PRN) on the posterior primary ramus (PPR) with at least two years follow-up. ⋯ PRN on the PPR has long-term beneficial effects. Long-term good results can be achieved after proper selection of patients with facet joint related low back pain.
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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
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.