Acta neurochirurgica. Supplement
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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
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
Controlled Clinical TrialTraumatic brain edema in diffuse and focal injury: cellular or vasogenic?
The objective of this study was to confirm the nature of the edema, cellular or vasogenic, in traumatic brain injury in head-injured patients using magnetic resonance imaging techniques. Diffusion-weighted imaging methods were quantified by calculating the apparent diffusion coefficients (ADC). Brain water and cerebral blood flow (CBF) were also measured using magnetic resonance and stable Xenon CT techniques. ⋯ In contrast, in patients with significant brain swelling ADC values were reduced and averaged 0.74 +/- 0.05 (p < 0.0001), consistent with a predominantly cellular edema. We also found that the CBF in these regions was well above ischemic threshold at time of study. Taking these findings in concert, it is concluded that the predominant form of edema responsible for brain swelling and raised ICP is cellular in nature.
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Acta Neurochir. Suppl. · Jan 2006
Controlled Clinical TrialClinical characteristics of postoperative contralateral intracranial hematoma after traumatic brain injury.
To investigate the clinical characteristics of contralateral intracranial hematoma (ICH) after traumatic brain injury. ⋯ The B-ICH patients had a worse outcome than the U-ICH patients. Contralateral ICH was difficult to forecast based on pre- and intraoperative clinical conditions. Subdural hematoma or contusional ICH was frequently observed as a contralateral ICH.
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Acta Neurochir. Suppl. · Jan 2006
Decompressive craniectomy for severe head injury in patients with major extracranial injuries.
Neurosurgical therapy aims to minimize secondary brain damage after a severe head injury. This includes the evacuation of intracranial space-occupying hematomas, the reduction of intracranial volumes, external ventricular drainage, and aggressive therapy in order to influence increased intracranial pressure (ICP) and decreased P(ti)O2. ⋯ The prognosis after decompression depends on the clinical signs and symptoms at admission, patient age, and the existence of major extracranial injuries. Our guidelines for decompressive craniectomy after failure of conservative interventions and evacuation of space-occupying hematomas include: patient age below 50 years without multiple trauma, patient age below 30 years in the presence of major extracranial injuries, severe brain swelling on CT scan, exclusion of a primary brainstem lesion or injury, and intervention before irreversible brain stem damage.