Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2006
Case ReportsFifteen year experience of intrathecal baclofen treatment in Japan.
Intrathecal baclofen administration is a fully established treatment for severe spasticity. However, it is scarcely known that Baclofen, an agonist of GABA-B receptor, has other potential effects on pain, restoration coma, dystonia, tetanus, and hypothalamic storm. Sporadic episodes of dramatic recovery from persistent vegetative state are reported after intrathecal administration of baclofen. ⋯ On the other hand, epidural spinal cord stimulation has been used for pain, spasticity, dystonia, or attempt to improve deteriorated consciousness, though the effects seem variable and modest. Similarity between baclofen and spinal cord stimulation is interesting in that both involve the spinal GABAergic system. Based on the 15-year personal experience of intrathecal baclofen, I would stress importance of this treatment not only for spasticity but also for other difficult neurological disorders.
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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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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
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
Randomized Controlled Trial Multicenter StudyDecompressive craniectomy in traumatic brain injury: the randomized multicenter RESCUEicp study (www.RESCUEicp.com).
The RESCUEicp (Randomized Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of intracranial pressure) study has been established to determine whether decompressive craniectomy has a role in the management of patients with traumatic brain injury and raised intracranial pressure that does not respond to initial treatment measures. We describe the concept of decompressive craniectomy in traumatic brain injury and the rationale and protocol of the RESCUEicp study.