Aneurysm of the anterior inferior cerebellar artery producing hearing loss.
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Biomedical subjects
Publications and source records attributed to R A Roski.
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Extradural meningeal cysts are rare spinal lesions. The clinical presentation is most often characterized by a slowly progressive spastic paraparesis, frequently associated with pain. Adequate drainage of the cyst with obliteration of the neck of the cyst or complete removal of the cyst can bring about a permanent resolution of the symptoms. The use of somatosensory cortical evoked responses also has an important role in the surgical management of this problem.
A beneficial effect of dimethyl sulfoxide (DMSO) in the treatment of acute focal cerebral ischemia has not been proven. In the present study, two established experimental models of acute focal cerebral ischemia were treated with DMSO. Twenty adult cats lightly anesthetized with ketamine hydrochloride underwent right middle cerebral artery (MCA) occlusion for 6 hours. Ten cats were not treated and 10 cats received DMSO (2.5 g/kg i.v.) immediately after occlusion. No improvement of EEG findings, erythrocyte transit, regional cerebral blood flow (rCBF), blood-brain barrier permeability, or morphological findings were demonstrated in the DMSO-treated cats. In a second study, 15 conscious adult baboons underwent temporary left MCA occlusion (6 or 12 hours) using an implanted occluding device. Seven baboons were not treated and 8 baboons received continuous intravenous infusions of DMSO for 10 hours beginning 30 minutes after occlusion. Four of the baboons that were treated with DMSO also were treated with pentobarbital coma for 96 hours starting 4 hours after occlusion. Analysis of the neurological scores after 1 week survival indicated that treatment with DMSO alone and DMSO and pentobarbital coma did not improve the outcome. Morphological changes were similar in the 3 groups. The findings of our investigation indicate that DMSO is ineffective in treating acute focal cerebral ischemia.
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Extracranial-intracranial arterial bypass was performed in five baboons to assess the effectiveness of the procedure in preventing acute cerebral ischemia following middle cerebral artery occlusion in our primate model. Thirty minutes following middle cerebral artery occlusion, the animals were placed in barbiturate coma while the extracranial-intracranial artery bypass was being completed. In the three animals with patent extracranial-intracranial arterial bypasses, infarction was prevented. In the two with occluded extracranial-intracranial arterial bypasses, a large infarction in the territory of the middle cerebral artery occurred. In a clinical correlate, postoperative ischemia was presumably prevented in three patients by barbiturate administration and revascularization for unanticipated intracranial vessel occlusion.
This boy first contracted atypical trigeminal neuralgia at the age of 6 years. Four years later, he underwent a microvascular decompression of a venous loop from his trigeminal nerve. He remains asymptomatic 2 years after surgery.
The therapeutic application of barbiturate-induced coma was evaluated in a primate model of focal cerebral ischemia. A standardized regimen of pentobarbital was used, and the times of initiation of administration were varied following a 6-hour middle cerebral artery occlusion in baboons. Three groups of five animals were treated at 30, 120, and 240 minutes after occlusion, while one group of five animals received no barbiturate therapy. Complete protection from intracranial pressure (ICP) elevation and ischemic damage was seen only in the group treated at 30 minutes. Those treated at 120 minutes, while doing better than untreated animals, still had ICP elevation and a marked neuropathological deficit. Animals treated at 240 minutes suffered a detrimental effect, in that malignant ICP and marked ischemic damage occurred earlier than in the untreated animals. The safe "therapeutic window" for barbiturate-induced coma in this animal model does not extend beyond 2 hours. Delayed administration results in a deleterious response and not merely a lack of protection.
Fourteen patients who underwent occipital to posterior inferior cerebellar arterial bypass are reviewed. All of the patients were treated for severe vertebrobasilar ischemia secondary to lesions of the distal vertebral artery. There was no operative death or permanent postoperative morbidity. On follow-up evaluation (averaging 13 months after operation), there has been 100% graft patency and a noticeable improvement in the neurological function in all patients. Operating with the patient in the prone position and avoiding intraoperative hypotension help to minimize the operative morbidity from this procedure.
Barbiturate therapy has been shown to be of benefit in certain instances for focal cerebral ischemia. This therapy can, however, result in a deleterious outcome. Early institution in combination with revascularization appears to be important for successful barbiturate application. Whether combinations of agents designed to act on different mechanisms in the pathophysiology of cerebral ischemia can prolong the 'therapeutic window' of barbiturate application is an area for future investigation.
Extracranial to intracranial bypass surgery was used in 27 cases of intracranial giant aneurysm to prevent ischemic complications. In 19 of 21 patients the aneurysm was considered unfit for a direct clipping or ligation, and an EC-IC bypass was done in conjunction with staged clipping of the internal carotid artery or occlusion of the middle cerebral artery. All bypass grafts have remained patent postoperatively. None of the patients have developed ischemic complications in the 6--14 month period of follow-up.
A case in which obstructive hydrocephalus was relieved by spontaneous ventriculo-cisternostomy is presented and the pertinent literature reviewed. Management of acquired obstructive hydrocephalus by percutaneous stereotactic or endoscopic third ventriculo-cisternostomy is discussed.
An unusual case of a vermian hematoma from the rupture of an angioma in a four-year-old child is presented. The lesion was treated successfully with complete recovery.
We measured the MCAP (middle cerebral artery pressure)/MSBP (mean systemic blood pressure) ratio in 76 patients who underwent an EIAB (extracranial-intracranial arterial bypass). Patients were divided into groups on the basis of angiographic findings. We found a definite correlation between increasing angiographic cerebral vascular occlusive disease and lower MCAP/MSBP ratios. Six of 32 patients with a preoperative neurologic deficit demonstrated mild but definite postoperative neurologic improvement. The mean MCAP/MSBP ratio in these six patients was significantly lower than that for the remainder of this group (p less than .05). Finally, postoperative filling of the middle cerebral artery territory through the graft was found to correlate in an inverse linear relationship with MCAP/MSBP. Evidence is presented that hypoperfusion produced by occlusion of major cranial vessels plays an important role in temporary and permanent neurological deficits seen in patients with cerebrovascular disease.