We describe an operative approach to lumbar canal stenosis which, unlike laminectomy, takes into account the segmental pathology of the disease. At each level involved, a bilateral subarticular fenestration is performed under high magnification. The medial third of each facet joint is first removed with an air-powered drill; then the remaining two-thirds of the joint is undercut with the drill to allow a generous fenestration in the thickened ligamentum flavum and adjacent laminae. All tissue responsible for neural compression is removed, but the spinous processes, interspinous ligaments, and much of the facet joints and laminae are preserved. Spinal stability is maintained and, because tissue disruption is minimized, postoperative discomfort is usually reduced, promoting early mobility and reduced hospital stay. The operation is described in detail, and the results of operation in 32 patients are assessed. The follow-up periods now range from 17 to 58 months. Of 23 patients who presented with neurogenic claudication, 14 (61%) obtained complete relief and 7 (30%) improved significantly. The mean hospital stay was 9 days (range, 4 to 17 days).
SummarySubarachnoid haemorrhage from intracranial aneurysms has a poor prognosis. Operative management of intracranial aneurysms was once considered ineffective. The first 100 cases treated by microsurgery were analysed to see whether mortality and morbidity were reduced. Modern surgical techniques halved the total mortality but the morbidity was unaltered. Results can be improved by delaying surgery seven days and by treating any hypertension before surgery.
The authors reviewed 100 consecutive survivors of aneurysm operations and identified 3 patients who developed postoperative epilepsy. The use of prophylactic phenytoin in the first 67 cases did not seem to influence the patient's risk of developing epilepsy. It is concluded that with present microneurosurgical techniques the risk of postoperative epilepsy is small and unselective use of phenytoin prophylaxis should be reconsidered.
Twenty-six patients who presented with spinal cord compression due to cervical disc prolapse (herniation of the nucleus pulposus) were treated by anterior discectomy. There was a high incidence of disc prolapse at the C3-4 level. The most severe degrees of preoperative disability were associated with prolapse at that level. Impairment of posterior column function, particularly in the upper limbs, played a major part in producing disability. High cervical disc prolapse can produce a clinical picture that is predominantly like that of a posterior cord syndrome. Preexisting fusion of vertebral bodies in the cervical spine and a history of cervical spinal trauma appear to be predisposing factors. Discectomy is an effective treatment of this condition. Spinal cord compression due to cervical disc prolapse should be distinguished from spondylotic myelopathy.
Most surgically treated cases of brain-stem hematomas have been attributed to rupture of cryptic arteriovenous malformations (AVM's); however, very few cases have been histologically proven. Similarly, there are very few reports of surgically treated spontaneous hematomyelia, in which the hemorrhage has been histologically confirmed as being due to a purely intramedullary AVM. The authors report three cases with surgically treated, histologically confirmed AVM's, of which two were in the brain stem and the third was in the spinal cord. In all these cases, abnormal vascular tissue in the wall of the hematoma cavity was recognized at operation and excised.
Eighty patients with subarachnoid hemorrhage underwent computerized tomography (CT) scanning before and after administration of Conray contrast medium. Abnormal enhancement was seen in visual evaluation of the CT scans in 26 cases, in the regions bordering the subarachnoid spaces. Abnormal enhancement was associated with a poor clinical condition, angiographic spasm, and a poor outcome. Measurements of absorption values in the thalamus revealed significant increases in density after contrast enhancement in those patients whose scans showed abnormal enhancement in the regions bordering the subarachnoid spaces on visual evaluation. The authors suggest that the abnormal enhancement is parenchymal, in the gyri, and is not "subarachnoid." They suggest that it is due to gyral hyperemia or extravasation of contrast material into the cortex resulting from breakdown of the blood-brain barrier, or a combination of both factors.
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