✓ Thirteen patients with schwannomas of the jugular foramen were operated on at the Cleveland Clinic between 1974 and 1983. The authors' experience in managing these rare tumors is presented. Three major growth patterns of jugular foramen schwannoma were seen, and it is postulated that the position of the tumor depends on its point of origin from the nerves as they pass through the pars nervosa of the jugular foramen. The more distal lesions will expand inferiorly out of the base of the skull, and the more proximal lesions will enlarge into the posterior fossa. Tumors in the mid region will tend to expand primarily into bone. The schwannoma was primarily intracranial in six patients. In five patients the tumor expanded the bone at the base of the skull, with only a small intracranial component, and in two patients the tumor was primarily extracranial, with a small extension into the bone or posterior fossa. The presentation of the patients varied according to the tumor growth pattern. Deafness, vertigo, and ataxia were present in all patients with a major intracranial component, and in most of these there were only minimal deficits of the jugular foramen nerves. By contrast, lower cranial nerve involvement, including hoarseness and weakness of the trapezius and sternocleidomastoid muscles, occurred in patients in whom the tumor was primarily within the bone or extracranial. Three of the five patients with the major component of the schwannoma within the bone also had deafness. Symptomatic history was longest in those with tumor mainly involving the bone at the base of the skull, and shortest in patients with entirely extracranial tumor. Surgical resection was accomplished with a joint neurosurgical-otological approach, usually combining a posterior fossa exploration with either a translabyrinthine transcochlear or infralabyrinthine procedure. The exact nature of the operation depended upon the presence of intracranial tumor and on the extent of bone or extracranial involvement. Total excision was performed in all cases. There was no operative mortality, and surgery resulted in loss of function of the ninth, 10th, and 11th cranial nerves in most patients. The major postoperative morbidity consisted of swallowing difficulties and sputum aspiration.
Andrew H. Kaye, Joseph F. Hahn, Sam E. Kinney, Russell W. Hardy Jr. and Janet W. Bay
Gene H. Barnett, Russell W. Hardy Jr., John R. Little, Janet W. Bay and George W. Sypert
✓ Hypertrophy of the posterior spinal elements leading to compromise of the spinal canal and its neural elements is a well-recognized pathological entity affecting the lumbar or cervical spine. Such stenosis of the thoracic spine in the absence of a generalized rheumatological, metabolic, or orthopedic disorder, or a history of trauma is generally considered to be rare. Over a 2-year period the authors have treated six cases of thoracic myelopathy associated with thoracic canal stenosis. In four patients the deficits developed gradually and painlessly. The three older patients had a clinical profile characterized by complaints of pseudoclaudication, spastic lower limbs, and evidence of posterior column dysfunction. Two patients were younger adults with low thoracic myelopathy associated with local back pain after minor trauma. Both patients also had congenital narrowing of the thoracic spinal canal.
Oil and metrizamide contrast myelography in the prone position were of limited value in diagnosing this condition; in fact, myelography may be misleading and result in erroneous diagnosis of thoracic disc protrusion, when the principal problem is dorsal and lateral compression from hypertrophied facets. Magnetic resonance imaging and computerized tomography sector scanning were more useful in the diagnosis of this disorder than was myelography. Thoracic canal stenosis may be more common than is currently recognized and account for a portion of the failures in anterior and lateral decompression of thoracic disc herniations.