Cauda equina syndrome as a neurological complication of long-standing ankylosing spondylitis was first reported in 1961. The syndrome is relatively uncommon and its pathophysiology is still poorly understood. Based on their experience with such a case, the authors review the clinical, electrographic, histological, and radiographic features of the syndrome, including the findings of magnetic resonance (MR) imaging. The addition of MR imaging to the evaluation of patients with ankylosing spondylitis and the cauda equina syndrome not only aids in the diagnosis of the syndrome but may also provide valuable insight into the pathophysiology of this condition.

Rotation-induced vertebrobasilar artery hypoperfusion causes transient ischemic attacks (TIAs), affecting the cerebellum, brainstem and spinal cord. When these symptoms occur transiently due to head movement, compression of the vertebral artery by an extraluminal lesion should be suspected. Cervical spondylotic spurs and anterior scalene muscle or deep cervical fascia are among the factors which can compress the vertebral artery. When symptoms of vertebrobasilar insufficiency occur with rotational head movement, subclavian angiography for visualization of the entire vertebral artery in both neutral and rotated head positions should be undertaken.

Eight patients undergoing an end-to-side vertebral artery (VA) to common carotid artery transposition between August, 1979, and July, 1982, had a polytetrafluoroethylene (PTFE) interposition graft placed when a direct anastomosis was believed not to be satisfactory. Five of these patients are living; clinical and radiographic follow-up studies over periods ranging between 54 and 82 months show that their transpositions are patent. Two patients died perioperatively, one from an acute anterior myocardial infarction and the other from acute VA occlusion with a propagating thrombus. A third patient died of myocardial infarction 20 months after graft placement; the anastomosis had been found patent at 12 months. This report gives the clinical and radiographic follow-up results in a previously reported group of patients with PTFE interposition grafts. Some of these patients have been followed for over 6 years after surgery: the average radiographic follow-up period in the five survivors is 60 months, and all grafts are patent without evidence of progressive stenosis. Expanded PTFE appears to be an acceptable material for short interposition grafts in operations involving the VA; however, direct artery-to-artery anastomosis is preferred. The results of longer PTFE grafts in reconstructive cerebrovascular surgery have not been adequately studied.

The biomechanical effects on the cranial contents after craniectomy and immediate soft-tissue flap reconstruction are substantial and potentially life threatening. Once the rigid protective covering of the skull is removed, the cerebral component of the cranial contents is vulnerable to rising extrinsic pressure. Intracranial pressure falls, brain compliance rises, and contralateral cerebral shift may occur by virtue of the craniectomy alone. However, if flaps filling the defect should compress by weight or swelling, even greater midline or craniocaudal shift of the brain may occur. We present three cases in which midline cerebral shift was documented by CT scan after flap reconstruction of lateral craniofacial/craniotemporal resection. Three other patients undergoing anterior craniofacial resection during the same time period for skin cancer (one patient) and esthesioneuroblastoma (two patients) had no shift in intracerebral contents. Symptomatic or asymptomatic intracranial shift may occur soon after substantial craniectomy and soft-tissue flap reconstruction. Midline shift from lateral resection and reconstruction is more likely than anteroposterior shift from anterior craniofacial resection. Strategies for minimizing this compression or shift are described.