This approach has certain drawbacks; recanalization occurs months later in many instances, as does distal occlusion of the venous drainage system with worsening of the myelopathy. For these reasons, surgical ligation of the arterial supply is still preferred as the initial procedure for larger AVMs. Some surgeons advise a staged approach in which the size of the malformation is first reduced by endovascular techniques, thereby making the surgery less complicated. Intradural fistulas are usually treated by endovascular methods but they can be excised if visualized intraoperatively. Interventional techniques have also been used to advantage in the intramedullary malformations, either as the sole treatment or in combination with surgery. Focused radiation has been tried but the results have been difficult to evaluate.
Naiman and coworkers described the case of an adolescent boy who died of sudden paralysis after a fall in a seated position. Postmortem examination revealed extensive myelomalacia as a result of occlusions of numerous spinal vessels by emboli of nucleus pulposus material. The clinical picture is essentially one of spinal apoplexy; after spinal trauma of even mild degree the patient experiences the abrupt onset of pain in the back or neck, accompanied by the signs of a transverse cord lesion affecting all sensory, motor, and sphincteric functions and evolving over a period of a few minutes to 1 h or more. Occasionally, the syndrome spares the posterior columns, thus simulating an anterior spinal artery occlusion. The CSF is normal. As with other types of cord infarction, the changes may not appear on MRI for a day or more.
In some of the reported instances there was said to have been no excessive activity or spinal trauma preceding the spinal cord symptoms. However, this has not been true of our patients, most of who had been participating in some strenuous activity, but often earlier in the day rather than at the time of the paraplegia. Others had fallen and injured themselves on preceding days; a direct blow to the back during contact athletic sports was the antecedent event in several others and is the easiest-to-understand cause.
At autopsy, numerous small arteries and veins within the spinal cord are occluded by fibrocartilage, with necrosis of the spinal cord over 1 or 2 segments. A ruptured disc of the usual type is usually not found in these patients, but high-resolution radiographs have exposed a discontinuity of the cortical bone of the vertebral body adjacent to a collapsed disc and herniation of disc tissue into a vertebral body in a few instances (Tosi et al). The explanation suggested by Yogananden and colleagues is that the high intravertebral pressure forces nucleus pulposus material into venules and arteries of the marrow of the vertebral body, and thence into the adjacent radicular vessels. This mechanism has probably been overlooked in some otherwise unexplained cases of acute ischemic myelopathy.
Caisson Disease (Decompression Sickness, “Bends”)
This extraordinary myelopathy, which is well known to the scuba diving community, is observed in persons who are subjected to high underwater pressure and then ascend too rapidly. It affects mainly the upper thoracic spinal cord as a result of nitrogen bubbles that form and are trapped in spinal vessels. There may be little or no involvement of the brain. Haymaker, who provided the most complete account of the neuropathologic changes, observed ischemic lesions mainly in the white matter of the upper thoracic cord; the posterior columns were more affected than lateral and anterior ones. We have encountered instances in which an almost complete transverse myelopathy was evident soon after the patient resurfaced but the syndrome then improved, leaving the patient with an asymmetrical and incomplete albeit permanent residual deficit. The smallest degree of damage is manifest as a minor myelopathy that affects the anterior or the posterior funiculi, leaving either spasticity or numbness of the legs. Immediate treatment consists of recompression in a hyperbaric chamber; later treatment is symptomatic, with antispasticity drugs and physical therapy.