Ischemic Spinal Vascular Diseases: Clinical Analysis Of Cases

We performed retrospective analysis of the original data of the 60 patients suffered from ischemic spinal vascular diseases from Feburary 1993 to October 2003. There were 37 men and 23 women aged from 15 to 80 years old (mean 44.8). Risk factors for spinal stroke included hypertension, atherosclerosis, nonspecific inflammatory diseases, cervical sopondylosis, disc herniation, hyperlipidemia, diabetes mellitus, coronary heart diseaseas, myocardial infarction, rheumatic heart diseases, cigarette smoking, habitual alchohol drinking, AVM and so on. Pathogenic mechanisms of ischemic myelopathy are spinal artery atherothrombosis in most patients, disc herniation and cardiogenic embolism in few patients. The most common first symptom was radicular pain. The secondary was weakness and numbness. ASAS makes the greatest propotion, which is characterized with abrupt onset of weakness and, below the level of the lesion, flaccid tetraplegia or paraplegia, areflexia, loss of spinothalamic perception of pain and temperature, and autonomic deficits comprising sphincter flaccidity, atonic urinary baldder and paralytic ileus. Sometimes cervical cord ischemic patients present with respiratory insufficiency and Horner syndrome. Transient radicular or back pain may herald these findings. Spasticity eventually ensues, with exaggerated deep tendon reflexes, Babinski responses, and clonus, except when ischemia involves anterior horn cells or motor nerver roots, or the cauda equina in which case mixed or lower motoneuron deficits may occur. Some patients may suffer central pain in the choronic stage. 48 of our patients suffered from radcular pain, of which 38 patients presented with it as the first symptom. We had ten patients who had stayed in hospital for more than one month. And 6 out of the 10 developed painful burning dysaesthesias below the level of spinal cord lesion, refractory to opiate, anticonvulsant and tricyclic antidepressant therapy. Patterns of sensory dysfunction in our patients were composed of the following: â‘ dissociated sensory loss: decreased or absent pain and temperature sensation below a sensory level with sparing of vibratory sense and proprioception; â‘¡all sensory loss below the level. Posterior spinal artery infarcton is rare. So we did not find a patient whose deep sense was abolished only. We had 4 patients who presented with Brown-sequard syndrome. Spinal cord hemisection orginates from a lesion obstructing the sulcocommissural arery. In this case ipsilateral paralysis accompanies contralateral loss of spinothalamic sensibility. As in the anterior spinal artery syndrome, the dorsal columns are spared. RI was sensitive after 24 hours from ictus. The classical image was hyperintensity on T2WIs, accompanied with hypointensity on T1WI and cord swelling. In the chronic period the spinal cord may become thin on T1WIs. In summary Ischemic vascular diseases spares neither yang nor old people. But the most patients were old people with the risking factors of cardiovascular diseases. The most common cinical findings were sudden radicular pain, tetraplegia or paraplegia, dissociated sensory loss, bladder and bowel paralysis. MRI was sensitive after 24 hours from ictus. The classical image is hyperintensity on T2WIs, accompanied with hypointensity on T1WI and cord swelling. Up to now there is no effective treament method and the prognosis is not good.