BACKGROUND: The mild type of anterior spinal artery syndrome (ASAS) is characterized by motor loss with an absent or insignificant sensory deficit due to a disturbance in the blood supply to the anterior horn of the spinal cord. The clinical symptoms of cervical spondylotic amyotrophy (CSA) are motor loss or atrophy with an absent or insignificant sensory deficit or a long tract sign; however, the pathophysiology has not been clarified. METHODS: Three patients who suffered from palsy of the deltoid and biceps brachii are presented. Magnetic resonance imaging confirmed the intrinsic cord disease as the cause of the paresis. We measured the central motor conduction time (CMCT) and the latencies of the tendon reflex (T waves) of the biceps and triceps and those of the F waves of the abductor pollicis brevis and abductor digiti minimi before, 2 weeks after, and 3 months after starting intravenous injections of prostaglandin E(1) (PGE(1)). RESULTS: In these 3 cases, restoration of muscle strength began after starting injection of PGE(1). The electrophysiologic diagnosis revealed a disturbance of the motor conduction, in the CMCT and the latencies of the T waves, in the paretic muscle, which is more severe than that in other muscles. The radiological diagnosis suggested damage in the spinal cord. Improvements in the disturbance of the motor conduction and those of symptoms were parallel. CONCLUSION: From symptomatologic or radiological viewpoints, it is difficult to differentiate CSA from ASAS with cervical spondylosis. This suggests that there have been patients with ASAS whom we have diagnosed as CSA, and we may add administration of PGE(1) to the treatment for the patients with CSA. The present 3 patients showed improvement of muscle strength after starting injections of PGE(1). Although this improvement was measured by an electrophysiologic method, the mechanisms of PGE(1) require further study.
BACKGROUND: The mild type of anterior spinal artery syndrome (ASAS) is characterized by motor loss with an absent or insignificant sensory deficit due to a disturbance in the blood supply to the anterior horn of the spinal cord. The clinical symptoms of cervical spondylotic amyotrophy (CSA) are motor loss or atrophy with an absent or insignificant sensory deficit or a long tract sign; however, the pathophysiology has not been clarified. METHODS: Three patients who suffered from palsy of the deltoid and biceps brachii are presented. Magnetic resonance imaging confirmed the intrinsic cord disease as the cause of the paresis. We measured the central motor conduction time (CMCT) and the latencies of the tendon reflex (T waves) of the biceps and triceps and those of the F waves of the abductor pollicis brevis and abductor digiti minimi before, 2 weeks after, and 3 months after starting intravenous injections of prostaglandin E(1) (PGE(1)). RESULTS: In these 3 cases, restoration of muscle strength began after starting injection of PGE(1). The electrophysiologic diagnosis revealed a disturbance of the motor conduction, in the CMCT and the latencies of the T waves, in the paretic muscle, which is more severe than that in other muscles. The radiological diagnosis suggested damage in the spinal cord. Improvements in the disturbance of the motor conduction and those of symptoms were parallel. CONCLUSION: From symptomatologic or radiological viewpoints, it is difficult to differentiate CSA from ASAS with cervical spondylosis. This suggests that there have been patients with ASAS whom we have diagnosed as CSA, and we may add administration of PGE(1) to the treatment for the patients with CSA. The present 3 patients showed improvement of muscle strength after starting injections of PGE(1). Although this improvement was measured by an electrophysiologic method, the mechanisms of PGE(1) require further study.