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1) Steinbrocker, O.: The shoulder-hand syndrome in reflex dystrophy of the upper ex- tremity, Ann. Intern. Med., 29: 22, 1948. 5) Greenfield, A. D. M., Whitney, R. J. and Mowbray, J. F.: Methods for the investigation of peripheral blood flow, Brit. Med. Bull., 19: 101, 1963. 7) Steinbrocker, O.: The shoulder-hand syndrome, associated painful homolateral dis- ability of the shoulder and swelling and atrophy of the hand, Amer. J. Med., 3: 402,

1947. 8) Hilker, A.: Shoulder-hand syndrome: complication of coronary artery disease, Ann. Intern. Med., 31: 303, 1949. 9) Edeiken, J.: Shoulder-hand syndrome following myocardial infarction with special reference to prognosis, Circulation, 16: 14, 1957. 17) McCarty, K. and Woodcock, J. P.: Frequency modulated ultrasonic Doppler flowmeter, Med. Biol. Engi., 13: 59, 1975. 11) Moskowitz, E., Bishop, H. F., Pe, H. et al.: 18) Sunderland, S.: Pain mechanisms in causalgia, Posthemiplegic reflex sympathetic dystrophy, J. A. M. A., 167: 836, 1958. 12) Moskowitz, E.: Complications in the rehabilitation of hemiplegic patients, Med. Clin. N. Amer., 53: 541, 1969. 13) Swan, D. M.: Shoulder-hand syndrome following hemiplegia, Neurol., 4: 480, 1954. 14) Johnson, E. W. and Pannozzo, A. N.: Management of shoulder-hand syndrome, J. A. M. A., 195: 108, 1966. 15) Russek, H. I.: Shoulder-hand syndrome following myocardial infarction, Med. Clin. N. Amer., 42: 1555, 1958. J. Neurol. Neurosurg. Psychiat., 39: 471, 1976. 19) Pak, T. J., Martin, G. M., Magness, J. L. et al.: Reflex sympathetic dystrophy, Minnesota Med., 53: 507, 1970. 20) Sato, A. and Schmidt, R. F.: Somatosympathetic reflexes: afferent fibers, central pathways, discharge characteristics, Physiol. Rev., 53: 916, 1973.

Abstract Shoulder-Hand Syndrome Following Hemiplegia -1. Vasomotor Disturbances in the Paralysed Upper Extremity- Fumio Eto The shoulder-hand syndrome occurrs in about twenty per cent of patients following hemiplegia, being not a rare complication of cerebrovascular disease and often interfering with stroke rehabilitation process. This syndrome is considered as reflex neurovascular conditions involving the shoulder and hand, but its pathophysiological mechanism is not definitely proved. In early phase of this syndrome the vasomotor changes may be the most characteristic and important phenomenon. The skin temperature and plethysmographic pulse wave height of the paralysed hand is significantly higher in hemiplegics with this syndrome than that in those without it. In most cases with this syndrome the first symptom may develop within three months after onset of Department of Geriatrics, Faculty of Medicine, University of Tokyo, Tokyo, Japan hemiplegia, when some suggestive findings of a significant increase of blood flow in the paralysed hand are observed. The increase of peripheral blood flow in the affected upper extremity of hemiplegic patients is sometimes observed prior to such other symptoms as pain and loss of range of motion in the shoulder and the hand. The reduction of blood flow due to reflex vasoconstriction is observed during local body cooling, which is one of somatosympathetic reflexes. Such a reflex activity is decreased in hemiplegic patients with this syndrome. There seems to be a disturbance of autonomic vasomotor regulation mechanism in peripheral circulation in the affected extremity with the shoulder-hand syndrome. The most important mechanism in pathogenesis of this syndrome following hemiplegia is considered to be associated with vaso motor paralysis due to damage of the central nervous systemabove the spinal cord, especially in the cerebrum.