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Protective effect of neural lesion on rheumatoid arthritis To the Editor:In response to a recent letter entitled "Unilateral Rheumatoid Arthritis" by Hammoudeh et al (I), we would like to report a case of seropositive nodular rheumatoid arthritis that developed in a patient with poliomyelitis. We confirmed Hammoudeh's observation that rheumatoid arthritis symptoms do not occur in the paralyzed extremity.A 73-year-old man had a history of poliomyelitis, which developed when he was 3 years old and resulted in a flail left leg. He was first seen by one of us in 1979 after he had developed Raynaud's phenomenon, morning stiffness, and pain in his right knee. Arthritic changes were noted in proximal interphalangeal, metacarpophalangeal, and both wrist joints, and in the knee and metatarsophalangeal joints of the right side. No signs of arthritis could be found in the left leg. Subcutaneous nodules were found on both elbows. Roentgenograms of the hands and right foot showed periarticular osteoporosis; there was an erosion in the first left metacarpophalangeal joint, as well as osteoporosis, atrophy, and thin cortices in the left foot. The patient's rheumatoid factor latex titer was I : 1,280.In September 1981 he developed intermittent claudication of the right leg. Radioisotopic angiography showed nearly complete obliteration of the left common iliac artery and moderate narrowing of the right iliac artery.The effect of hemiplegia on the development of various types of arthritis has been described (2,3). In rheumatoid arthritis the protective effect is seen with both upper and lower motor lesions (43). The mechanism for this protection against the local development of arthritis is not known, although the reduction of movement or disuse of the paralyzed limbs has been proposed as one possible explanation. In studies of capillary resistance, response to cutaneous vasodilators, and temperature gradients, however, no striking differences between the 2 sides (one paralyzed and one nonparalyzed) were shown (4). Glick (6) reported this phenomenon in patients previously paralyzed by poliomyelitis and suggested that decreased intraarticular pressure is an important factor.In patients with nodular rheumatoid arthritis, varying degrees of arterial occlusion have been shown by brachial arteriography. This occlusion seemed to be primarily ,a lesion of the vessel wall. Microvascular disease is also thought to be responsible for the proliferative process that produces rheumatoid nodules or synovial hyperplasia (7,8). However, in 1 patient with rheumatoid arthritis and hemiplegia, uniformly diminished main vessels on the paralyzed side and small vessel occlusions on both sides were shown by arteriography.Our patient had nearly complete obstruction of the iliac artery on the paralyzed side, possibly from atherosclerosis, and retained blood flow fairly well on the nonparalyzed side. These changes in the main vessel blood flow may be associated with the mechanism of the protective effect. However, we believe that in addition to relative i...
Protective effect of neural lesion on rheumatoid arthritis To the Editor:In response to a recent letter entitled "Unilateral Rheumatoid Arthritis" by Hammoudeh et al (I), we would like to report a case of seropositive nodular rheumatoid arthritis that developed in a patient with poliomyelitis. We confirmed Hammoudeh's observation that rheumatoid arthritis symptoms do not occur in the paralyzed extremity.A 73-year-old man had a history of poliomyelitis, which developed when he was 3 years old and resulted in a flail left leg. He was first seen by one of us in 1979 after he had developed Raynaud's phenomenon, morning stiffness, and pain in his right knee. Arthritic changes were noted in proximal interphalangeal, metacarpophalangeal, and both wrist joints, and in the knee and metatarsophalangeal joints of the right side. No signs of arthritis could be found in the left leg. Subcutaneous nodules were found on both elbows. Roentgenograms of the hands and right foot showed periarticular osteoporosis; there was an erosion in the first left metacarpophalangeal joint, as well as osteoporosis, atrophy, and thin cortices in the left foot. The patient's rheumatoid factor latex titer was I : 1,280.In September 1981 he developed intermittent claudication of the right leg. Radioisotopic angiography showed nearly complete obliteration of the left common iliac artery and moderate narrowing of the right iliac artery.The effect of hemiplegia on the development of various types of arthritis has been described (2,3). In rheumatoid arthritis the protective effect is seen with both upper and lower motor lesions (43). The mechanism for this protection against the local development of arthritis is not known, although the reduction of movement or disuse of the paralyzed limbs has been proposed as one possible explanation. In studies of capillary resistance, response to cutaneous vasodilators, and temperature gradients, however, no striking differences between the 2 sides (one paralyzed and one nonparalyzed) were shown (4). Glick (6) reported this phenomenon in patients previously paralyzed by poliomyelitis and suggested that decreased intraarticular pressure is an important factor.In patients with nodular rheumatoid arthritis, varying degrees of arterial occlusion have been shown by brachial arteriography. This occlusion seemed to be primarily ,a lesion of the vessel wall. Microvascular disease is also thought to be responsible for the proliferative process that produces rheumatoid nodules or synovial hyperplasia (7,8). However, in 1 patient with rheumatoid arthritis and hemiplegia, uniformly diminished main vessels on the paralyzed side and small vessel occlusions on both sides were shown by arteriography.Our patient had nearly complete obstruction of the iliac artery on the paralyzed side, possibly from atherosclerosis, and retained blood flow fairly well on the nonparalyzed side. These changes in the main vessel blood flow may be associated with the mechanism of the protective effect. However, we believe that in addition to relative i...
The origin of sympathetic and sensory innervation of the knee joint was investigated by the intra-axonal transport method. After injection of horseradish peroxidase (HRP) or horseradish peroxidase conjugated to wheat germ agglutinin (WGA-HRP) into the knee joint unilaterally in adult rats, labelled neurons were found ipsilaterally both in sympathetic and dorsal root ganglia at the lower thoracic and lumbosacral levels. A maximum of 1500 and 1000 peroxidase-positive cells were observed in the sympathetic and dorsal root ganglia, respectively; in the former they were mainly located at the levels of L2-L4, and in the latter mainly at L3-L5. The functional implications of the above observations are discussed in relation to pain mechanisms in joints and to the earlier hypothesis that a nervous component might be involved in the pathogenesis of chronic joint inflammation.
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