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Findings: Marked joint space narrowing, extensive osteoporosis with thin tubular diaphyseal structures. Additionally, there is muscle atrophy of the lower leg.
Diagnosis: Neuromuscular arthropathy secondary to poliomyelitis.
Discussion: Poliomyelitis is caused by an enterovirus termed the poliovirus. The virus has an affinity for the central nervous system, which it reaches by crossing the blood brain barrier. Motor neurons are particularly vulnerable to infection and destruction.1
Musculoskeletal manifestations of polio include osteoporosis, soft tissue atrophy, growth disturbances, joint infections and synovitis.
As seen in this case, osteoporosis is a profound effect of this disease. Its etiology is thought to be similar to that which follows muscular inactivity with long-standing immobilization.
Muscle atrophy and growth disturbances are also felt to be the result of decreased activity. Premature closure of the growth plate is a well known sequelae of poliomyelitis. This is felt to be the result of angular deformity with muscular and osseous weakening. Joint infections are due to immobilization with subsequent skin breakdown over pressure points.
The disease process is different from that seen in neuroarthropathic changes. In such diseases there is a loss of deep sensation and proprioception which results in relaxation and hypotonia of supporting structures. This leads to recurrent injury with malalignment and subsequent erosions of the subchondral surface, subchondral sclerosis, fractures and fragmentation of cartilage. Eventually with loss of a large portion of the chondral coat, sclerosis can become extreme and bony shards can dissect along tissue planes. The causes of neuroarthropathy are numerous. A Charcot joint which is the manifestation of the above changes is very typically seen as a result of diabetes mellitus.
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