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Biomedical subjects

L A Childs

Publications and source records attributed to L A Childs.

3 recordsLinked to original sources

The association of pain with physical activities in chronic low back pain.

Most patients with chronic low back pain associate strenuous physical activities with increased pain. This association can cause avoidance of those activities believed to cause intolerable discomfort. This study explored the relationship of performance of physical activities with self-reported pain measures in 40 consecutive patients with disabling low back pain (mean duration 17 months) during a functional restoration rehabilitation program (mean treatment period 7 weeks). Evaluations were performed at initial presentation and at program completion. Measures included quantification of performance on eight physical tests assessing flexibility, lifting capacity and endurance. Before physical testing patients were asked to complete a pain analog scale, a quantified pain drawing, and a rating of the pain anticipated to result from the performance of each physical test. Results showed that pain measures did not generally correlate with measured physical performance. At completion of treatment, significant improvement in performance on all physical tests was found, but these were not associated with consistent changes in pain measures. These results demonstrate that subjects with chronic low back pain can increase their physical performance abilities within their same pain experiences. Medical recommendations for subjects' involvement in physical activities should not be based solely on the reported association of pain with those activities.

Adult↗

Complement-dependent toxicity of serum from myasthenic patients to muscle cells in culture.

The toxicity of myasthenic sera to rat myotubes in monolayer culture was examined by measuring the release of [Me-3H]carnitine from pre-loaded cells. In the presence of guinea pig complement, heat-inactivated serum samples from 9 out of 13 myasthenic patients showed clear myotoxicity, in contrast to 0 out of 11 normal controls and 0 out of 6 polymyositis patients. Neither heat-inactivated sera alone nor guinea pig complement sera alone showed myotoxicity. Removal of anti-acetylcholine receptor (anti-AChR) antibodies from a myasthenic serum sample by affinity absorption led to loss of myotoxicity. Myotoxicity of myasthenic sera could, in most cases, be confirmed by light microscopy. These results support the idea that complement-mediated cell damage, initiated by anti-AChR antibodies, contributes to post-synaptic membrane degeneration in myasthenia gravis.

Animals↗