Whether joint receptors contribute demonstrably to proprioception has remained uncertain. Therefore, we tested whether an articular contribution to movement sense could be revealed if the total sensory input available to signal joint movement were reduced by eliminating movement signals from muscles. With a reduced sensory input, whatever contribution articular receptors made to proprioception ought to assume a greater-than-normal importance, and any effect of eliminating articular inputs should become more apparent. The distal interphalangeal joint of the middle finger was used, because the muscles could be decoupled from this joint by positioning the fingers to slacken the tendons. To further enhance the possibility for observing an effect of eliminating articular contributions, we planned to test movement sense at positions of the joint in which the articular receptors would be most active. However, the response properties of receptors in primate finger joints were unknown, so we examined activity of receptors in finger joints of monkeys prior to testing humans. Activity of receptors in interphalangeal joints of monkeys was measured over a wide range of positions before and during local anesthasia of the joint. Little response was seen over intermediate positions, but activity increased as the joint approached full flexion of full extension in much the same manner as responses previously observe with receptors in the knee, elbow, wrist, and hip joints. Local anesthetic injected into the joint space abolished the nerve activity. Proprioception was tested in humans before and during local anesthesia of the joint using a movement-detection paradigm. The joint was rotated 10° at different velocities into either flexion or extension from a base-line position near maximum extension, a position which articular receptors should be active. Joint anesthesia produced a modest but statistically significant impairment in subjects' ability to detect the displacements compared to the unanesthetized condition. The anesthesia also produced slight numbness in the fingertip with several subjects. Four additional subjects were tested with only the skin of the figertip slighly numbed to check whether the impairment seen with joint anesthesia might have been due to numbing of the skin. No impairment was seen during anesthesia of the fingertip alone. Therefore, we conclude the anesthetic block of articular receptors can produce a deficit in joint movement sense. However, considering the deficit was modest and required a reduced sensory input to be observed, we concluded that articular receptors likely contribute little if anything to normal proprioception. After completion of the above tests, we received a report of a similar experiment by Ferrell et al. They found a reduction in performance as a result of joint anesthesia about fourfold greater than what we saw suggesting that joint receptors can play an important role in proprioception. In an attempt to resolve this disparity, we repeated our experiment using a protocol similar to theirs. We found a modest but nonsignificant decrease in performance scores with this protocol.
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