Neural mechanisms of kinesthesia
Our primary interest is in where the signals for position and movement of the limbs originate and how the information is encoded. Humans can independently sense the positions and movements of their limbs in the absence of vision, and their senses are derived from mechanoreceptors located in the limbs. Receptors in muscles, skin and joints are potential sources of position and movement signals, but how (and whether) each of these groups contributes to kinesthesia remains uncertain. Recent evidence indicates that a sense of static-position derives from length receptors in muscle, whereas receptors in the skin, and possibly though not likely the joints, can signal movement of a limb but not its static position. At present, we are examining the consequences of not having a static-position sense at the fingers apart from an inability to detect very slow displacements. Using a more demanding test, we have found no substantial difference in the accuracy of reproducing target positions passively imposed on the MCP joint and the proximal interphalangeal (PIP) joint of the index finger. Our working hypothesis is that subjects normally use movement sense mechanisms to detect displacements, probably because they are faster, but how (or whether) subjects manage to obtain an absolute position reference with only a movement sense available remains unknown and is an issue under investigation.