Relative contributions of neural mechanisms versus muscle mechanics in promoting finger extension deficits following stroke.

The origins of impaired finger and hand function were examined in 10 stroke survivors with chronic spastic hemiparesis, with the intent of assessing whether mechanical restraint or altered neurophysiological control mechanisms are responsible for the well-known impairment of finger extension. Simultaneous extension of all four metacarpophalangeal (MCP) joints of the impaired hand was either externally imposed using a rotary actuator or attempted voluntarily by the subject. Trials were conducted both before and after administration of a local anesthetic, blocking the median and ulnar nerves at the elbow. The anesthetic was administered to reduce the activity of the muscles flexing the MCP joints, in order to distinguish mechanical from neuronal resistance to imposed MCP rotation. We found that the nerve blockade resulted in a reduction in velocity-dependent torque (P = 0.01), thereby indicating significant joint impedance due to spasticity. Blockade also produced a posture-dependent reduction in static torque in declaratively relaxed subjects (P = 0.04), suggesting some tonic flexor activity for specific hand postures. No change in either extensor isometric (P = 0.33) or isokinetic (0.53) torque was apparent, but 3 of the 10 subjects did exhibit substantial (>10 degrees ) improvement in voluntary MCP extension following the blockade. This improvement seemed largely due to a decrease in inappropriate flexor activity during the movement, rather than an increase in extensor activity. We argue that persistent and inappropriate flexor activation plays a role in limiting voluntary finger extension, and that this activation is potentially a reflection of altered supraspinal control of key spinal pathways. In all cases, this inappropriate activation was compounded by weakness, apparent in both the extensor and flexor muscles.