Contribution of muscle afferents to prolonged flexion withdrawal reflexes in human spinal cord injury.

The contribution of force-sensitive muscular afferents to prolonged flexion withdrawal reflexes, or flexor spasms, after human spinal cord injury (SCI) was investigated. In three separate experimental conditions, flexion reflexes were triggered in subjects with SCI using trains of electrocutaneous stimuli delivered at the foot and lower leg and compared with reflexes elicited via intramuscular (i.m.) electrical stimuli. In the first experiment, flexion reflexes were elicited using i.m. stimuli to the tibialis anterior (TA) in the majority of subjects tested. The ratio of peak isometric ankle to hip torques during i.m.-triggered reflexes were proportionally similar to those evoked by electrocutaneous foot or shank stimulation, although the latency to onset and peak flexion torques were significantly longer with i.m. stimulation. In the second experiments, the amplitude and frequency of i.m. TA stimulation were varied to alter the stimulus-induced muscle torque. Peak ankle and hip torques generated during the flexion reflex responses were correlated to a greater extent with stimulus-induced muscle torques as compared with the modulated stimulus parameters. In the third experimental series, i.m. stimuli delivered to the gastrocnemius (GS) elicited flexion reflexes in approximately half of the subjects tested. The combined data indicate a potentially prominent role of the stimulus-induced muscle contraction to the magnitude and latency of flexor reflex behaviors after i.m. TA stimulation. Results after i.m. GS stimulation indicate multi-joint flexion reflexes can also be elicited, although to a lesser extent than i.m. TA stimulation.

Windup of flexion reflexes in chronic human spinal cord injury: a marker for neuronal plateau potentials?

The physiological basis of flexion spasms in individuals after spinal cord injury (SCI) may involve alterations in the properties of spinal neurons in the flexion reflex pathways. We hypothesize that these changes would be manifested as progressive increases in reflex response with repetitive stimulus application (i.e., "windup") of the flexion reflexes. We investigated the windup of flexion reflex responses in 12 individuals with complete chronic SCI. Flexion reflexes were triggered using trains of electrical stimulation of plantar skin at variable intensities and inter-stimulus intervals. For threshold and suprathreshold stimulation, windup of both peak ankle and hip flexion torques and of integrated tibialis anterior electromyographic activity was observed consistently in all patients at inter-stimulus intervals < or =3 s. For subthreshold stimuli, facilitation of reflexes occurred only at intervals < or =1 s. Similarly, the latency of flexion reflexes decreased significantly at intervals < or =1 s. Patients that were receiving anti-spasticity medications (e.g., baclofen) had surprisingly larger windup of reflex responses than those who did not take such medications, although this difference may be related to differences of spasm frequency between the groups of subjects. The results indicate that the increase in spinal neuronal excitability following a train of electrical stimuli lasts for < or =3 s, similar to previous studies of nociceptive processing. Such long-lasting increases in flexion reflex responses suggest that cellular mechanisms such as plateau potentials in spinal motoneurons, interneurons, or both, may partially mediate spinal cord hyperexcitability in the absence of descending modulatory input.