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J Neurophysiol (January 1, 2003). 10.1152/jn.00979.2001
Submitted on Submitted 29 November 2001; accepted in final form 26 July 2002
1Department of Physical Medicine and Rehabilitation and 2Department of Physical and Biomedical Engineering, Northwestern University Medical School, Chicago, IL 60611; 3Sensory Motor Performance Program, Rehabilitation Institute of Chicago, Chicago, Illinois 60611; and 4Department of Biomedical Engineering, Marquette University, Milwaukee, Wisconsin 53201-1881
Hornby, T. G.,
W. Z. Rymer,
E. N. Benz, and
B. D. Schmit.
Windup of Flexion Reflexes in Chronic Human Spinal Cord Injury: A
Marker for Neuronal Plateau Potentials?. J. Neurophysiol. 89: 416-426, 2003. 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 
3 s. For subthreshold stimuli, facilitation of reflexes occurred only at intervals 1 s.
Similarly, the latency of flexion reflexes decreased significantly at
intervals 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
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.
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