Knikou M^1-3, Rymer WZ^1-2; ¹Feinberg School of Medicine Northwestern University; ²Rehabilitation Institute of Chicago, Sensory Motor Performance Program, Chicago IL; ³CUNY, The College of Staten Island, Staten Island, NY. m-knikou@northwestern.edu; knikou@mail.csi.cuny.edu; NIDDR.

PURPOSE: The purpose of this research study was to examine the modulation of the soleus H reflex following static changes in the hip joint angle in persons with complete spinal cord injury (SCI). Changes in reflex latency and duration were also determined. SUBJECTS: Seven persons with complete paraplegia participated in the present study. IRB was approved from the local ethics committee. METHODS: The soleus H reflex was evoked by electrical stimulation of the right posterior tibial nerve at the popliteal fossa, using a 1 ms rectangular pulse triggered once every 10 s. The anode (a stainless steel plate, 4×4 cm²) was positioned just above the patella. With the leg brace secured to the limb, the hip joint could be moved passively by the experimenter in the sagittal plane. The H reflex recorded with the hip positioned at 10° of flexion constituted the control reflex (or Ho). Reflexes recorded with the hip positioned at 30° and 40° of flexion and at 10° of extension were considered as the conditioned reflexes (Hcond). ANALYSIS: The conditioned H reflexes were expressed as percentages of the mean size of the Ho recorded with hip positioned at 10° of flexion. One-way analysis of variance (ANOVA) was applied to the data. When statistical significance was encountered, post hoc Bonferroni tests for multiple comparisons were performed to determine at which hip angle the conditioned reflex was different. The latency and the duration of the M waves and of the H reflexes were also determined using customized written software. RESULTS: Hip extension to 10° resulted in facilitation of the H reflex with the Hcond size to range from 130 ± 3.4 to 200 ± 8.7 % of the Ho. Furthermore, the H reflex reached an overall amplitude of 70 ± 8.1% of Ho at 30° of hip flexion, while for 40° of hip flexion the reflex reached an amplitude of 65 ± 9.4 % of Ho (P < 0.05). In addition, reflex latency was found to be prolonged (by 1.3 ms) following inhibitory conditioning (hip flexion) and to be shortened (by 0.98 ms) following facilitatory conditioning (hip extension). Reflex duration appeared to be modulated inversely to the reflex latency. CONCLUSIONS: Changes in hip angle can powerfully modulate spinal reflex excitability in persons with SCI, promoting a switch between inhibitory and facilitatory pathways that depend primarily on spinal segmental mechanisms. These actions could possibly underlay the extensor spasms that are prevalent in many persons with SCI.

"Reprinted from CLINICAL NEUROPHYSIOLOGY, V113:1698-1708, Knickou M et al: "Hip angle induced ...", Copyright (2002), with permission from the International Federation of Clinical Neurophysiology."

Some of the above material have been presented at the Annual Meeting of the Society for the Neural Control of Movement, Naples, FL, USA, April 16-21, 2002 and all have been published: Maria Knikou and William Zev Rymer (2002) Hip angle induced modulation of H reflex amplitude, latency and duration in spinal cord injured humans. Clinical Neurophysiology, November 113; 11: 1698-1708.

Copyright 2004 by the American Physical Therapy Association

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