Interneuronal pathways play a significant role in the origin of spasticity in spinal cord injury (SCI.). Following SCI, the interruption of key descending spinal pathways results in uncontrolled reflex movements of the legs. These reflex movements consist of coordinated flexion or extension of the hip, knee and ankle in response to specific exteroceptive or proprioceptive cues. We postulate that SCI releases functional interneuronal circuits, making them accessible to afferent inputs. These circuits include interneuronal pathways responsible for the well-know flexion withdrawal reflex, which Is exaggerated in SCI, and the emergence of a novel reflex response, the extensor spasm. Knowledge of the afferent pathways and interneuronal systems responsible for flexor spasms is based on this analogy to the flexion withdrawal reflex. However, there is virtually no information about the origins of extensor spasms in SCI.
Our first aim i s to test whether flexor spasms are peripherally mediated by load-sensitive muscle afferents of the flexors. We postulate that hvperexcitability of the interneuronal pathways associated with load sensitive afferents could produce self excitation, effectively establishing a positive feedback loop. This mechanism would provide an explanation for the prolonged, repetitive muscle activation associated with flexor spasms. We will test this hypothesis in SCI subjects by altering the muscle load during the flexor reflex using muscle stimulation and imposed movements. Effects will be measured using joint torque and electromyographic measurements. For extensor spasms, we hypothesize that the observed motor behavior results from the release of spinal locomotor pathways following SCI. We will test this hypothesis by investigating whether extensor spasms are modulated by afferent information from hip flexors and ankle extensors. Since the proprioceptive hip flexor afferents and group lb ankle extensor afferents play a prominent role in the modulation of locomotion, by analogy we expect to show that extensor spasms are the manifestation of these locomotor reflexes. Extensor spasms will be quantified using a novel apparatus that measures the joint torque response to imposed movement triggers. The principles developed in this study will form the basis for new treatment modalities for spasticity in spinal cord injury.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
1R01NS040901-01
Application #
6232631
Study Section
Special Emphasis Panel (ZNS1-SRB-L (01))
Program Officer
Heetderks, William J
Project Start
2000-09-28
Project End
2005-08-31
Budget Start
2000-09-28
Budget End
2001-08-31
Support Year
1
Fiscal Year
2000
Total Cost
$301,230
Indirect Cost
Name
Rehabilitation Institute of Chicago
Department
Type
DUNS #
068477546
City
Chicago
State
IL
Country
United States
Zip Code
60611
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Garrison, M Kevin; Ng, Alexander V; Schmit, Brian D (2008) Leg sympathetic response to noxious skin stimuli is similar in high and low level human spinal cord injury. Clin Neurophysiol 119:466-74
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Knikou, Maria; Chaudhuri, Debjani; Kay, Elizabeth et al. (2006) Pre- and post-alpha motoneuronal control of the soleus H-reflex during sinusoidal hip movements in human spinal cord injury. Brain Res 1103:123-39
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Deutsch, Katherine M; Hornby, T George; Schmit, Brian D (2005) The intralimb coordination of the flexor reflex response is altered in chronic human spinal cord injury. Neurosci Lett 380:305-10

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