Publication Date

2011-12-05

Availability

Open access

Embargo Period

2011-12-05

Degree Type

Dissertation

Degree Name

Doctor of Philosophy (PHD)

Department

Physical Therapy (Medicine)

Date of Defense

2011-07-18

First Committee Member

Edelle C. Field-Fote

Second Committee Member

Kathryn E. Roach

Third Committee Member

Christine K. Thomas

Fourth Committee Member

T. George Hornby

Abstract

Spinal cord injury (SCI) manifests signs of spasticity, plantar flexor (PF) hyperreflexia and ankle clonus, and deficits in motor function. In individuals with motor-incomplete SCI (MISCI), ankle clonus may limit independent walking function. Ankle clonus is attributed to enhanced soleus stretch reflex (SSR) excitability due to decreased supraspinal input and maladaptive reorganization of spinal reflex circuitry. We explored these questions: 1. What are the biomechanical, clinical, and neurophysiologic correlates of ankle clonus? 2. Does locomotor training improve ankle clonus and walking function? 3. Will operant conditioning-based interventions that increase tibialis anterior activation or decrease soleus reflex excitability improve ankle motor control and walking function? In Chapter 2 we compared Ankle Clonus Drop Test (Drop Test) measures with clinical and neurophysiologic measures. Drop Test measures were highly reliable and exhibited moderate to strong correlations with clinical and neurophysiologic measures. Analysis of EMG activity during clonus revealed a predominant pattern of antagonist coactivation. In Chapter 3 we investigated the effects of locomotor training on PF and quadriceps spasticity, and walking function. We assessed responsiveness of the PF reflex threshold angle, a Drop Test measure of PF spasticity. PF and quadriceps spasticity decreased after locomotor training and were moderately correlated with increased walking speed. The PF reflex threshold angle measure discriminated between individuals with and without clonus. In Chapter 4 we compared the effects of two operant-conditioning based interventions to, (1) increase TA EMG activation (TA↑) and (2) decrease SOL H-reflex amplitude during active dorsiflexion (SOL↓), on reflex modulation, ankle motor control, and walking function. Each intervention improved walking function; however, modulated the variables in unique ways. TA↑ improved deficits of strength and range of motion, and SOL↓ improved modulation of SSR and SOL/TA coactivation. In Chapter 5 we discussed implications of our conclusions: (1) Drop Test ankle clonus measures are valid, reliable, and responsive; (2) antagonist coactivation was predominant during ankle clonus; (3) in individuals with chronic MISCI, locomotor training decreased PF and quadriceps spasticity and improved walking function; and (4) an operant conditioning-based intervention to either increase TA strength or decrease SOL reflex excitability improved spinal reflex modulation and walking function.

Keywords

plantar flexor spasticity; ankle clonus; reflex modulation; EMG activation; operant conditioning; spinal cord injury

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