Support: NIH Grant R01HD059895 Craig H Neilson Foundation
Authors: *L. D. DUFFELL1, M. M. MIRBAGHERI2; 1Univ. Col. London, London, United Kingdom; 2Rehabil. Inst. Chicago, Chicago, IL Disclosures: L.D. Duffell: None. M.M. Mirbagheri: None.
An incomplete spinal cord injury (SCI) results in the partial loss of motor and sensory function below the level of the injury. One secondary consequence is neuromuscular abnormalities causing hypertonia of muscle groups, which are thought to be the result of a combination of intrinsic and reflex-mediated muscle stiffness. Hypertonia commonly affects ankle-joint muscles, which have important roles during gait, however the relationship between hypertonia and gait function remains controversial in people with SCI. Clinical indications of spasticity have been proposed to be unrelated to gait impairment, however these tests do not provide information regarding the origin of spasticity. This study aimed to compare gait function of people with SCI, with and without reflex-mediated hypertonia. This study had IRB approval and 45 subjects with chronic, incomplete SCI were recruited. Neuromuscular properties were assessed with subjects seated in an isokinetic dynamometer with one ankle strapped to a footplate. Ankle position, torque and electromographic (EMG) activity of ankle muscles were measured during a series of passive isokinetic movements to maximum dorsi-flexion (DF) at two velocities: 5 and 100°/sec. Maximum voluntary isometric contractions (MVICs) and active range of motion (AROM) at the ankle joint were also measured. Functional scores (WISCI II) and clinical measures of walking speed (10 meter walk test), endurance (6 minute walk test) and mobility (timed up and go) were assessed. Based on EMG activity during isokinetic DF at 100°/sec, 19 subjects were classified as having reflex-mediated hypertonia (reflex on) and 26 without (reflex off).