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OBJECTIVES: I. Assess the ability of patients with and without sensorimotor loss below the thoracic spinal cord injury to execute coordinated whole-limb synergies sufficient for walking with full or partial weight support.
II. Promote weight bearing, balance, and reciprocal leg movement in these patients.
III. Elicit synchronized motor output within and between limbs in these patients.
PROTOCOL OUTLINE: This is a controlled, prospective study. Patients pairs matched for strata are randomly assigned to 1 of 2 treatment groups. Patients are stratified into pairs by age, time since onset, Frankel grade, and Motor Score Index.
One group receives body weight-supported treadmill training immediately after baseline clinical, biomechanical, and physiological measures. The second group is the control; baseline measures are identical but training is delayed for 3 months.
Patients in both groups receive training 3 days/week for 3 months. Initial treadmill velocity is 18 meters/minute; velocity is increased in increments of 6 meters/minute until the maximum speed is achieved at which each patient exhibits the best locomotor capability at full weight bearing. Patients are trained with the minimal weight support assistance necessary for effective limb progression without excessive knee flexion or hyperextension. Polypropylene ankle-foot orthosis is allowed.
Patients are re-tested after maximal treadmill velocity is achieved: following clonidine once a day for 3 days; clonidine twice a day for 3 days; cyproheptadine for 3 days; and an increased dose of cyproheptadine for 3 days. There is a 3-day washout between clonidine and cyproheptadine testing.
Patients are not advanced if they experience adverse cardiovascular effects during therapy. No concurrent therapeutic exercise for the lower extremities is allowed.
Kinematic, temporal, kinetic, spasticity, Frankel grading, Motor Index Score, metabolic, and functional outcome measures are evaluated at 3 and 6 months.
Primary Purpose: Treatment
Spinal Cord Injury
Office of Rare Diseases (ORD)
Published on BioPortfolio: 2014-08-27T03:58:09-0400
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Repair of the damaged neuron function after SPINAL CORD INJURY or SPINAL CORD DISEASES.
A syndrome associated with traumatic injury to the cervical or upper thoracic regions of the spinal cord characterized by weakness in the arms with relative sparing of the legs and variable sensory loss. This condition is associated with ischemia, hemorrhage, or necrosis involving the central portions of the spinal cord. Corticospinal fibers destined for the legs are spared due to their more external location in the spinal cord. This clinical pattern may emerge during recovery from spinal shock. Deficits may be transient or permanent.
Pathologic conditions which feature SPINAL CORD damage or dysfunction, including disorders involving the meninges and perimeningeal spaces surrounding the spinal cord. Traumatic injuries, vascular diseases, infections, and inflammatory/autoimmune processes may affect the spinal cord.
Reduced blood flow to the spinal cord which is supplied by the anterior spinal artery and the paired posterior spinal arteries. This condition may be associated with ARTERIOSCLEROSIS, trauma, emboli, diseases of the aorta, and other disorders. Prolonged ischemia may lead to INFARCTION of spinal cord tissue.
Ischemia or infarction of the spinal cord in the distribution of the anterior spinal artery, which supplies the ventral two-thirds of the spinal cord. This condition is usually associated with ATHEROSCLEROSIS of the aorta and may result from dissection of an AORTIC ANEURYSM or rarely dissection of the anterior spinal artery. Clinical features include weakness and loss of pain and temperature sensation below the level of injury, with relative sparing of position and vibratory sensation. (From Adams et al., Principles of Neurology, 6th ed, pp1249-50)
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