Decreasing Spasticity with Intensive Locomotor Training in Para- and Quadriplegic Patients

Elena Yu. Shapkova
Dept. Kinesiology/Penn State University and Childrens Surger

Ekaterina V. Starodub
Childrens Surgery Clinic, Institute of Phtysiopulmonology

Andrew Pershin
Childrens Surgery Clinic, Institute of Phtysiopulmonology

Svetlana A. Kuklina
Childrens Surgery Clinic, Institute of Phtysiopulmonology

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     Last modified: March 1, 2007

Abstract
Our program of locomotor recovery for patients with vertebrogenic paralysis routinely included electrostimultion of the midlumbar enlargement resulting in rhythmic alternating leg movements (40-90 min/day); the ?propriospinal? stimulation: air-stepping in a parachute system evoked by rhythmic arm movements imitating walking and running (15-30min/day), the treadmill training with partial body weight support (30-40%, 30-40 min/day), tetrapedal walk and kneeling (30-60 min/day or more), and training of vertical posture with a rhythmic displacement of the center of mass in either frontal or sagittal plane (the parachute system without unloading, 20-40 min/day). The total time of passive, simulation-evoked and self-induced motor activity was about 4-8 hours a day depending on the age and functional ability of the patients and stage of rehabilitation. The course of training lasted for 6-10 weeks. In most spastic patients (initial spasticity of 2-3 points on the Ashworth scale), during the course of training we observed a temporary increase in spasticity (up to plus one point on the Ashworth scale) during the first week and its smooth decrease over the next 4-6 weeks up to a level 1-2 points less than the initial level. The spasticity decrease continued for about 3-4 months after the training course ended. No antispastic drugs or other special therapy was used for these patients. We ascribe this effect to the intensive locomotor training. In 5 patients (age 10-19) with high spasticity (4-5 on the Ashworth scale) such training during 4 weeks did not improve spasticity, which limited the treadmill training and disturbed the night sleep. For these patients we additionally used pharmacological locomotor and antispasticity stimulation with combination of clonidine (alfa2-noradrenergic agonist) and cyproheptadine (serotonergic antagonist) following a scheme of Fung et al (1990). Four of these patients showed a 1-2 point decrease in spasticity and one patient recovered the physiological muscle tone. At the end of the course all patients demonstrated improved locomotor and postural capabilities: facilitation and an increase of the step length, higher velocity and distance of treadmill and tetrapedal walk, as well as improved duration and stability of supported standing. All patients needed less help. The patients with incomplete paralysis increased muscle force during voluntary leg muscle contractions. Our experience shows that intensive locomotor training decreases spasticity and improves locomotor ability and force of voluntary leg muscle contraction in paraplegic patients. In cases of strong spasticity additional pharmacological treatment with clonidine and cyproheptadine gives good results.