PubMed · 14842083
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W R RUSSELL, E H J SCHUSTER. 1951-06-23. Apparatus for reducing contractures.. https://doi.org/10.1016/s0140-6736(51)92801-2
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Spastic paresis follows chronic disruption of the central execution of volitional command. Motor function in patients with spastic paresis is subjected over time to three fundamental insults, of which the last two are avoidable: (1) the neural insult itself, which causes paresis, i.e., reduced voluntary motor unit recruitment; (2) the relative immobilization of the paretic body part, commonly imposed by the current care environment, which causes adaptive shortening of the muscles left in a shortened position and joint contracture; and (3) the chronic disuse of the paretic body part, which is typically self-imposed in most patients. Chronic disuse causes plastic rearrangements in the higher centers that further reduce the ability to voluntarily recruit motor units, i.e., that aggravate baseline paresis. Part I of this review focuses on the pathophysiology of the first two factors causing motor impairment in spastic paresis: the vicious cycle of paresis-disuse-paresis and the contracture in soft tissues.
In the subacute and chronic stages of spastic paresis, stretch-sensitive (spastic) muscle overactivity emerges as a third fundamental mechanism of motor impairment, along with paresis and soft tissue contracture. Part II of this review primarily addresses the pathophysiology of the various forms of spastic overactivity. It is argued that muscle contracture is one of the factors that cause excessive responsiveness to stretch, which in turn aggravates contracture. Excessive responsiveness to stretch also impedes voluntary motor neuron recruitment, a concept termed stretch-sensitive paresis. None of the three mechanisms of impairment (paresis, contracture, and spastic overactivity) is symmetrically distributed between agonists and antagonists, which generates torque imbalance around joints and limb deformities. Thus, each may be best treated focally on an individual muscle-by-muscle basis. Intensive motor training of the less overactive muscles should disrupt the cycle of paresis-disuse-paresis, and concomitant use of aggressive stretch and focal weakening agents in their more overactive and shortened antagonists should break the cycle of overactivity-contracture-overactivity.
OBJECTIVE: To determine the efficacy of positioning the affected shoulder in flexion and external rotation to prevent contracture shortly after stroke. DESIGN: Prospective, parallel-group, randomized controlled trial. SETTING: Four metropolitan mixed rehabilitation units. PARTICIPANTS: A volunteer sample of 36 subjects (minus 5 dropouts), whose mean age was 68 years and had had their first stroke within the past 20 days. INTERVENTIONS: The experimental group received two 30-minute sessions a day, 5 days a week, for 4 weeks, during which the affected upper limb was placed in maximum comfortable external rotation and 90 degrees of flexion. Both the experimental and control groups received up to 10 minutes of shoulder exercises and standard upper-limb care. MAIN OUTCOME MEASURES: Contracture was measured as the maximum passive shoulder external rotation and flexion of the affected side as compared with the intact side. Measures were taken at 2 and 6 weeks after stroke by an assessor blinded to group allocation. RESULTS: The 30-minute program of positioning the shoulder in maximum external rotation significantly reduced the development of contractures in the experimental group, compared with the control group ( P =.03). The 30-minute program of positioning the shoulder in 90 degrees of flexion did not prevent contractures in the experimental group as compared with the control group ( P =.88). CONCLUSIONS: At least 30 minutes a day of positioning the affected shoulder in external rotation should be started as soon as possible for stroke patients who have little activity in the upper arm.