Contracture

Abstract: Background Dupuytren's disease limits hand function, diminishes the quality of life, and may ultimately disable the hand. Surgery followed by hand therapy is standard treatment, but it is associated with serious potential complications. Injection of collagenase clostridium histolyticum, an office-based, nonsurgical option, may reduce joint contractures caused by Dupuytren's disease. Methods We enrolled 308 patients with joint contractures of 20 degrees or more in this prospective, randomized, double-blind, placebo-controlled, multicenter trial. The primary metacarpophalangeal or proximal interphalangeal joints of these patients were randomly assigned to receive up to three injections of collagenase clostridium histolyticum (at a dose of 0.58 mg per injection) or placebo in the contracted collagen cord at 30-day intervals. One day after injection, the joints were manipulated. The primary end point was a reduction in contracture to 0 to 5 degrees of full extension 30 days after the last injection. Twenty-si...

Abstract: Summary It has become increasingly recognized that the major functional deficits following brain damage are largely due to 'negative' features such as weakness and loss of dexterity rather than spasticity. A variety of studies suggest that spasticity is a distinct problem and separate from the loss of dexterity, but that it may be implicated in the formation of muscle contracture and even in the recovery of strength. In order to address these issues, we examined the relationship between spasticity, contracture, strength and dexterity in the affected upper limb following stroke. Spasticity was measured both as increased tonic stretch reflexes and increased resistance to passive stretch (hypertonia). Twenty-four patients were recruited non-selectively from three rehabilitation units within 13 months of their stroke. Few patients exhibited increased tonic reflexes but half were found to have muscle contracture, the earliest at 2 months following stroke. Hypertonia was associated with contracture but not with reflex hyperexcitability. Increased tonic stretch reflexes were observed only in a subgroup of those with contracture and where present could usually be elicited only at the end of muscle range. This finding suggests that instead of spasticity causing contracture, contracture may actually potentiate spasticity in some patients. However, the majority of patients with contracture did not have increased tonic stretch reflexes. In addition, we found no relationship between spasticity and either weakness or loss of dexterity. Therefore, while hypertonia remains an important problem following cerebral lesions, it would appear that the amount of attention directed to reflex hyperexcitability associated with spasticity is out of proportion with its effects. Consequently, hypertonia needs to be clearly distinguished from reflex hyperexcitability in patients with spasticity.

Abstract: 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.

Abstract: 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.