What are the primary causes of contractures?

Primary Causes of Contractures

Contractures develop primarily from three mechanisms: prolonged immobilization with static positioning, muscle weakness preventing full active range of motion, and spasticity following upper motor neuron injury.

Neurological Causes

Stroke and Upper Motor Neuron Injury

• Stroke is the leading cause of unilateral contractures, particularly affecting the hemiplegic side where patients fail to recover functional hand use 1
• Disruption of upper motor neuron inhibitory pathways by stroke, brain trauma, or spinal cord injury leads to muscle spasticity, which is characterized by increased muscle tone, hyperactive reflexes, and possible clonus 2
• The presence of spasticity within the first 4 months post-stroke strongly predicts elbow contracture development within the first year 1
• Increased muscle tone from spasticity results in loss of joint motion, ultimately leading to fixed contractures 2

Neuromuscular Disease

• Progressive neuromuscular diseases, particularly dystrophic myopathies with excessive fibrosis and fatty infiltration into muscle, commonly cause contractures 3, 4
• Severe neuromuscular conditions resulting in significant weakness and wheelchair reliance (such as spinal muscular atrophy) frequently develop contractures 4
• Profound generalized weakness limits antigravity movement, preventing achievement of full active range of motion 3

Biomechanical and Pathophysiological Mechanisms

Muscle Weakness and Imbalanced Forces

• Less than antigravity strength produces inability to achieve full active range of motion, leading to static positioning of limbs (generally in flexion) and lack of weight bearing 4
• Imbalanced weakness across joints leads to alterations in posture and compensatory movement patterns 3
• With severe early weakness, the unopposed influence of gravity has the most profound effect on positioning and contracture development 3
• Persistent use of compensatory movement patterns over time leads to biomechanical disadvantage, contracture, and deformity, resulting in increasing weakness and disability 3

Immobilization-Induced Changes

• Prolonged immobilization causes pathological muscle changes including disuse skeletal muscle atrophy and skeletal muscle tissue fibrosis 5
• Proteolytic pathways involved in disuse muscle atrophy include the ubiquitin-proteasome-dependent pathway, caspase system, matrix metalloproteinase pathway, Ca2+-dependent pathway, and autophagy-lysosomal pathway 5
• Skeletal muscle fibrosis develops through intermuscular connective tissue thickening caused by transforming growth factor-β1 and anaerobic environments within skeletal muscle inducing hypoxia-inducible factor-1α 5
• Prolonged immobility may lead to contractures, orthopedic complications, or pressure palsies 3

Secondary Causes

Spasticity-Related Contractures

• Upper extremity contractures in spastic patients may result from muscle spasticity, secondary muscle contracture, or joint capsular contracture 6
• Lack of functional hand use following neurological injury is a significant risk factor for contracture development 1

Disease-Specific Factors

• Anterior capsular fibrosis and contracture occurs more frequently in conditions such as pseudoexfoliation syndrome, retinitis pigmentosa, diabetes, uveitis, and eyes with zonular pathology (in the context of ocular contractures) 3
• Myopathy from glycogen accumulation in muscle (as in Pompe disease) leads to compromised muscle function and progressive weakness, with imbalanced weakness across joints contributing to contracture development 3

Critical Clinical Pitfalls

• Contractures can be mistaken for active spasticity, but they represent fixed tissue changes rather than dynamic muscle activity 1
• Treatment of established contractures is difficult; prevention through joint mobilization should be emphasized as a primary goal in managing patients at risk 2
• Overlooking early signs of contracture development can lead to permanent disability and functional limitations 1