Structural and mechanical alterations in spastic skeletal muscle

Abstract

Spasticity, a neurological problem secondary to an upper motor neuron lesion, has a significant effect on skeletal muscle. The upper motor neuron lesions may be secondary to a cerebral vascular accident, head injury, spinal cord injury, or degenerative diseases such as multiple sclerosis, or perinatal brain injuries such as cerebral palsy. Functional ability in these patients can be severely compromised but the basic mechanisms underlying these deficits are not clearly understood. In this review we evaluate the current evidence in the literature that suggests that skeletal muscle tissue itself is altered in spastic conditions. Experimental studies were evaluated that included a variety of methods encompassing joint mechanics, tissue mechanics, and muscle morphology. Taken together, the literature strongly supports the assertion that 'spastic muscles’are altered in a way that is unique among muscle plasticity models and inconsistent with simple transformation due to chronic stimulation or disuse. Further studies are required to detail the intra‐ and extracellular modifications of skeletal muscle that occur secondary to spasticity so that novel therapeutic treatments can be developed for this impairment.

The role of co-activation in strength and force modulation in the elbow of children with unilateral cerebral palsy

“…One of the most frequently used definitions of spasticity defines it as ''a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex'' (Lance, 1980), and spasticity is typically measured as resistance to passive movement. However, it is generally accepted that the resistance felt during passive muscle stretch includes both passive and active muscular components that are changed in a spastic muscle (Foran et al, 2005). This makes it challenging to differentiate between what is ''true'' spasticity and what might be structural changes, by studying resistance only.…”

A Critical Evaluation of the Updated Evidence for Casting for Equinus Deformity in Children with Cerebral Palsy

“…Although not fully elucidated, emerging evidence suggests that contracture formation is a highly multifactorial process, with neural and muscular factors (Barrett and Lichtwark, 2010), as well as endocrinal, nutritional and mechanical influences all proposed to play a significant role (Gough and Shortland, 2012). The presumption that contractures are due to reduced muscle fibre length and number of in-series sarcomeres has been challenged (Foran et al, 2005), with inconsistent findings in the few studies that have directly evaluated fibre length in individuals with spastic CP (Barrett and Lichtwark, 2010). While Mohagheghi et al (2008) found significant shortening of fascicle length in the gastrocnemius of children with diplegic CP, several others did not (Shortland et al, 2002;Malaiya et al, 2007;Barber et al, 2011), suggesting that atrophy and shortening may result from a reduction in muscle fibre diameter.…”

Muscle rupture caused by exacerbated spasticity in a patient with multiple sclerosis

“…Furthermore, composition of ECM is changed and has an elasticity modulus which is only 1/40 that of the ECM in unaffected musculature. For these reasons, spasticity affects not only active movements but also results in inferior mechanical properties [4,6,11,12].…”