Neuromuscular determinants of muscle strength and passive range of motion in men with spastic cerebral palsy

Hussain, Ayser (2013) Neuromuscular determinants of muscle strength and passive range of motion in men with spastic cerebral palsy. Doctoral thesis (PhD), Manchester Metropolitan University.

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Abstract

Spastic cerebral palsy (SCP) relates to a specific movement-related impairment characterised by a velocity-dependent resistance to stretch. Muscle weakness and decreased range of motion (ROM) are characteristics of the paretic limb in individuals with SCP. However, there are no data on the in vivo determinants of strength and ROM in adults with SCP. The aim of the thesis was to examine the factors associated with impaired plantarflexion, maximal voluntary isometric contraction (MVIC) and joint ROM in the paretic limb of physically active men with SCP compared to the contralateral non-paretic limb and individuals without neurological impairment. Passive stiffness, myotendinous junction displacement and ROM of the paretic gastrocnemius medialis (GM) were not different from the control muscles. However, the elastic modulus of the paretic GM was two times stiffer than the control GM muscles. MVIC torque of the paretic plantarflexors was 42% and 52% less than the non-paretic (P = 0.007) and control limbs (P < 0.001), respectively. The paretic gastrocnemius ACSA was 20% smaller than the control group (P = 0.004) only. Paretic agonist activation was 36% and 39% less than the non-paretic (P < 0.001) and control groups (P < 0.001), whereas paretic antagonist coactivation was 3-fold higher compared to the non-paretic (P < 0.001) and control group (P < 0.001). Agonist muscle activation accounted for 57% of variation in paretic plantarflexion MVIC torque (P = 0.007). When accounting for GM architecture, neural properties and moment arm length, no difference in GM specific force was established. Finally when the tendon elastic properties and Young’s modulus were calculated at a standardised force, no difference was observed in tendon stiffness properties across all experimental groups. These findings suggest that in active adults with SCP, weakness is due to a reduction in muscle size and impaired muscle activation. Furthermore, in the presence of no decline in ROM there remained an alteration in the passive elastic properties of the muscle, but not the tendon.