Neuromuscular activation and motor-unit firing characteristics in cerebral palsy

Abstract

Muscle strength, neuromuscular activation, and motor-unit firing characteristics (firing rate, recruitment, and short-term synchronization) were assessed during voluntary contractions of the medial gastrocnemius (GAS) and tibialis anterior (TA) muscles of 10 participants with spastic diplegic or hemiplegic cerebral palsy (CP). The participants (six females, four males; age range 6 to 37y) walked with equinus gait at Gross Motor Function Classification System levels II to III. These were compared with 10 age-matched controls (five females; age range 7 to 35y). Neuromuscular activation was estimated by the ratio of surface electromyogram amplitude to M-wave amplitude elicited by supramaximal electrical nerve stimulation. Participants with CP produced significantly less torque (normalized by leg length) compared with controls (TA: mean 2.3, SD 1.6 vs mean 8.9, SD 3.4N m/m; GAS mean 13.7, SD 7.1 vs mean 28.6, SD 5.1Nm/m, p<0.001). Neuromuscular activation during maximum voluntary contraction was significantly reduced in the participants with CP compared with controls (mean 2.4, SD 1.5 vs mean 9.7, SD 2.7Nm/m for TA; mean 1.04, SD 0.41 vs mean 3.1, SD 1.2Nm/m for GAS, p<0.001). When compared at the same submaximal level of neuromuscular activation, motor-unit recruitment and firing rates were not different between the groups, although short-term synchronization in TA was reduced in the participants with CP. These data indicate that weakness, known to be an important component of the motor deficit in CP, has a strong central component. Although the relation between recruitment and firing rate remained substantially intact at the low and moderate force contractions tested, results suggest that the participants with CP were unable to recruit higher threshold motor units or to drive lower threshold motor units to higher firing rates.

Full Activation Profiles and Integrity of Corticospinal Pathways in Adults With Bilateral Spastic Cerebral Palsy

“…People with CP were unable to fully activate all their motor units and submaximal contractions required higher levels of voluntary effort to reach similar degrees of increased motor unit recruitment and firing rates. 4 Taken together with our results, this suggests that in people with CP, voluntary activity must be increased further before the proportion of the spinal motor neuron pool available for activation by TMS reaches a comparable magnitude to that of people without neurologic injuries.…”

“…We do know that following an injury to the developing brain resulting in a disorder of movement and posture, 1 people with spastic CP have muscular weakness 2,3 mediated, in part, by reduced activation of spinal motoneurons. 4-6 While it has long been postulated that damage to descending pathways from the brain that project to spinal motoneurons may contribute to motor impairments in spastic CP, 7 the evidence of this is incomplete. In this study, we used transcranial magnetic stimulation (TMS) to characterize the activation of corticospinal pathways in adults with bilateral spastic CP.…”

Transformational Technologies in Single-Event Neurological Conditions: Applying Lessons Learned in Stroke to Cerebral Palsy (August 14-15, 2008)

“…Gait and upper limb disorders in spastic CP arise from a set of interrelated motor deficits that include loss of selective motor control, muscle weakness, spasticity, short muscletendon length, and joint contracture. 70,71 Mechanisms underlying these motor deficits result from interruption of excitatory and inhibitory motor signals subsequent to a nonprogressive brain injury most commonly in the periventricular white matter around the time of birth. 72 Postural balance deficits also may impair motor function and are associated with lesions in the cerebellum.…”

Biomechanical Modeling of Children with Cerebral Palsy to Establish Recreational Rock Climbing Therapy

“…In patients with CP, type I fiber predominance has been observed and attributed to strong tonic spasticity and the selective recruitment of lower frequency motor units (Ito et al, 1996;Rose et al, 1994). Additionally, patients with CP are unable to fully activate all available motor units compared to age-controlled peers, which in turn impacts their force-generation capabilities leading to muscle weakness (Rose & McGill, 2005;Stackhouse, Binder-Macleod, & Lee, 2005).…”

“…Over time, physiological changes occur as a result of consistently shortened muscle, a state brought about by hypertonia, sedentary habits or immobilization, atrophy, lack of muscle growth in proportion to bone growth, spasticity, or other factors. Muscles working at shortened lengths reduce number of sarcomeres, add connective tissue between fibers that increase resistance to muscle compliance, and decrease the cross-sectional area of the muscle fibers (Farmer & James, 2001;Handsfield et al, 2015;Rose & McGill, 2005;Williams, Catanese, Lucey, & Goldspink, 1988;Williams & Goldspink, 1984). Lack of motion related to symptoms or surgical intervention can thin cartilage between articulated joints and induce ligament disorganization, which can lead to joint pain that discourages further motion that could otherwise reverse this trend (Akeson, Amiel, Abel, Garfin, & Woo, 1987).…”