Investigating physiological symptoms associated with mental health symptoms in youth with cerebral palsy: An observational study.

Over 50 % of children and youth with cerebral palsy (CP) experience mental health challenges, with anxiety and depression most common. Youth with CP also experience several physiological symptoms such as fatigue, pain, sedentary lifestyle, and sleep disturbances that impact their daily living; however, little is known about the impact of these symptoms on mental health outcomes in these youth. This study addressed this gap and examined the individual and cumulative impacts of physiological symptoms on anxiety and depression symptoms in youth with CP. Forty youth with CP aged 8 to 18 years, and their caregiver, participated in this cross-sectional observational study. Pain, fatigue, anxiety, and depressive symptoms were measured using caregiver- and self-reported questionnaires and participants wore accelerometers for seven consecutive days, providing non-invasive physical activity and sleep pattern data. Youth with CP experienced substantial physiological symptoms and elevated anxiety and depression symptoms. Linear regression models determined that all physiological factors were predictive of caregiver-reported youth anxiety (R2 = 0.23) and youth depressive symptoms (R2 = 0.48). Fatigue, pain severity, sleep efficiency, and physical activity outcomes individually and cumulatively contributed to caregiver-reported youth anxiety and depression symptoms. These findings highlight the important role of physiological symptoms as potential risk factors and potential targets for intervention for mental health issues for in youth with CP.

Associations of hamstring and triceps surae muscle spasticity and stance phase gait kinematics in children with spastic diplegic cerebral palsy.

Clinical decisions on interventions to improve function in children with cerebral palsy (CP) are based, in part, on hypothesized interactions amongst physical signs of CP and functional deficits. However, a knowledge gap exists regarding associations between spasticity and gait function. This study quantified associations of hamstring and triceps surae spasticity with hip, knee and ankle CP gait patterns. This is a cohort study of children and adolescents [n = 51; 31 male; 20 female; spastic diplegia; Gross Motor Function Classification System I (n = 23) and II (n = 28)] who participated in a clinical consult including gait (Motion Analysis, USA) and modified Tardieu scale (MTS) testing (hamstrings, triceps surae). Shape-based clustering was performed on stance phase sagittal hip, knee and ankle patterns using z-normalized and non-normalized data. Linear regression (R, v3.5.0, R Core Team, Austria) was conducted to assess associations between MTS measures and data clusters (α = 0.05). Shape-clustering revealed two hip and three knee and ankle clusters for z-normalized and non-normalized data. Significant associations of hamstring spasticity and joint patterns were observed for z-normalized knee clusters (CKnee A p = 0.002; CKnee B p = 0.006) and interactions amongst non-normalized hip and knee clusters (CHipA:CKnee B p = 0.033). Trends were observed for soleus spasticity and gastrocnemius range of motion angle and non-normalized ankle clusters (CAnkle B p = 0.051; CAnkle B p = 0.053 respectively). Significant associations of early knee extension and hamstring spasticity, observed using shape-clustering of z-normalized data, provide unique information that may inform the identification of individuals most likely to benefit from spasticity management and targets for spasticity management assessment.

Spinal inhibition and motor function in adults with spastic cerebral palsy.

KEY POINTS: Abnormal activation of motoneurons in the spinal cord by sensory pathways is thought to contribute to impaired movement control and spasticity in individuals with cerebral palsy. Here we use single motor unit recordings to show how individual motoneurons in the spinal cord respond to sensory inputs in a group of participants with cerebral palsy having different degrees of motor dysfunction. In participants who had problems walking independently and required assistive devices such as wheelchairs, sensory pathways only excited motoneurons in the spinal cord. In contrast, in participants with cerebral palsy who walked independently for long distances, sensory inputs both inhibited and excited motoneurons in the spinal cord, similar to what we found in uninjured control participants. These findings demonstrate that in individuals with severe cerebral palsy, inhibitory control of motoneurons from sensory pathways is reduced and may contribute to motor dysfunction and spasticity. ABSTRACT: Reduced inhibition of spinal motoneurons by sensory pathways may contribute to heightened reflex activity, spasticity and impaired motor function in individuals with cerebral palsy (CP). To measure if the activation of inhibitory post-synaptic potentials (IPSPs) by sensory inputs is reduced in CP, the tonic discharge rate of single motor units from the soleus muscle was plotted time-locked to the occurrence of a sensory stimulation to produce peri-stimulus frequencygrams (PSFs). Stimulation to the medial arch of the foot was used to activate cutaneomuscular afferents in 17 adults with bilateral spastic CP and 15 neurologically intact (NI) peers. Evidence of IPSP activation from the PSF profiles, namely a marked pause or reduction in motor unit firing rates at the onset of the cutaneomuscular reflex, was found in all NI participants but in only half of participants with CP. In the other half of the participants with CP, stimulation of cutaneomuscular afferents produced a PSF profile indicative of a pure excitatory post-synaptic potential, with firing rates increasing above the mean pre-stimulus rate for 300 ms or more. The amplitude of motoneuron inhibition during the period of IPSP activation, as measured from the surface EMG, was less in participants with poor motor function as evaluated with the Gross Motor Functional Classification System (r = 0.72, P < 0.001) and the Functional Mobility Scale (r = -0.82, P < 0.001). These findings demonstrate that in individuals with CP, reduced activation of motoneuron IPSPs by sensory inputs is associated with reduced motor function and may contribute to enhanced reflexes and spasticity in CP.