BoNT-A is an effective adjunct to therapy and surgery in managing muscle imbalance, cocontractions, and contractures in neonatal brachial plexus palsy. Use of BoNT-A can result in averting, modifying, or deferring surgical interventions in a number of affected children.

Therapeutic Level IV.

Purpose To determine the impact on families of children with brachial plexus injuries in order to best meet their clinical and social needs. Methods Our cross-sectional study included families with children between the ages of 1 and 18 with birth or non-neonatal brachial plexus injuries (BPI). The consenting parent or guardian completed a demographic questionnaire and the validated Impact on Family Scale during a single assessment. Total scores can range from 0-100, with the higher the score indicating a higher impact on the family. Factor analysis and item-total correlations were used to examine structure, individual items, and dimensions of family impact. Results One hundred two caregivers participated. Overall, families perceived various dimensions of impact on having a child with a BPI. Total family impact was 43. The 2 individual items correlating most strongly with the overall total score were from the financial dimension of the Impact on Family Scale. The strongest demographic relationship was traveling nationally for care and treatment of the BPI. Severity of injury was marginally correlated with impact on the family. Parent-child agreement about the severity of the illness was relatively high. Conclusion Caretakers of children with a BPI perceived impact on their families in the form of personal strain, family/social factors, financial stress, and mastery. A multidisciplinary clinical care team should address the various realms of impact on family throughout the course of treatment. Level of Evidence II Prognostic

Clinicians who work with children with NBPI should consider peer support and coping strategies when promoting the psychosocial functioning of these youth.

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IntroductionBrachial plexus birth injury (BPBI) and cerebral palsy (CP) both cause disabling contractures for which no curative treatments exist, largely because contracture pathophysiology is incompletely understood. The distinct neurologic nature of BPBI and CP suggest different potential contracture etiologies, although imbalanced muscle strength and insufficient muscle length have been variably implicated. The current study directly compares the muscle phenotype of elbow flexion contractures in human subjects with BPBI and CP to test the hypothesis that both conditions cause contractures characterized by a deficit in muscle length rather than an excess in muscle strength.MethodsSubjects over 6 years of age with unilateral BPBI or hemiplegic CP, and with elbow flexion contractures greater than 10 degrees on the affected side, underwent bilateral elbow flexion isokinetic strength testing to identify peak torque and impulse, or area under the torque-angle curve. Subjects then underwent needle microendoscopic sarcomere length measurement of bilateral biceps brachii muscles at symmetric joint angles.ResultsIn five subjects with unilateral BPBI and five with hemiplegic CP, peak torque and impulse were significantly lower on the affected versus unaffected sides, with no differences between BPBI and CP subjects in the percent reduction of either strength measurement. In both BPBI and CP, the percent reduction of impulse was significantly greater than that of peak torque, consistent with functionally shorter muscles. Similarly, in both conditions, affected muscles had significantly longer sarcomeres than unaffected muscles at symmetric joint angles, indicating fewer sarcomeres in series, with no differences between BPBI and CP subjects in relative sarcomere overstretch.DiscussionThe current study reveals a common phenotype of muscle contracture in BPBI and CP, with contractures in both conditions characterized by a similar deficit in muscle length rather than an excess in muscle strength. These findings support contracture treatments that lengthen rather than weaken affected muscles. Moreover, the discovery of a common contracture phenotype between CP and BPBI challenges the presumed dichotomy between upper and lower motor neuron lesions in contracture pathogenesis, instead revealing the broader concept of “myobrevopathy”, or disorder of short muscle, warranting increased investigation into the poorly understood mechanisms regulating muscle length.

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