Recovery potential after postnatal shoulder paralysis. An animal model of neonatal brachial plexus palsy.

摘要: Background: Injury to the brachial plexus during birth results in paralysis of upper extremity as many one 250 births and can lead substantial functional deficits shoulder. The goal this study was characterize development bone joint deformities paralyzed neonatal shoulders assess improvement these after muscle function recovery with use an animal model. Methods: Intramuscular injections botulinum toxin were used paralyze supraspinatus, infraspinatus, posterior deltoid left mice at birth. Seventy divided into three groups: Botox, recovery, normal. twenty-five Botox group received until they killed. twenty for different durations then allowed injection-free periods normal saline solution Radiographs measure shoulder elbow contractures. Microcomputed tomography examine anatomical parameters supraspinatus muscle, humerus, scapula. Results: showed including delayed mineralization flattening humeral head, hypoplasia, introversion (i.e., anteversion) contractures elbow, hypoplasia muscles, scapula, retroversion glenoid. In group, a significant trend toward properties observed longer (p < 0.05). However, only soft-tissue resolved completely longest period. Conclusions: This mouse model successfully simulates human palsy, reproducing most found condition. started develop early postnatal period progressed paralysis. Early restoration elbow. osseous humerus scapula never completely. These findings demonstrate time-dependence reversibility musculoskeletal developing neurological deficits. Clinical Relevance: information provides basis further mechanisms factors influencing upper-extremity development.