Abnormal development of biceps brachii phasic stretch reflex and persistence of short latency heteronymous reflexes from biceps to triceps brachii inspastic cerebral palsy

Co-contraction of antagonist muscles is characteristic of spasticity arisin g from perinatal brain damage but not in spasticity occurring after brain d amage in adulthood. Such co-contraction is a normal feature of early post-n atal motor development. Heteronymous, monosynaptic Group Ia projections fro m biceps brachii to both the antagonist triceps brachii and to other synerg ist and non-synergist muscles of the upper limb occur in the newborn baby a nd become restricted during the first 4 years to motor neurons of primarily synergistic muscles. Longitudinal and cross-sectional studies have been pe rformed to test the hypothesis that inappropriate heteronymous excitatory p rojections persist in children with perinatal brain damage who develop spas ticity. Subjects with spasticity, from brain damage acquired in adulthood w ere also studied to determine if these projections simply become unmasked a s part of spasticity, independent of the age of occurrence of the brain dam age. Twenty-nine healthy newborn babies and 29 at high risk for cerebral pa lsy, 12 of whom developed spastic quadriparesis, were studied longitudinall y for 4 years. Thirty-eight subjects, aged 8-30 years, with spasticity of p erinatal origin (11 hemiplegic, 11 quadriplegic, 16 with Rett syndrome) and 11 subjects with stroke in adulthood and spastic hemiplegia were also stud ied. The results were compared with those obtained in 372 normal subjects a ged from birth to 55 years. Small taps were delivered to the tendon of bice ps brachii using an electromechanical tapper. Surface EMG was recorded from biceps and triceps brachii, pectoralis major and deltoid. In the longitudi nal study, those developing spastic quadriparesis showed persistent low thr esholds for the homonymous phasic stretch reflex, which had abnormally shor t onset latencies. There was persistence of short onset heteronymous excita tory responses in triceps brachii, while a normal pattern of restriction of heteronymous responses to pectoralis major and deltoid occurred. The same pattern was observed in older subject groups with spasticity of perinatal o rigin. In adults with hemiplegia following stroke the threshold of the homo nymous phasic stretch reflex was low, but it had a normal onset latency. Th ere was no evidence of abnormal heteronymous excitatory responses. In concl usion, exaggerated excitatory responses to primary muscle afferent input we re observed in the homonymous (biceps brachii) and antagonist (triceps brac hii) motor neurons in subjects with spasticity arising from perinatal brain damage. They are likely to play an important role in the predominant co-co ntraction of agonist/antagonist muscles during voluntary movement observed in subjects with spastic cerebral palsy.