Blink Reflex in Cerebral Palsy: Evaluation of Late Components in Patients With Normal Auditory Brainstem ResponsesDepartment of Developmental Disorders National Institute of Mental Health, National Center of Neurology and Psychiatry, Chiba
Department of Developmental Disorders National Institute of Mental Health, National Center of Neurology and Psychiatry, Chiba
Division of Child Neurology Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago
Division of Child Neurology National Center Hospital for Mental, Nervous and Muscular Disorders, National Center of Neurology and Psychiatry, Tokyo, Japan
Division of Child Neurology National Center Hospital for Mental, Nervous and Muscular Disorders, National Center of Neurology and Psychiatry, Tokyo, Japan The electrically elicited blink reflex was examined and evaluated quantitatively in 60 controls and seven patients with cerebral palsy due to perinatal asphyxia who exhibited normal auditory brainstem responses. In the controls, the early component (R1) latency changed slightly from infancy to adulthood, and the late component (R2 and R2') latencies decreased to adult values by 4 to 6 years of age. The electromyographic activity of R2 and R2' increased later and became mature in the young adolescent period. Prolonged R2 latency and decreased R2 amplitude were observed more frequently than R1 abnormalities in the patients. The electromyographic activity of R2 in the patients was lower than that in control subjects more than 13 years old. Almost all patients showed bilateral cerebral atrophy and dilated lateral ventricles, but only one patient exhibited distinct pontine atrophy on cranial computed tomographic scan. These electrophysiologic abnormalities suggest that decreased excitability of intemeurons of the reflex arc was present in the patients, particularly in older ones. The blink reflex test seems to be more sensitive than the auditory brainstem response for detecting brainstem dysfunction in patients with cerebral palsy due to neonatal asphyxia. (J Child Neurol 1996;11:205-209).
Journal of Child Neurology, Vol. 11, No. 3,
205-209 (1996) |
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||

