The findings in paediatric obstetric brachial palsy differ from those in older patients: a suggested explanation
Article first published online: 13 FEB 2007
Developmental Medicine & Child Neurology
Volume 42, Issue 3, pages 158–161, March 2000
How to Cite
Vredeveld, J. W., Blaauw, G., Slooff, B. A. C. J., Richards, R. and Rozeman, S. C. A. M. (2000), The findings in paediatric obstetric brachial palsy differ from those in older patients: a suggested explanation. Developmental Medicine & Child Neurology, 42: 158–161. doi: 10.1111/j.1469-8749.2000.tb00063.x
- Issue published online: 13 FEB 2007
- Article first published online: 13 FEB 2007
- Accepted for publication 7th October 1999.
An EMG and nerve-conduction-study protocol has been developed and used in all patients with brachial plexus lesions since 1985. The findings of EMG and nerve-conduction studies in obstetric brachial palsy (OBP) mostly suggest a falsely optimistic prognosis. To analyse this, all subjects were selected with complete avulsion of both roots C5 and C6 and/or complete rupture of the upper trunk verified during operation from a group of 162 infants with OBP (aged 4 to 14 months) and a group of 184 child and adult patients (aged 6 to 74 years) with a traumatic brachial plexus lesion. Fourteen infants, approximately 4 months old, with OBP, and 19 adults (aged 16 to 30 years) met the selection criteria. The infants from the group with OBP had at 4 months a nearly normal recruitment pattern of motor units in the biceps brachii and deltoid muscles, with little or no denervation. However, in the older group with traumatic brachial palsy, the same lesion caused complete denervation of both muscles. From the group with OBP, a third group (N=3) with the same lesion plus an additional lesion of C7 or a rupture of the middle trunk was selected. This additional lesion resulted in nearly complete denervation of both muscles. This means that C7 largely contributes to the innervation of both muscles at the time of birth, but this innervation is lost during later life in normally developing individuals (apoptosis). A central mechanism might be responsible for the clinical palsy and later spontaneous improvement which is always found in the infants with OBP.