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Double nerve transfer for restoring external rotation of the glenohumeral joint after neonatal brachial plexus injury
Author(s) -
Soldado Francisco
Publication year - 2020
Publication title -
microsurgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.031
H-Index - 63
eISSN - 1098-2752
pISSN - 0738-1085
DOI - 10.1002/micr.30616
Subject(s) - medicine , brachial plexus , brachial plexus injury , external rotation , shoulder joint , reinnervation , surgery , scapula , motor nerve , anatomy , anesthesia
The probability of spontaneous recovery of shoulder external rotation in neonatal brachial plexus injury (NBPI) is very low after the age of 18 months. We report the outcomes of double nerve transfers to restore active external rotation of the glenohumeral joint in children with NBPI after this age. Patients and methods Retrospective analysis of 20 children of mean age of 23.8 months with a mean follow‐up of 14.8 months. Inclusion criteria were: age > 18 months, full passive glenohumeral external rotation in abduction, and absence of severe joint deformity on MRI. The spinal accessory nerve was transferred to the infraspinatus motor branch and the long head of the triceps motor branch to the teres minor motor branch. Anterior shoulder release was associated when passive shoulder external rotation in adduction (pERADD) was <30° ( n = 13, Group R vs. Group N‐no release n = 7). Active shoulder elevation and external rotation in abduction (aERABD) of the glenohumeral joint were evaluated pre‐ and postoperatively. Results All children except two in Group R, recovered aERABD 4–6 months after surgery. Mean postoperative aERABD was 70 ± 32.4 and 82.9 ± 11.1° and shoulder elevation gain was 24.6 ± 22.2 and 27.1 ± 29.2° for Group R and N, respectively, without statistically significant differences. Conclusions Late nerve transfers to external rotator muscles are effective in children with NBPI. This might be explained not only by muscle reinnervation, but also by the interruption of a previous co‐contraction or developmental apraxia. Level of evidence Therapeutic IV.

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