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Changes to medial gastrocnemius architecture after surgical intervention in spastic diplegia
Author(s) -
Shortland Adam P,
Fry Nicola R,
Eve Linda C,
Gough Martin
Publication year - 2004
Publication title -
developmental medicine and child neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.658
H-Index - 143
eISSN - 1469-8749
pISSN - 0012-1622
DOI - 10.1111/j.1469-8749.2004.tb00979.x
Subject(s) - spastic diplegia , medicine , muscle architecture , aponeurosis , ankle , diplegia , fascicle , gastrocnemius muscle , physical therapy , spastic , cerebral palsy , physical medicine and rehabilitation , anatomy , skeletal muscle
We assessed the architecture of the medial gastrocnemius in nine children (five males, four females; age range 6 to 15 years; mean 10 years 10 months, SD 3 years 6 months) with spastic diplegia by ultrasound imaging before and after a gastrocnemius recession. The children were ambulant (seven independent, one with a posterior walker, one using crutches) before and after surgical intervention. We compared values for fascicle lengths and deep fascicular‐aponeurosis angles with those from a group of normally developing children (five males, five females; age range 6 to 11 years; mean 8 years 4 months, SD 1 year 4 months). Despite a variable interval between assessments (from 56 to 610 days), fascicles were shorter ( p =0.00226) and the deep fascicular‐aponeurosis angle increased ( p =0.0152) after intervention. Fascicle lengths of patients were similar to those in the group of normally developing children before surgery. After surgery, fascicles in the group of children with spastic diplegia were shorter than in their normally developing peers ( p =0.00109). The gastrocnemius recession procedure alters muscle architecture, though the degree of fascicular shortening varied, with four of the participants in our study losing less than 10% of their original fascicular length at maximum dorsiflexion. Increases in ankle‐joint power in walking, observed after surgical intervention in children with spastic diplegia, may be due to a more normal ankle position rather than to improvements in the active mechanical performance of the gastrocnemius.

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