The morphology of the medial gastrocnemius in typically developing children and children with spastic hemiplegic cerebral palsy.

We collected 3D ultrasound images of the medial gastrocnemius muscle belly (MG) in 16 children with spastic hemiplegic cerebral palsy (SHCP) (mean age: 7.8 years; range: 4-12) and 15 typically-developing (TD) children (mean age: 9.5 years; range: 4-13). All children with SHCP had limited passive dorsiflexion range on the affected side with the knee extended (mean+/-1SD: -9.3 degrees +/-11.8). Scans were taken of both legs with the ankle joint at its resting angle (RA) and at maximum passive dorsiflexion (MD), with the knee extended. RA and MD were more plantar flexed (p<0.05) in children with SHCP than in TD children. We measured the volumes and lengths of the MG bellies. We also measured the length of muscle fascicles in the mid-portion of the muscle belly and the angle that the fascicles made with the deep aponeurosis of the muscle. Volumes were normalised to the subject's body mass; muscle lengths and fascicle lengths were normalised to the length of the fibula. Normalised MG belly lengths in the paretic limb were shorter than the non-paretic side at MD (p=0.0001) and RA (p=0.0236). Normalised muscle lengths of the paretic limb were shorter than those in TD children at both angles (p=0.0004; p=0.0003). However, normalised fascicle lengths in the non-paretic and paretic limbs were similar to those measured in TD children (p>0.05). When compared to the non-paretic limb, muscle volume was reduced in the paretic limb (p<0.0001), by an average of 28%, and normalised muscle volume in the paretic limb was smaller than in the TD group (p<0.0001). The MG is short and small in the paretic limb of children with SHCP. The altered morphology is not due to a decrease in fascicle length. We suggest that MG deformity in SHCP is caused by lack of cross-sectional growth.

[1]  Overstretching of sarcomeres may not cause cerebral palsy muscle contracture , 2004, Journal of orthopaedic research : official publication of the Orthopaedic Research Society.

[2]  P D Neilson,et al.  Mechanisms of Muscle Growth Related to Muscle Contracture in Cerebral Palsy , 1989, Developmental medicine and child neurology.

[3]  M. Smeulders,et al.  Myofascial force transmission and tendon transfer for patients suffering from spastic paresis: a review and some new observations. , 2007, Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology.

[4]  Richard L Lieber,et al.  Spasticity causes a fundamental rearrangement of muscle–joint interaction , 2002, Muscle & nerve.

[5]  Jürgen Mitternacht,et al.  MRT-measurements of muscle volumes of the lower extremities of youths with spastic hemiplegia caused by cerebral palsy , 2006, Brain and Development.

[6]  P. Huijing,et al.  Substantial effects of epimuscular myofascial force transmission on muscular mechanics have major implications on spastic muscle and remedial surgery. , 2007, Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology.

[7]  J. Engsberg,et al.  Ankle spasticity and strength in children with spastic diplegic cerebral palsy , 2000, Developmental medicine and child neurology.

[8]  Y. Duval Limitations of This Study , 2019, Because of You: Understanding Second-Person Storytelling.

[9]  P. Cerretelli,et al.  In vivo human gastrocnemius architecture with changing joint angle at rest and during graded isometric contraction. , 1996, The Journal of physiology.

[10]  Peter A Huijing,et al.  Epimuscular myofascial force transmission between antagonistic and synergistic muscles can explain movement limitation in spastic paresis. , 2007, Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology.

[11]  M Gough,et al.  Architecture of the medial gastrocnemius in children with spastic diplegia , 2001, Developmental medicine and child neurology.

[12]  Constantinos N. Maganaris,et al.  Ultrasonographic assessment of human skeletal muscle size , 2003, European Journal of Applied Physiology.

[13]  P. Uvebrant,et al.  HEMIPLEGIC CEREBRAL PALSY AETIOLOGY AND OUTCOME , 1988, Acta paediatrica Scandinavica. Supplement.

[14]  Stuart A Binder-Macleod,et al.  Voluntary muscle activation, contractile properties, and fatigability in children with and without cerebral palsy , 2005, Muscle & nerve.

[15]  A. Vianello,et al.  Functional status of adults with cerebral palsy and implications for treatment of children , 2001, Developmental medicine and child neurology.

[16]  D. Damiano,et al.  Lower‐Extremity strength profiles in spastic cerebral palsy , 1998, Developmental medicine and child neurology.

[17]  C. Maganaris,et al.  Muscle fibre length-to-moment arm ratios in the human lower limb determined in vivo. , 2006, Journal of biomechanics.

[18]  T N Theologis,et al.  Collagen accumulation in muscles of children with cerebral palsy and correlation with severity of spasticity. , 2001, Developmental medicine and child neurology.

[19]  L. Leahey,et al.  Contributing factors to muscle weakness in children with cerebral palsy , 2003 .

[20]  R. Lieber,et al.  Inferior mechanical properties of spastic muscle bundles due to hypertrophic but compromised extracellular matrix material , 2003, Muscle & nerve.

[21]  P Facchin,et al.  Predictors of Independent Walking in Children With Spastic Diplegia , 2000, Journal of child neurology.

[22]  M Gough,et al.  Three-dimensional realisation of muscle morphology and architecture using ultrasound. , 2004, Gait & posture.

[23]  P A Huijing,et al.  Effects of short length immobilization of medial gastrocnemius muscle of growing young adult rats. , 1992, European journal of morphology.