Trunk and leg growth in children with paraplegia caused by spinal cord injury

Duval-Beaupère, G; Lougovoy, J.; Trocellier, L; Lacert, P

doi:10.1038/sc.1983.58

Cited by 12 publications

(9 citation statements)

References 20 publications

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“…The mean growth defects of children with myelomeningocele are of the same order of magnitude as those of patients with paraplegia caused by spinal-cord injury (Duval-Beaupere et al 1983) or damage to anterior horn cells as may occur in poliomyelitis (Duval-Beaupere and Soulignac 1975). Although paralysis may extend to the trunk in victims of neurological level of paralysis Fig.…”

Section: Discussionmentioning

confidence: 92%

Growth of Trunk and Legs of Children With Myelomeningocele

Duval-Beaupère¹,

Kaci²,

Lougovoy

et al. 1987

Develop Med Child Neuro

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SUMMARY Total body length and body segments (crown‐rump length, sub‐ischeal length) of 78 children with myelomeningocele were measured at regular intervals during growth for a mean duration of 4‐4 years. These children were shown to have defective growth, with an increased upper segment/lower segment ratio. It was found that the higher the level of the meningocele the greater the growth defects. However, the relationship was statistically significant only for the first seven years of life. It is concluded that neurological damage was mainly responsible for defective growth during the first years of life, but that other factors independent of the level of the meningocele also come into play in later years. RÉSUMÉ L'étude conceme les valeurs anthropométriques de longueur couche et de segments de 78 sujets atteints de myelomingocele mesurés régulièrement au cours de la croissance pendant une durée moyenne de 4 ans et demi. II est mis en evidence un defaut de croissance avec augmentation du rapport segment supérieur, segment inférieur. Plus le niveau myèlomérique des paralysies est haut, plus de défaut de croissance est important: mais cette corrélation n'est statistiquement significative que jusqu'a l'âge de 7 ans. Des tables de prédictions sont proposées pour ces classes d'âge. Les auteurs concluent que si l'atteinte neurologique est le principal responsable des défauts de croissance dans les 7 premières années de la vie, d'autres facteurs indépendants du niveau lésionnel interviennent ensuite en plus ou en moins et masquent alors le rôle persistant de l'extension paralytique. ZUSAMMENFASSUNG Wachstum von Rumpf und Beinen bei Kindern mil Myelomeningocele Bei 78 Kindern mit Myelomeningocele wurden während der Wachstumsphase in regelmäßigen Abständen, im Mittel über 4‐4 Jahre, die Gesamtkörperlange und Körpersegmente (Scheitel‐Steiß‐Länge, sub‐ischeale Länge) gemessen. Je höher die Meningocele lokalisiert war, desto größer war die Wachstumsverminderung. Diese Relation war jedoch nur in den ersten sieben Lebensjahren signifikant. Die Autoren vertreten die Meinung, daß in den ersten sieben Jahren hauptsächlich die neurologische Schädigung für die Wachstumsverminderung verantwortlich ist, daß aber in den späteren Jahren andere Faktoren ins Spiel kommen, die von der Lokalisation der Meningocele unabhängig sind. RESUMEN Crecimiento de tronco y piernas en niños con mielomeningocele La longitud total del cuerpo y de segmentos del cuerpo (coronilla‐rabadilla y subisquial) de 78 niflos con mielomeningocele, fueron medidas a intervalos regulares durante el crecimiento por un promedio de 4‐4 años. Se halló que cuanto más alto era el meningocele, tanto mayores eran los defectos de crecimiento. Sin embargo, la relatión era estadísticamente significativa sólo durante los primeros siete años de edad. Se concluye que la lesión neurológica era el mayor responsable del defecto de desarrollo durante el primer año de vida, pero que otros factores independientes del nivel del meningocele juegan también un papel en los años posteriores.

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Section: Discussionmentioning

confidence: 92%

Growth of Trunk and Legs of Children With Myelomeningocele

Duval-Beaupère¹,

Kaci²,

Lougovoy

et al. 1987

Develop Med Child Neuro

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“…This finding suggests that spinal cord injury may result in altered cartilage differentiation and/or signaling between cartilage and growing bone. Children with spinal cord injury are known to have stunted growth of the long bones that are distal to the neurological injury [37]. The growth plate arrest with chondrocyte columnar derangement may represent a histopathogical basis for the growth deficiency seen in human patients.…”

Section: Discussionmentioning

confidence: 99%

Spinal cord injury causes rapid osteoclastic resorption and growth plate abnormalities in growing rats (SCI-induced bone loss in growing rats)

et al. 2007

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“…Stunting of long bone skeletal growth has been reported in children with neurological impairment due to poliomyelitis [29, 30] as well as spinal cord injury [14, 15]. Delayed fracture union and non-union have also been reported following SCI [10, 11].…”

Section: Discussionmentioning

confidence: 99%

“…The combination of the injury and this treatment results in prolonged immobility, worsening disability, and serious medical complications including fracture non-union [9–11] and amputation [12, 13]. Long bone growth arrest [14, 15] has also been reported following SCI in children.…”

Section: Introductionmentioning

confidence: 99%

Severe Spinal Cord Injury Causes Immediate Multi-cellular Dysfunction at the Chondro-Osseous Junction

Morse

Solomon

et al. 2011

Transl. Stroke Res.

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Spinal cord injury is associated with rapid bone loss and arrested long bone growth due to mechanisms that are poorly understood. In this study, we sought to determine the effects of severe T10 contusion spinal cord injury on the sublesional bone microenvironment in adolescent rats. A severe lower thoracic (vertebral T10) spinal cord injury was generated by weight drop (10 g×50 mm). Severely injured and body weight-matched uninjured male Sprague–Dawley rats were studied. At 3 and 5 days post-injury, we performed histological analysis of the distal femoral metaphysis, TUNEL assay, immunohistochemistry, real-time PCR, and western blot analysis compared to uninjured controls. We observed severe hindlimb functional deficits typical of this model. We detected uncoupled remodeling with increased osteoclast activity in the absence of osteoblast activity. We detected osteoblast, osteocyte, and chondrocyte apoptosis with suppressed osteoblast and chondrocyte proliferation and growth plate arrest due to spinal cord injury. We also detected altered gene expression in both whole bone extracts and bone marrow monocytes following spinal cord injury. We conclude that spinal cord injury results in altered gene expression of key regulators of osteoblast and chondrocyte activity. This leads to premature cellular apoptosis, suppressed cellular proliferation, growth plate arrest, and uncoupled bone remodeling in sublesional bone with unopposed osteoclastic resorption.

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Trunk and leg growth in children with paraplegia caused by spinal cord injury

Cited by 12 publications

References 20 publications

Growth of Trunk and Legs of Children With Myelomeningocele

Growth of Trunk and Legs of Children With Myelomeningocele

Spinal cord injury causes rapid osteoclastic resorption and growth plate abnormalities in growing rats (SCI-induced bone loss in growing rats)

Severe Spinal Cord Injury Causes Immediate Multi-cellular Dysfunction at the Chondro-Osseous Junction

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