1977
DOI: 10.1097/00007632-197712000-00003
|View full text |Cite
|
Sign up to set email alerts
|

Ultrastructural Changes of the Back Muscles of Idiopathic Scoliosis

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

2
4
0

Year Published

1980
1980
2019
2019

Publication Types

Select...
6
2

Relationship

0
8

Authors

Journals

citations
Cited by 11 publications
(6 citation statements)
references
References 0 publications
2
4
0
Order By: Relevance
“…Subcellular changes such as general increase in glycogen and lipid contents, derangement of myofilaments and Z band seen in the present study have been also reported by Wong et al (1977) in their study of two adolescent scoliotic patients. Dystrophic changes were observed in four of our cases on both sides of the curvatures.…”
Section: Discussionsupporting
confidence: 89%
See 1 more Smart Citation
“…Subcellular changes such as general increase in glycogen and lipid contents, derangement of myofilaments and Z band seen in the present study have been also reported by Wong et al (1977) in their study of two adolescent scoliotic patients. Dystrophic changes were observed in four of our cases on both sides of the curvatures.…”
Section: Discussionsupporting
confidence: 89%
“…However, only a few histological (Gruca 1958, Saito 1964, Kaneko 1968, Spencer & Zorab 1976) and ultrastructural studies (Hirano 1972, Wong et al 1977, Yarom & Robin 1979a are available. The pathogenesis and etiology of idiopathic scoliosis are still not clearly known.…”
mentioning
confidence: 99%
“…Others believed that the increased myoelectric activities on the convex side were only a secondary effect of the muscles adapting to a higher load demand in larger curves (Zetterberg et al, 1984). This would be consistent with the reported findings of differences in the morphology of the paravertebral muscles between the left and right sides ( Saltin et al, 1977;Spenser & Eccles, 1976;Wong et al, 1980;Yarom & Robin, 1979). However, the increase of type 1 muscle fibres on the convex side can be explained on the basis of muscle denervation ( Ford et al, 1984;Webb, 1973Webb, & 1981Zetterberg et al, 1984), produced by an alteration of the motor drive arising at the spinal cord level, either from altered sensory input at the same level ( Pincott, 1980;Pincott & Taffs, 1982; or from a central mechanism ( Barrack et al, 1984;Dubousset et al, 1982;Michelsson, 1965;Whitecloud et al, 1984).…”
Section: Neuromuscular Factorssupporting
confidence: 68%
“…Abnormalities in the paraspinal muscles have been implicated by several investigators as a possible causative factor in the production and progression of adolescent idiopathic scoliosis (Fidler et al, 1974;Fidler & Jowett, 1976;Ford et al, 1984;Spenser & Eccles, 1976;Yarom & Robin, 1979). An increased myoelectric response on the convex side of the curve, near its apex, was the main finding reported by various authors ( Alexander & Season, 1978;Butterworth & James, 1969;Guth & Abbink, 1980;Henssge, 1962;Redford et al, 1969;Spenser & Eccles, 1976;Wong et al, 1980;Yarom & Robin, 1979;Zetterberg et al, 1984), but not all agreed on the meaning of these findings. In early reports a fatigue mechanism was suggested (Riddle & Roaf, 1955), while others explained the difference as an effect of the stretching of the erector spinae muscles on the convex side (Butterworth & James, 1969).…”
Section: Neuromuscular Factorsmentioning
confidence: 80%
“…It has been suggested that idiopathic scoliosis is a primary and diffuse muscle disease, with a significant decrease in muscle fiber type II as well as myopathic alterations, as shown by histochemical and morphometric analysis using electron microscopy (Sahgal et al, 1983). Other muscle alterations include an increase in type I fibers in the convexity of the scoliotic curve associated with loss of type II fibers in the concavity (Fidler et al, 1974;Maffuli, 1989;Chagas et al, 1998); elevated intracellular concentrations of glycogen and lipids (Wong et al, 1977); structural changes in the sarcolemma and myotendineous junction (Kohsla et al, 1980;Ovalle et al, 1983); altered muscle enzyme activity (Cotic et al, 1983); and elevated intracellular calcium concentrations (Blatt et al, 1984). The histological changes in muscle fibers suggest a congenital origin for AIS (Wajchenberg et al, 2015), that include the development of central core myopathy, atrophy, necrosis, preponderance of type I fibers, perimisial and endomysial fibrosis and fatty proliferation more evident in the concavity of the deformity.…”
Section: Introductionmentioning
confidence: 99%