This is a study of children who first attended as infants with either progressive infantile idiopathic scoliosis or congenital scoliosis. All had a pattern of scoliosis in which early and damaging deterioration is inevitable. The infants were treated from before the age of three, initially by plaster casts and then a Milwaukee brace, followed at about the age of ten by correction and fusion. The cases were then observed to the end of growth or near that point. In the main study there were twelve cases, six of progressive infantile idiopathic scoliosis and six of congenital scoliosis, which were followed through this long period. Only one of the twelve had a curve worse at the end of growth compared with the initial radiograph as an infant; this one curve had increased only 16 degrees in almost as many years. Although small, the series does show that it is nearly always possible to control even the most serious scoliosis in an infant, if it is tackled early and unremittingly. There are supportive studies of children who have partially completed this regime, and interim results in a newer group of children with spina bifida and scoliosis.
1. Resolving infantile scoliosis is transient and unimportant; progressive infantile idiopathic scoliosis can be catastrophic. 2. To be able to differentiate the two at an early stage is a considerable advance. This is important for many reasons, but particularly for parents who are anxious for the future of an infant with a small curve which looks so innocent but which can be so malignant. 3. With the new observations reported by Mehta on the difference of the angles between the apical vertebra and its two ribs, and on the radiological relationship of these rib heads to the vertebral body, the prognosis is now almost wholly reliable. 4. Our former clinical impression that all cases with compensatory curves are progressive has now been verified. 5. At last an early distinction between progressive and resolving scoliosis can be made with confidence.
1. Skeletal and other clinical features in twenty-three patients with homocystinuria have been compared with those in sixteen patients with Marfan's syndrome. 2. The two diseases are clinically similar but florid arachnodactyly and scoliosis are commoner in Marfan's syndrome, whereas widening of epiphyses and metaphyses of long bones is a distinctive feature of homocystinuria. 3. Patients with homocystinuria frequently have osteoporosis at a young age with a high incidence of vertebral involvement including biconcavity and flattening. Patients with Marfan's syndrome do not have osteoporosis and may have excessively tall vertebrae. 4. Mental retardation and thrombosis are common in homocystinuria and uncommon in Marfan's syndrome. 5. Homocystinuria is most probably inherited as an autosomal recessive and Marfan's syndrome as an autosomal dominant. 6. The two diseases should be differentiated because of the thrombotic risk in homocystinuria, and also because in this disease there is a possibility of treating the biochemical defect. 7. Although patients with homocystinuria may present to the orthopaedic surgeon with osteoporosis, severe genu valgum or scoliosis, the disease is an uncommon cause of these defects.
1. The results in 138 hands operated on for Dupuytren's contracture are analysed and compared with those in other series. 2. Contracture ofthe metacarpo-phalangeal joint can be expected to respond well to operation, whereas the outlook in the case of contracture of the proximal interphalangeal joint is generally poor. 3. The reasons for this difference are examined. 4. The advantages of early operation for contracture of the proximal interphalangeal joint are stressed.
