INJURY to the spinal cord and the ensuing extensive paralysis of skeletal muscle is known to give rise to many metabolic changes (Cooper and Hoen, 1952; O'Connell and Gardner, 1953; Arieff et al., 1960). Some of these changes are generally reversible, such as the catabolic reaction resulting in marked loss of nitrogen, potassium and calcium (Cooper, et al., 1950), impairment of bromsulfalein clear ance (Cooper and Hoen, 1952) and development of gynecomastia in males. These abnormalities may disappear in the course of a few months, especially with modern treatment (Arieff et al., 1960). On the other hand, some changes seem to be essen tially permanent and these include disturbance of the distribution of serum proteins (Robinson, 1954; Arieff e t al., 1960), a tendency to creatinuria and decreased creatine tolerance (Pollock et at., 1954), a lowered excretion of creatinine and sub normal serum glutamic-oxalacetic transaminase levels (Arieff et al., 1960). The aim of the present work is to determine to what extent the gross body composition of spinal cord injured patients is altered as a result of such metabolic changes. The patients available in this hospital for the care and rehabilitation of the chronically ill were treated elsewhere during the acute post-injury phase. Consequently only the effects of relatively long-term metabolic changes would be apparent from these studies. In one approach, observations made on groups of paraplegic and quadriplegic patients were compared with those from groups of other chronically ill patients in this hospital in order to delineate differences specifically due to spinal cord injury. Comparison with data from the literature on healthy normal controls was also possible. In a second approach, in which the patient served as his own control, periodic observations were made on spinal cord injured subjects over a period of up to 51 months in order to follow changes in their body composition. Previous work on the variability in measurement of the selected parameters allowed assess ment of the statistical significance of the changes observed in the latter study (Greenway et al., 1965). METHODS Patient Selection. All patients were chronically ill, but in no acute distress. The spinal cord injured patients had no large decubitus ulcers and were all either 1 These studies have been supported in part by USPHS Grants A-1886, HD-00669 and VRA Grant RD-II44-M.

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Pigs were fed alternately tryptophan deficient diet and the same diet supplemented with tryptophan. The deficient diet depressed food intake, caused changes in the pattern of plasma amino acids, increased plasma glucose levels and increased plasma urea levels per unit food intake. Plasma levels of insulin and growth hormone gave no indication that either hormone was involved in the suppression of food intake.

1. Cytoplasmic aldehyde dehydrogenase was shown to be free of contamination by the mitochondrial enzyme by isoelectric focusing.2. Both enzymes showed inultiple banding in activity stains. The cytoplasmic enzyme gave two very close bands pI = 5.22 0.03 whereas the mitochondrial enzyme showed seven bands, a pair at pI 3. Disulfiram in a fourfold excess reduced the activity of the cytoplasmic enzyme to 9 2, of the initial valuc.The residual activity represents the activity of the disulfiram-modified enzyme and is not due to mitochondrial contamination. This casts doubt on the role of an essential thiol group. 4. The mitochondrial enzyme shows a low amplitude (22'11() burst in the production of 4-nitrophenoxide ion during the hydrolysis of 4-nitrophenyl acetate at pH 7.6. The burst rate constant was 7.3 & 1 s and the steady-state rate constant was 0.2 s-I , values similar to those previously reported for the cytoplasinic enzyme.5. The mitochondrial enzyme shows a burst in the release of protons during thc oxidation of propionaldehyde at pH 7.6. The burst rate constant was 6 sC1 and.the amplitude was equal to half the formal enzyme concentration.

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