Steady State Hormonal Secretion in Traumatic Quadriplegia

Abstract

Physiologically complete cervical spinal cord transection results in motor and sensory quadriplegia and interruption of the sympathetic neural pathways; this condition leads to metabolic deficiencies suggestive of abnormal endocrine function. An investigation of the non-stimulated secretion of some of the hormones influencing metabolism was undertaken by evaluating thyroxine, iodothyronine binding index, testosterone, growth hormone, calcitonin, and parathyroid hormone in venous blood of fasting healthy subjects and quadriplegic patients. The effect of the duration of the paralysis was examined by repeating the evaluations at different periods after onset. The results show that 1) thyroxine was low for 2 months after onset in 21 patients and normal thereafter in 53 patients, 2) testosterone was low throughout the study in 62 patients; the decrease is greatest during the first 2 months, 3) growth hormone was often increased in 46 patients for 8 months after onset, and nearly normal afterward in 25 patients, 4) calcitonin was normal in 22 patients throughout the study, and 5) parathyroid hormone was normal in relation to normal serum calcium as early as 6 days after onset in 79 out of 83 patients. These data do not preclude a parathyroid hormone increase at onset or alterations in the patterns of circadian secretion and in the responses to specific stimulation for the hormones evaluated. Therefore, it may be concluded only that the steady state secretion of these hormones is not altered by traumatic quadriplegia per se, but is temporarily modified by the original insult to the nervous system, and by changes in life pattern and the heavy sedation that follows. The results suggest that the minor endocrin changes occurring in quadriplegic patients during the early period of paralysis will be rapidly overcome by rehabilitation to an active life pattern.

Considerations for Studying Sex as a Biological Variable in Spinal Cord Injury

“…Indeed, Kikuchi et al ( 154 ) found that all but one male SCI patient ( n = 15) were within normal range when compared with age-matched controls. A possible explanation for this discrepancy comes from evidence showing that testosterone is lowest acutely after SCI and gradually increases over 18 months' time ( 156 ). A recent review found the prevalence of men with low testosterone acutely after SCI ranged from 69 to 83% of patients, which contrasts a prevalence of 10–46% of men with chronic SCI ( 157 ).…”

Mechanisms of osteoporosis in spinal cord injury

“…Medications, especially corticosteroid administration, frequently prescribed immediately after SCI, may also alter serum thyroid hormone levels 149 . It has been demonstrated that serum T3 and T4 levels remain depressed in acute SCI patients 150–154 . After acute stress, there may also be associated changes in thyroid hormone binding that could lower serum thyroid hormone levels 155 .…”

“…149 It has been demonstrated that serum T3 and T4 levels remain depressed in acute SCI patients. [150][151][152][153][154] After acute stress, there may also be associated changes in thyroid hormone binding that could lower serum thyroid hormone levels. 155 Similarly, in chronic SCI patients, serum T3 and T4 levels were also reduced as compared with controls.…”

High Incidence of Impaired Glucose Tolerance in Spinal Cord Injuries.

“…Physicians who care for patients with spinal cord injuries (SCI) have long had the clinical impression that some of them had high percentage of body fat, despite lack obesity, due to paraplegia or quadriplegia. Studies on this question, however, have been insufficient, and few investigators have reported [1][2] the factors that potentiate the development of glucose intolerance in patients with a stable, established SCI.…”