Is the Use of Growth hormone and Melatonin Justified in Spinal Cord Injuries?

Abstract

In this review we analyzed the possibility that tetraplegic patients suffer a deficient GH secretion occurring as a consequence of the loss of adrenergic control of somatostatin release, the inhibitor of pituitary GH synthesis and release. A deficient GH secretion can contribute to enhance the metabolic abnormalities seen in tetraplegics, increase the cardiovascular risk and osteopenia/osteoporosis. We also analyzed why orthostatic hypotension exists in tetraplegics, because of the loss of sympathetic afferences to the cardiovascular system. In addition we examined why the pineal production of melatonin is absent in tetraplegics, as a result of the loss of adrenergic signals from the upper cervical ganglion to the pineal gland; this results in sleep disorders and poor quality of life, but also in increased oxidative stress and the loss of the multiple beneficious effects that melatonin plays in the human body (oncostatic, anti-inflammatory, neuroprotective, etc). Lastly we describe a case of exaggerated allergic response to an allergen in a young tetraplegic girl. We conclude that because of the decreased production of the natural inhibitors of histamine (adrenaline and ACTH-independent corticosteroids), tetraplegic patients may have a special enhanced sensitivity to allergens that should be studied. In summary, GH and Melatonin are useful and safe in the treatment of tetraplegic patients.

Usefulness of Melatonin and Other Compounds as Antioxidants and Epidrugs in the Treatment of Head and Neck Cancer

“…In fact, sympathetic denervation leads to loss of pineal gland function [ 34 ], while NA administration rapidly increases MT synthesis in these situations. At this point, it is important to note that the cervical region of the spinal cord is essential for normal secretion of pineal MT in humans [ 35 ]; therefore, this secretion is lost in tetraplegic patients [ 36 , 37 ] due to loss of sympathetic stimuli from the spinal cord to the superior cervical ganglion and from this to the pineal gland, as shown in Figure 1 A. A similar loss occurs in pathologies that present with total blindness due to the lack of activation of the retino-hypothalamic tract.…”

Growth Hormone Deficiency: Is It Just a Problem of Growth Impairment? Part I

“…In the case of the spinal cord, injuries above T5-T6, there is a loss of the afferent inputs from the spinal cord to the sympathetic ganglionic chain resulting in a decreased or absent supply of catecholamines to the hypothalamus. The result of this situation would be an increased hypothalamic somatostatin release and, consequently, deficient or insufficient GH secretion [82]. This GHD in patients with spinal cord injuries had been reported years ago [83,84], but never were they treated with GH, until 2007, when we began to treat these patients with the hormone and rehabilitation, based on the fact that there are neural stem cells in the spinal cord ependyma whose proliferation and differentiation is stimulated by GH, with good or very good results in many cases (Figure 4), although we still have not published our results.…”