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.

Paroxysmal sympathetic hyperactivity is a frequent condition in patients that suffered a TBI, but also other kinds of brain damage, characterized by a myriad of signs and symptom such as high temperature, tachycardia, tachypnea, hypertension, profuse sweating and spastic extension of legs and arms. The presence of high temperature may lead to suspect about any infective process whose analysis can put at risk the life of the patient, while in fact these symptom appear as a consequence of an increased release of catecholamines occurring because of the disruption of central pathways. Muscle spasticity produces a great heat that contributes to the central origin of hyperthermia. Here we describe two cases that presented PSH after different brain injuries. Both were in coma. One of them after a severe TBI and the other one because of a very important brain infection. PSH in the first case was due to a renal colic and PSH was resolved with propofol. The second case developed PSH suddenly before a session of physiotherapy. The rapid detection of the problem led us to use propranolol and in 40 minutes the patient was in normal conditions. We conclude that the knowledge of PSH and its rapid treatment should be mandatory in hospitals and centers devoted to rehabilitate neurological patients.