Question: What is the role of Thyrotropin Releasing Hormone in the treatment of comatose patients?

Context:
Despite the correction of these metabolic disorders, the patient became comatose, and MRI, on T2 weighted image, showed hyperintense signals in the basal ganglia consistent with extra-pontine myelinolysis. The patient's state remained unchanged for six weeks. Since S. Konno and H. Wakui published cases of myelinolysis who dramatically improved after TRH treatment, the patient was given 0.6 mg i.v daily of TRH for six weeks. Improvement began within a few days, and continued until complete recovery.
His CNS symptoms improved dramatically after administration of thyrotropin-releasing hormone tartrate (TRH-T).
[Montirelin hydrate (NS-3), a TRH analog, improved the disturbance of consciousness caused by head concussion and pentobarbital in mice].
NS-3 shortened the latent periods to the recovery of the righting reflex (0.03-0.1 mg/kg, i.v.) and spontaneous motor activity (0.1 mg/kg, i.v.) following the head concussion. In the case of TRH, higher doses were needed to induce such effects. NS-3 (0.1-0.3 mg/kg, i.v.) reversed the pentobarbital-induced narcosis in a dose-dependent manner. A similar effect was elicited by 30- to 100-fold higher doses of TRH than NS-3.
Taken together with the finding that NS-3 did not bind to dopamine, adrenaline or muscarine receptors, it is suggested that NS-3 may restore the disturbance of consciousness by activating the brain dopamine, noradrenaline and acetylcholine neurons without stimulating these receptors directly.
A 46-year-old female motorcyclist, who suffered injuries to the brain stem in a traffic accident, showed hypotensive and bradycardiac responses to thyrotropin-releasing hormone (TRH) given to counter consciousness disturbance.
The direct TRH (thyrotropin releasing hormone) stimulation to the anterior lobe was responded to well. 
The neuropharmacological activities of TRH include an interesting arousal effect and an analeptic action on generalized depression of the CNS whether this depression is of natural origin, such as hibernation, or induced pharmacologically (barbiturates, ethanol) or of a traumatic origin (coma). This analeptic action is attributable to stimulation of cholinergic neurons in the septo-hippocampal area and to the presence of terminals containing TRH in the lateral septum and TRH receptors concentrated especially in the medial septum and diagonal band of Broca. It has also been suggested that TRH localized in the pineal gland has a part in activating the neuronal mechanisms of arousal. Associated with the arousal effect and especially evident in variously originated shock conditions are the activating effects of TRH on vegetative functions (body temperature, circulation, the gastrointestinal tract). These stimulatory activities on the CNS were the rationale for therapeutic use of TRH in the initial treatment of coma due to brain trauma and for the treatment of endogenous depression. 
In the vegetative group, TRH caused significant increases in MBP (from 91 +/- 8 mm Hg to 110 +/- 10 mm Hg) at 2 min after the injection [p < 0.05, analysis of variance (ANOVA) with a Scheffé F-test]. In contrast, five of the seven BD patient showed no alterations in the measured parameter in response to the TRH injection. However, the remaining two BD patients, who had spinal reflexes, exhibited an elevation in MBP. 
These results indicate that in comatose patients, the hemodynamic effects of TRH may differ depending on impairments in the central nervous system; the results support previous reports indicating a mediation of the central sympathetic nervous system in the development of pressor effects of TRH. 

Answer: Thyrotropin Releasing Hormone and its analogs are used for treatment of comatose patients. In animal models, Thyrotropin Releasing Hormone and its analogs have been shown to improve the disturbance of consciousness caused by head concussion and pentobarbital. This analeptic action is attributable to stimulation of cholinergic neurons in the septo-hippocampal area and to the presence of terminals containing TRH in the lateral septum and TRH receptors concentrated especially in the medial septum and diagonal band of Broca. It has also been suggested that TRH localized in the pineal gland has a part in activating the neuronal mechanisms of arousal. Associated with the arousal effect and especially evident in variously originated shock conditions are the activating effects of TRH on vegetative functions (body temperature, circulation, the gastrointestinal tract). These stimulatory activities on the CNS were the rationale for therapeutic use of TRH in the initial treatment of coma due to brain trauma. Thyrotropin Releasing Hormone has been shown to induce recovery in comatose patients with extrapontine and pontine myelinosis syndromes.