Thyrotropin-releasing hormone (TRH) is naturally produced by the hypothalamus. Under normal conditions, it is involved in regulating the release of thyroid stimulating hormone and prolactin. Among individuals with SCI, TRH can take on several functions to remediate secondary injuries such as increasing blood flow, acting as an antioxidant and stabilizing membranes (Fehlings & Baptiste, 2005). The exact mechanism of action of this pharmaceutical agent is still unknown. Animal studies examining TRH for acute SCI have found it to contribute to significant long-term motor recovery (Faden et al. 1981a; Faden et al. 1984b), even when the first treatment administration was delayed up to one week (Hashimoto & Fukuda, 1991). Animal studies have found that when compared to naloxone and dexamethasone, TRH is significantly more effective than either drug (e.g., Akdemir et al. 1992; Faden et al. 1981b; Faden et al. 1983). In humans, preliminary TRH clinical studies have also been conducted to examine its effect on amyotrophic lateral sclerosis (Brooks et al. 1987).
In one, small RCT conducted by Pitts et al. (1995), TRH was effective in promoting neurological recovery in patients with incomplete SCI, however not for those with complete SCI. Despite this promising observation, larger clinical trials are required to validate these results.
There is level 1b evidence (from one RCT; Pitts et al. 1995) that thyrotropin-releasing hormone may be effective in promoting neurological recovery in individuals with incomplete acute SCI.
Thyrotropin-releasing hormone may be effective for neurological recovery during the acute phase post SCI in individuals with incomplete injuries.