Gacyclidine is a non-competitive antagonist for the NMDA receptor, such that its binding deactivates the receptor and blocks the negative effects of significant downstream influx of calcium into the cells. It was developed to inhibit excitotoxicity by reducing excessive glutamate concentrations surrounding neurons. Investigations of animal SCI models treated with gacyclidine have reported the animals to recover significantly more motor skills and have less damage around the spinal cord compared to animals that received a placebo (Gaviria et al. 2000). Gacyclidine has also been suggested as being more effective for neurological recovery compared to other NMDA antagonists (Feldblum et al. 2000). To date, one RCT has examined the neuroprotective effectiveness of gacyclidine in humans (Tadie et al. 2003).
The only RCT to investigate the neuroprotective effectiveness of gacyclidine in acute SCI found no significant improvement in neurological recovery among individuals with acute SCI (Tadie et al. 2003). Even though patients showed a trend toward neurological improvement over time, this was seen across all groups including the control group. It is currently not recommended that patients receive gacyclidine as treatment for acute SCI. Further trials examining gacyclidine for SCI in humans have been terminated (Fehlings & Baptiste, 2005).
There is level 2 evidence (from one RCT; Tadie et al. 2003) that gacyclidine is not effective in promoting neurological recovery in acute SCI individuals.
Gacyclidine is not effective for neurological recovery during the acute phase post SCI.