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Neuroprotection (Acute Phase)

Gacyclidine

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).

Author Year
Country
Research Design
PEDro
Sample Size		 Methods Outcomes
Tadie et al. (2003)
France
RCT
PEDro=4
Ninitial=280, Nfinal=228		 Population: Age range=18-65 yr; Gender: male=87%, female=13%; Level of injury: cervical-thoracic; Severity of injury: complete=72%, incomplete=28%.
Treatment: Patients were randomly assigned to receive either 0.005 mg/kg gacyclidine, 0.01 mg/kg gacyclidine, 0.2 mg/kg gacyclidine, or placebo, administered intravenously within 2 hr of injury and followed by a second dose given within the next 4 hr.
Outcome Measures: The following after 1 month and after 1 year: ASIA motor function, ASIA sensory function (pinprick and light touch), Functional Independence Measure (FIM), adverse event outcomes.
Chronicity: Individuals were studied beginning within 2 hr of sustaining injury.
  1. There was an overall trend toward increased motor function in all groups, especially among those with incomplete injuries, but there were no significant differences among the four groups after 1 month (p=0.09) and after 1 year (no statistical analyses provided).
  2. There were no significant differences among groups with regards to pinprick score or light touch score after 1 month (p=0.68 and p=0.85, respectively) and 1 year (no statistical analyses provided).
  3. There were no significant differences in FIM scores among the four groups after 1 month (p=0.07) and 1 year (p=0.87).
  4. There were no significant differences in adverse event outcomes among the groups (p>0.05).

Discussion

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).

Conclusion

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.

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