Granulocyte-colony stimulating factor (G-CSF), a pharmaceutical agent that is normally used to treat neutropenia, has recently been investigated for its potential role in the treatment of acute SCI. The main function of G-CSF is apoptosis inhibition and stimulation of neuron differentiation from new bone marrow-derived cells (Schneider et al. 2005). It also suppresses the expression of inflammation-causing cytokines and protects the myelin sheath surrounding the axons of neurons (Takahashi et al. 2012). Recent studies in animal models have found G-CSF to enhance neurological recovery (Koda et al. 2007; Nishio et al. 2007), and its potential use in other neurological disorders, such as stroke, is under investigation (Schneider et al. 2005).
Two clinical trials (Takahashi et al. 2012; Kamiya et al. 2014) have been recently conducted to examine whether G-CSF improves neurological recovery in acute SCI. It is promising to see initial improvements in neurological function compared to baseline measurements, especially in those experiencing incomplete injuries (Kamiya et al. 2014). However, despite positive findings, it is important to note that the sample sizes were small and the protocols lacked blinding and randomization. While the authors noted significantly fewer episodes of pneumonia using G-CSF instead of MP, there is still a concern with other side effects such as elevated levels of white blood cells. It is known that white blood cell counts in the levels of 50 000 cells/mm3 can cause splenic rupture, and significantly higher white blood cell counts were observed in both groups receiving treatment, with one patient experiencing counts in this dangerous level (Kamiya et al. 2014). Additional RCTs examining the role of G-CSF in acute SCI are recommended.
There is level 2 evidence (from one cohort study and one prospective controlled trial: Kamiya et al. 2014; Takahashi et al. 2012) that a moderate dose (10 µg/kg/day) of granulocyte-colony stimulating factor may be effective in promoting motor and sensory recovery in acute SCI individuals.