Axonal damage is remarkable in patients with acutely worsening symptoms of compression myelopathy: biomarkers in cerebrospinal fluid samples.

PURPOSE

To determine levels of biomarkers reflecting damage to axon, myelin, astrocytes, and neuron in cerebrospinal fluid (CSF) of patients with cervical compression myelopathy.

METHODS

We collected 69 CSF samples from patients before spinal surgery for acutely worsening compression myelopathy (AM, 20), chronic compression myelopathy (CM, 20), and lumbar canal stenosis (LCS 29; control). We measured levels of phosphorylated neurofilament subunit H (pNF-H), tau (reflecting axonal damage), myelin basic protein (MBP) (reflecting demyelination), S100b (reflecting astrocyte damage), and neuron-specific enolase (NSE) (reflecting neuronal damage). Change of neurological function by surgery was determined using a Japanese Orthopaedic Association (JOA) score for cervical myelopathy.

RESULTS

Significantly higher levels of pNF-H were detected in AM compared with those in either CM or LCS (P < 0.01). Significantly higher levels of tau were detected in AM compared with those in CM (P < 0.05). Levels of MBP were undetectable in almost all the patients. Levels of S100b were equivalent in the three groups. Levels of NSE in AM and CM were significantly lower than those in LCS (P < 0.01). The recovery rate of JOA score was significantly greater for patients with AM than CM. We found a positive correlation between pNF-H and recovery of JOA score (r = 0.381, P = 0.018).

CONCLUSION

The present results suggest that axonal damage is remarkable compared with demyelination, astrocytic, and neuronal damage in AM. Better clinical outcome in AM with high CSF levels of pNF-H indicates that axonal compensatory plasticity in spinal cord is preserved, and pNF-H can be predictive of good surgical outcome for AM. These slides can be retrieved under Electronic Supplementary Material.