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Both traumatic and slow-onset disc herniation can directly compress and/or chemically irritate cervical nerve roots, and both types of root injury elicit pain in animal models of radiculopathy. This study investigated the relative contributions of mechanical compression and chemical irritation of the nerve root to spinal regulation of neuronal activity using several outcomes. Modifications of two proteins known to regulate neurotransmission in the spinal cord, the neuropeptide calcitonin gene-related peptide (CGRP) and glutamate transporter 1 (GLT-1), were assessed in a rat model after painful cervical nerve root injuries using a mechanical compression, chemical irritation or their combination of injury. Only injuries with compression induced sustained behavioral hypersensitivity (p≤0.05) for two weeks and significant decreases (p<0.037) in CGRP and GLT-1 immunoreactivity to nearly half that of sham levels in the superficial dorsal horn.

Cervical nerve roots are susceptible to compression injuries of various durations. The duration of an applied compression has been shown to contribute to both the onset of persistent pain and also the degree of spinal cellular and molecular responses related to nociception. This study investigated the relationship between peripherally evoked activity in spinal cord neurons during a root compression and the resulting development of axonal damage. Electrically evoked spikes were measured in the spinal cord as a function of time during and after (post-compression) a 15 minute compression of the C7 nerve root. Compression to the root significantly (p=0.035) reduced the number of spikes that were evoked over time relative to sham. The critical time for compression to maximally reduce evoked spikes was 6.6±3.0 minutes. A second study measured the post-compression evoked neuronal activity following compression applied for a shorter, sub-threshold time (three minutes).