Sustained Neuronal Hyperexcitability Is Evident in the Thalamus After a Transient Cervical Radicular Injury

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Study Design.

This study used extracellular electrophysiology to examine neuronal hyperexcitability in the ventroposterolateral nucleus (VPL) of the thalamus in a rat model of painful radiculopathy.


The goal of this study was to quantify evoked neuronal excitability in the VPL at day 14 after a cervical nerve root compression to determine thalamic processing of persistent radicular pain.

Summary of Background Data.

Nerve root compression often leads to radicular pain. Chronic pain is thought to induce structural and biochemical changes in the brain affecting supraspinal signaling. In particular, the VPL of the thalamus has been implicated in chronic pain states.


Rats underwent a painful transient C7 nerve root compression or sham procedure. Ipsilateral forepaw mechanical allodynia was assessed on days 1, 3, 5, 7, 10, and 14 and evoked thalamic neuronal recordings were collected at day 14 from the contralateral VPL, whereas the injured forepaw was stimulated using a range of non-noxious and noxious mechanical stimuli. Neurons were classified on the basis of their response to stimulation.


Behavioral sensitivity was elevated after nerve root compression starting at day 3 and persisted until day 14 (P < 0.049). Thalamic recordings at day 14 demonstrated increased neuronal hyperexcitability after injury for all mechanical stimuli (P < 0.024). In particular, wide dynamic range neurons demonstrated significantly more firing after injury compared with sham in response to von Frey stimulation (P < 0.0001). Firing in low threshold mechanoreceptive neurons was not different between groups.


These data demonstrate that persistent radicular pain is associated with sustained neuronal hyperexcitability in the contralateral VPL of the thalamus. These findings suggest that thalamic processing is altered during radiculopathy and these changes in neuronal firing are associated with behavioral sensitivity.


Level of Evidence: N/A

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