Functional exploration for neuropathic pain

Abstract

Neuropathic pain (NP) may become refractory to conservative medical management, necessitating neurosurgical procedures in carefully selected cases. In this context, the functional neurosurgeon must have suitable knowledge of the disease he or she intends to treat, especially its pathophysiology. This latter factor has been studied thanks to advances in the functional exploration of NP, which will be detailed in this review. The study of the flexion reflex is a useful tool for clinical and pharmacological pain assessment and for exploring the mechanisms of pain at multiple levels. The main use of evoked potentials is to confirm clinical, or detect subclinical, dysfunction in peripheral and central somato-sensory pain pathways. LEP and SEP techniques are especially useful when used in combination, allowing the exploration of both pain and somato-sensory pathways. PET scans and fMRI documented rCBF increases to noxious stimuli. In patients with chronic NP, a decreased resting rCBF is observed in the contralateral thalamus, which may be reversed using analgesic procedures. Abnormal pain evoked by innocuous stimuli (allodynia) has been associated with amplification of the thalamic, insular and SII responses, concomitant to a paradoxical CBF decrease in ACC. Multiple PET studies showed that endogenous opioid secretion is very likely to occur as a reaction to pain. In addition, brain opioid receptors (OR) remain relatively untouched in peripheral NP, while a loss of ORs is most likely to occur in central NP, within the medial nociceptive pathways. PET receptor studies have also proved that antalgic Motor Cortex Stimulation (MCS), indicated in severe refractory NP, induces endogenous opioid secretion in key areas of the endogenous opioid system, which may explain one of the mechanisms of action of this procedure, since the secretion is proportional to the analgesic effect.

Brain-network mechanisms underlying the divergent effects of depression on spontaneous versus evoked pain in rats: A multiple single-unit study

“…Clinical observations have found that the exacerbation of pain is closely associated with abnormal functioning of medial pathway structures (Grande et al, 2004; Maarrawi et al, 2011; Seifert et al, 2013). In our study, rats with the depressive-like phenotype plus spontaneous pain showed a prominent neuronal change, namely the reduction of inhibitory responses in the medial thalamus.…”

The Application of Functional Magnetic Resonance Imaging in Neuropathic Pain

“…At the late stage of injury (20 weeks after surgery), ACC, prefrontal, insula, basal ganglia, and S1 activity was significantly enhanced, while activity in the medial thalamus and PAG areas was inhibited [33]. It can be seen that the formation of neuropathic pain is related to the inhibition of the function of the descending regulation system of pain [34]. ACC activity is inhibited in the early stages of nerve injury, and with the chronic process of pain, ACC activity is gradually enhanced, which may be related to the unpleasant emotional experience of neuropathic pain [29,35,36].…”