Pain anticipatory phenomena in patients with central poststroke pain: a magnetoencephalography study

Abstract

Gopalakrishnan R, Burgess RC, Lempka SF, Gale JT, Floden DP, Machado AG. Pain anticipatory phenomena in patients with central poststroke pain: a magnetoencephalography study. J Neurophysiol 116: 1387-1395, 2016. First published June 29, 2016 doi:10.1152/jn.00215.2016.-Central poststroke pain (CPSP) is characterized by hemianesthesia associated with unrelenting chronic pain. The final pain experience stems from interactions between sensory, affective, and cognitive components of chronic pain. Hence, managing CPSP will require integrated approaches aimed not only at the sensory but also the affective-cognitive spheres. A better understanding of the brain's processing of pain anticipation is critical for the development of novel therapeutic approaches that target affectivecognitive networks and alleviate pain-related disability. We used magnetoencephalography (MEG) to characterize the neural substrates of pain anticipation in patients suffering from intractable CPSP. Simple visual cues evoked anticipation while patients awaited impending painful (PS), nonpainful (NPS), or no stimulus (NOS) to their nonaffected and affected extremities. MEG responses were studied at gradiometer level using event-related fields analysis and timefrequency oscillatory analysis upon source localization. On the nonaffected side, significantly greater responses were recorded during PS. PS (vs. NPS and NOS) exhibited significant parietal and frontal cortical activations in the beta and gamma bands, respectively, whereas NPS (vs. NOS) displayed greater activation in the orbitofrontal cortex. On the affected extremity, PS (vs. NPS) did not show significantly greater responses. These data suggest that anticipatory phenomena can modulate neural activity when painful stimuli are applied to the nonaffected extremity but not the affected extremity in CPSP patients. This dichotomy may stem from the chronic effects of pain on neural networks leading to habituation or saturation. Future clinically effective therapies will likely be associated with partial normalization of the neurophysiological correlates of pain anticipation.

Randomized clinical trial of deep brain stimulation for poststroke pain

“…34 Because pain anticipation is highly linked to pain chronification phenomena and to pain-related limited use of the affected extremities (and therefore linked to disability), we also believe that clinically effective VS/ALIC DBS will likely be associated with partial normalization of the neurophysiological correlates of pain anticipation. 35 In conclusion, VS/ALIC DBS was safe and effective in addressing the affective component of pain in patients with PSPS but not in reducing disability. We demonstrated that active versus sham VS/ALIC DBS produced significant improvements in multiple outcome measures related to the affective sphere of chronic pain.…”

“…We hypothesize that clinically effective DBS will be associated with significant changes in the pain neuromatrix . Because pain anticipation is highly linked to pain chronification phenomena and to pain‐related limited use of the affected extremities (and therefore linked to disability), we also believe that clinically effective VS/ALIC DBS will likely be associated with partial normalization of the neurophysiological correlates of pain anticipation …”

Functional Magnetic Resonance Imaging Correlates of Ventral Striatal Deep Brain Stimulation for Poststroke Pain

“…To investigate the neural substrates of pain affect and its modulation by DBS of the ventral striatum, we previously studied the same patient cohort using an event‐related magnetoencephalography (MEG) paradigm (18‐20). Our findings were twofold.…”

Deep Brain Stimulation for the Treatment of Dejerine-Roussy Syndrome

“…Patients with DRS no longer experience heightened anxiety from the anticipation of pain at the affected location compared to the unaffected side, possibly indicating neuronal habituation to painful stimuli [19]. In this instance, the patient already experiences unrelenting pain, and thus the threat of further stimuli loses salience [19].…”

“…In this instance, the patient already experiences unrelenting pain, and thus the threat of further stimuli loses salience [19]. Larger neuronal losses after an infarct, in combination with proliferation of glia or microglia in the perilesional area, can lead to more severe allodynia [20].…”