Central pain mechanisms in chronic pain states – Maybe it is all in their head

Abstract

Mechanisms underlying chronic pain differ from those underlying acute pain. In chronic pain states, central nervous system (CNS) factors appear to play particularly prominent roles. In the absence of anatomical causes of persistent pain, medical sub-specialties have historically applied wide-ranging labels (e.g. fibromyalgia -FM, irritable bowel syndrome, interstitial cystitis, somatization) for what now is emerging as a single common set of CNS processes. The hallmark of these “centrally-driven” pain conditions is a diffuse hyperalgesic state identifiable using experimental sensory testing, and corroborated by functional neuroimaging. The characteristic symptoms of these central pain conditions include multifocal pain, fatigue, insomnia, memory difficulties, and a higher rate of co-morbid mood disorders. In contrast to acute and “peripheral” pain states that are responsive to NSAIDs and opioids, central pain conditions respond best to CNS neuromodulating agents such as serotonin-norepinephrine re-uptake inhibitors (SNRIs) and anticonvulsants.

Altered Brain Complexity in Women with Primary Dysmenorrhea: A Resting-State Magneto-Encephalography Study Using Multiscale Entropy Analysis

“…Brain complexity in the left thalamus and the right hippocampus were positively associated with depression level. On the other hand, the amygdala is a well-known region related to the affective-motivational dimension of pain [122] and shows altered resting-state activities in chronic pain conditions [123]. The complexity of the amygdala was also found to be decreased in PDMs in this study, implying that emotional processing could be altered.…”

Rethinking chronic pain in a primary care setting

“…[32][33][34][35] While no clear consensus presently exists on the terminology, the hallmark of this type of pain appears to be generalized hypersensitivity to a variety of stimuli including mechanical, thermal, olfactory, auditory, and visual cues. [36][37][38][39] Unlike traditional central sensitization triggered by persistent nociceptive and/or neuropathic input, it is often impossible to pinpoint the cause of sensory hypersensitivity. It is thought to occur throughout the CNS and may involve additional mechanisms such as a decrease in descending inhibition and neuroplasticity in pain processing areas of the brain.…”

Delayed pain decrease following M1 tDCS in spinal cord injury: A randomized controlled clinical trial

“…Evidence suggests that the resulting chronic pain is associated with the phenomenon of central sensitization involving a large neural network that includes limbic structures, such as the anterior cingulate cortex, hippocampus and amygdala, and thalamic nuclei [4][5][6]. However, the precise mechanisms leading to central sensitization in SCI are not yet understood.…”