Central sensitization: implications for the diagnosis and treatment of pain. (2011)

Abstract
Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk in both developing conditions with pain hypersensitivity, and their chronification. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity.

My comments:
This paper isn’t a study but is a review of 279 other papers regarding the concept of central sensitization. The idea, which this paper shows is well established in research, is that certain types of painful stimuli that travel up the nervous system make it more sensitive to future painful stimuli. Thus, making what should be a normal touch sensation a painful one. This is often seen in patients with fibromyalgia. The mechanism of action described in the paper sounds a lot like gate control theory in reverse. This seems to be associated with A LOT of chronic pain conditions where pain felt seems to exceed apparent physiological damage.

Conditions described in this paper include rheumatoid arthritis, osteoarthritis, temporomandibular disorders, fibromyalgia, headache, neuropathic pain, complex regional pain syndrome, post surgical pain and visceral pain hypersensitivity syndromes. What the paper also discussed, and what I have often seen in my physical therapy practice, is that these conditions while seemingly unrelated happen often in the same individuals. This indicates a likely common cause or contributor.

The author spoke about numerous studies using “brief (10-20s) , low frequency (1-10 Hz) bursts of action potentials into the CNS” which increased synaptic efficiency of nociceptors in the dorsal horn of the spinal cord for tens of minutes afterwards.  At this point I’m not sure how this relates to gate control theory, but it might indicate low rate TENS isn’t ideal if your goals is to reduce central sensitization.  In my observation patients find higher rate TENS and EMS more comfortable and more effective at decreasing pain, and perhaps this is part of the reason why.  I’ll have to research this area further.

Unfortunately, the paper says there is still a lot to be learned about genetic and environmental factors that increase the risk of development central sensitization, or exactly what triggers and sustains it in particular patients. The paper is definitely a good read for physical therapists working with chronic pain patients who might otherwise think their patients are malingerers, lazy, exaggerating their symptoms, have psychosomatic problems, or just don’t want to get better. Instead, central sensitization is a real neurobiological phenomenon.