Chronic Pain & Central Sensitization

Overview

When an individual experiences long-term pain, or persistent inflammation, the way the pain signal is processed within the body is changed.

This can lead to a number of additional disorders, which, though not intuitively associated with the original problem, constitute a related group of disorders collectively known as Central Sensitization Syndrome.

human nervous systemTMD and certain types of headache are commonly found within central sensitization syndrome. Once established, simply treating the symptoms of the individual disorders within the syndrome complex is unlikely to lead to significant overall improvement in patient outcomes.

An experienced multi-disciplinary team, assembled to address specific patient needs, offers the best prognosis.

Central Sensitization

Chronic pain is a multidimensional experience encompassing biological, psychological and social elements. Each of these elements is entangled bi-directionally with the neuromatrix as a whole.

There is a growing consensus that chronic pain is a disease entity. This disease has been termed maldynia by the American Medical Association. This new designation has come about in recognition that acute and chronic pain are fundamentally different experiences, demanding a fresh approach to diagnosis, therapy, and prognosis.

It has been repeatedly demonstrated that many chronic pain disorders have a major component of central sensitization. Assessment and therapy for these several disorders is dependent on an understanding of central sensitization.

What is Central Sensitization (CS)?

Central sensitization is thought to occur when "Sensory-afferent signals overwhelm the body's ability to filter them".[1,2] When this occurs a number of pathophysiologic changes occur including neuro-immune dysfunction, neuro-endodrine dysfunction, NMDA (N-methyl-D-aspartate) dysregulation, sympatho-afferent coupling; and altered serotonin and norepinephrine production and utilization. These events are thought to occur predominantly in the mid-brain and associated structures and are influenced by elements of the neuromatrix delineated by Melzack, Woolf, and others.

These pathophysiologic changes are associated with decreased descending inhibition, dysautonomia, and altered serotonin production/utilzation. The resulting depression, anxiety, sleep fragmentation, allodynia, and hyperalgesia characterize a number of chronic pain disorders.

At least two etiological pathways are posited for central sensitization. The first is chronification of nociceptive pain; and involves neuroplastic changes, and peripheral sensitization as precursors to central sensitization and the resulting clinical pain. A more psychologically centered pathway is offered as an alternative to this transformed nociception. This alternate pathway begins with elevated levels of chronic stress, and encompasses elements of anxiety, sleep fragmentation, decreased pain thresholds, and dysautonomia. It is common to find both axes actively involved in the etiology of a central sensitization syndrome. Central sensitization syndromes can be thought of as the archetypical exemplars of a chronic biopsychosocial pain disorder.