Mechanisms of chronic pain – key considerations for appropriate physical therapy management

Abstract

In last decades, knowledge of nociceptive pain mechanisms has expanded rapidly. The use of quantitative sensory testing has provided evidence that peripheral and central sensitization mechanisms play a relevant role in localized and widespread chronic pain syndromes. In fact, almost any patient suffering with a chronic pain condition will demonstrate impairments in the central nervous system. In addition, it is accepted that pain is associated with different types of trigger factors including social, physiological, and psychological. This rational has provoked a change in the understanding of potential mechanisms of manual therapies, changing from a biomechanical/medical viewpoint, to a neurophysiological/nociceptive viewpoint. Therefore, interventions for patients with chronic pain should be applied based on current knowledge of nociceptive mechanisms since determining potential drivers of the sensitization process is critical for effective management. The current paper reviews mechanisms of chronic pain from a clinical and neurophysiological point of view and summarizes key messages for clinicians for proper management of individuals with chronic pain.

Clinical Reasoning Behind Non-Pharmacological Interventions for the Management of Headaches: A Narrative Literature Review

“…Proper management of chronic pain syndromes, including headaches, have begun to target various pain mechanisms as one strategy for combatting chronic pain [17]. In fact, clinical and basic science evidence support that proper management of patients with headache should be multimodal, and consider individualized and personalized patient's perspectives by including passive and/or active strategies, active listening, empathy, and psycho-social issues.…”

Duration of symptoms is associated with conditioned pain modulation and somatosensory measures in knee osteoarthritis

“…Peripheral sensitization is defined as the facilitated response of nociceptive neurons located at the site of tissue injury or disease; it is limited to these nociceptors and will resolve as tissues heal and inflammation recedes. Central sensitization is mediated via amplification of signaling to the central nervous system, potentially at both spinal and supraspinal levels, and is associated with heightened pain, spontaneous pain without trigger, expanded distribution of pain, and potentially the presence of altered non‐nociceptive findings, including diminished vibration perception threshold (VPT) particularly in region of most pain . Altered somatosensory findings in persons with chronic knee OA, such as VPT may serve as a clinical correlate of pain‐related central neurophysiological changes.…”

“…Central sensitization is mediated via amplification of signaling to the central nervous system, potentially at both spinal and supraspinal levels, and is associated with heightened pain, spontaneous pain without trigger, expanded distribution of pain, and potentially the presence of altered non-nociceptive findings, including diminished vibration perception threshold (VPT) particularly in region of most pain. 18 Altered somatosensory findings in persons with chronic knee OA, such as VPT may serve as a clinical correlate of pain-related central neurophysiological changes. Besides heightened pain sensitivity, impaired descending pain inhibition may also contribute to the development of chronic pain generally, 19 and in knee OA specifically.…”

Predicting the outcome of the greater occipital nerve block – an observational study on migraine patients with and without musculoskeletal cervical impairment

“…However, these indicators might not be sensitive to detect differences between different hyperalgesic states. Pain hypersensitivity from the trigeminal region might be extended via the TCC to the upper cervical system, expressing widespread pain and hyperalgesia as known for other chronic pain conditions (59). Our current results suggest that a GON-block may be less effective in a hypersensitive cervical system and thus may have a greater effect on migraine in a less altered system.…”