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KINESIOLOGY TAPE FOR RECOVERY / PERFORMANCE / PREVENTION

  • Imaging pain modulation in health and disease

    Bingel U, Schoell E, Bùˆchel C. Imaging pain modulation in health and disease. Curr Opin Neurol. 2007 Aug;20(4):424-31.

    PURPOSE OF REVIEW: In this review, we discuss recent advances in pain imaging research. We focus on the involvement of endogenous pain control mechanisms in the healthy central nervous system and the potential contribution of failure within this system for chronic pain states. RECENT FINDINGS: Nociceptive information processing and related pain perception is subject to substantial pro and antinociceptive modulation. Recent studies demonstrate that this modulation can take place at any stage of ascending information processing. A network of cortical, predominantly mesial and frontal areas, in combination with specific brainstem nuclei, appear to be the key players in the context of endogenous pain modulation. Recent findings from functional and anatomical neuroimaging support the notion that an altered interaction of pro and antinociceptive mechanisms may contribute to the development or maintenance of chronic pain states. The additional use of pharmacological intervention in pain imaging research provides an alternative tool for investigating mechanisms of pain modulation. SUMMARY: Top-down pain modulation relies on both cortical and subcortical structures. Research on the involved circuitry, including the implemented mechanisms, is a major focus of contemporary neuroscientific research in the field of pain and will provide new insights into the prevention and treatment of chronic pain states.

  • Central sensitization in fibromyalgia and other musculoskeletal disorders

    Arendt-Nielsen L, Graven-Nielsen T. Central sensitization in fibromyalgia and other musculoskeletal disorders. Curr Pain Headache Rep. 2003 Oct;7(5):355-61.

    Muscle hyperalgesia and referred pain play an important role in chronic musculoskeletal pain. New knowledge on the involved basic mechanisms and better methods to assess muscle pain in the clinic are needed to revise and optimize treatment regimens. Increased muscle sensitivity is manifested as pain evoked by a normally non-nociceptive stimulus (allodynia), increased pain intensity evoked by nociceptive stimuli (hyperalgesia), or increased referred pain areas with associated somatosensory changes. Some manifestations of sensitization, such as expanded referred muscle pain areas in patients with chronic musculoskeletal pain, can be explained from animal experiments showing extrasegmental spread of sensitization. An important part of the pain manifestations (eg, tenderness and referred pain) related to chronic musculoskeletal disorders may result from peripheral and central sensitization, which may play a role in the transition from acute to chronic pain.

  • Mechanisms of pain modulation in chronic syndromes

    Bolay H, Moskowitz MA. Mechanisms of pain modulation in chronic syndromes. Neurology. 2002 Sep 10;59(5 Suppl 2):S2-7.

    Transmission of pain from the periphery to the cortex depends on integration and signal processing within the spinal cord, brainstem, and forebrain. Sensitization, a component of persistent or chronic pain, may develop either through peripheral mechanisms or as a consequence of altered physiology in the spinal cord or forebrain. Several molecular and biophysical mechanisms contribute to the phenomenon of sensitization and persistent pain, including upregulation of sensory neuron- specific sodium channels and vanilloid receptors, phenotypic switching of large myelinated axons, sprouting within the dorsal horn, and loss of inhibitory neurons due to apoptotic cell death. Recently, forebrain structures have been implicated in the pathophysiology of persistent pain. Although a number of treatment options are used, unfortunately pharmacotherapy for neuropathic pain is often ineffective. Unraveling the mysteries of chronic pain may lead to better treatment options, such as drugs that act specifically on sensory neuron-specific sodium channels or as NR2B-subunit-selective N-methyl-D- aspartate receptor antagonists.