Monthly Archives: August 2011
Read my monthly blog post @ SportEX discussing my review of an article published discussing core balance vs. core strengthening for the treatment of LBP
Central sensitization is a phenomenon caused by a prolonged but reversibile increase in the excitability and synaptic efficacy of neurons triggered by nociceptive inputs. Several conditions, which are pain dominant, have a contribution from this process and it is important that we recognize when it occurs. Below are several conditions which have associated prolonged pain from this process:
1. Juvenile rheumatoid arthritis: a study on this condition reported enhanced sensitivity to noxious stimuli at joints and remote areas in patients with and without an active disease.
2. Osteoarthritis: Due to the degree of pain not always correlating with the degree of joint damage, it is suspected that there is a central component to the pain. It has been shown that patients with high pre-operative pain and a low pain threshold have a higher risk of pain following a total knee arthroplasty. So despite a peripheral pathology, a central component appears to regulate prolonged symptoms and slows outcomes. As PTs, we often make the mistake of attributing pain following the arthroplasty to decreased motion or weakness, when in actuality, its of central origin.
3. Fibromyalgia: Individuals diagnosed with this condition have been shown to have altered heat/cold thresholds and reduced toelrance to pain, as well as reduced nociceptive reflex threshold, which is a measure of central excitability.
4. Musculoskeletal disorders: diverse musculoskeletal disorders (especially chronic conditions) are often characterized by a spread of pain sensitivity to deep uninjured tissues.
5. Heachaches: Individuals with chronic tension-type headaches have been found to have reduced thresholds for pressure, pin-prick, blink and nociceptive flexion reflexes. Cutaneous allodynia also was found to develop in 79% of patients during migraine attacks.
Other conditions: TMJ disorders, neuropathic pain, CRPS, post-surgical pain, visceral pain hypersensitivity syndromes, etc.
Woolf CJ. Central Sensitization: Implications for the diagnosis and treatment of pain. Pain 2011: 152; S2-15.
I just ran across a new article examining the prevalance of hand osteoarthritis (OA) in habitual knuckle crackers. I have to admit, not only did I find this article amusing, but I am also not at all surprised by the results.
The examiners of this study performed a retrospective case-control study, in which participants had x-rays taken of their hands over a five year period. They compared individuals with diagnosed hand OA and those without, and had each group document their knuckle cracking behavior.
The results: A history of habitual knucle cracking does not appear to be a risk-factor for hand OA.
I suspect these results occured due to effects of knuckle cracking being chemical/neurophysiological vs. biomechanical. Does this further support the effects of manipulation being neurophysiological? Maybe. Let me know what you guys think.
deWeber K, Olszewski M, Ortolano R. Knuckle Cracking and Hand Osteoarthritis. The Journal of the American Board of Family Medicine 2011: 24 (2); 169-174.