Unrestrained: Dr. Peter Rowe on Neuromuscular Strain in Chronic Fatigue Syndrome (ME/CFS) By Cort Johnson on July 8, 2014
The study suggested that healthy people can have restricted ranges of motion and exceed them without symptoms, but when adolescents with Chronic Fatigue Syndrome exceed their ROM’s they feel pain and other symptoms. Why would that be?
Great question. Healthy individuals have to adapt to areas of mechanical dysfunction in daily life, such as after a fall or an ankle sprain. We usually do so with localized symptoms, and don’t typically develop overwhelming fatigue and other ME/CFS symptoms. Beyond a certain threshold of injury or biomechanical strain, additional stressors—such as from infectious mononucleosis or other illness—might create further adverse neural tension. This can have negative consequences, including increased noxious input to the nervous system.
In a sensitized nervous system, further neuromuscular strain would be expected to lead to greater physiological consequences, including altered pain signaling, fatigue, and autonomic nervous system changes.
Could connective tissue problems be affecting nerve elongation in Chronic Fatigue Syndrome (ME/CFS)?
We think these issues are related. One possible explanation for the apparent paradox of joint hypermobility and connective tissue laxity on the one hand, and the adverse neural strain on the other, is that some of the positions of the spine in those with ligamentous laxity (slumped chest, head-forward posture, exaggerated lumbar lordosis) impose a length demand on the spinal canal and its contents.
This in turn increases the load on the peripheral nerves, making them less able to elongate, more likely to be associated with reflex muscle guarding, and therefore more likely to sensitize the nervous system to further stresses. In those with tightness and reduced mobility of the connective tissues, nerve elongation is likely to be more directly impaired.
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