This is and interesting article that I read yesterday showing that there may be more going on with trigger point than previously thought.  It makes sense that the pain would be more of a neuralgic pain and not originating from muscle tissue that needs to be worked out with deep pressure, thumb pressure, stretch, or other techniques that are often used by therapist. The article explains how there is a layer of fat, vascular tissue, smooth muscle, fascia, nerve and connective tissue that is superior to the muscle and likely a source of potential nociception from metabolic and inflamatory markers that may not necessarily be originating from muscle tissue. In fact, the majority of “trigger point” pain may not be muscular pain but nerve entrapment and sensitization of nociceptors from metabolic and inflammation around the area of pain.  It is an interesting read and our hope is to understand further in order to accurately treat pain syndromes.

Dr. Ramirez

A Spinal Health and Movement Center (505-247-2373).


Secondary hyperalgesia and presynaptic inhibition: an update.
Cervero F1, Laird JM, García-Nicas E.
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One of the most prominent features of secondary hyperalgesia is touch-evoked pain, i.e., pain evoked by dynamic tactile stimuli applied to areas adjacent or remote from the originating injury. It is generally accepted that the neurobiological mechanism of this sensory alteration involves the central nervous system (CNS) so that incoming impulses in low-threshold mechanoreceptors from the area of secondary hyperalgesia can evoke painful sensations instead of touch. Some years ago we proposed a mechanistic model for this form of pain based on presynaptic interactions in the spinal dorsal horn between the terminals of low-threshold mechanoreceptors and of nociceptors. Here we review the evidence gathered in support of this model in the intervening years with special reference to experimental studies of antidromic activity (Dorsal Root Reflexes–DRRs) in nociceptive afferents and on the acquisition of low-threshold inputs by nociceptor-specific neurons in the spinal dorsal horn. We also discuss and identify potential molecular mechanisms that may underlie the presynaptic interaction model and therefore that could be responsible for the development of secondary hyperalgesia.