Neurological Piece of the Fibromyalgia Puzzle

These same findings of hyperalgesia and allodynia have been noted in most of the other conditions acknowledged to be part of this continuum, including irritable bowel syndrome (IBS), temporomandibular joint disorder, tension type headache, idiopathic low back pain, vulvodynia, and interstitial cystitis.^19-25

Brain imaging studies also demonstrate the existence of central pain augmentation in FM, IBS, low back pain, and several other central sensitivity syndromes (CSSs).^26-29

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FIGURE 1: Neural Influences on Pain and Sensory Processing. Recent studies have made it clear that an individual’s “set point” or “volume control setting” for pain is determined by a variety of factors, including the levels of neurotransmitters on the left that either facilitate pain transmission (turn up the gain or volume control) or those on the right that reduce pain transmission. High levels of neurotransmitters on the left, or low levels of those on the right, could cause the diffuse hyperalgesia (increased volume control) seen in a variety of chronic pain states. The arrows indicate the levels of these neurotransmitters in the CSF of individuals with FM. You can see that there are high levels (two to three times higher than in healthy controls) of a number of neurotransmitters on the left, and low levels of one set of neurotransmitters (serotonin, norepinephrine, dopamine) on the right. The only neurotransmitter system that has been studied in FM and not shown to be abnormal in a direction that would cause hyperalgesia or an increased volume control is the opioidergic system, which seems to be appropriately increased in FM. This may help explain why opioidergic drugs do not seem to work very well for these central pain states such as FM.

The Role of Specific Neurotransmitters

Rheumatologists might best understand pain and sensory processing by considering that this type of processing is controlled in a manner very similar to immune function. Just as high levels of proinflammatory cytokines, or low levels of antiinflammatory cytokines, can move an individual towards hyperimmune function, there are neurotransmitters that are similarly known to either increase or decrease pain transmission in the central nervous system (CNS). Overall, the analogy of an increased “volume control” or “gain” setting on pain and sensory processing is supported by studies from a variety of sources. Similar to essential hypertension, where a variety of root causes can lead to elevated systemic blood pressure, these disorders represent essential hypertension of pain and sensory processing pathways. Elevated levels of neurotransmitters that tend to be pro-nociceptive (see the left side of Figure 1, above) or reduced levels of neurotransmitters that inhibit pain transmission (see the right side of Figure 1) have a tendency to increase the volume control, and drugs that block neurotransmitters on the left or augment activity of those on the right will typically be effective treatments, at least for a subset of individuals with this spectrum of illness.