Studying the Brain in Fibromyalgia
The article in question is the work of Marco L. Loggia, PhD, an instructor in radiology at Harvard Medical School and assistant in neuroscience at Massachusetts General Hospital, Boston. Loggia and colleagues undertook a comparison of neural activity between patients with fibromyalgia and healthy controls using functional magnetic resonance imaging (fMRI) to observe brain activity, finding what appear to be signficant differences between the two groups.
What Causes Fibromyalgia?
The researchers noted that prior studies have observed differences between pain responses in those with fibromyalgia, including a finding that around half of those with the condition have small fiber polyneuropathy, a potentially treatable problem. There has, however, been little research done on the underlying brain activity that is involved in creating anticipation of pain and pain relief, which affects how patients respond to painkilling medications.
Brain Abnormalities in Fibromyalgia
Interestingly, what Loggia and colleagues found was that those with fibromyalgia “exhibit reduced brain activity in response to visual cues informing them of impending pain onset (pain anticipation) and pain offset (relief anticipation).” The patients had a reduced response in areas of the brain associated with processes such as reward and punishment, as has been seen in other research looking at the phenomenon of chronic pain.
Some 31 patients with fibromyalgia were compared with 14 healthy controls and those with fibromyalgia had a diminished response in the brain ventral tegmental area as they anticipated pain and deactivation of this area when anticipating pain relief (visual cues told them when to expect pain onset from a pressure cuff, and when the pain would stop). The VTA has also been implicated in the processing of romantic love, in addition to pain.
In addition, there were abnormalities in the fibromyalgia patients’ brains in the supplementary motor area, middle and posterior cingulate cortices, periaqueductal gray, caudate nucleus and globus pallidus on the left and in the second somatosensory cortex and posterior insula on the right. These changes are a possible explanation for why opioids are less effective or ineffective for the pain of fibromyalgia. These medications are not actually recommended for treating fibromyalgia but many patients are prescribed such drugs at some point during management of their condition.
Anticipating Pain and Pain Relief
This kind of research allows physicians and neuroscientists to consider how working with our existing knowledge of the brain may help in formulating treatments that focus on augmenting normal brain signalling, shifting focus from medications that work with other types of pain to creating new therapies originating from the underlying pain response mechanisms. This kind of shift in thinking could also have ramifications for other chronic pain conditions, helping those with neck pain caused by things other than fibromyalgia and for which traditional conservative treatments have proven ineffective.
The VTA becomes active in healthy people when pain is expected or experienced and is deactivated upon relief. This area of the brain is closely tied to dopamine activity and the activity of gamma amino butyric acid (GABA) often referred to as the reward and relaxation neurotransmitters. This study shows a stark contrast between activity in this area of the brain in fibromyalgia, the extent of which surprised the researchers.
New Treatments for Fibromyalgia
It may be that psychological interventions can work with these results to restore normal activity in the VTA, and that further confirmation of this GABA/dopaminergic connection can be found in trials using medications targeting these neurotransmitters for fibromyalgia. Uncovering these alterations in central processing of pain may help explain the ineffectiveness of opioids in fibromyalgia treatment and could also be useful to physicians looking to prescribe post-surgical medications for those with fibromyalgia.