As many readers already know, and as has been written so many times, fibromyalgia (FM) is a chronic functional pain syndrome characterized by widespread pain, significant catastrophizing of that pain, and in the minds of some, dysfunction.
And while chronic pain patients experience pain as mostly a somatosensory phenomenon, it is also important to recall the importance of emotions and cognition in the experience of chronic pain. However, there is a missing link in the consideration of chronic pain: Where and what is the interface between the physical, somatic sensation of pain, and the emotional and cognitive components of a human being?
While several studies have demonstrated altered resting brain connectivity in FM, studies have not specifically probed the somatosensory system and its role in both somatic and non-somatic FM symptoms. The objective of a study published in the May, 2015, issue of “Arthritis and Rheumatology” was to evaluate resting primary somatosensory cortex connectivity and to explore how sustained, evoked deep tissue pain modulates this connectivity.
The researchers acquired functional magnetic resonance imaging and electrocardiography data on fibromyalgia patients and healthy control patients during rest and during sustained mechanical pressure-induced pain over the lower leg. They then calculated functional connectivity associated with different areas of the somatosensory part of the brain; in particular, the part of the brain that processes the lower leg pain was compared to the experience of pain during the active stimulation of pain, and after the introduction of such pain stimuli.
Interestingly, during the period after the application of the pain stimulus, there was less evidence of connectivity between the multiple areas of the brain involved with the processing of somatic pain, and this correlated with the perceived severity of pain. On the other hand, compared to this so-called rest phase, the pain phase produced increased somatosensory brain connectivity to the area called the anterior insula—on both the right side and the left side of the brain; this same activity was not seen in the healthy controls.
More, the researchers noted that the association between somatosensory connectivity and pain, the emotionally charged response to pain, and the other physical responses to pain (such as a rapid heart rate), were localized to the right anterior insula; but the cognitive attention to pain was localized to the left anterior insula.
So, based on this research report, it would seem that chronic pain that is experienced as a noxious physical stimulant, and is often hand-in-hand with symptoms whose origin lie in the emotional and cognitive parts of the human being, is fueled by neural links between the somatosensory part of the brain and those parts that process and express emotional and cognitive brain output.
The next step is to try to manipulate these connections to produce a patient who experiences less pain, or at least more tolerance of pain.
And while chronic pain patients experience pain as mostly a somatosensory phenomenon, it is also important to recall the importance of emotions and cognition in the experience of chronic pain. However, there is a missing link in the consideration of chronic pain: Where and what is the interface between the physical, somatic sensation of pain, and the emotional and cognitive components of a human being?
While several studies have demonstrated altered resting brain connectivity in FM, studies have not specifically probed the somatosensory system and its role in both somatic and non-somatic FM symptoms. The objective of a study published in the May, 2015, issue of “Arthritis and Rheumatology” was to evaluate resting primary somatosensory cortex connectivity and to explore how sustained, evoked deep tissue pain modulates this connectivity.
The researchers acquired functional magnetic resonance imaging and electrocardiography data on fibromyalgia patients and healthy control patients during rest and during sustained mechanical pressure-induced pain over the lower leg. They then calculated functional connectivity associated with different areas of the somatosensory part of the brain; in particular, the part of the brain that processes the lower leg pain was compared to the experience of pain during the active stimulation of pain, and after the introduction of such pain stimuli.
Interestingly, during the period after the application of the pain stimulus, there was less evidence of connectivity between the multiple areas of the brain involved with the processing of somatic pain, and this correlated with the perceived severity of pain. On the other hand, compared to this so-called rest phase, the pain phase produced increased somatosensory brain connectivity to the area called the anterior insula—on both the right side and the left side of the brain; this same activity was not seen in the healthy controls.
More, the researchers noted that the association between somatosensory connectivity and pain, the emotionally charged response to pain, and the other physical responses to pain (such as a rapid heart rate), were localized to the right anterior insula; but the cognitive attention to pain was localized to the left anterior insula.
So, based on this research report, it would seem that chronic pain that is experienced as a noxious physical stimulant, and is often hand-in-hand with symptoms whose origin lie in the emotional and cognitive parts of the human being, is fueled by neural links between the somatosensory part of the brain and those parts that process and express emotional and cognitive brain output.
The next step is to try to manipulate these connections to produce a patient who experiences less pain, or at least more tolerance of pain.
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