A Randomized, Controlled Neuroimaging Trial of Cognitive-Behavioral Therapy for Fibromyalgia Pain 2023 Lee et al

Andy

Retired committee member
Objective

Fibromyalgia (FM) is characterized by pervasive pain-related symptomatology and high levels of negative affect. Mind-body treatments such as cognitive-behavioral therapy (CBT) appear to foster improvement in FM via reductions in pain-related catastrophizing, a set of negative, pain-amplifying cognitive and emotional processes. However, the neural underpinnings of CBT's catastrophizing-reducing effects remain uncertain. This randomized, controlled, mechanistic trial was designed to assess CBT's effects on pain catastrophizing and its underlying brain circuitry.

Methods
Of 114 enrolled participants, 98 underwent a baseline neuroimaging assessment and were randomized to 8 weeks of individual CBT or a matched fibromyalgia education control condition (EDU).

Results
Compared with EDU, CBT produced larger decreases in pain catastrophizing at post-treatment (P < 0.05), and larger reductions in pain interference and symptom impact. Decreases in pain catastrophizing played a significant role in mediating those functional improvements in the CBT group. At baseline, brain functional connectivity between ventral posterior cingulate cortex (vPCC), a key node of the default mode network, and somatomotor and salience network regions was increased during catastrophizing thoughts. Following CBT, vPCC connectivity to somatomotor and salience network areas was reduced.

Conclusion
Our results suggest clinically important and CBT-specific associations between somatosensory/motor- and salience-processing brain regions and the default mode network in chronic pain. These patterns of connectivity may contribute to individual differences (and treatment-related changes) in somatic self-awareness. CBT appears to provide clinical benefits at least partially by reducing pain-related catastrophizing and producing adaptive alterations in default mode network functional connectivity.

Paywall, https://acrjournals.onlinelibrary.wiley.com/doi/10.1002/art.42672
 
Intro opens with —

Fibromyalgia (FM) is a nociplastic pain disorder characterized by function-impairing symptoms such as widespread pain, fatigue, cognitive difficulties, and psychosocial distress (1). FM predominantly affects women, and the broad array of FM symptoms and contributory factors suggests a strong biopsychosocial basis (2).

The supporting references are:

1. Nociplastic pain: towards an understanding of prevalent pain conditions (2021, The Lancet) noted previously here
2. Treatment of Fibromyalgia in the 21st Century (2021, JAMA Internal Medicine)
 
CBT uses structured techniques to alter distorted thoughts and negative moods, and within only a few sessions, can produce lasting changes in pain-related outcomes.

... or your brain-washing convinces people to score their symptoms lower, and where by "lasting" you mean "a few weeks or months".

One mechanistic pathway supporting CBT’s benefits appears to involve reductions in negative affective processes such as pain-related catastrophizing. Catastrophizing, commonly measured by the Pain Catastrophizing Scale (PCS), is a pain-specific psychosocial construct comprised of cognitive and emotional processes such as helplessness, rumination, and magnification of pain complaints.

Well I guess when we're being accused of catastrophising, we can reply that that's a pain-specific psychosocial construct don't-ya-know, so has no bearing on any non-pain symptoms we might be "catastrophising" about.

(They seem to have dropped the 'bio' with this psychosocial construct.)

While catastrophizing is related to general measures of negative affect, it also has a unique and specific influence on pain-related outcomes. Prior CBT studies have identified catastrophizing as a crucial process variable contributing to the pain reducing benefits of mind-body therapies. Thus, changes in the brain circuitry underlying pain catastrophizing may underpin the clinical improvements and putative “normalization” of brain function following CBT.

Or it might be the brain-washy questionnaire thingy.
 
Objective

Fibromyalgia (FM) is characterized by pervasive pain-related symptomatology and high levels of negative affect. Mind-body treatments such as cognitive-behavioral therapy (CBT) appear to foster improvement in FM via reductions in pain-related catastrophizing, a set of negative, pain-amplifying cognitive and emotional processes. However, the neural underpinnings of CBT's catastrophizing-reducing effects remain uncertain. This randomized, controlled, mechanistic trial was designed to assess CBT's effects on pain catastrophizing and its underlying brain circuitry.

Methods
Of 114 enrolled participants, 98 underwent a baseline neuroimaging assessment and were randomized to 8 weeks of individual CBT or a matched fibromyalgia education control condition (EDU).

Results
Compared with EDU, CBT produced larger decreases in pain catastrophizing at post-treatment (P < 0.05), and larger reductions in pain interference and symptom impact. Decreases in pain catastrophizing played a significant role in mediating those functional improvements in the CBT group. At baseline, brain functional connectivity between ventral posterior cingulate cortex (vPCC), a key node of the default mode network, and somatomotor and salience network regions was increased during catastrophizing thoughts. Following CBT, vPCC connectivity to somatomotor and salience network areas was reduced.

Conclusion
Our results suggest clinically important and CBT-specific associations between somatosensory/motor- and salience-processing brain regions and the default mode network in chronic pain. These patterns of connectivity may contribute to individual differences (and treatment-related changes) in somatic self-awareness. CBT appears to provide clinical benefits at least partially by reducing pain-related catastrophizing and producing adaptive alterations in default mode network functional connectivity.

Paywall, https://acrjournals.onlinelibrary.wiley.com/doi/10.1002/art.42672

"However, the neural underpinnings of CBT's catastrophizing-reducing effects remain uncertain." I think unknowable would be better than uncertain.

No clue wot they are measuring nor impossible to establish validity. (I've not read the paper).

So, in conclusion 'we' showed some stuff changed a bit when the patients had cbt making it look sciency with some brain scans. Perhaps talking and problem solving with an empathetic person results in some changes. Whoopee. No qualitative data to see what was meaningful for patients. I bet what was helpful to patients wasn't their so called 'catastrophising'. And no mention of reduction in pain or symptoms. Maybe that is in there but I suspect not, if it's not in the abstract 'cos surely you'd wanna shout about that :sneaky:
 
From the Supporting Information S1, the patient is in the scanner and reads the following statements on a screen. Change in blood flow in certain brain regions is then evaluated.

The Pain Catastrophizing fMRI task consisted of visually presenting 6 pain-catastrophizing (CAT) statements (i.e., “I become afraid that the pain will get worse”, “I keep thinking of other painful events”, “I anxiously want the pain to go away”, “I keep thinking about how badly I want the pain to stop”, “There’s nothing I can do to reduce the intensity of the pain”, “The pain is awful and I feel that it overwhelms me”) drawn from the PCS, and 6 control neutral (NEU) statements (i.e., “Our body is made up mostly of water”, “There is a rug and two baskets on the floor”, “Tablecloths and utensils are in the basket”, “There are four drawers in the cabinet containing folders”, “There are a lot of containers that have a blue lid and a clear base”, “The glasses are on the table and the keys are in the bag”) which were of similar lexical difficulty and word count.

At baseline, FM patients showed significantly increased ‘pain catastrophizing-specific’ brain responses (i.e., CAT > NEU contrast) in several DMN subregions: ventral and dorsal posterior cingulate cortex (vPCC and dPCC, respectively), precuneus (PC), medial prefrontal cortex (mPFC), ventrolateral and dorsolateral prefrontal cortex (vlPFC and dlPFC, respectively), angular gyrus/inferior parietal lobule (IPL), and superior temporal sulcus (STS). When compared with our previously-reported findings from a smaller cohort (N=31) (20), the results from our current analysis showed significant overlap, but also showed an extension of CAT>NEU activation to other areas of the DMN (e.g., dlPFC and STG) as outlined by Yeo et al. (31)

20. Encoding of Self-Referential Pain Catastrophizing in the Posterior Cingulate Cortex in Fibromyalgia (2018, Arthritis & Rheumatology, PubMed)
31. The organization of the human cerebral cortex estimated by intrinsic functional connectivity (2011, Journal of Neurophysiology)

I'm not sure how everyone is convinced that the brain responses they see are not due to the patient actually suffering from severe chronic pain that is peripherally (or at least below the brain) generated. Are there any similar studies with positive controls, ie people who are known to have a disorder of peripheral pain generation (eg the voltage-gated sodium channels)? Or is this something that simply "doesn't exist"?
 
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Could the FM subjects in this research while under the scanner and reading those pain catastrophizing statements, be reacting merely to the word "pain" contained in those statements?

They could be reacting to the fact that they were expected to be reacting to the fact that they were expecting to be reacting to the word pain!

fMRI becomes useless in these situations. Would we expect people with FM to have different thoughts from others, or from earlier on, during these experiments. Of course they would. They know what is going on. Perhaps the fMRI signal is for the bit of the brain that thinks 'God, these people are daft'.
 
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