Review Migraine and functional neurological disorder (FND)—a review of comorbidity and potential overlap 2025 Stone et al

Andy

Andy

Senior Member (Voting rights)

Abstract​

Migraine and functional neurological disorder (FND) are two of the most common conditions in neurological practice. It is assumed that the two conditions have distinct underlying mechanisms. However, it can be clinically challenging to disentangle their relative contributions to a patient's symptoms. In addition, apart from the relationship between persistent postural perceptual dizziness (PPPD) and migraine, the frequency of co-occurrence has not been characterized in detail. Contemporary conceptualizations of FND have driven a re-evaluation of its relationship to other neurological disorders, including migraine. We carried out a narrative review of the literature examining the co-occurrence of migraine and FND. We also explored their comorbidities, aetiological risk factors and mechanisms, focusing especially on areas of potential overlap.

Our review suggests increased frequency of migraine in people with functional seizures compared to epilepsy, but data from people with functional motor symptoms is mixed. Robust epidemiological studies evaluating the frequency of FND in migraine are lacking. Similar to other neurological disorders, migraine is an established trigger of FND. Female gender, adverse childhood experiences and comorbid psychiatric and functional disorders, such as irritable bowel syndrome and fibromyalgia, are more common in both conditions than in controls, but perhaps more so in FND. Mechanistic research in both conditions highlights converging frameworks of dysregulated allostatic/stress responses in the context of predictive processing models of the brain. This has implications for pharmaceutical and rehabilitation treatments.

The relationship between migraine and FND is poorly studied. An overview of their overlap offers a model of non-dualistic thinking within a clinical neuroscience framework for future studies.

Open access
 
"Functional disorder comorbidity

A considerable amount of epidemiological evidence indicates substantial overlap between common functional (somatic) disorders, including irritable bowel syndrome, persistent fatigue states and chronic primary pain syndromes such as fibromyalgia.85 A similar overlap for both FND and migraine would support a mechanistic connection."

Ref 85 is to https://www.s4me.info/threads/migra...omatic-disorders-2022-henningsen-et-al.30474/
 
Forget the FND but maybe the 2-3x female predominance for migraine can tell us more about ME/CFS. In our Qeios article we suggested that this sort of ratio is largely seen in autoimmune diseases. But migraine seems to show a similar major female predominance.

Migraine may be more about blood vessels than nerves but it does suggest that CNS physiology is different in women.
 
How they explain migraines:
Allostasis and predictive processing have also been recently integrated into a mechanistic account of migraine,99,100 which proposes that symptoms arise from multimodal sensory amplifications of prediction errors initiated as forms of a ‘failsafe’ procedure to maintain allostasis. Put more simply, the brain shuts itself down, in anticipation or as a consequence of being overloaded, so it can ‘reset’.100 In chronic migraine, there may be a similar ‘learnt’ component corresponding to overweighted predictions.
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This next part is outrageous. They acknowledge that predictive processing and allostasis are theoretical unproven concepts, but claim that they still have use in rehabilitation and treatment.
We recognize that predictive processing and allostasis are broad frameworks that have been applied to many neurological and psychiatric disorders, and that while conceptually appealing, they remain one of many competing frameworks that still require more substantiation. Nonetheless, such frameworks are directly applicable to treatment, for example, to rehabilitation approaches to both conditions.
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Even more insanity: they say that the understanding of migraines have evolved due to people doing actual science. Apparently, they seem to be saying that this has not been done yet in FND. But they still conclude that predictive processing models «are likely to be relevant in FND and migraine».
Overall, different paradigms and experimental approaches limit current comparison or meaningful synthesis, but we would encourage further investigation like this. Treatment for migraine has advanced by studying concrete neurophysiological and testable scientific hypotheses. Similar evolving neurophysiological, genetic, neuroimaging and neurotransmitter research in FND could lead to similar advances in that disorder. The scientific field does not have to choose between ‘top-down’ predictive processing models and ‘bottom-up’ neurophysiological perspectives, since both are likely to be relevant in FND and in migraine.
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This is not science. It’s propaganda.
The function of propaganda is . . . not to weigh and ponder the rights of different people, but exclusively to emphasize the one right which it has set out to argue for. Its task is not to make an objective study of the truth, in so far as it favors the enemy, and then set it before the masses with academic fairness; its task is to serve our own right, always and unflinchingly.
 
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I googled 'pathophysiology of migraine'. The AI summary response is interesting in that it is really terrible - complete bullshit that ultimately says 'nobody has any real idea, or if they do the research community as a whole isn't aware of it'.

Surprise surprise it mentions mediators as inducing inflammation - which of course isn't there in migraine either. It talks of neural dysregulation - pretty much like BACME. It talks of activation of the trigeminal nerve - which is meaningless because the trigeminal nerve contains a whole range of different afferent and efferent neuron populations.

If anyone needs convincing that AI summaries are worse than useless this does it.
 
Jon Stone reports honoraria from UptoDate, personal fees from Expert Witness Work and grants from Chief Scientist Office, outside the submitted work, and runs a self-help website, www.neurosymptoms.org, for patients with functional neurological disorder; he is the president elect of the FND Society and on medical advisory boards to FND Hope, FND Hope UK and FND Action.

Jan Coebergh reports personal fees from Expert Witness Work and speaker fees from Merck Serono and Bial.

Lujain Khoja reports no potentially relevant conflicts of interest.

Matthew Butler reports no potentially relevant conflicts of interest.

Timothy R Nicholson reports honoraria for textbooks and talks on FND and other medical topics, personal fees from Expert Witness Work and research grants from the UK National Institute for Health and Care Research on FND and other disorders.

David W Dodick reports consulting, AbbVie, Genentech and Nocira, and honoraria, Wolters Kluwer, Oxford University Press and Cambridge University Press. Stock options/shareholder/patents/board of directors: Ctrl M (options), Aural analytics (options), Axon Therapeutics (board/options), ExSano (options), Palion (options), Keimon Medical (Options), Man and Science, Healint (options), Theranica (options), Second Opinion/Mobile Health (options), Epien (options), Nocira (options), Matterhorn (shares), Ontologics (shares), King-Devick Technologies (options/board), Precon Health (options/board), ScotiaLyfe (board), EigenLyfe (options/board), AYYA BioSciences (options), Nuvie Bio (options/board), Cephalgia Group (options/board) and Atria Health (options/employee). Patent 17189376.1-1466:vTitle: Onabotulinum Toxin Dosage Regimen for Chronic Migraine Prophylaxis (non-royalty bearing).
 
Jonathan Edwards said:
I googled 'pathophysiology of migraine'. The AI summary response is interesting in that it is really terrible - complete bullshit that ultimately says 'nobody has any real idea, or if they do the research community as a whole isn't aware of it'.

Surprise surprise it mentions mediators as inducing inflammation - which of course isn't there in migraine either. It talks of neural dysregulation - pretty much like BACME. It talks of activation of the trigeminal nerve - which is meaningless because the trigeminal nerve contains a whole range of different afferent and efferent neuron populations.

If anyone needs convincing that AI summaries are worse than useless this does it.
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Is anything actually properly known about migraines? Or is there only rubbish?
 
The first migraine I remember was about age 5, I thought my brain was breaking and something was seriously wrong, but I was alone in bed and unable to move to ask for help.
At 7 I was sent home from school with one, and was confused with everyone saying “it’s her first migraine” it certainly wasn’t.
I’m getting really fed up of the overlap between people who want to psychologise medical problems and people who write research papers.
 
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