Mark Hallett and the renaissance of functional neurological disorder, 2026, Stone

Dolphin

Senior Member (Voting Rights)

Clinical Parkinsonism & Related Disorders

Volume 15, 2026, 100464
Clinical Parkinsonism & Related Disorders

Mark Hallett and the renaissance of functional neurological disorder​


Author links open overlay panelJon Stone
Show more
Add to Mendeley
Share
Cite
https://doi.org/10.1016/j.prdoa.2026.100464Get rights and content
Under a Creative Commons license
Open access

Abstract​

This article traces the contributions of Mark Hallett (1943–2025) to Functional Neurological Disorder (FND) from 2003 to his death.
Mark brought his expertise in motor physiology, free will, volition and agency to this neglected but common condition.

He raised awareness of our need to understand its pathophysiology, natural history and treatment, and then became a key researcher investigating abnormalities of brain networks found in individuals with the condition, as well as its multifactorial aetiology.

He played a pivotal role in organising international meetings and books on functional movement disorder and FND, culminating in his role as the first president of the International FND Society (2019–2022).

In 2024, Mark Hallett gave the 2024 American Academy of Neurology Wartenberg lecture, recalling “la lésion dynamique” proposed by Charcot as the pathophysiology of FND in the 19th century.

This lecture was emblematic of the renaissance of interest in FND after a long period of neglect and his huge contribution to our understanding of the disorder.

Keywords​

Functional neurological disorder
Mark Hallett
Psychogenic
Conversion disorder
Pathophysiology
Volition
 

4. Havana syndrome and post-infectious myalgic encephalomyelitis/chronic fatigue syndrome​

In the last few years of his time at NIH, Mark contributed to related research on two contested syndromes. NIH carried out a reassessment of the controversial “Havana syndrome”, mostly US diplomatic staff posted in Cuba who developed a range of symptoms including sensory sensitivity, headache, fatigue and cognitive symptoms [49]. My understanding is that his second author position on this paper reflected the fact that Mark saw most of these patients himself as part of extensive week-long testing. Initial studies of these patients published in JAMA [50], [51] suggested they had evidence of brain damage, perhaps consistent with some kind of remote weapon. The final NIH conclusion was that 24% had functional neurological disorder, mostly persistent postural perceptual dizziness and a range of other sometimes non-specific symptoms, but no evidence of brain damage or unusual findings on structural or functional neuroimaging.

In a similarly thorough deep phenotyping study of individuals with post-infectious myalgic encephalomyelitis/chronic fatigue syndrome, 17 individuals with the condition underwent an enormous battery of tests including functional neuroimaging, immune, autonomic, cognitive, cardiopulmonary, cerebrospinal fluid and muscle strength testing [52]. One of the key findings was a motor physiology one. Compared to healthy volunteers, there was a reduction in ability to maintain a moderate grip force, which correlated, as in FND, with decreased activity of the right temporoparietal junction. There was an increase in sympathetic but a decrease in parasympathetic activity, which could not be attributed to anxiety, as well as downregulations of cerebrospinal fluid tryptophan metabolites and some interesting immunological leads, although no consistent pattern of immune dysregulation.
 
Back
Top Bottom