# Ultra-high field brain MRI for functional neurological disorder: opportunities and challenges

**Authors:** Sverre Myren, Johannes Jungilligens, Ibai Diez, Erlend Bøen, Torbjørn Elvsåshagen, Birte Forstmann, Maryam Ziaei, Thanh P. Doan

PMC · DOI: 10.1016/j.nicl.2026.103972 · 2026-02-19

## TL;DR

Ultra-high field MRI (UHF) can improve understanding of brain network dysfunctions in functional neurological disorder (FND) by offering higher sensitivity and resolution than standard MRI.

## Contribution

A biophysical multimodal MRI framework is proposed to capture FND symptom construction using UHF MRI techniques.

## Key findings

- UHF MRI provides better spatial resolution and contrast sensitivity to study microcircuit and neurochemical mechanisms in FND.
- Abnormalities in FND may be below the detection limits of standard MRI field strengths.
- A multimodal framework integrating multiple MRI techniques can yield biologically interpretable markers for FND.

## Abstract

Figures adapted from BioRender.

•FND arises from brain network dysfunctions, yet imaging findings are inconsistent.•UHF MRI offers higher sensitivity to reveal alterations underlying FND.•We outline the opportunities and challenges of applying UHF MRI to FND research.•We propose a biophysical multimodal MRI framework capturing FND symptom construction.•Most of the underlying principles are also applicable at standard field strengths.

FND arises from brain network dysfunctions, yet imaging findings are inconsistent.

UHF MRI offers higher sensitivity to reveal alterations underlying FND.

We outline the opportunities and challenges of applying UHF MRI to FND research.

We propose a biophysical multimodal MRI framework capturing FND symptom construction.

Most of the underlying principles are also applicable at standard field strengths.

Functional neurological disorder (FND) is a common condition with debilitating neurological symptoms emerging from brain network alterations; yet, neuroimaging findings are often of unclear neurobiological significance. Contemporary mechanistic accounts indicate disturbances in hierarchical brain processing involving arousal, interoception, salience attribution, affective-motor integration, and self-agency. The findings of abnormal brain function with only partially consistent neuroimaging abnormalities imply that relevant pathology may occur below the resolution or contrast capabilities of conventional clinical MRI. Ultra-high field MRI (UHF, 7T and above) provides substantially improved spatial resolution, contrast sensitivity, and physiological specificity needed to interrogate microcircuit-, mesoscale-, and neurochemical-level mechanisms. We review how UHF-enhanced structural, diffusion, functional, and spectroscopic techniques can address long-standing mechanistic questions in FND. Selected targets that operate at different spatial scales are used to illustrate how UHF MRI can resolve features that are either inaccessible or not fully reliable at standard magnetic field strengths (1.5–3T). To synthesize these advances, we propose a biophysical multimodal MRI framework that integrates quantitative MRI, diffusion MRI, functional MRI, and MR spectroscopy to derive biologically interpretable markers spanning microstructure, white matter architecture, circuit dynamics, and neurometabolic domains. This approach aligns with contemporary computational and neurobiological models of FND and offers a scalable roadmap for future research. Together, UHF MRI and biophysically grounded multimodal imaging can enable a new generation of mechanistic studies in FND, with potential implications for diagnosis, subtype stratification, and biomarker development.

## Linked entities

- **Diseases:** functional neurological disorder (MONDO:0002104), FND (MONDO:0002104)

## Full-text entities

- **Genes:** PAG1 (phosphoprotein membrane anchor with glycosphingolipid microdomains 1) [NCBI Gene 55824] {aka CBP, PAG}
- **Diseases:** panic (MESH:D016584), structural abnormalities (MESH:C566527), multiple sclerosis (MESH:D009103), FND (MESH:D003291), myelin loss (MESH:D003711), gait disturbances (MESH:D020233), dystonia (MESH:D004421), movement disorders (MESH:D009069), loss of control over movements (MESH:D006963), metallic taste (MESH:D013651), atrophy (MESH:D001284), arousal dysregulation (MESH:D020921), Volume loss (MESH:D016388), abnormal brain function (MESH:D001927), hallucinations (MESH:D006212), dizziness (MESH:D004244), Impaired sense of agency (MESH:D020886), sensory deficits (MESH:D012678), limb disuse (MESH:D020966), emotion dysregulation (MESH:D021081), deficits in attention and inhibitory control (MESH:D001289), major depressive disorder (MESH:D003865), tremor (MESH:D014202), communication and swallowing disorders (MESH:D003680), seizure (MESH:D012640), anxiety (MESH:D001007), iron dysregulation (MESH:D000090463), hyperactivity (MESH:D006948), cognitive disorder (MESH:D003072), LC (OMIM:601308), Alzheimer's Disease (MESH:D000544), neurological and psychiatric disorders (MESH:D001523), pain (MESH:D010146), weakness (MESH:D018908), neurological disorder (MESH:D009461)
- **Chemicals:** Gln (MESH:D005973), neuromelanin (MESH:C014121), glutathione (MESH:D005978), 13C (MESH:C000615229), carbon (MESH:D002244), Glu (MESH:D018698), 1H (-), GABA (MESH:D005680), creatine (MESH:D003401), serotonin (MESH:D012701), Cho (MESH:C034482), sodium (MESH:D012964), noradrenaline (MESH:D009638), phosphorus (MESH:D010758), water (MESH:D014867), N-acetyl aspartate (MESH:C000179), iron (MESH:D007501), choline (MESH:D002794), myo-inositol (MESH:D007294)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** glutamate from glutamine

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13010964/full.md

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Source: https://tomesphere.com/paper/PMC13010964