COURSE · PART 1 · MODULE 3
Module 3 — What May Cause or Affect FND?
There is not one complete explanation for why FND begins or continues in every person. This module separates what researchers have observed from what they have proposed, and it shows how to consider possible influences without turning them into blame or unsupported certainty.
What this module teaches
- Cause, risk factor, trigger, mechanism and maintaining factor do not mean the same thing. [1][3][4]
- The event near the beginning of symptoms may differ from what affects symptoms now. [1][3]
- Physical, psychological and social factors may have different roles in different people. [3][4]
- Trauma, stress and mental illness are not required for an FND diagnosis. [1]
- Brain-network and predictive-processing research offers possible explanations, not one settled cause or individual biomarker. [1][2][5]
- A useful treatment or explanation does not automatically prove why FND began. [1][3]
- Research claims can be judged by what was measured, who was studied, what remains uncertain and whether the result applies to an individual. [3][4][5]
Research into brain networks and group-level structural differences can coexist: “functional” and “structural” are not simple opposites. Neither provides one settled cause or an individual diagnostic biomarker. The brain-networks page explains an imaging example and its limits.
Pages
- Causes, Risk Factors, Triggers, and Maintaining Factors — how the terms differ, why the beginning and the present may differ, and how to keep facts separate from possibilities.
- Brain Networks, Prediction, Attention, and Agency — what these research ideas mean, what has been measured and what remains a proposed model.
- Physical, Psychological, and Social Factors—and How to Judge Claims — how possible influences may fit an individual life and how to recognize claims that go beyond the evidence.
Inside each page: Person with FND · Supporters · Clinicians · Research
Every page in this module uses these same four main sections.
Research and Sources
| Citation | Figure | Full citation |
|---|---|---|
| [1] | — | Hallett M, Aybek S, Dworetzky BA, McWhirter L, Staab JP, Stone J. Functional neurological disorder: new subtypes and shared mechanisms. The Lancet Neurology. 2022;21(6):537–550. FND-CIT-0003. https://doi.org/10.1016/S1474-4422(21)00422-1 |
| [2] | — | Drane DL, Fani N, Hallett M, Khalsa SS, Perez DL, Roberts NA. A framework for understanding the pathophysiology of functional neurological disorder. CNS Spectrums. 2021;26(6):555–561. FND-CIT-0006. https://doi.org/10.1017/S1092852920001789 |
| [3] | — | Pick S, Goldstein LH, Perez DL, Nicholson TR. Emotional processing in functional neurological disorder: a review, biopsychosocial model and research agenda. Journal of Neurology, Neurosurgery & Psychiatry. 2019;90(6):704–711. FND-CIT-0005. https://doi.org/10.1136/jnnp-2018-319201 |
| [4] | — | Butler M, Shipston-Sharman O, Seynaeve M, et al. International online survey of 1048 individuals with functional neurological disorder. European Journal of Neurology. 2021;28(11):3591–3602. FND-CIT-0014. https://doi.org/10.1111/ene.15018 |
| [5] | — | Bègue I, Adams C, Stone J, Perez DL. Structural alterations in functional neurological disorder and related conditions: a software and hardware problem? NeuroImage: Clinical. 2019;22:101798. FND-CIT-0004. https://doi.org/10.1016/j.nicl.2019.101798 |