Functional Neurological Disorders after Head Injury Edition
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Functional Neurological Disorder after Head Injury
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BRAIN INJURY
Traumatic Brain Injury and Functional Neurological Disorder: When a Concussion is No Longer a Concussion
Ginger Polich • Ny-Ying Lam • Daniel Goodman
Laura
Functional Seizures and Traumatic Brain Injury: Biopsychosocial Assessment and Treatment
Ryan Van Patten, PhD • W. Curt LaFrance Jr., MD, MPH
Corresponding Author: Ryan Van Patten, PhD, ABPP-CN
Jocelyn Brystorm
Functional Dizziness After Traumatic Brain Injury
Jeffrey P. Staab, MD, MS
Corresponding Author: Jeffrey P. Staab, MD, MS
NORTH AMERICAN BRAIN INJURY SOCIETY
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BRAIN INJURY PROFESSIONAL
PUBLISHER J. Charles Haynes, JD
CO-EDITOR IN CHIEF Beth Slomine, PhD - USA
CO-EDITOR IN CHIEF Nathan Zasler, MD - USA
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TECHNOLOGY EDITOR Stephen K. Trapp, PhD - USA
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Editor Bio
Dr. Beth Slomine is CoDirector of the Center for Brain Injury Recovery and Assistant Vice President of Psychology at Kennedy Krieger Institute. She is Professor of Psychiatry & Behavioral Sciences at Johns Hopkins University School of Medicine and has a secondary appointment in the Department of Physical Medicine & Rehabilitation. She is a licensed psychologist, board certified clinical neuropsychologist, and board certified subspecialist in pediatric neuropsychology. Research interests include neurobehavioral measurement, outcomes, and interventions following pediatric neurological injury Dr. Slomine has authored >100 peer-reviewed manuscripts, numerous book chapters, and co-edited a textbook entitled Cognitive Rehabilitation for Pediatric Neurological Conditions.
editor from the
As Co-Editor-in-Chief, I am pleased to introduce this special issue of Brain Injury Professional, which shines a spotlight on Functional Neurological Disorder (FND) after head injury, a topic that is gaining overdue attention in the brain injury rehabilitation community. Our guest editor, Dr. Noah Silverberg, a board certified clinical neuropsychologist, brings deep expertise in brain injury rehabilitation and has curated an exceptional collection of articles that explore the complex interface between traumatic brain injury (TBI), concussion, and injury to the head without TBI and their relationship to FND.
As highlighted by Dr. Silverberg, FND is often described as the most common neuropsychiatric condition you’ve never heard of, and its relevance to neurorehabilitation is frequently underrecognized. This issue addresses that gap by providing clinicians with practical insights into identifying, diagnosing, and treating FND in patients with persisting post-concussive symptoms. Articles in this issue cover a wide range of topics.
Polich, Lam & Goodman outline how FND can emerge after concussion, stressing early recognition and positive diagnosis using rule-in signs. McWhirter and Carson describe the features of functional cognitive disorder (FCD) and present their approach to the clinical assessment and treatment of patients with FCD after TBI. Van Patten and LaFrance review functional seizures and advocate for biopsychosocial assessment and evidence-based psychotherapy. Staab examines functional dizziness, particularly persistent posturalperceptual dizziness (PPPD), highlighting triggers of PPPD and effective treatment approaches. Bystrom provides a patient perspective underscoring the importance of compassionate communication and instilling hope when delivering an FND diagnosis. The tech column by Ranford reviews neurosymptoms.org as a trusted resource for patient education and clinical support. Lastly, Dr. Silverberg’s expert interview with behavioral neurologist, Matthew Burke, highlights shared risk factors between concussion and FND and strategies for prevention through early education and reframing negative beliefs. Collectively, these articles underscore the importance of recognizing functional symptoms early, delivering clear and compassionate diagnoses, and employing multidisciplinary, FNDinformed rehabilitation strategies. This special issue serves as a unique and valuable resource for clinicians, researchers, and advocates committed to optimizing care for individuals with FND cared for by brain injury specialists.
Finally, mark your calendars for upcoming conferences, including the 2026 Collaborative Brain Injury Summit, in Arlington, VA, March 11-15, and the 6th International Paediatric Brain Injury Society Conference, in Calgary, AB, Canada, April 29-May 2nd 2026.
Beth S. Slomine, PhD, ABPP
Noah Silverberg
Editor Bio
Dr. Noah Silverberg is an Associate Professor at the University of British Columbia and scientist with the Djavad Mowafaghian Centre for Brain Health and Vancouver Coastal Health Research Institute’s Centre for Aging SMART. He is also a board-certified neuropsychologist (ABPP-CN) with 15 years of brain injury rehabilitation experience, primarily at GF Strong Rehabilitation Centre. Dr. Silverberg’s research program focuses on psychological
from the
guest editor
Functional neurological disorder (FND) is often introduced as the most common neuropsychiatric condition you have never heard of. Even brain injury professionals who know FND by name typically underappreciate its relevance to traumatic brain injury (TBI) rehabilitation. Many fail to spot it in their patients, hold views about FND that have not kept pace with the quickly evolving science, and/or feel unsure about how to approach its treatment.
There has been an overdue and welcomed surge of interest in FND in the recent medical literature, but little has been written specifically about FND as a complication of TBI or head impact without TBI. The clinical presentation of FND can include seizures, dizziness, gait abnormalities, and/or cognitive difficulties that mimic the effects of TBI but are distinct in ways that will hopefully become clear by reading this special issue. FND typically starts after an event that perturbs brain function, such as a major stressor, illness, medical procedure, or in this case, a traumatic injury, typically coinciding with stressor(s). The event gives rise to symptoms that perpetuate, becoming decoupled from their origin cause. The brain essentially misinterprets sensory information from, and sends faulty signals to, the body. Unlike TBI, FND often does not gradually improve on its own, but rather requires rehabilitation to retrain the brain to do what it had been capable of all along, because FND is not an irremediable consequence of structural brain injury.
I am grateful to the editors of Brain Injury Professional for the opportunity to shine a spotlight on FND after TBI with this Special Issue and to the world-class interdisciplinary group of contributing authors for providing this light. Polich provides an overview of FND following mild-spectrum TBI, its cause(s), and the fundamentals of its clinical management. Bystrom shares her personal experience as a patient, highlighting what was helpful (and not) about how her FND diagnosis was communicated, offering insights for clinicians faced with this task. Articles by McWhirter & Carson (cognitive), Staab (dizziness), and Van Patten & LaFrance (seizures) sharpen the spotlight on the most common subtypes, or clinical presentations of FND after TBI. Ranford reviews the Neurosymptoms.org website as a resource for patient education and treatment planning. Finally, Burke, as one of a small number of clinician-scientists whose practice focuses on the intersection of FND and TBI, tackles pressing questions in the field. Our hope is that this Special Issue provides a launching pad for brain injury professionals to learn more about FND, provide “FND-aware” care (to quote Bystrom), and advocate to their colleagues to do the same.
determinants of recovery from concussion/traumatic brain injury (TBI) and effectiveness of rehabilitation therapies. Over the past few years, the intersection of concussion and functional neurological disorder has become a major interest. Dr. Silverberg has held several leadership positions (e.g., Chair of the American Congress of Rehabilitation Mild TBI Task Force and Co-Chair of Working Groups with the National Academies’ Action Collaborative on TBI and National Institutes of Health TBI Classification Initiative) and contributed to clinical practice guideline development in the field of concussion/TBI. He is an Associate Editor with the Journal of Neurotrauma.
Introduction
In the classic concussion presentation, a patient sustains a head strike resulting in range of clinical signs and symptoms 1, with recovery taking place within weeks to months. While most individuals improve relatively quickly, a substantial minority report persisting symptoms after concussion (PSaC) 2. Patients may also display highly unusual neurologic symptoms subsequent to a head strike, some of which cannot easily be attributable to a concussive etiology 3. Here clinicians may need to look for alternative symptom explanations, including a diagnosis of functional neurological disorder (FND).
FND is a neuropsychiatric condition that may present with a broad range of symptoms, involving motor (e.g. weakness, tremors, gait abnormalities, speech difficulties), sensory (e.g. dizziness, visual disturbance, functional seizures), and/or cognitive domains 4 FND may exist in isolation or be co-morbid with other neurologic disorders, and present with single or multiple functional symptoms, which often fluctuate over time. The reach of FND is also widespread, existing across cultures, affecting pediatric, adolescent, adult, and geriatric populations 5
There is a growing body of literature associating PSaC and FND. Concussed individuals have endorsed atypical neurologic symptoms (e.g. paralysis, dysphagia, aphonia, inability to recognize family members, tunnel vision) and somatic symptoms (e.g. shortness of breath, stomach pain) that do not typically overlap with PSaC 3 Case reports and case series have highlighted specific phenotypes developing after a concussion, including functional gait disorders, stuttering, functional weakness, functional vision and oculomotor disorders, persistent postural-perceptual dizziness (PPPD), functional cognitive disorders, and functional seizures 3,6–9. Prevalence rates of FND after concussion are not known, though in one case series from a pediatric concussion clinic, nearly 6% of individuals met criteria for a functional gait disorder 8 .
Below we will review the literature on PSaC, FND, and their intersection with regards to predisposition, pathogenesis, differential diagnosis, and treatment planning. Given the relative scarcity of literature on some of these topics, clinical observations from the authors will also be included.
Mild Traumatic Brain Injury and Functional Neurological Disorder: When a Concussion is No Longer a Concussion
Ginger Polich • Ny-Ying Lam • Daniel Goodman
While identifying functional post-concussion symptoms, communicating this information to patients, and adapting treatment approaches can be challenging, many new resources now exist to guide the clinician through the process.
Predisposing, Precipitating, and Perpetuating Factors in FND and PSaC
Conceptual models incorporating predisposing, precipitating, and perpetuating factors are commonly applied in FND and PSaC 10,11 . These factors can span the entire lifespan and biopsychosocial spectrum.
Predisposing Factors
Underlying predisposing factors shared between PSaC and FND include mental health disorders (e.g. anxiety, depression), personality factors (e.g. perfectionism, personality disorders), beliefs and expectations regarding illness, tendencies toward somatization, healthcare seeking behaviors, as well as difficult life circumstances including early life adversity, and stressors 4,12–15
Precipitating Factors
Injuries, illnesses, and/or medical procedures are more common precipitants for FND than psychological events, especially in the rehabilitation setting 16. Following a head injury, PSaC symptoms, psychosocial burden of functional impairments, and co-occurring stressors may all be relevant contributors 10 .
Perpetuating Factors
Perpetuating factors can fuel symptom persistence and/or prevent recovery in PSaC or FND. Perpetuating factors for FND might include an ongoing symptom burden that ‘perpetuates’ itself 17 , psychological comorbidities, diagnostic delays, feeling disbelieved, and compensation benefits 4. Similar overlap with perpetuating factors for PSaC can be found, including ongoing symptomatology, development or worsening of psychiatric conditions, symptom misattribution, and ongoing medicolegal pursuits 10,11,18,19
Etiological Models
Dysfunction in emotion processing and excessive self-directed attention have been implicated in both FND and PSaC. Both emotional under-regulation (e.g. emotional lability) and overregulation (e.g. emotional avoidance or impaired emotional awareness) have been noted 20–23. Impaired attentional capabilities, including focus on one physiologic system to the neglect of others, have been regularly documented in FND 21,22 and PSaC 24 as well.
Ultimately, new post-concussion symptoms may shift attention toward the symptoms. Interpreting the symptoms as threatening along with maladaptive coping mechanisms (hypervigilance, avoidance) may perpetuate the symptoms 25. Strongly held negative concussion-related beliefs 26 or concussion-related nocebo effects 27 may further reinforce sensations as symptom complexes and solidify one’s conviction of ‘brain injury’ as the cause.
These processes could generate novel functional neurological symptoms or magnify more typical post-concussive symptoms following a head strike—e.g. mild balance difficulties becoming a functional gait disorder, word-finding difficulty becoming a functional stutter, vestibular disorder transforming into PPPD. These symptoms may start out as physiological 28, but through a variety of cognitive-emotional processes, evolve into a functional disorder over time.
Current psychodynamic theories in FND consider that some functional symptoms serve a core “function” for an individual—to suppress an emotion, sustain a relationship, resolve a dilemma, or escape interpersonal conflict 29. Their relevance to PSaC is unclear at this time 28,30
Making and Delivering a FND Diagnosis
Post-concussion symptoms tend to peak within 24 hours following a head injury event. The natural history of FND after a head injury impact can vary 9,25. Some individuals manifest acute atypical symptoms (e.g. gait disorder, paralysis, stutter) that mimic stroke, while others may develop new functional neurologic symptoms after exposure to a second, often more minor event (e.g. a subsequent very mild bump to the head, whiplash, migraine, loud noise, a stressor). In yet other cases, functional symptoms evolve slowly and insidiously over the course of treatment for PSaC.
Diagnosing FND
Certain elements of the clinical history may raise suspicion for FND and cue one into the need to perform a careful physical exam to further support the diagnosis 25—see Box 1.
Box 1: Elements of a concussion history that may raise suspicion for FND
• Implausible mechanism of injury—e.g. event with only minimal impact to the head
• Atypical neurological symptoms otherwise unexplained by brain injury
• Severe appearing symptoms out of proportion with what would be expected following a concussion
• Delayed onset of symptoms, beginning days or weeks after the incident event
• Atypical natural history with symptoms abruptly or gradually worsening rather than improving over time
• Symptoms that extensively wax or wane (may fluctuate between nearly absent to severe)
• Discrepancy between reported symptoms and daily functional capabilities (e.g. substantial difficulty walking in clinic, but hiking long distances on the weekends)
• Pre-injury or comorbid trauma/abuse history, posttraumatic stress disorder, or functional somatic syndromes (e.g. IBS, fibromyalgia)
Recent literature emphasizes the importance of making a positive diagnosis of FND, rather than treating it as a diagnosis of exclusion. General rule-in features include distractibility, variability, inconsistency, enhancement with attention, and incongruency. Many examination techniques rely heavily on distraction, which may help unmask more normal neurologic function through the reduction of excessive self-directed attention 31. With use of modern technology and validated rule-in signs, misdiagnosis rates of FND are low 32 . High yield exam features that distinguish FND from traumatic brain injury (TBI) are noted in Table 1.
Table 1: Differentiating exam features for FND versus TBI symptoms
Weakness pattern neuroanatomically congruent with orthopedic injury sustained (e.g. RTC injury). Concussion or uncomplicated mTBI should not have overt weakness.
Abnormalities in vestibuloocular exam, positive Dix Hallpike or nystagmus Cooccurring lower limb injury.
Abnormal vestibular or oculomotor exam, positive Dix Hallpike, nystagmus, abnormal saccades; dizziness induced by rapid head or eye motion (e.g. on VOMS)
Stutter, difficulty talking
Difficulty reading, blurry vision, difficulty fixating on near objects
Speech should be fluent in mTBI though patients may report slowed processing speed or word-finding difficulties.
PPPD: dizziness, unsteadiness, or nonspinning vertigo on most days for at least 3 months; worse with upright posture, motion without regard to direction or position, or exposure to moving visual stimuli
Functional stutter: Effortful speech, pauses, word or syllable repetitions, child-like speech quality; may differ by topic or social setting
Convergence paralysis: Normal adduction, but unable to converge when visual target is presented at close range. Convergence spasm: normal abduction with intermittent convergence, miosis, accommodation.
Functional eye oscillations (voluntary nystagmus)
Functional tremor: Entrainment; variability in amplitude, frequency, or direction; whack-a-mole sign
Functional seizures: forced eye closure, response to external stimuli, fluctuating course (pauses, waxing/waning tempo), ictal crying, awareness retained during episode
Functional cognitive disorder: Inconsistencies in symptoms that can vary across contexts or with mood or anxiety
In a case series on post-concussive FND, nearly 75% presented with multiple functional symptoms 9. When one functional symptom is identified, it may be appropriate to look more closely for others. Mixed organic-functional symptoms presentations are also common.
Watch for differences in strength on confrontational testing versus when performing tasks. (e.g. 1/5 leg strength but able to stand) Pain can also cause give-way weakness.
Have patient walk backwards and sideways to see if functional abnormalities improve with different walking tasks. Watch gait in other contexts (when leaving clinic, heading to bathroom)
Consider VNG testing for more objective measurement of vestibular dysfunction.
Listen carefully to shifts in speech pattern when different topics are discussed
Casually observe for inconsistency, whether a patient can look at watch, phone, or read paperwork. Consider more dedicated vision testing by ophthalmology or optometry
Enhancement of physiologic or essential tremor may present if anxiety worsens after injury
Urinary incontinence and tongue biting are nonspecific
Neuropsychological testing with inconsistent performance across domains and/or failed validity testing
Communicating the Diagnosis
Communicating the diagnosis is the first step in FND treatment. Many resources are now available to help with diagnostic delivery 33. Key elements to delivering a FND diagnosis are shared in Box 2. To supply a brief conceptual explanation of FND, common analogies may include “a software not a hardware problem”, “brain overload”, “mind-body disconnection”, or “malfunction or disconnection of the nervous system.” Instead of emphasizing it as a diagnosis of exclusion, point out ‘rule in’ features on their exam.
Inquire if patients are still worrying that their symptoms are due to TBI or another specific neurological disorder. Explain why further testing is no longer needed 31
Box 2: Key elements in delivering a FND diagnosis
• Validate patient experience as genuine and common
• Name the condition: Functional Neurological Disorder
• Explain why the patient’s concussion history alone does not fully account for their symptoms
• Make a positive diagnosis of FND highlighting ‘rule-in’ exam findings
• Provide an explanatory model of FND mechanism
• Highlight potential for improvement and emphasize effective treatment approaches
• Explain how the treatments for PSaC and FND differ
In the setting of multiple neurologic symptoms and exam findings, it is important to delineate which specifically are attributable to FND and thus appropriate for FND-focused treatment. In some cases, FND may be the cause of only a subset of symptoms or amplify TBI-related symptoms. In others, FND may be replacing PSaC as the primary cause of ongoing symptoms and require a complete shift in the patient’s understanding of their disorder. Using an FND model centered on brain network dysfunction often helps patients accept the rationale behind why their head injury preceded the development of FND.
In FND at large, patients who are openly skeptical toward or reluctant to accept the diagnosis are much less likely to respond to FND-focused treatment 34. This is likely true for individuals with postconcussive FND or a PSaC/FND overlap as well.
Treatment Approach
Data supporting treatment for FND after head strike is limited. Conventional rehabilitation strategies for PSaC may require adaptations 8. Treatment should incorporate consensus- and evidencebased rehabilitative and/or psychotherapeutic strategies for FND 35–38 These typically include efforts at redirection of attention away from symptoms, minimizing fear and anxiety regarding movements, and enhancing agency 38. See Box 3 for an example on how conventional PSaC versus FND-focused rehabilitation differ, using an example of gait training 37–40
Cognitive behavioral therapy (CBT) is the most widely studied psychotherapy for FND. CBT can help address unhelpful cognitions, negative illness beliefs, health related anxiety, distress or worry regarding symptoms, impaired coping strategies, maladaptive behaviors and help patient identify FND triggers and perpetuating factors. Additional psychotherapeutic approaches such as mindfulness-based therapy, acceptance and commitment theory, and psychodynamic therapy are also frequently utilized 36,41 . Psychotherapeutic self-help books for FND are now available as well 42 Similar psychotherapeutic strategies have shown benefit for PSaC 40,43
Treatment Challenges
Treating PSaC and FND presents a unique and complex challenge that requires equally complex recognition and insight.
Diagnostic Resistance and Stigma
Patients can differ widely in their response to the FND diagnosis. The diagnosis may provide relief, empowerment, or renewed hope for some. Individuals who are strongly enmeshed with and identify as a chronically brain-injured individual may find diagnostic revision threatening, however. Potential sources of diagnostic resistance are highlighted in Box 4.
<< INSERT BOX 3. HERE >>
Box 3: Example of divergent PSaC versus FND strategies for gait rehabilitation
PSaC
Rehabilitation exercises Address vestibular-oculomotor abnormalities if present.
• Example: gaze stabilization exercises to improve the vestibuloocular reflex.
For specific deficits, introduce progressively challenging tasks
• Example: for balance, progress from stable to uneven surfaces, progress from static to dynamic exercises, progress from single to dual task exercises.
Employ a physical exercise program with stepwise progression. Stages are advanced as performance improves and symptoms reduce.
• Follow Return to Sport guidelines
FND
Retrain movement with diverted attention. This can be done by encouraging automatically generated movements and minimizing self-focused attention Employing fast, rhythmic, or unfamiliar movements can be of benefit. Externally-directed, task-oriented exercises are preferred.
• Example: if forward walking is difficult, try running, tandem gait, walking backwards, walking to music, walking while throwing a ball back and forth
Minimize fear/hyperarousal regarding movements by incorporating CBT or mindfulness techniques
• Engage patients in breathing and/or grounding exercises in session.
Help patients observe normal movements to demonstrate symptom reversibility.
• Respectfully point out normal movements when they occur
Cognitive behavioral therapy (CBT) is the most widely studied psychotherapy for FND. CBT can help address unhelpful cognitions, negative illness beliefs, health related anxiety, distress or worry regarding
Box 4: Potential sources of resistance when revising a PSaC diagnosis to concomitant FND
• Fixed negative beliefs about head injury as the sole cause of symptoms
• High level of investment in brain injury identity (e.g. participation in brain injury support groups or advocacy work, brain injury-related social media engagement)
• Limited psychological mindedness, tendency to attribute physiological symptoms of stress to medical disease
• Misunderstanding and stigma surrounding FND
• Concerns about losing concussion-related accommodations at school or work (e.g. reduced hours or responsibilities)
• Comfortably adapted to life of disability (e.g. has already made structural environmental modifications such as a wheelchair ramp in the home)
• Financial concerns regarding worker’s compensation, medical disability, or a pending personal injury lawsuit
Stigma can be another significant barrier to care and recovery. Within healthcare settings, external stigma often presents through skepticism about the legitimacy of symptoms, misattribution of symptoms to malingering or attention-seeking, and insufficient support from medical providers. These perceptions can be harmful to patients and delay access to appropriate medical care 44. Stigma that is internalized by a patient can worsen symptoms on account of increased shame and embarrassment, erode self-esteem, undermine treatment engagement, and contribute to social avoidance 44 .
Counteracting stigma requires a patient-centered and systemic approach. Validating the diagnosis through respectful, transparent communication is foundational. At the point of diagnosis—often a pivotal moment in the treatment trajectory in FND—it is essential to provide clarity, offer resources, and establish a shared understanding among the patient, caregivers, and clinical team. Education of both patients and healthcare providers fosters a more accurate understanding of comorbid FND and helps reframe the diagnosis as legitimate and treatable. When patients feel heard, believed, and supported, the psychological relief can itself become a therapeutic catalyst, promoting greater engagement and better outcomes.
Structural Barriers
Access to care remains a persistent challenge in most regions. Providers who commonly manage or are comfortably managing PSaC, may not feel as comfortable managing FND. While FNDfocused interdisciplinary clinics may be limited to academic centers in large communities, core elements can nevertheless be delivered through traditional neurorehabilitation programs.
Conclusion
Sometimes the symptoms patients attribute to their “concussion” can no longer be accounted for by PSaC and alternative diagnoses, including FND, need to be explored. Risk factors for PSaC and FND are overlapping in many circumstances, and a concussive event (along with its accompanying and ensuing challenges) can be a precipitant for FND. For clinicians treating PSaC, identifying functional symptoms and explicitly delivering the FND diagnosis, may provide new and potentially efficacious treatment avenues for PSaC patients suffering from chronic symptoms. The alternative of remaining complicit in perpetuating false patient narratives regarding one’s ‘injured brain’ may well be iatrogenic.
References
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18. Binder LM, Rohling ML. Money matters: a meta-analytic review of the effects of financial incentives on recovery after closed-head injury. Am J Psychiatry. 1996;153(1):7-10. doi:10.1176/ajp.153.1.7
19. Gunstad J, Suhr JA. “Expectation as etiology” versus “the good old days”: postconcussion syndrome symptom reporting in athletes, headache sufferers, and depressed individuals. J Int Neuropsychol Soc. 2001;7(3):323-333. doi:10.1017/s1355617701733061
20. Buzzanca-Fried KE, Snyder AR, Bauer RM, et al. Psychological Constructs From the Fear Avoidance Model and Beyond as Predictors for Persisting Symptoms After Concussion: An Integrative Review. Arch Phys Med Rehabil. 2024;105(12):2362-2374. doi:10.1016/j.apmr.2024.04.007
21. Drane DL, Fani N, Hallett M, Khalsa SS, Perez DL, Roberts NA. A Framework for Understanding the Pathophysiology of Functional Neurological Disorder. CNS spectrums. Published online September 4, 2020:1. doi:10.1017/S1092852920001789
22. Mavroudis I, Kazis D, Kamal FZ, et al. Understanding Functional Neurological Disorder: Recent Insights and Diagnostic Challenges. Int J Mol Sci. 2024;25(8):4470. doi:10.3390/ijms25084470
23. Wood RL, O’Hagan G, Williams C, McCabe M, Chadwick N. Anxiety sensitivity and alexithymia as mediators of postconcussion syndrome following mild traumatic brain injury. J Head Trauma Rehabil. 2014;29(1):E9-E17. doi:10.1097/HTR.0b013e31827eabba
24. Teodoro T, Edwards MJ, Isaacs JD. A unifying theory for cognitive abnormalities in functional neurological disorders, fibromyalgia and chronic fatigue syndrome: systematic review. Journal of Neurology, Neurosurgery and Psychiatry. 2018;89(12). doi:10.1136/jnnp-2017-317823
25. Burke MJ, Silverberg ND. New framework for the continuum of concussion and functional neurological disorder. Br J Sports Med. 2025;59(3):145-147. doi:10.1136/bjsports-2024-108154
26. Snell DL, Hay-Smith EJC, Surgenor LJ, Siegert RJ. Examination of outcome after mild traumatic brain injury: the contribution of injury beliefs and Leventhal’s common sense model. Neuropsychol Rehabil. 2013;23(3):333-362. doi:10.1080/09658211.2012.758419
27. Polich G, Iaccarino MA, Kaptchuk TJ, Morales-Quezada L, Zafonte R. Nocebo Effects in Concussion: Is All That Is Told Beneficial? Am J Phys Med Rehabil. 2020;99(1):71-80. doi:10.1097/PHM.0000000000001290
28. Lishman WA. Physiogenesis and psychogenesis in the “post-concussional syndrome.” Br J Psychiatry. 1988;153:460-469. doi:10.1192/bjp.153.4.460
29. Carson A, Ludwig L, Welch K. Psychologic theories in functional neurologic disorders. Handb Clin Neurol. 2016;139:105-120. doi:10.1016/B978-0-12-801772-2.00010-2
30. Macleod S. Post concussion syndrome: the attraction of the psychological by the organic. Med Hypotheses. 2010;74(6):1033-1035. doi:10.1016/j.mehy.2010.01.002
31. Aybek S, Perez DL. Diagnosis and management of functional neurological disorder. BMJ. 2022;376:o64. doi:10.1136/bmj.o64
32. Stone J, Smyth R, Carson A, et al. Systematic review of misdiagnosis of conversion symptoms and “hysteria.” British Medical Journal. 2005;331(7523). doi:10.1136/bmj.38628.466898.55
33. Bennett K, Diamond C, Hoeritzauer I, et al. A practical review of functional neurological disorder (FND) for the general physician. Clin Med (Lond). 2021;21(1):28-36. doi:10.7861/clinmed.2020-0987
34. Adams C, Anderson J, Madva EN, LaFrance WC, Perez DL. You’ve made the diagnosis of functional neurological disorder: now what? Pract Neurol. 2018;18(4):323-330. doi:10.1136/practneurol-2017-001835
35. Baker J, Barnett C, Cavalli L, et al. Management of functional communication, swallowing, cough and related disorders: Consensus recommendations for speech and language therapy. Journal of Neurology, Neurosurgery and Psychiatry. 2021;92(10):1112-1125. doi:10.1136/jnnp-2021-326767
36. Gutkin M, McLean L, Brown R, Kanaan RA. Systematic review of psychotherapy for adults with functional neurological disorder. J Neurol Neurosurg Psychiatry. Published online November 5, 2020:jnnp-2019321926. doi:10.1136/jnnp-2019-321926
37. Nicholson C, Edwards MJ, Carson AJ, et al. Occupational therapy consensus recommendations for functional neurological disorder. Journal of Neurology, Neurosurgery & Psychiatry. 2020;91(10):1037-1045. doi:10.1136/jnnp-2019-322281
38. Nielsen G, Stone J, Matthews A, et al. Physiotherapy for functional motor disorders: a consensus recommendation. Journal of Neurology, Neurosurgery & Psychiatry. 2015;86(10):1113-1119. doi:10.1136/ jnnp-2014-309255
39. Marwaa MN, Klakk Egebæk H, Dalgaard Guldager J. Occupational and Physiotherapy modalities used to support interdisciplinary rehabilitation after concussion: A Scoping Review. J Rehabil Med. 2023;55:jrm4512. doi:10.2340/jrm.v55.4512
Author Bios
40. Rytter HM, Graff HJ, Henriksen HK, et al. Nonpharmacological Treatment of Persistent Postconcussion Symptoms in Adults: A Systematic Review and Meta-analysis and Guideline Recommendation. JAMA Network Open. 2021;4(11):e2132221. doi:10.1001/jamanetworkopen.2021.32221
41. Baslet G, Ridlon R, Raynor G, Gonsalvez I, Dworetzky BA. Sustained improvement with mindfulnessbased therapy for psychogenic nonepileptic seizures. Epilepsy Behav. 2022;126:108478. doi:10.1016/j. yebeh.2021.108478
42. Williams C, Kent C, Smith S, Carson A, Sharpe M, Cavanagh J. Overcoming Functional Neurologic Symptoms a Five Areas Approach. Hodder Arnold; 2011.
43. Smith A, King NS, Carrigan N, Reed N. What psychological interventions are effective for individuals with prolonged post-concussion symptoms of at least 12 months following mild traumatic brain injury? A systematic review. Neuropsychol Rehabil. Published online December 16, 2024:1-31. doi:10.1080/0960201 1.2024.2435283
44. McLoughlin C, McWhirter L, Pisegna K, et al. Stigma in functional neurological disorder (FND) - A systematic review. Clin Psychol Rev. 2024;112:102460. doi:10.1016/j.cpr.2024.102460
Ginger Polich is an Assistant Professor of Physical Medicine and Rehabilitation at Spaulding Rehabilitation Hospital / Mass General Brigham. She received a BA in Sociocultural Anthropology from Amherst College in 2006, a MS from UC-Berkeley in 2011, and a MD from UC-San Francisco in 2013. Dr. Polich completed her Physical Medicine and Rehabilitation residency in 2017 and her Brain Injury Medicine fellowship at Spaulding Rehabilitation Hospital in 2018. She is interested in neurorecovery, resiliency and psychological wellbeing after brain injury, and functional neurological disorders. She is part of an outpatient multidisciplinary team treating functional disorders at Brigham and Women’s Hospital.
Ny-Ying Lam, MD, is a board-certified physiatrist and Associate Professor of Rehabilitation Medicine at the University of Washington School of Medicine. Dr. Lam is the Vice Chair for Clinical Affairs in the Department of Rehabilitation Medicine and Service Chief of Rehabilitation Medicine at UW Medical Center. Dr. Lam earned a Bachelors of Science degree in Bioengineering in 2007 at Rice University. Dr. Lam earned her medical degree from Emory University School of Medicine in 2011 and completed residency training at the Rehabilitation Institute of Chicago in 2015. She is also board certified in Brain Injury Medicine. In her clinical practice she cares for a wide range of neurological disorders including adults with acquired brain injuries while also co-directing the outpatient functional movement disorder rehabilitation program at UW Medical Center.
Daniel Goodman is an Associate Professor at Northwestern Feinberg School of Medicine. He is the medical director for the Physical Medicine and Rehabilitation consultation service at Northwestern Memorial Hospital and serves as the physiatry lead for the functional movement disorder clinic at Shirley Ryan AbilityLab. Dr. Goodman earned a bachelor of arts degree in kinesiology and applied physiology in 2000 and a master of science degree in applied anatomy and physiology 2005. Dr. Goodman earned his medical degree from the Chicago Medical School in 2012 and completed residency training at the Rehabilitation Institute of Chicago in 2016. Dr. Goodman’s medical practice is focused on optimizing function and mobility for patients across all diagnosis with an additional focus those with neurological disorders.
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Functional Cognitive Disorder After TBI
Laura McWhirter • Alan Carson
Background
Cognitive complaints are prominent in the substantial minority of those who remain highly symptomatic after mild traumatic brain injury (mild TBI). Clinical experience of seeing many patients who are symptomatic after mild TBI indicates that this is a group in whom functional cognitive disorder (FCD) is common. FCD is a term for a condition where persistent memory or thinking problems are present, associated with distress or impairment, and are due to dynamic alterations in attention, meta-cognitive beliefs, and cognitive control, rather than structural damage or disease. Although the clinical presentation now called FCD is not new, use of this unified diagnostic term has been helpful in drawing attention to the frequent clinical problem of distressing and incapacitating cognitive symptoms in the absence of (or greatly in excess of) any structural brain injury (McWhirter et al., 2020). Those FCD symptoms developing after TBI have often been subsumed without curiosity under the Persistent Post Concussion Symptoms (PPCS) heading, under which discrete and potentially treatable conditions (migraine, benign positional vertigo, FCD) seem to become a diffuse and unmanageable condition. However with improved understanding of functional neurological disorders more generally there is much to be gained from collaboration with FND researchers in this area (Burke & Silverberg, 2025).
Crucially, the presence of FCD, or an element of functional ‘overlay’, can indicate that improvement is possible. The identification of this potentially-reversible condition has important implications for quality of life and return to employment. Becoming familiar with FCD presentations therefore allows us to minimise disability in the post mild-TBI population as a whole. Here, we hope to summarise our approach to the clinical assessment and treatment of patients with FCD after traumatic brain injury.
Severity and Prognosis
In the clinical assessment of a patient presenting with self-reported cognitive difficulties after head injury, an important first step is establishing the severity of the index injury. In doing so it is important to have some understanding of the differing purposes, and so potential limitations, of widely used methods for classifying brain injury severity.
Readers will be familiar with the traditional mild/moderate/severe classification system for TBI, based on Glasgow Coma Score (GCS) on arrival at hospital, duration of loss of consciousness (LOC) and duration of post-traumatic amnesia (PTA). We should be reminded that the purpose of this classification system was aimed at triaging patients to guide the very earliest treatment decisions, such as which patients required a CT scan, and which might require surgery or critical care. GCS, particularly, does not translate well into prognosis, particularly for patients who have sustained objectively milder injuries.
The future looks likely to bring a more nuanced multidimensional approach to brain injury classification, incorporating biomarkers and neuroimaging findings as well as a broader range of clinical features (Manley et al., 2025), but it is important to remember that biomarkers that are reliable enough for clinical use do not currently exist. Even when they do it is going to be important, however, that the addition of biomarker profiles does not replace thorough clinical assessment. With widening availability of increasingly sensitive – but not always specific – blood and cerebrospinal fluid biomarkers, and with increasingly high-resolution neuroimaging, the likelihood of findings not directly related to the brain injury also increases. Clinical correlation (i.e. “what does this white dot mean in this patient?”) requires the skill and experience obtained by having thoroughly assessed many patients.
Clinical Assessment
Clinical assessment is particularly important in enabling us to identify the internally inconsistent patterns of FCD after mild TBI. Attempts to operationalise FCD diagnosis have given a starting point for treatment trials and are also useful in clinic (Ball et al., 2020; Cabreira et al., 2023). In FCD, cognitive symptoms are present and often deeply distressing, but are also experienced and evidenced inconsistently. The complaints are typically of frequent inattentive lapses, poor concentration, forgetfulness, word-finding difficulties, and spells of ‘autopilot’. Thinking feels hard and slow, and may be accompanied by somatic symptoms (headache), fatigue, or emotional upset, all of which the patient tends to explain is a consequence and not a cause of the cognitive difficulty. Examination of the symptom trajectory often suggests an evolving bidirectional relationship between distressing emotional and physical symptoms and cognitive difficulty.
FCD is not a diagnosis of exclusion and (like functional neurological disorders) may be present comorbidly with other pathologies. Key positive clinical features, and common clinical observations, are listed in Table 1
The initial clinical assessment of a patient with suspected FCD should include a detailed history of the index event to establish the likely
Table 1: Clinical features of functional cognitive disorder
Functional cognitive disorder
Interactional features:
Usually attends alone, having travelled to the appointment independently
More concerned about the symptoms than family members
Detailed and linguistically rich account
Detailed recall of specific forgetting events
Examples of difficulties:
Poor concentration, cognitive lapses, minor wordfinding difficulties
Subjective difficulty with the highest level tasks compared to previous, others unconcerned with performance
Reports previous outstanding memory
Physical symptoms: fatigue, headache, unsteadiness, ‘dizziness’ etc may be prominent.
Index injury:
Mild injury, usually with very short duration of PTA
FCD less likely with more severe TBI requiring hospital admission, neurosurgery, etc
Circumstances of injury may or may not have been psychologically distressing. There may be a profound sense of injustice or embitterment about the circumstances of the injury and following events.
Cognitive testing:
Becomes autonomically aroused (sweating, flushing) or tearful during cognitive testing
severity of the injury and with an ear for patterns of escalating cognitive avoidance and anxiety about mentally demanding tasks. Comorbid migraine, depression, phobic anxiety, Post-traumatic Stress Disorder (PTSD), motor FND, or Persistent Postural Perceptual Dizziness (PPPD), if present, are likely to cause their own depletion of available ‘concentration’ resources and so exacerbate the cognitive symptoms.
‘Structural’ post-TBI impairment
Brought by others, requiring assistance; may be late or miss appointment
Unconcerned or dismissive regarding suggested difficulties; accompanying family members much more concerned
Sparse or disorganised account
Unable to give examples of the difficulties
Limited description; often unaware. Whereas family members may report socially inappropriate, impulsive, or disorganised behaviour.
Either limited engagement with high level tasks; or continuing without awareness of difficulties while impairment apparent to others.
Can normalise difficulties compared with others “just the same as everyone else”
Physical complaints may be present but are less bothersome.
More severe cognitive deficits on testing with longer duration of PTA
Negative “Can’t do it” or “Gone blank” comments during cognitive testing
May perform well; or extremely poorly (inconsistent with overall presentation); or with patchy inconsistency within domains.
Trajectory over time:
Subjective worsening and withdrawal from activities over weeks to months gives impression of early worsening.
Ultimately stable, fluctuating, or improving. Nonprogressive.
Undistressed or distractible; may become frustrated with the testing process but not with own performance. Occasionally severe cognitive impairment may be accompanied by acceptance rather than distress.
Few comments. Generally unaware of deficits or poor performance
Performance in keeping with abilities and engagement. Inconsistency within single domain less likely.
Improvement over early weeks and months (unless complications arise)
Ultimately stable except in case of neurodegenerative disease.
The history is usually of cognitive difficulties getting worse, or at least more apparent, over time as a result of the individual becoming more and more vigilant to cognitive lapses and in turn altering their behaviour. There have usually been adjustments to activities in order to avoid cognitive tasks, which in turn become increasingly anxiety-provoking and fatiguing. Family members may act to protect the individual from difficulty or perceived risk by taking on cognitive or even basic domestic tasks; in contrast or may become dismissive and impatient, thereby amplifying the difficulties. As a result, the individual developing FCD after mild TBI becomes isolated and incapacitated to the extent that others will assume the injury severe and permanent. Taking a detailed history of the evolution of the problem over time in this way can aid collaborative formulation with the patient.
Cognitive assessment should be carefully considered and the results carefully interpreted. As per Table 1, a wide range of scores can be expected on cognitive testing, and of course there is also value in documenting the test scores for the benefit of longitudinal review. However, equally or more important clinical information can be gathered in watching the patient’s approach to and experience of the tests: tearfulness and autonomic arousal being common in FCD and (where approached sensitively) providing an example of the effects of altered emotional or arousal states on attention which can be used in explaining the condition later. Internal inconsistencies, such as superior delayed recall compared with immediate recall, can be helpful in diagnosis and explanation. Clinical experience in a multidisciplinary team setting is that functional assessments tasks tend to give better ‘real world’ profiles than highly abstracted pen and paper tests. In FCD, such assessments can also help the therapist to identify inconsistent patterns, areas of preserved high-level cognitive function, and help with insights into the patient’s beliefs and attitudes to their symptoms.
Management
Evidence for specific treatments is limited so far, although there is room for optimism with several pilot or feasibility trials completed for both isolated and post-mild TBI FCD, modalities including Acceptance and Commitment Therapy (ACT), Cognitive Behavioural Therapy, manualized therapist led neurobehavioural therapy, and computerised app-based intervention(Cabreira et al., 2025; Cotton et al., 2024; Poole et al., 2025; Rioux et al., 2024).
In the absence, yet, of much data on which to guide treatment, clinical experience suggests taking a similar initial treatment approach as to functional neurological disorder. The first part of treatment consists clear explanation of the problem; this may take more than one appointment, especially if the diagnosis is unexpected. Written, printed and/or online information may be helpful, with a printable pdf leaflet available at https:// neurosymptoms.org/en/symptoms/fnd-symptoms/functionalcognitive-symptoms/ and relevant information also at www. headinjurysmptoms.org.
The diagnosis of FCD is likely to require some explanation of the function of attention (using metaphor, like ‘spotlight’) for registration and later recall, and the impact of environmental, emotional, and cognitive demands on this process.
Beyond the explanation, treatment should be tailored to the individual; but in most cases, gradual re-exposure to cognitive challenges is necessary in order to regain feelings of competence.
Early identification of psychiatric (or other) comorbidities is important. The patient who is significantly depressed may require pharmacological treatment. PTSD is common after a mild TBI and requires trauma-focussed treatment if it does not resolve over time. Migraine treatment can be optimised. Obstructive sleep apnoea may cause an unpleasant combination of cognitive inefficiency, poor sleep, and daytime fatigue/sleepiness.
There remain a number of unanswered questions for future research in this area. There are issues of terminology and ‘caseness’; where, for example, is the borderline between cognitive symptoms in depression and FCD; when is the problem better described as an anxiety disorder? Broadly, however, increasing recognition of FCD as a ‘ball-park’ diagnosis with a number of clear common features has been positive to date in encouraging attempts at treatment and follow-up of a group of patients who have been discharged from clinics with reassurance but remaining highly symptomatic; or who have been assumed to have severe and untreatable impairments.
References
1. McWhirter, L., Ritchie, C., Stone, J., & Carson, A. Functional cognitive disorders: A systematic review. The Lancet Psychiatry. 2020;7(2):191–207.
2. Burke, M. J., & Silverberg, N. D. New framework for the continuum of concussion and functional neurological disorder. British Journal of Sports Medicine. 2025; 59(3):145–147). doi:https://bjsm.bmj.com/ content/59/3/145.abstract?casa_token=I-vRAOkLleQAAAAA:5s_fZpfo3IQn-VmPH1Ae_Kh6n05nYuWex8cap1_ jQ4MJeXs2kyWmcEsxXmiPe5RVBQUnUboCncAuPA.
3. Manley, G. T., Dams-O’Connor, K., Alosco, M. L., Awwad, H. O., Bazarian, J. J., Bragge, P., Corrigan, J. D., Doperalski, A., Ferguson, A. R., Donald, C. L. M., Menon, D. K., McNett, M. M., Naalt, J. van der, Nelson, L. D., Pisică, D., Silverberg, N. D., Umoh, N., Wilson, L., Yuh, E. L., … Yurgelun-Todd, D. A new characterisation of acute traumatic brain injury: The NIH-NINDS TBI Classification and Nomenclature Initiative. The Lancet Neurology. 2025; 24(6), 512–523. https://doi.org/10.1016/S1474-4422(25)00154-1.
4. Ball, H. A., McWhirter, L., Ballard, C., Bhome, R., Blackburn, D. J., Edwards, M. J., Fleming, S. M., Fox, N.C., Howard, R., & Huntley, J. Functional cognitive disorder: Dementia’s blind spot. Brain. 2020;143(10),2895–2903.
5. Cabreira, V., Frostholm, L., McWhirter, L., Stone, J., & Carson, A. Clinical signs in functional cognitive disorders: A systematic review and diagnostic meta-analysis. Journal of Psychosomatic Research. 2023;173, 111447.
6. Cabreira, V., Frostholm, L., Stone, J., & Carson, A. Feasibility trial of a self-help digital intervention for functional cognitive disorder. Brain Communications. 2025; fcaf248.
7. Cotton, E., Mordecai, K. L., McWhirter, L., Cabreira, V., Van Patten, R., Silverberg, N. D., Kaat, A. J., & LaFrance Jr, W. C. Taking Control of Your Functional Cognitive Symptoms Workbook: A Novel Intervention. medRxiv. 2024; 2024–10.
8. Poole, N., Cope, S., Vanzan, S., Duffus, A., Williams, T., Mantovani, N., Smith, J. G., Barrett, B., Scicluna, M., & Beardmore, S. Randomised controlled feasibility trial of online group acceptance and commitment therapy for functional cognitive disorder. BJPsych Open. 2025; 11(3), e91.
9. Rioux, M., Mamman, R., Byworth, M. T., Panenka, W. J., Howard, A. K., Perez, D. L., Schmidt, J., Courchesne, C., LeMoult, J., & Heran, M. K. Pilot feasibility randomised controlled trial of cognitive–behavioural therapy for functional cognitive disorder after concussion. BMJ Neurology Open. 2024;6(2), e000666.
Author Bios
Dr. Laura McWhirter is a Consultant Neuropsychiatrist and core member of the acute Traumatic Brain Injury rehabilitation team at Edinburgh Royal Infirmary. She is a member of the Edinburgh Functional Neurological Disorder research group and has a particular research interests in Functional Cognitive symptoms.
Professor Alan Carson works as a Consultant Neuropsychiatrist at the Royal Infirmary of Edinburgh where he splits his time between a general neuropsychiatry service and an acute service for brain trauma. He is an Honorary Professor in Neuropsychiatry at the University of Edinburgh. The Functional Disorders Research group in Edinburgh, which he set up along with Jon Stone, has produced a range of influential work. He was awarded the President’s Medal of the Royal College of Psychiatrists in 2017, the British Neuropsychiatry Association Medal in 2025 and was visiting Professor of Neurology at the University of Toronto in 2024.
March
9 – 13: 2026 Collaborative Brain Injury Summit, March 9 – 13, 2026, Hilton Arlington National Landing Hotel, Washington, DC. For more information visit braininjurysummit2026.org/about/
11 – 13: North American Brain Injury Society 18th Annual Conference in Brain Injury, March 11 - 13, 2026, Hilton Arlington National Landing Hotel, Washington, DC. For more information visit braininjurysummit2026.org/about/
9 – 11: National Brain Injury Conference and Awareness Day, March 9 – 11, 2026, Hilton Arlington National Landing Hotel, Washington, DC. For more information visit braininjurysummit2026.org/about/
10 – 12: State Government & Partners Track, March 10 – 12, 2026, Hilton Arlington National Landing Hotel, Washington, DC. For more information visit braininjurysummit2026.org/about/
April
29 – 2: 6th International Paediatric Brain Injury Society Conference, April 29 – May 2, Calgary, AB, Canada. For more information, visit ipbis.org/calgary-2026.
October
30 – 2: ACRM 103rd Annual Fall Conference & Expo, October 30 –November 2, Washington, DC. For more information, visit acrm.org.
Introduction
Functional seizures (FS) are paroxysmal events that resemble epileptic seizures but do not display ictal epileptiform discharges and are instead associated with underlying neural network dysfunction. The neuropathophysiology of FS is still a matter of active investigation,1 with emerging evidence suggesting abnormal structural and functional connectivity between emotion processing circuits and motor and executive control regions,2 which could explain why negative affect states can serve as seizure triggers. Nearly half of patients with FS have a TBI history,3 and TBI can serve as a precipitating factor for some patients. Up to 90% of TBIs preceding FS are in the mild (mTBI) range,4 whereas post-traumatic epilepsy is much more strongly associated with moderate/severe TBI.5 Patients with FS and TBI have greater psychopathology and disability relative to FS without TBI.6 Moreover, having a mental health history increases the chance of FS relative to epilepsy in patients who have seizures.7 Patients with FS tend to have particularly complex and difficult to treat mental health profiles, including somatization, alexithymia, and dissociation,8 which can be more prominent/severe when TBI is also present.6
Link Between TBI and FS
TBI can be a contributing factor in the development of FS.3 That is, TBI often occurs in the context of an emotionally laden event, such as a motor vehicle accident or intimate partner violence. In mTBI, the psychological context associated with the event (e.g., fear, anxious arousal), together with expectations for brain damage and dysfunction (nocebo effects), can increase the risk for developing FS. This is particularly true in Western societies where there are widespread beliefs that concussion leads to permanent brain diseases,9 including seizures.10
From a clinical perspective, the risk for FS following mild TBI can be understood in the context of a biopsychosocial model, which
Functional Seizures and Traumatic Brain Injury: Biopsychosocial Assessment and Treatment
Ryan Van Patten, PhD
W. Curt LaFrance Jr., MD, MPH
Corresponding Author: Ryan Van Patten, PhD, ABPP-CN
considers contributions of predisposing, precipitating, perpetuating, and protective factors in the development and maintenance of the disorder (Table 1).11 For clinicians, an ideal approach to case formulation in FS involves a comprehensive neuropsychiatric/ neuropsychological evaluation identifying those experiences that contribute to seizures and overall clinical symptoms.
Management and Treatment
Evidence-based treatments such as psychotherapy can reduce seizures and improve mental health and quality of life in FS.12 Specific to patients with both TBI+FS, the individual 12-session multimodal Neurobehavioral Therapy (NBT) approach for seizures has been examined in a nonrandomized, controlled trial design that accounted for TBI history.13 In this approach, 89 patients with TBI+FS and 29 patients with TBI+epilepsy were treated with NBT and standard medical care (SMC) and were compared to 75 nonseizure TBI participants treated with SMC alone. NBT was associated with reduced seizure frequency, better mental health, decreased TBIrelated symptoms, and improved quality of life during treatment (primarily moderate effect sizes), with changes in seizures, mental health, and quality of life persisting for the TBI+FS group at 12 months post-enrollment.
Clinical Recommendations
Below we provide evidence-based recommendations for neurotrauma clinicians. Suggestions are based on a biopsychosocial framework and are most effectively implemented by an interdisciplinary team. This section assumes that the patient has a history of TBI and is organized based on two scenarios: (i) a patient with mTBI who has confirmed FS, or (ii) a patient with TBI who has seizures not yet diagnosed.
Scenario 1: Patients with mTBI and Confirmed FS
• Assess predisposing, precipitating, perpetuating, and protective factors using a comprehensive chart review and clinical interview. Account for these factors in the individualized case formulation.
• Document circumstances surrounding TBIs that preceded FS. Note the patient’s illness beliefs and expectations related to TBI, seizures, and current symptoms. Formulate tentative hypotheses about relationships among the patient’s experiences, symptoms, and illness narratives.
• Inquire as to the patient’s attributional cause(s) of their seizures, which can be relevant for clinical formulation and treatment planning.
• Account for cultural factors (e.g., military/sport history; religious beliefs regarding illness and healing), which may color a patient’s interpretation of TBI and seizure sequelae.
• Provide the patient and their family with clear psychoeducation about the natural history of mTBI, the link between TBI and seizures, the different types of seizures (epileptic/functional/ physiologic), and your individualized case conceptualization.
• Validate the patient’s symptoms and disability concerns associated with FS. For example, say, “these are real seizures. The seizures may impact how you feel and perform at work.”
• Adopt a compassionate and hopeful perspective with respect to mTBI and FS. That is, although the symptoms are real and can be disabling, there is potential for significant growth and recovery.
• Consider offering relevant psychotherapy (e.g., NBT, seizurefocused CBT) to improve symptoms and quality of life.
• Acknowledge the individual’s existential concerns (e.g., moral injury in Veterans), addressing spirituality and referring for care, when indicated.
• Consider offering treatments for co-occurring symptoms, as indicated (e.g., cognitive processing therapy for PTSD; CBT for insomnia).
Scenario 2: Patients with TBI and Seizures Not Yet Diagnosed
• Consider risk factors for FS (e.g., psychological trauma) versus epilepsy (e.g., severe TBI).
• Discuss different types of seizure presentations with the patient and their family as early as possible: epileptic, functional (FS), and physiologic/nonepileptic (e.g., syncope) events. Inform the patient that all three types are valid, all can occur following TBI, and diagnostic tests (e.g., video EEG) can determine which seizure type(s) they are experiencing.
• Ensure appropriate diagnosis (i.e., don’t assume epilepsy) by referring to an epilepsy specialist and long-term video EEG monitoring for confirmation with high diagnostic certainty 14
• Determine the appropriate course of action based on seizure diagnosis.
• Exercise caution when considering antiseizure medications, given that they do not have therapeutic benefit for treating FS (and can have problematic side effects).
Clinical Case
Background
Ms. Jones is a 32-year-old single, white woman with a bachelor’s degree who is a U.S. Veteran with multiple overseas deployments. Since discharge three years ago, she has been employed full-time in customer service. She has a history of remote childhood abuse, chronic depression, and irritable bowel syndrome. She has never been married (no children), but has several supportive friends.
One year after discharge from the military, she was involved in a car accident leading to multiple orthopedic injuries requiring surgery, mTBI (without loss of consciousness), hospitalization (with significant financial costs), and several months of missed work. A head CT scan soon after the mTBI was unremarkable. She reports prolonged neurological and cognitive symptoms (e.g., headaches, brain fog) after the injuries, with the onset of video EEG-confirmed FS about one month after the car accident. Following discharge from the hospital and several weeks of physical/occupational therapy, her physical status improved, but she continued experiencing several seizures per day and noted ongoing headaches, brain fog, back pain, and fatigue, which prevent her from working. She was referred to an outpatient neurotrauma clinic for neuropsychiatric assessment and treatment recommendations.
During the evaluation, Ms. Jones reports feeling “overwhelmed” and “exhausted.” She believes that she has brain damage from her car accident and is worried about her seizures, which she perceives as uncontrollable and unpredictable. Her depression has worsened since the car accident, and she experiences stress and frustration related to chronic pain, inability to drive, and financial pressure (hospital bills and missed work). She also recalls witnessing events during her military deployments that violate her moral compass, and she describes herself as “broken” and “useless.” She attributes most of her seizures, brain fog, and headaches to her TBI during the car accident. When discussing the possibility of treatment, she expresses curiosity and a willingness to try anything.
Case Formulation and Approach
A focused case formulation is provided in Table 1. Clinical recommendations would include providing unambiguous education about expected neurobiological recovery from mTBI (i.e., the brain is resilient and is likely healed from the mTBI) and about the validity of FS (a “real disorder”). Although it would be explained that the exact cause of her seizures is not entirely known, predisposing, precipitating, and perpetuating factors may be reviewed as hypothesized contributors to FS onset and maintenance. Additionally, the clinician can work to better understand Ms. Jones’ sociocultural background (e.g., personal relationships, developmental history) and engage Ms. Jones in an exploration of the associations among her symptoms. For example, her brain fog and fatigue may be the result of acute and chronic pain, psychological distress, and worry/anxiety. Assessing her sleep quality/quantity would be beneficial, as this is often impacted by anxious arousal and pain. We suggest that psychoeducation be framed carefully in order to instill hope for recovery rather than invalidate current symptoms. Her seizures, though frightening and apparently unpredictable, may have reliable triggers (e.g., stress, headaches, brain fog). These triggers may be identifiable via journaling, possibly leading to a reduction in seizure frequency and/ or an increase in a sense of predictability and control.
Critically, the clinician can communicate that Ms. Jones has experienced very difficult life events that would likely be distressing for anyone. Many other people like her who have experienced severe depression and seizures have improved tremendously with targeted treatment, returning to work, and learning to manage their seizures. The clinician could end an initial appointment with a deeper discussion about treatment options, which may include psychotherapy for depression and somatization, NBT for seizures and co-occurring symptoms, psychotherapy (and/or chaplain services) for moral injury, non-pharmacological approaches for chronic pain, and/or vocational rehabilitation.
Conclusion
FS and TBI co-occur frequently, and both can contribute to complex, interacting, and impairing symptoms that are best understood using a biopsychosocial framework.
Assessing, managing, and treating FS and TBI requires a comprehensive clinical approach to mapping out symptoms and creating a
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Table 1. Preliminary Case Formula4on for Ms. Jones.
Label Defini+on
Predisposing factors
PrecipitaAng factors
Background risk factors that increase vulnerability to FS.
Acute/subacute events that trigger the iniAal presentaAon of FS.
PerpetuaAng factors Life events/stressors that serve as barriers to recovery.
ProtecAve factors
Buffers or resilience factors that can facilitate healing.
personalized formulation about interactions among symptoms, which can be collaboratively addressed in conjunction with patients, their families, and allied clinicians and community supports. Evidence-based treatments, including NBT, are available that consider the whole person with seizures, their individual background, and critical psychological/existential factors, which can lead to reductions in seizures and comorbid symptoms, and improvements in quality of life for people with FS and TBI.
References
1. Szaflarski JP, LaFrance Jr. WC. Psychogenic Nonepileptic Seizures (PNES) as a Network Disorder – Evidence from Neuroimaging of Functional (Psychogenic) Neurological Disorders. Epilepsy Curr. 2018;18(4):211-216. doi:10.5698/1535-7597.18.4.211
2. Foroughi AA, Nazeri M, Asadi-Pooya AA. Brain connectivity abnormalities in patients with functional (psychogenic nonepileptic) seizures: A systematic review. Seizure. 2020;81:269-275. doi:10.1016/j. seizure.2020.08.024
3. Popkirov S, Carson AJ, Stone J. Scared or scarred: Could ‘dissociogenic’ lesions predispose to nonepileptic seizures after head trauma? Seizure. 2018;58:127-132. doi:10.1016/j.seizure.2018.04.009
4. Chen DK, LaFrance CW. Traumatic brain injury and psychogenic nonepileptic seizures. In: Mula M, ed. PostTraumatic Epilepsy. Cambridge University Press; 2021.
5. Jenkins P, Cock H. Post-traumatic epilepsy: Epidemiology, definition, and terminology. In: Post-Traumatic Epilepsy. Cambridge University Press; 2021.
6. LaFrance Jr. WC, DeLuca M, Machan JT, Fava JL. Traumatic brain injury and psychogenic nonepileptic seizures yield worse outcomes. Epilepsia. 2013;54(4):718-725. doi:10.1111/epi.12053
7. Salinsky M, Rutecki P, Parko K, et al. Psychiatric comorbidity and traumatic brain injury attribution in patients with psychogenic nonepileptic or epileptic seizures: A multicenter study of US veterans. Epilepsia 2018;59(10):1945-1953. doi:10.1111/epi.14542
8. Brown RJ, Reuber M. Psychological and psychiatric aspects of psychogenic non-epileptic seizures (PNES): A systematic review. Clinical Psychology Review. 2016;45:157-182. doi:10.1016/j.cpr.2016.01.003
9. Merz ZC, Van Patten R, Lace J. Current Public Knowledge Pertaining to Traumatic Brain Injury: Influence of Demographic Factors, Social Trends, and Sport Concussion Experience on the Understanding of Traumatic Brain Injury Sequelae. Arch Clin Neuropsychol. Published online October 20, 2016:acn;acw092v1. doi:10.1093/arclin/acw092
10. Salinsky M, Parko K, Rutecki P, Boudreau E, Storzbach D. Attributing seizures to TBI: Validation of a brief patient questionnaire. Epilepsy & Behavior. 2016;57:141-144. doi:10.1016/j.yebeh.2016.02.003
11. LaFrance Jr. WC, Devinsky O. Treatment of nonepileptic seizures. Epilepsy & Behavior. 2002;3(5):19-23.
12. Goldstein LH, Robinson EJ, Mellers JDC, et al. Cognitive behavioural therapy for adults with dissociative seiures (CODES): a pragmatic, multicentre, randomised controlled trial. The Lancet Psychiatry. 2020;7(6):491505. doi:10.1016/S2215-0366(20)30128-0
13. Van Patten R, Blum A, Correia S, et al. One-year follow-up of neurobehavioral therapy in functional seizures or epilepsy with traumatic brain injury: A nonrandomized controlled trial. Epilepsia 2024;65(12):3545-3560. doi:10.1111/epi.18137
14. LaFrance Jr. WC, Baker GA, Duncan R, Goldstein LH, Reuber M. Minimum requirements for the diagnosis of psychogenic nonepileptic seizures: A staged approach: A report from the International League Against Epilepsy Nonepileptic Seizures Task Force. Epilepsia. 2013;54(11):2005-2018. doi:10.1111/epi.12356
Author Disclosures
R. Van Patten engages in profit sharing with the International Neuropsychological Society for Continuing Education proceeds from the Navigating Neuropsychology podcast. He receives royalties from publication of the book, Becoming a Neuropsychologist: Advice and Guidance for Students and Trainees (Springer, 2021). He also serves as Associate Editor for the journal, Neuropsychology.
Common Examples Examples for Ms. Jones
Adverse childhood experiences; chronic illnesses.
Mild TBI, acute life stressor, surgery, vaccine.
Job loss, nocebo effects, liAgaAon.
Self-efficacy, support from friends/family.
Childhood trauma, chronic health condiAons (depression, irritable bowel syndrome), moral injury.
Mild TBI with physical injuries, psychosocial stress, financial strain.
Illness beliefs, temporary disability, negaAve expectaAons for recovery, worsening depression.
Social support, interest in treatment.
The research reported/outlined here was supported by the Department of Veterans Affairs, Veterans Health Administration, VISN 1 Career Development Award to R. Van Patten (V1CDA2023-70).
W.C. LaFrance Jr. has served on the editorial boards of Epilepsia, Epilepsy & Behavior; Journal of Neurology, Neurosurgery and Psychiatry, and Journal of Neuropsychiatry and Clinical Neurosciences; receives editor’s royalties from the publication of Gates and Rowan’s Nonepileptic Seizures, 3rd ed. (Cambridge University Press, 2010) and 4th ed. (2018); author’s royalties for Taking Control of Your Seizures: Workbook and Therapist Guide (Oxford University Press, 2015); has received research support from the Department of Defense (DoD W81XWH-17-0169), NIH (NINDS 5K23NS45902 [PI], VA Providence HCS, Center for Neurorestoration and Neurorehabilitation, Rhode Island Hospital, the American Epilepsy Society (AES), the Epilepsy Foundation (EF), Brown University and the Siravo Foundation; has served on the Epilepsy Foundation of America and the EF New England Professional Advisory Board, the Functional Neurological Disorder Society Board of Directors, the American Neuropsychiatric Association Advisory Council and on the International League Against Epilepsy Commission; has received honoraria for the AES and AAN Annual Meetings; has served as a clinic development consultant at University of Colorado Denver, Cleveland Clinic, Spectrum Health, Emory University, Oregon Health Sciences University and Vanderbilt University; and has provided medico legal expert testimony.
Author Bios
Ryan Van Patten, PhD, ABPP, is an Assistant Professor at Brown University and a Board Certified Clinical Neuropsychologist at VA Providence. He completed his PhD in Clinical Psychology from Saint Louis University, internship at Brown University, and fellowships at UC San Diego and Harvard Medical School. As an early career neuropsychologist, Dr. Van Patten has a VA-funded research program in FND, TBI, digital neuropsychology, and cognitive rehabilitation. He has published >70 peer reviewed papers, books, and book chapters (>30 first authored). His achievements to date were recognized with the 2023 Levitt Early Career Award in Neuropsychology from APA Division 40.
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W. Curt LaFrance Jr., MD, MPH, earned his MD from Medical College of Georgia and MPH from Brown University. He is boarded in both neurology and psychiatry by ABPN. He is Director of the VA Mind Brain Program, and Clinical Lead for the VA Tele-Seizures Clinic. He is Inaugural Director of Neuropsychiatry and Behavioral Neurology at Rhode Island Hospital and a Professor of Psychiatry and Neurology at Brown University. Dr. LaFrance has >160 peer reviewed publications, >20 book chapters, and is an internationally recognized expert in developing and evaluating biomarkers and interventions for neuropsychiatric conditions, including FND.
Offering Hope: A Patient’s Perspective on FND Diagnosis
Jocelyn Brystorm
My curious, intelligent brain still wonders: How did I end up diagnosed with Functional Neurological Disorder, or FND? Disease arrives without stigma, unlike getting an FND diagnosis. Don’t tell me I have FND, give me two web addresses, and send me home to figure it out by myself.
First, listen: Prioritize the therapeutic relationship. Choose curiosity without judgement. When a psychiatrist finally diagnosed with me FND, after listening and earning my trust, I more easily accepted the diagnosis. Be aware that there can be negative impacts after a patient is dismissed or when assumptions are made. Provide compassionate and whole-person care. Then healing will feel possible.
Tell me what FND is: It’s a severe condition at the intersections of neurology and psychiatry that impacts the function of the nervous system and the way your brain sends and receives messages. FND involves mixed-up messages communicated through your neural networks. Although we don’t know everything about FND, we know the symptoms are real.
Help me understand “why me”: We’re not sure exactly why FND symptoms are triggered. Recent vetted research informs us that the physical symptoms you’re currently experiencing may have varied prompting events. These may include, although are not limited to unexpected life-altering situations, traumatic incidents, occurrences post-surgery, post-vaccination, or following unexpected losses, a death of a loved one or grief. None of which, are your fault.
Give hope: State with confidence that hope is possible. Share a success story, e.g., other patients with this diagnosis who have done well. Reassure me, in the presence of my loved ones, that I can be well, even though my recent experience indicates otherwise. Reassure me that with time, hard work, and self-advocacy and your support, improvements can and does occur.
Explain how recovery can happen: Like an individual who’s suffered a stroke, I want to know that my brain’s neuroplasticity enables me the same opportunity for retraining. Learning that my brain has a miraculous capacity to reduce and diminish current functional symptoms, including daily non-epileptic seizures, migraines, and myoclonic jerks, exponentially increases that I’ll accept my FND diagnosis.
Be confident but humble: Explain your confidence in the diagnosis after using rule-in diagnostic procedures. “We’ve been able to positively identify signs and symptoms indicative of Functional Neurological Disorder.”
Acknowledge that misdiagnosis is possible and that brain disease may coexist alongside functional symptoms.
Recognize my journey: Summarize how my symptoms have evolved and may continue to. We recognize that it’s likely you may have experienced anticipatory grief, anger and/or fear during your diagnostic investigations. Your symptoms have impacted your expected lifestyle, career, and abilities prior to our determination of an FND diagnosis.
Invite questions: Answer my question with as much clarity as possible, recognizing that I may be in a state of overwhelm and information overload. I’ve just learned I have FND, that it’s a severe condition and that there’s no cure. Ask me: What’s your biggest concern heading home with this FND diagnosis? Offer a followup appointment post-FND diagnosis to provide an opportunity to ask questions after I’ve had time to process and discuss my FND diagnosis with loved ones and trusted allies. This gives me time to consider follow-up questions within a reasonable timeline and builds therapeutic trust.
Reiterate:
You’ve got this. There’s hope that you can be well again. Let’s talk in a week or two.
Please, don’t give me two web addresses and send me home to figure it out by myself.
Author Bios
Jocelyn Bystrom, M.Ed., is a published author, health advocate, and founder of Thrive-Together-Network. With over 30 years as an educational leader, Jocelyn empowers individuals navigating new or challenging medical diagnoses to build resilience, shift limiting beliefs, and thrive with confidence. Her book, FiNDing Hope: The Mind-Body Connection & Importance of Being Seen and Heard, offers a compassionate lens into the patient experience, making it a valuable resource for practitioners to recommend to newly diagnosed patients. Drawing on her personal journey with Functional Neurological Disorder (FND) and training in Dialectical Behavioral Therapy (DBT) techniques, Jocelyn emphasizes the power of embodied storytelling, listening, and connection to foster healing. For free resources and community support, visit thrive.thrive-together-network.com, and to learn more, visit jocelynbystrom.com.
Introduction
Vestibular symptoms of vertigo, unsteadiness, dizziness, and balance difficulties are common after traumatic brain injuries (TBI) and among the leading causes of post-TBI disability.1-3 The specific mechanisms underlying chronic post-TBI vestibular and balance symptoms are unknown.3-6 Additionally, a sizeable proportion of patients first report post-TBI vestibular symptoms well after the acute post-injury period. In the prospective TRACK-TBI study, 132/582 (22.7%) patients who reported dizziness at 3 months postinjury and 136/484 (28.1%) who reported dizziness at 6 months post-injury endorsed it for the first time at those time points.1
Among patients with moderate-severe TBI, acute vestibular and balance symptoms often can be attributed to identifiable structural deficits of the vestibular labyrinth or brain, especially acutely.4-5 Among the far more numerous patients with mild TBI, by contrast, only one-quarter of those with dizziness have any acute vestibular abnormalities.5 Especially for these patients, the severity of chronic dizziness-related handicap is correlated more strongly with abnormalities on tests of dynamic posture and gait functioning (e.g., Sensory Organization Test, Dynamic Gait Index) than tests of structural injury or basic reflexes (e.g., head impulse test, caloric irrigation). 6 Performance deficits on dynamic tests may result from changes in postural control strategies with or without co-existing structural injuries.
Functional Dizziness
Persistent postural-perceptual dizziness (PPPD), a functional neuro-otologic disorder, was defined in 2017.7,8 PPPD manifests with unsteadiness and non-vertiginous dizziness, present nearly continuously for >3 months and exacerbated by upright posture, active or passive motion, and exposure to environments with moving objects or complex visual patterns. PPPD is precipitated by conditions that cause acute or recurrent bouts of vestibular or balance symptoms such as peripheral vestibular disorders, migraine, anxiety disorders, dysautonomias, cardiac dysrhythmias, and TBI. Evidence suggests that pathophysiologic mechanisms of PPPD involve functional changes in physiological processes that govern spatial orientation and motor control as well as changes in brain activity and connectivity in networks that subserve these essential activities.8 Triggering events increase vigilance about body motion that induces overestimation of movement and over-reliance on visual versus vestibular and somatosensory stimuli for judging position and movement of self and surrounding objects. These changes drive stiffening of posture and gait and reductions in the speed of gaze shifts.
Functional Dizziness After Traumatic Brain Injury
Jeffrey P. Staab, MD, MS
Corresponding Author: Jeffrey P. Staab, MD, MS
The typical patient with PPPD scores in the moderately to severely impaired range on the patient-reported Dizziness Handicap Inventory (DHI).9
Functional Dizziness Post-TBI
Descriptions of vertigo, unsteadiness, and dizziness affecting patients post-TBI have been published,10-13 but there is not yet a consensus on definitions of these symptoms. Among patients with PPPD diagnosed at a tertiary neuro-otology center, 134/1503 (8.9%) had TBI (85.8% mild) as their triggering event.13 Those individuals fully met the diagnostic definition of PPPD. Conversely, there are no published data on the prevalence of PPPD among patients with TBI, but estimates can be inferred from published reports. A DHI score of 61100 (severe handicap) is 88% specific for PPPD or psychiatric causes of chronic dizziness, with or without co-existing structural deficits.9 Several studies of patients with post-TBI vestibular symptoms reported DHI scores.5,10,11 From their means and standard deviations, it can be estimated that about 17% of patients at 3 months postinjury11 and about 3.5-8% of patients at 12 months post-injury5,12 have DHI scores >60 (i.e., probable PPPD), estimates that roughly match the percentages of patients who reported moderate or severe dizziness at those time intervals on the Rivermead Questionnaire in the TRACK-TBI investigation.2 More directly, researchers studying military service members who sustained blast injuries in Iraq described two syndromes with similarities to PPPD.12 Postblastinduced dizziness manifested a constant feeling of unsteadiness when upright that was worse in challenging environments, plus constant headache. Postblast-induced dizziness with vertigo added recurrent episodes of vertigo to constant dizziness and headache. Together, they accounted for 86% of patients with postblast vestibular symptoms lasting longer than 30 days. These conditions are strikingly similar to PPPD with co-existing chronic headache or vestibular migraine, which are encountered frequently in civilian populations. TBI also may induce posttraumatic stress disorder, often with delayed onset after injury,3,6,13 autonomic dysregulation in the form of orthostatic intolerance (separate from sympathetic storm that can follow severe TBI),14 and cervical injury.4,6 All of these are known triggers of PPPD in patients without TBI.7 Thus, TBI can cause sequelae that are established precipitants of PPPD (Figure 1), including PPPD with chronic headache or episodic vertigo (Figure 1, red arrows).
Comorbid Functional Symptoms
Posttraumatic stress disorder and other psychosocial factors have been associated with post-TBI vestibular morbidity, but may not be the sole genesis of functional dizziness, per se, except as depicted in Figure 1.8
Patients with PPPD often have a slightly cautious gait, but a portion (not yet determined) develop additional functional movement disorders including stifflegged stance with exaggerated truncal sway in Romberg position and stifflegged, wide-based, excessively slow gait with unnecessary reliance on gait aids.8 They also describe functional cognitive symptoms (brain fog, problems with working memory) and perform poorly on tests of
Posttraumatic headache
Peripheral labyrinthine injury
Central grey matter injury
Diffuse axonal injury
Posttraumatic stress disorder
Autonomic dysregulation
Musculoskeletal injury
spatial cognition (e.g., marked impairment on the virtual Morris Water Maze test).15
Treatment of Functional Dizziness (PPPD)
Three treatments for PPPD are supported by numerous case series, retrospective studies, and prospective investigations, but no definitive randomized clinical trials.16 Vestibular habituation exercises (in clinic and at home), selective serotonin reuptake inhibitors and serotonin norepinephrine reuptake inhibitors, and cognitive behavioral therapies, including in patients without psychiatric comorbidity, have been shown to reduce symptoms by >50%, from moderate-severe to mild-moderate handicap on the DHI. Two-thirds of patients achieve this clinically meaningful benefit. Combinations of treatment modalities may produce better results.16
A retrospective review of treatment outcomes for patients with post-TBI PPPD showed positive results with this multi-modality strategy, but a numerically lower percentage had a meaningful clinical response (53% vs. 65%) and mean improvement on the Clinical Global Impressions-Improvement Scale was significantly lower compared to outcomes in patients with PPPD due to other precipitants.10
Vestibular suppressants such as meclizine, dimenhydrinate, and benzodiazepines are not recommended for patients with post-TBI vestibular symptoms because they do not improve the course of illness and may interfere with recovery.3
Summary
For most patients with TBIs, vestibular and balance symptoms lasting >3 months have the clinical phenotype of functional dizziness, specifically PPPD or PPPD-like syndromes with chronic headache. Structural injury to the vestibular labyrinth or brain are neither necessary nor sufficient to trigger these persistent symptoms. Physiological alterations in spatial cognition, control of locomotion, and associated changes in brain activity and connectivity may underlie PPPD. Existing treatments adapted for PPPD, may offer clinically meaningful reductions in dizziness-related handicap, making it worthwhile to include this clinical condition in the differential diagnosis of patients with post-TBI dizziness.
Vestibular migraine
Chronic headache
Acute or recurrent vertigo
Unsteadiness
Gait ataxia
Panic attacks or generalized anxiety
Orthostatic intolerance
Neck or back pain
References
Functional deficits in spatial cognition
PPPD-type functional dizziness
Functional gait disorder
1. Machamer J, et al. Symptom frequency and persistence in the first year after traumatic brain injury: A TRACK-TBI study. J Neurotrauma. 2022;39(5-6):358-370. doi: 10.1089/neu.2021.0348.
2. Chae R, et al. Dizziness after traumatic brain injury: A prospective TRACK-TBI analysis of risk factors, quality of life, and neurocognitive effects. Otol Neurotol. 2022;43:e1148–e1156. doi: 10.1097/ MAO.0000000000003710.
3. VA/DoD clinical practice guideline for the management and rehabilitation of post-acute mild traumatic brain injury, 2021. Published online at: https://www.healthquality.va.gov/guidelines/Rehab/mtbi/ VADODmTBICPGFinal508.pdf, accessed 29 June 2025.
4. Marcus, HJ, et al. Vestibular dysfunction in acute traumatic brain injury. J Neurology. 2019;266:2430–2433. doi.org/10.1007/s00415-019-09403-z
5. Skóra W, et al. Vestibular system dysfunction in patients after mild traumatic brain injury. Ann Agric Environ Med. 2018;25(4):665-668. doi:10.26444/aaem/81138.
6. Akin FW, et al. Vestibular and balance function in veterans with chronic dizziness associated with mild traumatic brain injury and blast exposure. Front. Neurol. 2022:13:930389. doi: 10.3389/fneur.2022.930389.
7. Staab JP, et al. Diagnostic criteria for persistent postural-perceptual dizziness (PPPD): Consensus document of the committee for the Classification of Vestibular Disorders of the Bárány Society. J Vestib Res 2017;27(4):191-208. doi: 10.3233/VES-170622.
8. Staab JP. Persistent postural-perceptual dizziness: Review and update on key mechanisms of the most common functional neuro-otologic disorder. Neurol Clin. 2023;41(4):647-664. DOI: 10.1016/j.ncl.2023.04.003
9. Graham MK, et al. A comparison of dizziness handicap inventory scores by categories of vestibular diagnoses. Otol Neurotol. 2021 Jan;42(1):129-136. doi: 10.1097/MAO.0000000000002890.
10. Kleffelgaard I, et al. Dizziness-related disability following mild-moderate traumatic brain injury. Brain Inj 2017;31(11):1436-1444. doi: 10.1080/02699052.2017.1377348.
11. Kleffelgård I, et al. Dizziness-related disability one year after a mild-to-moderate TBI-a follow-up study. J Clin Med. 2023;12(16):5192. doi: 10.3390/jcm12165192.
12. Hoffer ME, et al. Blast exposure: vestibular consequences and associated characteristics. Otol Neurotol 2010;31(2):232-6. doi: 10.1097/MAO.0b013e3181c993c3.
13. Johnson B, et al. Prevalence and treatment outcomes of persistent postural-perceptual dizziness after traumatic brain injury. PMR. 2025;17(6):621-627. doi: 10.1002/pmrj.13339.
14. Pearson R, et al. Post-concussive orthostatic tachycardia is distinct from postural orthostatic tachycardia syndrome (POTS) in children and adolescents. Child Neurology Open. 2022;9. doi:10.1177/2329048X221082753
15. Breinbauer HA, et al. Spatial navigation is distinctively impaired in persistent postural perceptual dizziness. Frontiers Neurol 2020;10:1361. DOI: 10.3389/fneur.2019.01361
16. Trinidade A, et al. Treatment of persistent postural-perceptual dizziness (PPPD). Curr Treat Op Neurol 2023;25(9):281-306. https://doi.org/10.1007/s11940-023-00761-8
Author Bios
Jeffrey P. Staab, MD, MS, is Professor and Chair of the Department of Psychiatry and Psychology and holds a joint appointment as a Consultant in the Department of Otorhinolaryngology – Head and Neck Surgery at Mayo Clinic, Rochester, MN USA. Dr. Staab received a Bachelor of Science in Chemical Engineering from Northwestern University, Doctor of Medicine from the University of Pittsburgh, and Master of Science in Bioengineering from Carnegie-Mellon University. He completed an internship in internal medicine and residency in psychiatry at Walter Reed National Military Medical Center in Bethesda, MD, followed by a fellowship in traumatic stress disorders at the Uniformed Services University of the Health Sciences. His research centers on problems at the interface of neurology, otology, and psychiatry.
expert interview BIP
Interview with Matthew J. Burke
Dr. Burke has no conflicts of interest to disclose
Dr. Matthew Burke is a Cognitive Neurologist at Sunnybrook Health Sciences Center and an Assistant Professor at the University of Toronto (cross appointed between Psychiatry and Neurology). He holds positions as the Director of Sunnybrook’s Traumatic Brain Injury Recovery Program, Director of Sunnybrook’s Functional Neurological Disorder Clinic and the Neuropsychiatry Lead for the University of Toronto Neurology Residency Program. Prior to his current appointments, Dr. Burke completed medical school and neurology training at the University of Toronto and then a fellowship in Cognitive Neurology and Neuropsychiatry at Harvard Medical School. Dr. Burke’s research focuses on investigating complex topics at the interfaces between psychiatry, neurology and neuroscience, and he was recently recognized with the 2025 American Academy of Neurology Norman Geschwind Prize for his contributions to emerging areas of neuropsychiatry.
1. How did you become interested in the overlap between traumatic brain injury (TBI) and FND?
I am Behavioral Neurologist specializing in Neuropsychiatry and hold cross-appointments between the Departments of Psychiatry and Neurology. FND and TBI have emerged as two disorders exemplifying the complex interfaces between these disciplines. For the past five years, my core clinical practice has involved leading separate clinics dedicated to both patient populations. Seeing high volumes of these patients in parallel, I started noticing the strong overlap in the clinical profiles between those with persisting post-concussive symptoms and FND (with no history of head injury). This includes similar themes of premorbid comorbidities, neuropsychiatric symptom constellations and maladaptive psychological coping styles. I also began identifying that an increasing number of our “concussion” referrals were actually FND presentations triggered by mild head injuries. Such referrals commonly would not meet updated diagnostic criteria for concussion/mTBI (e.g., no acute clinical signs of brain injury) but were still triaged accordingly due to the presence of non-specific neuropsychiatric symptoms (labelled as “post-concussion syndrome”). I was surprised by the lack of research and clinical guidelines for navigating this complex spectrum between TBI, head injury and FND so I decided to jump in!
2. Can FND occur after TBI of any severity? What’s the relationship between TBI severity and risk of FND?
Theoretically any severity of TBI could trigger FND. While incompletely understood, we believe that TBI may precipitate FND by introducing the brain to new symptoms, shifting attentional processes (what a person’s attention is drawn to) and activating threat response systems (e.g., so bodily sensations tend to be interpreted as threatening). TBIs of any severity have the potential to induce these factors. However, in my clinical experience, it is much more common to see FND triggered after concussion (“mild” TBI) or even a head/neck injury that may not meet diagnostic criteria for TBI. Further research is needed on this topic.
3. Does FND after TBI look different than FND precipitated by another kind of event, experience, or injury?
I think the best answer is that it depends. In general, the core FND clinical characteristics/signs usually look the same but there may be a different contextual symptom milieu. For example, a patient presenting with functional seizures triggered by a TBI may have semiology that is indistinguishable from functional seizures following other precipitants. However, such patients may also have
concurrent clusters of symptoms that fall in the complex border zones between TBI and FND, including cognitive complaints, fatigue, dizziness, chronic headaches and so on. While the latter symptoms are commonly seen in FND more broadly (with non-injury related triggers), in my experience they occur at a higher frequency when there is a concurrent TBI.
4. Are there “yellow flags” in the clinical presentation that make you suspicious for FND after TBI?
Yes, we have presented such “yellow flags” in a recent article on this topic (Burke and Silverberg, 2024). The flags are relevant to the context of a patient with persisting symptoms after head injury and may be used as guideposts for a clinical presentation suspicious of FND.
i. Low likelihood of brain injury (e.g., low-velocity mechanism, no LOC, no post-traumatic amnesia)
ii. Symptom onset delayed (e.g., >48 hours after head injury)
iii. Fluctuating, worsening, or remit/relapse course
iv. Internal inconsistencies and/or attention-mediated fluctuations in (e.g. patients with functional cognitive disorder report memory lapses with vivid detail)
v. Atypical symptoms incongruent with structural neurological disease (e.g., stuttering, abnormal movements, non-epileptic events)
vi. Pre-injury or comorbid functional somatic syndromes (e.g., irritable bowel syndrome, fibromyalgia)
vii. Presence of contributory psychological mechanisms (e.g., posttraumatic stress disorder, dissociation)
Please see the referenced article for further details.
5. Is “post-concussion syndrome” a type of FND or a distinct condition? Can patients have both?
This remains a very controversial topic and I think arguments could be made supporting both sides. There is no doubt that significant overlap exists and probably much more than the field has historically recognized. However, whether or not PCS is best positioned as a subtype of FND comes down to whether you are a lumper (versus splitter) and how broad your diagnostic bucket for FND is. If a splitting approach is taken (categorizing them as distinct conditions), then at a minimum a high degree of overlap and potential for co-occurrence between PCS and FND should be acknowledged. Sometimes simple labelling cannot do justice to characterizing a patient’s condition.
As an aside, I have informally polled many clinicians and scientists when lecturing on this subject and I would say opinions on this matter remain split.
6. Is there anything that healthcare professionals can do early on (in the hours to weeks following TBI) to help prevent FND?
Yes, this is a hot topic and different strategies are currently being evaluated. I will highlight one approach that is of particular interest to me and my clinical research efforts. We are increasingly understanding how positive or negative expectancies can contribute to symptom alleviation (placebo effects) or generation/worsening (nocebo effects) in medicine. In FND and other neuropsychiatric disorders, brain circuit dysfunction implicated in FND pathophysiology may be modulated by placebo/nocebo effects.
In the present context, clinicians could potentially help prevent FND by mitigating nocebo effects surrounding concussion. For example, clinicians could engage in education and counseling to identify if negative expectancies/beliefs exist and then help reframe them. This could include positively framing that most patients make a full recovery from concussion, prolonged brain rest is not helpful, and symptom flair-ups are a typical in normal recovery. Specific negative beliefs such as that their concussion might cause dementia/chronic traumatic encephalopathy could also be addressed. This could include reassurance that explains the nature of the association between these topics and that most data raising alarms (i.e., that they may have seen covered in the media) are based on studies of professional athletes suffering numerous (sometimes thousands) of concussive and/or sub-concussive blows.
The above education/counseling will be generally beneficial to all patients but it is critical that clinicians try to identify patients that may be at particular high risk of FND (based on their medical history and/or the injury event - see yellow flags above) and make extra efforts for this sub-population. Anecdotally, such education and counseling can make a big difference for their recovery trajectory and there are ongoing research efforts trying to quantify this.
7. How might the treatment plan differ for a patient with FND after TBI compared to another patient with typical TBI symptoms?
Existing evidence-based TBI guidelines such as those found here (https://concussionsontario.org/) would still generally apply to all patients across this spectrum. They emphasize the importance of multidisciplinary care and offer approaches for symptom-based management.
However, patients with TBI-triggered FND may also benefit from more specialized FND-informed rehabilitation strategies. For example, this could include earlier and/or more intensive psychological therapy (e.g., cognitive-behavioral therapy) and/ or targeted physiotherapy (e.g., protocols for Persistent PosturalPerceptual Dizziness [PPPD]). It may also be important to minimize any proposed therapeutic interventions that involve close tracking or hypervigilance of symptoms. While usually well-intentioned, such therapies could be maladaptive by promoting attentional direction towards symptoms and contributing to symptom preoccupation or catastrophizing. FND treatments typically aim to reverse such cognitions/behaviors.
References
1. Aybek S, Perez DL. Diagnosis and management of functional neurological disorder. BMJ. 2022;24;376.
2. Burke MJ, Silverberg ND. New framework for the continuum of concussion and functional neurological disorder. British Journal of Sports Medicine. 2025;59(3):145-7.
3. Clark CN, Edwards MJ, Ong BE, Goodliffe L, Ahmad H, Dilley MD, Betteridge S, Griffin C, Jenkins PO. Reframing postconcussional syndrome as an interface disorder of neurology, psychiatry and psychology. Brain. 2022:1906-1915.
4. Fiorio M, Braga M, Marotta A, Villa-Sánchez B, Edwards MJ, Tinazzi M, Barbiani D. Functional neurological disorder and placebo and nocebo effects: shared mechanisms. Nat Rev Neurol. 2022;18(10):624-35.
5. Hallett M, Aybek S, Dworetzky BA, McWhirter L, Staab JP, Stone J. Functional neurological disorder: new subtypes and shared mechanisms. Lancet Neurol. 2022;21(6):537-50.
6. Picon EL, Perez DL, Burke MJ, Debert CT, Iverson GL, Panenka WJ, Silverberg ND. Unexpected symptoms after concussion: Potential links to functional neurological and somatic symptom disorders. J Psychosom Res 2021;151:110661.
7. Silverberg ND, Cairncross M, Brasher PMA, Vranceanu AM, Snell DL, Yeates KO, Panenka WJ, Iverson GL, Debert CT, Bayley MT, Hunt C, Baker A, Burke MJ; Canadian Traumatic Brain Injury Research Consortium (CTRC). Feasibility of Concussion Rehabilitation Approaches Tailored to Psychological Coping Styles: A Randomized Controlled Trial. Arch Phys Med Rehabil. 2022;103(8):1565-1573.
8. Silverberg ND, Iverson GL, Group AB, Cogan A, Dams-O-Connor K, Delmonico R, Graf MJ, Iaccarino MA, Kajankova M, Kamins J, McCulloch KL. The American congress of rehabilitation medicine diagnostic criteria for mild traumatic brain injury. Arch Phys Med Rehabil. 2023;104(8):1343-55.
About the Interviewer
Dr. Beth Slomine is Co-Director of the Center for Brain Injury Recovery and Assistant Vice President of Psychology at Kennedy Krieger Institute. She is Professor of Psychiatry & Behavioral Sciences at Johns Hopkins University School of Medicine and has a secondary appointment in the Department of Physical Medicine & Rehabilitation. She is a licensed psychologist, board certified clinical neuropsychologist, and board certified subspecialist in pediatric neuropsychology. Research interests include neurobehavioral measurement, outcomes, and interventions following pediatric neurological injury Dr. Slomine has authored >100 peer-reviewed manuscripts, numerous book chapters, and co-edited a textbook entitled Cognitive Rehabilitation for Pediatric Neurological Conditions.
Tech Column
Neurosymptoms.org is a comprehensive, evidence-based resource for patients, families and healthcare professionals seeking to understand Functional Neurological Disorder (FND). Created by Dr. Jon Stone, a neurologist, researcher and worldleading expert on FND, the website aims to reduce stigma and promote better outcomes through education about FND symptoms, causes, and treatment. This review evaluates the quality of the content and useability of the website by both patients and healthcare professionals, as well as its utility as a clinical tool.
Content Evaluation
The content on neurosymptoms.org is based on current clinical understanding and reflects a biopsychosocial approach to FND. It is structured into clear sections, including explanations of symptoms, diagnostic procedures, treatment approaches, frequently asked questions, patient stories, and video resources. The site covers a wide range of symptoms such as functional seizures, limb weakness, speech and cognitive disturbances, gait problems, and sensory changes, with each section offering plain-language explanations and helpful illustrations and/or diagrams. Common questions about how and why FND happens are addressed using a neuroscience framework that avoids overly technical or stigmatizing language. The website emphasizes the legitimacy and reversibility of symptoms by citing current diagnostic practice including specific ‘rule-in’ criteria and clarifying misconceptions that FND is a diagnosis of exclusion and imagined.
The site’s content reflects modern approaches to managing FND, which may include treatment with a multidisciplinary team of psychotherapy providers, physiotherapists (PTs), occupational therapists (OTs) and speech therapists (SLTs). Each therapy offers practical information from clinical and research experts in the field. Videos, diagrams, and real patient narratives enhance the clarity and relatability of the material. There are several links to patient and professional organizations as additional resources. The overall tone is reassuring and empathetic, while maintaining scientific accuracy.
Usability and Functionality
From a usability standpoint, the website is straightforward, with intuitive navigation and clear tabs that make it easy to find relevant content. The inclusion of multimedia elements— particularly explanatory videos created in collaboration with medical professionals—adds value, especially for visual learners. The site is accessible across desktop and mobile devices. While most content across the site translates to thirteen different languages, some of the translations are spotty and videos and testimonials are not available in some of the languages.
Clinical Utility
While primarily patient-facing, neurosymptoms.org also serves as a valuable educational tool for clinicians of various disciplines, in diverse settings. In the hospital setting, a patient’s direct time with physicians can be brief as it tends to focus on communicating a diagnosis, treatment approach and discharge plan.
Directing patients to the website after the clinical encounter allows them to process information at their own pace which can reduce anxiety and establishes a framework for consistent messaging from the interdisciplinary team. Printable fact sheets outlining specific symptoms, causes, and treatments are valuable tools for team members who interact with patients during their hospital stay. Specifically, they can facilitate symptom discussions using a common language and reinforce the diagnosis. For patients, this knowledge can create a sense of autonomy and engagement with treatment and providers.
The website is a valuable complement to outpatient clinical care, supporting collaboration among neurology, psychiatry, and therapy teams. Patients with FND often struggle to understand or accept their diagnosis, and reviewing content or videos together during clinic appointments can improve communication and build trust. Patient testimonials offer validation and help individuals feel understood. Introductory videos like “What is FND?” and the 'Causes' tab are especially helpful for educating patients so they can be prepared for the clinical encounter and set realistic expectations for treatment and recovery.
Strengths and Limitations
The key strengths of neurosymptoms.org lie in its credibility, accessibility of language, and patient-centered approach. It is one of the few resources that successfully translate clinical knowledge about FND into a format that patients can easily understand. It should be cautioned, however, that reliance on this resource alone cannot substitute for the essential faceto-face time needed to explain the diagnosis, listen to patient concerns, answer questions, and offer reassurance and hope. Additionally, the website would benefit from a more modern web interface and interactive or customizable content. As with any website, it requires regular updates to stay current which can be time consuming.
Conclusion
Overall, neurosymptoms.org is an excellent resource that fills a critical gap in patient education and clinical support for FND. Its content is clear, credible, and compassionate. It is a highly recommended tool for clinicians to use in practice, offering a way to extend conversations beyond the clinic and support patients in understanding and managing their condition.
Author Bios
Jessica Ranford, MS, OTR/L, is an Occupational Therapist with 25 years of clinical experience specializing in the assessment and treatment of individuals with neurologic, neuropsychiatric, and psychiatric conditions. She earned her Master of Science in Occupational Therapy from College Misericordia in 2000 and currently serves as the Clinical Specialist for outpatient OT at Massachusetts General Hospital. A member of the MGH Functional Neurological Disorder (FND) Unit and Research Lab since its inception, she has co-investigated NIH-funded studies and published extensively on sensory processing and sensorybased OT treatment approaches for FND. Jessica is a co-author of the OT consensus recommendations for FND, a founding member of the FND Society, and a frequent invited speaker on sensory-based rehabilitation in FND.
SEEKING RESEARCH PARTICIPANTS WITH MILD TRAUMATIC BRAIN INJURY
ABOUT THE STUDY:
WHO IS ELIGIBLE?*
1. Between 18-80 years of age
2. Diagnosis of mild traumatic brain
injury or concussion with or without post-traumatic stress disorder
3. At least 3 months post-injury
4. No history of epilepsy or active seizures
5. Ability to safely participate in MRI
STUDY ACTIVITIES
• Tests of thinking, memory, and attention
• Self - report of daily function and mental health
• MRI
• Eye-tracking
• Experimental brain stimulation (transcranial magnetic stimulation)
STUDY LOCATIONS
Additional
MORE INFORMATION
6. No other neurologic conditions that affect thinking or moving https://clinicaltrials.gov/study/NCT03819608
Time commitment includes up to 9 weeks of with 4 of these weeks involving treatment.
You will be compensated for your time and, as indicated, for travel/parking
S t u dy Title: Neuromodulation and Neurorehabilitation for Treatment of Functional Deficits after m TB I plus PTSD
PI: Theresa Bender Pape NU IRB # : STU 00203773
Northwestern University , Chicago, IL Moody Neurorehabilitation, Houston TX
STUDY PURPOSE
The purpose of this study is to determine the effect of brain stimulation paired with cognitive intervention has on improving functional outcomes after m
