By Dr Ioannis Mavroudis – Consultant Neurologist & Researcher
Based on our new publication in Brain Sciences brainsci-15-00755
Post-Concussion Syndrome (PCS) and Functional Neurological Disorder (FND), including its cognitive subtype Functional Cognitive Disorder (FCD), have historically been treated as two separate clinical worlds—one rooted in biomechanical brain injury, the other in functional network dysfunction.
But as our team shows in our latest peer-reviewed paper, these conditions share far more common ground than previously appreciated. In fact, many patients seen in concussion clinics or neurology settings sit in the overlap zone, where persistent symptoms are shaped by both organic and functional mechanisms.
This article breaks down what we found—focusing especially on the shared predisposing factors, the overlapping symptom patterns, and the Functional Overlay Model that can help clinicians navigate this diagnostic interface.
1. Two Diagnoses, One Symptom Language
PCS is triggered by a mild traumatic brain injury, whereas FND/FCD involves altered brain network functioning without structural damage. Yet the lived experience of patients can be remarkably similar.
Shared symptom profiles include:
- Cognitive fog and slowed processing
- Attention and memory complaints
- Fatigue and sleep disturbance
- Heightened symptom awareness
- Anxiety, irritability, emotional lability
- Dizziness, headaches, sensory sensitivities
Both groups often report symptoms out of proportion to objective findings, especially months after the initial trigger.
2. The Overlap of Predisposing Factors: What Makes People Vulnerable?
A key finding of the paper is the striking similarity in predisposing psychological and demographic traits across PCS and FND/FCD.
Shared predisposing traits and backgrounds include:
1. High neuroticism
Both PCS and FND/FCD patients frequently exhibit elevated neuroticism—meaning:
- emotional sensitivity
- stress reactivity
- heightened vigilance to bodily sensations
In PCS, this predicts prolonged symptom burden; in FND/FCD it fuels symptom amplification and misinterpretation.
2. Pre-existing anxiety or depression
Psychiatric history strongly predicts:
- persistent PCS after concussion
- emergence of functional neurological symptoms
3. Trauma history
Childhood emotional neglect/abuse is a known risk factor in FND and is also increasingly recognised in chronic PCS.
4. Maladaptive coping & catastrophising
Both groups often over-interpret benign physical or cognitive sensations:
- “My headache means I have brain swelling.”
- “I forgot a word—maybe I have permanent brain damage.”
These beliefs deepen symptom vigilance and slow recovery.
5. Personality traits such as perfectionism or over-conscientiousness
These traits drive over-monitoring of cognitive performance in FCD and fuel post-injury hyperfocus on symptoms in PCS.
6. Female sex
Consistently linked with:
- higher PCS severity and duration
- higher prevalence of FND/FCD
3. Precipitating and Perpetuating Factors: Why Do Symptoms Become Chronic?
Precipitating events
- For PCS: mild traumatic brain injury
- For FND/FCD: stress, minor injuries, conflict, uncertainty
Yet both can be triggered by events that disrupt bodily trust.
Perpetuating loops
Both conditions can become chronic due to:
- avoidance behaviours
- hypervigilance to symptoms
- reduced physical activity
- inconsistent messaging from healthcare providers
- fear of worsening symptoms
- legal/litigation stress (strongly documented in PCS)
In FND, positive signs of inconsistency are key indicators. In PCS, persistent symptoms despite normal investigations are red flags for functional contribution.
4. Shared Neurobiological Ground: When Brain Networks Stop Communicating Efficiently
Advanced neuroimaging increasingly reveals that both PCS and FND involve network dysfunction, particularly:
- Default Mode Network (DMN)
- Fronto-limbic circuits
- Emotion–motor pathways
- Attention and executive control networks
PCS
Shows:
- microstructural white matter changes
- altered functional connectivity
- hypoconnectivity in attentional networks
- metabolic and neuroinflammatory changes
FND/FCD
Shows:
- abnormal self-monitoring
- limbic hyperactivation
- disrupted agency and movement initiation networks
- DMN overactivity linked to excessive introspection
These shared circuits explain why patients with different diagnoses can look so similar.
5. Subjective Cognitive Impairment: The Great Diagnostic Overlap
In PCS:
Patients may have:
- slowed processing
- reduced mental stamina
- subtle memory encoding inefficiencies
But neuropsychological tests often normalise over time.
In FCD:
Patients describe:
- severe forgetfulness
- poor concentration
- word-finding problems
Yet testing shows:
- normal performance
- inconsistency
- improvement under distraction
Both groups overestimate the severity of their cognitive dysfunction.
The reason is different – but the experience is shared.
6. The Functional Overlay Model: Bridging the Gap
One of the key contributions of our paper is the Functional Overlay Model, which provides a framework for understanding cases where:
- PCS begins with a real biomechanical injury
- Symptoms persist beyond the expected recovery period
- No structural or cognitive deficits explain the severity
- Functional mechanisms gradually take over
This does not mean symptoms are “not real.”
It means the maintenance mechanisms shift from biological to functional, much like chronic pain.
This model helps clinicians:
- validate symptoms
- avoid unnecessary investigations
- tailor rehabilitation
- integrate psychology early
7. Why This Matters for Clinicians and Patients
1. It reduces misdiagnosis.
Patients with FND are often mistakenly labelled with chronic PCS—and vice versa.
2. It improves treatment planning.
Both groups benefit from:
- early, graded physical activity
- cognitive behavioural approaches
- education about symptom mechanisms
- reducing fear and avoidance
- restoring confidence in the body
3. It reduces stigma.
Understanding shared vulnerabilities helps break the false divide of:
- “organic” (real) vs
- “functional” (not real)
Both are real. Both are treatable.
Conclusion: PCS and FND/FCD Are Different – But Not Opposites
Our research shows that PCS and FND/FCD sit on a continuum of brain–mind interaction, shaped by:
- injury
- stress
- personality traits
- cognitive biases
- network vulnerabilities
- lived experiences
By recognising their shared risk factors and overlapping mechanisms, clinicians can better diagnose, educate, and support patients—leading to faster recovery and fewer chronic cases.
