Susceptibility to functional seizures in temporal lobe epilepsy: the interplay between psychological and somatoform dissociation, trauma, and sense of agency

Introduction

Temporal Lobe Epilepsy (TLE) frequently co-occurs with Functional Seizures (FS), this overlap complicates drug-resistant cases, often leading to unnecessary polypharmacy and increased psychological burden [1]. Despite its clinical significance, the mechanisms driving comorbid FS remain unclear. While clinical assessments typically focus on dissociation, the neurocognitive mechanism of Sense of Agency (SoA)[2]—the implicit monitoring of action control— remains under-explored in this population. This study investigates if FS in TLE stems from SoA disruption or somatoform trauma. We hypothesized that the SoA remains intact in TLE patients, while somatoform dissociation driving FS development.

Methods

We analyzed data from 31 participants: Isolated TLE (n=11), Comorbid TLE+FS (n=9), and Healthy Controls (HC)(n=11). In the comorbid group, FS diagnosis was confirmed via Video-EEG monitoring.

No significant differences were found between groups regarding age (H = 0.979, p = 0.613), sex (Χ² = 3.428, p = 0.180), or education (H = 1.239, p = 0.538).
Clinical cohorts were well-matched for pharmacological load (Isolated TLE: Mean=2.18, SD=0.75; Comorbid TLE+FS: Mean=2.00, SD=1.58); no significant difference was observed in the number of anti-seizure medications (ASMs) (p = 0.632).
Current and lifetime psychiatric comorbidities were assessed using the SCID (Structured Clinical Interview for DSM). Psychological dissociation was measured with the Dissociative Experiences Scale (DES), somatoform dissociation with the Somatoform Dissociation Questionnaire (SDQ-20), and trauma history with the Traumatic Experiences Checklist (TEC). Implicit SoA was measured via an Intentional Binding Task based on the Libet Clock Paradigm.
Statistical analyses were performed using JASP (Kruskal-Wallis and Spearman’s correlation tests, r_s; p<0.05).

Results

Isolated TLE patients matched controls (p=0.403), while the TLE+FS group exhibited significantly higher SDQ-20 scores (r_rb=0.788, p=0.017), marking it a specific FS indicator.
Within clinical cohorts, SDQ-20 scores strongly correlated with physical abuse history (p=0.005). Conversely, psychological dissociation (DES) showed no trauma link (p=0.880), suggesting FS is mediated by somatic rather than psychological dissociation.
No significant differences emerged in SoA parameters across all groups (Action binding: p=0.604, Outcome binding: p=0.276, Overall binding: p=0.471). This proves that FS do not stem from a disruption in implicit agency. A marginal trend (p=0.075) between action binding and current psychiatric illness suggests that general psychopathology may weaken action control as the sample expands.
Psychiatric comorbidity differed significantly across groups (Χ²=8.86, p=0.012), concentrating in the TLE+FS cohort (standardized residual = 2.02), and linking somatic burden to general psychopathology.

Conclusions

Comorbid FS in TLE stems from somatoform dissociation rather than a neurocognitive Sense of Agency (SoA) deficit. Since both patient groups shared similar medication loads, these findings suggest a post-traumatic somatic reorganization rather than drug side effects. In essence, the pathology reflects a faulty “software” algorithm (somatoform dissociation) rather than a “hardware” failure (SoA). Routine SDQ-20 assessment is vital for early FS detection and directing patients toward trauma- and body-oriented psychotherapy. These preliminary data highlight a critical clinical trajectory for managing treatment-resistant epilepsy.

References

Widyadharma, I.P.E., Soejitno, A., Samatra, D. P. G.P., Sinardja, A. M. G., 2021. Clinical differentiation of psychogenic non-epileptic seizure: a practical diagnostic approach. Egypt J Neurol Psychiatry Neurosurg 57, 19.
Haggard, P., Clark, S., Kalogeras, J., 2002. Voluntary action and conscious awareness. Nat Neurosci Apr. 5(4), 382-5.