Cognitive and Sensory Profiles in Patients with Epilepsy, Migraine, and Their Comorbidity: A Quantitative Study

Background Epilepsy and migraine are highly comorbid neurological disorders with shared pathophysiological features. However, their combined impact on cognitive, emotional, and sensory processing remains insufficiently characterized. This study aimed to quantitatively compare these domains across patients with epilepsy, migraine, their comorbidity, and healthy controls. Methods​: The study recruited 27 patients with epilepsy, 27 with migraine, 20 with comorbid epilepsy and migraine, and 25 healthy controls. Cognitive function, anxiety, and depression were assessed using the Montreal Cognitive Assessment (MoCA), Self-Rating Anxiety Scale (SAS), and Self-Rating Depression Scale (SDS), respectively. Disease-specific scales were also administered. Sensory function was evaluated by measuring the pain perception threshold (PPT) with von Frey filaments and by quantifying the current perception threshold (CPT) and pain tolerance threshold (PTT) using a Neurometer® at 2000 Hz (Aβ fibers), 250 Hz (Aδ fibers), and 5 Hz (C fibers). Results​: All patient groups showed significantly lower MoCA scores and higher SAS/SDS scores compared to controls (all P  < 0.05). The comorbidity group had the most pronounced cognitive deficits, particularly in attention, executive function, and visuospatial memory. While PPT and CPT did not differ between groups, PTT was significantly reduced in all patient groups at 250 Hz and 5 Hz (all P  < 0.05), with the comorbidity group also showing lower PTT at 2000 Hz. Correlation analyses revealed positive associations between VAS score and headache attack duration, as well as between both MIDAS and HIT-6 scores and VAS score. LSSS score positively correlated with seizure duration. MoCA score positively correlated with both headache attack duration and HIT-6 score. Conclusion​: Patients with epilepsy, migraine, or their comorbidity exhibit significant cognitive and emotional impairments, with comorbid patients demonstrating additive deficits. The broad reduction in pain tolerance implicates shared sensory processing abnormalities and central sensitization as a potential mechanism linking the two disorders. These results support an integrated clinical approach that targets cognitive, emotional, and sensory dysfunction.