Revisiting Hughlings Jackson’s dreamy state: dissociative symptoms in temporal lobe epilepsy

Transient, dissociative experiences have been attributed to temporal lobe epilepsy (TLE) since at least the time of John Hughlings Jackson in the 1870s, who described how different dissociative symptoms might have distinct clinical potential. While dissociative symptoms are well-understood as a semiological feature of mesial TLE, they can also occur interictally yet remain poorly understood. We systematically examined the frequency, nature, and clinical correlates of dissociative experiences in TLE in an initial effort to better understand their phenotypic features. 157 adults with TLE and 57 healthy controls participated (N = 214). A data-driven statistical approach determined the underlying factor structure of the Wessex Dissociation Scale in this cohort and delineated phenotypic symptom clusters. We then examined group differences in rates of dissociation symptoms, as well as the influence of epilepsy-related and mood factors. People with TLE reported more frequent dissociative experiences (M = 0.96, SD = 0.61) than controls (M = 0.69, SD = 0.38; p < 0.001). A novel five-factor solution of dissociative symptoms emerged, namely intrusive, affective, memory, somatic, and numbing. Memory blanks and somatic distortions were uniquely elevated in TLE. Memory blanks and numbing dissociative symptoms were associated with increased seizure frequency, epilepsy duration, and number of anti-seizure medications. Higher depression and anxiety symptoms were linked to elevated overall dissociative symptoms and scores on each subfactor (r = 0.26-.64; p < 0.01-<.001). People with TLE experience elevated rates of dissociative symptoms in their daily lives. Rather than a general dissociative phenotype, memory- and sensory-related symptoms predominate. The data-driven five-factor model refines earlier understandings and aligns well with contemporary neurocognitive models of epilepsy as a disorder of large-scale network dysfunction, with psychological and epilepsy-specific mechanisms underpinning dissociative experiences in TLE. While the aetiology of these symptoms is complex and multidetermined, TLE nevertheless remains an insightful model for understanding the neurological basis of dissociation more broadly.