Summary Objective Research suggests that individuals with chronic epilepsy display differences in their self‐identity. The mechanisms by which self‐identity is altered, however, are not well understood. Neural networks supporting autobiographical memory retrieval in the mesial temporal (MT) lobe are thought to be fundamental to self‐identity processes. Thus, we examined differences in self‐identity and autobiographical memory in patients with either MT or non–mesial temporal (NMT) foci with early or late age of habitual seizure onset. Methods Participants included 102 adults: 51 healthy individuals and 51 patients with drug‐resistant focal seizures (19 MT, 32 NMT). We used the Ego Identity Process Questionnaire to profile the identity development of participants, and examined how this related to memory function assessed using the Autobiographical Memory Test. Results Patients and controls had strikingly different self‐identity profiles, with early onset MT patients showing the least identity development compared to controls and other patient groups. In contrast, late‐onset NMT patients showed the highest level of identity development of the patient groups and closely resembled healthy controls (p < 0.05 for all comparisons). For all MT patients, poor autobiographical memory retrieval was correlated with altered self‐identity (p < 0.001). No associations between autobiographical memory and self‐identity were evident in the NMT group. Significance Self‐identity in epilepsy may be modulated by the extent to which seizure foci impinge on the autobiographical memory network and the timing of seizure onset. Early disruption to MT regions of the autobiographical memory network may constitute a neurocognitive mechanism by which self‐identity is altered in chronic focal epilepsy.

ObjectivePsychosis of epilepsy (POE) occurs more frequently in temporal lobe epilepsy, raising the question as to whether abnormalities of the hippocampus are aetiologically important. Despite decades of investigation, it is unclear whether hippocampal volume is reduced in POE, perhaps due to small sample sizes and methodological limitations of past research.MethodsIn this study, we examined the volume of the total hippocampus, and the hippocampal head, body and tail, in a large cohort of patients with POE and patients with epilepsy without psychosis (EC). One hundred adults participated: 50 with POE and 50 EC. Total and subregional hippocampal volumes were manually traced and compared between (1) POE and EC; (2) POE with temporal lobe epilepsy, extratemporal lobe epilepsy and generalised epilepsy; and (3) patients with POE with postictal psychosis (PIP) and interictal psychosis (IP).ResultsCompared with EC the POE group had smaller total left hippocampus volume (13.5% decrease, p<0.001), and smaller left hippocampal body (13.3% decrease, p=0.002), and left (41.5% decrease, p<0.001) and right (36.4% decrease, p<0.001) hippocampal tail volumes. Hippocampal head volumes did not differ between groups.ConclusionPosterior hippocampal volumes are bilaterally reduced in POE. Volume loss was observed on a posteroanterior gradient, with severe decreases in the tail and moderate volume decreases in the body, with no difference in the hippocampal head. Posterior hippocampal atrophy is evident to a similar degree in PIP and IP. Our findings converge with those reported for the paradigmatic psychotic disorder, schizophrenia, and suggest that posterior hippocampal atrophy may serve as a biomarker of the risk for psychosis, including in patients with epilepsy.

Epilepsy ABSTRACTThis systematic review critically assesses structural and functional neuroimaging studies of psychosis of epilepsy (POe). we integrate findings from 18 studies of adults with POe to examine the prevailing view that there is a specific relationship between temporal lobe epilepsy (TLe) and POe, and that mesial temporal lobe pathology is a biomarker for POe. Our results show: (1) conflicting evidence of volumetric change in the hippocampus and amygdala; (2) distributed structural pathology beyond the mesial temporal lobe; and (3) changes in frontotemporal functional network activation. These results provide strong evidence for a revised conceptualisation of POe as disorder of brain networks, and highlight that abnormalities in mesial temporal structures alone are unlikely to account for its neuropathogenesis. Understanding POe as a disease of brain networks has important implications for neuroimaging research and clinical practice. Specifically, we suggest that future neuroimaging studies of POe target structural and functional networks, and that practitioners are vigilant for psychotic symptoms in all epilepsies, not just TLe.

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