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Electroencephalographic abnormalities in the absence of any other major laboratory or imaging findings are a frequently encountered phenomenon in many psychiatric disorders. In some cases, clear-cut interictal epileptiform EEG abnormalities in patients with classic primary psychiatric disorders lead to referrals to epilepsy departments for diagnostic evaluation. Although video/EEG telemetry in these cases generally proves that there is no direct temporal link between the EEG pathologies and psychiatric symptoms, and therefore the psychiatric syndrome cannot be regarded as epilepsy, the relevance of the EEG abnormalities remains open to discussion. In this article we put forward the model of a paraepileptic pathomechanism, which might explain the pathogenetic role of such EEG pathologies, at least in subgroups of such patients. We propose that ictal or nonictal epileptic neurophysiological activity can lead to local area neuronal network inhibition (LANI). In this model clinical symptoms are related not to the excitatory epileptiform abnormalities themselves, but to the extent, site, and dynamics of the resulting local neuronal network inhibition. The LANI hypothesis is capable of explaining the complex relationship between EEG abnormalities and clinical symptoms in different neuropsychiatric syndromes and can be verified and falsified in empirical research., (Copyright © 2011 Elsevier Inc. All rights reserved.)

To properly address the psychosocial health of people with epilepsy, service and resource allocation, standards of care, and research should reflect the differing needs of patients presenting at different care levels and in different parts of the world. Ideally, people with epilepsy should have access, according to need, to adequately trained primary care physicians and nurse practitioners; to dedicated secondary care epilepsy clinics staffed by trained multidisciplinary teams; and to tertiary level dedicated staff, able to offer a range of psychosocial interventions and supported by comprehensive assessment tools for psychosocial screening, diagnosis, and management. Established protocols linking the various tiers of care would be important, as would a dedicated, nationally applicable online EMR system. In developing countries, best practice needs to be tailored to be realistic and achievable, and some potentially useful models are already available.

We assessed 228 people with epilepsy (PWE) in the residential care setting using the Neuropsychiatric Inventory (NPI) and Brief Psychiatric Rating Scale (BPRS) as caregiver- and observer-rated instruments. There was a significant burden of psychopathology, about half of all subjects surveyed scoring positive on either or both instruments. Psychopathology as measured by the NPI and BPRS was significantly greater in cognitively impaired subjects than in those with intact cognitive function. The NPI was found to be a valid caregiver-rated measure of psychopathology in PWE, with a principal components analysis yielding a reliable and interpretable four-factor solution, psychosis, interictal dysphoric disorder, depression, and anxiety being identified. Mental health service needs were found to be considerable in this population, with a significant hidden burden of psychiatric comorbidity. As this population has ongoing service needs through the life span, further research is necessary.

The classification of psychiatric disorders in epilepsy has evolved considerably from the first attempts in the 19th century. A dedicated subcommission of the ILAE Commission on Psychobiology of Epilepsy (now the Commission on Neuropsychiatric Aspects) has developed this classification proposal. The aim of this proposal is to separate disorders comorbid with epilepsy and those that reflect ongoing epileptiform activity from epilepsy-specific disorders, and to attempt to subclassify the epilepsy-specific disorders alone. Further, the classification of epilepsy-specific psychiatric disorders has largely followed their relationship to the ictus, with factors such as relationship to antiepileptic drug (AED) change being coded as additional information. Finally, this proposal presents a clinical and descriptive system of classification rather than an etiological classification on the grounds that there is currently inadequate information for the latter approach to be employed globally.

Epilepsy and behavior have a complex, often intriguing relationship. We report here the interesting case of Mrs. A, who presented with depression and developed seizures and an ictal psychosis precipitated by use of a selective serotonin reuptake inhibitor. She subsequently presented with forced normalization characterized by affective somatoform and hysterical manifestations.

Many people with epilepsy suffer from comorbid depression. Despite this, there have been few studies addressing the treatment of depression in this population, and the literature on psychiatric management techniques in patients with epilepsy is composed largely of opinions rather than evidence from randomized, controlled trials or other systematic investigations. Antidepressant drugs, including tricyclics and selective serotonin reuptake inhibitors, can be used to treat patients with epilepsy and comorbid depression. Nonpharmacological treatment options include vagus nerve stimulation, transcranial magnetic stimulation, and psychological therapies including cognitive-behavioral therapy, individual or group psychotherapy, patient support groups, family therapy, and counseling. Another important area that remains largely uninvestigated is psychiatric research in patients with epilepsy in non-Western cultures (with the exception of Japan). Factors such as problems with access to and acceptability of therapies in many developing nations have further implications for the treatment of psychiatric disorders in epilepsy.

Bilateral symmetrical hippocampal atrophy (BHA) has been implicated as a possible causal element in various neuropsychiatric disorders, in particular depressive disorder and schizophrenia. To test the hypothesis that bilateral symmetrical severe volume loss of the hippocampi is of causal relevance to these psychiatric syndromes rather than an epiphenomenon we assessed the psychopathology in a group of patients with temporal lobe epilepsy (TLE) and very severe bilateral symmetrical hippocampal atrophy and compared it with that of a patient control group. Patients with TLE and hippocampal volumes smaller than three standard deviations below the mean of a control population were identified and compared with a matched patient population with normal hippocampal volumes. Psychopathology was assessed by blinded trained psychiatrists using the Present State Examination and Neurobehavioral Inventory. The prevalence of psychiatric syndromes was high in both patient groups; however, there was no significant difference between the two groups. With use of the more specific Neurobehavioral Inventory a psychopathological pattern reminiscent of the Geschwind syndrome emerged when patients with BHA were characterized by caregivers. While BHA does not result in an increased prevalence of specific psychiatric syndromes, specific symptoms that characterize the Geschwind syndrome like hypergraphia and hyposexuality might be pathogenically related to hippocampal atrophy.

In 1953, Landolt described a group of patients with poorly controlled epilepsy who had psychotic episodes associated with remission of their seizures and disappearance of epileptiform activity on their EEGs. He called this phenomenon "forced normalization." Since then, neurologists and psychiatrists have been intrigued by this phenomenon, and although it has been also reported by others, its existence continues to be the source of much debate. In this article, we review the clinical characteristics and potential pathogenic mechanisms of forced normalization and illustrate the complexities inherent in reaching this diagnosis, as well as its differential diagnosis in two representative cases.

To study the nature of personality and psychopathology in nonepileptic attack disorder (NEAD) and epilepsy, we prospectively assessed 45 consecutive attendees to a specialist assessment unit for epilepsy. Patients with NEAD were more likely to report clinically significant symptoms of anxiety, worry, disordered eating, and somatoform disorder. An ICD-10 diagnosis of anxiety or phobic disorder was significantly more common in NEAD patients. Together DSM-IV personality Clusters A and C were more common in epilepsy than NEAD. Hierarchical logistic regression with diagnosis as the target variable found anxiety, eating, and worry but not somatoform symptoms were reliably associated with NEAD. Together the Present State Examination (PSE) eating, PSE worrying/tension, PSE expansive mood, past psychiatric history, and gender variables allowed for correct classification of more than 88% of all cases. Personality and psychopathology variables seem to be valid clinical predictors of epilepsy and NEAD, and should be examined in epidemiological studies.