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Lateral frontal lobe seizures.

P Kotagal·G S Arunkumar
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Abstract

On the basis of cytoarchitectural and functional studies, the frontal lobe can be subdivided into the primary motor cortex, premotor cortex, prefrontal cortex, and the limbic and paralimbic cortices. However, we are still a long way from clearly identifying individual frontal lobe epilepsies. Instead, we are limited to a discussion of frontal lobe seizures arising from various regions of the frontal lobe. Supplementary motor area epilepsy and perirolandic epilepsy have been quite well defined, in contrast to syndromes involving other regions of the frontal lobe. Recent technological advances in neuroimaging, electroencephalography, magnetoencephalography and detailed videotape analysis of seizure semiology may enable us to delineate these frontal lobe syndromes with better accuracy, thereby improving outcome after epilepsy surgery.

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Epilepsy, Frontal LobeFluorodeoxyglucose F18Frontal LobeHumansMagnetic Resonance ImagingMagnetoencephalographyMotor CortexPrefrontal CortexTerminology as TopicTomography, Emission-ComputedTomography, Emission-Computed, Single-PhotonTomography, X-Ray ComputedTreatment OutcomeJournal ArticleReview

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P Kotagal, G S Arunkumar. 1998. Lateral frontal lobe seizures.. https://doi.org/10.1111/j.1528-1157.1998.tb05126.x

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PubMed2003

Schizophrenia, psychotic illness and other psychiatric symptoms in families with autosomal dominant nocturnal frontal lobe epilepsy caused by different mutations.

OBJECTIVES: Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is characterized by a strong family history of epileptic seizures, which predominantly occur during sleep. ADNFLE has been associated with mutations in two genes coding for the nicotinic acetylcholine receptor (CHRNA4 and CHRNB2). Thus far, three different mutations have been detected in the CHRNA4 gene, and two in the CHRNB2 gene. The aim of this study was to compare the frequency of psychiatric disorders in two ADNFLE families with different CHRNA4 mutations (776ins3 and Ser248Phe). METHODS: Information was gathered from hospital charts and therapists, and the family members were assessed by clinical interviews and structured clinical interviews. RESULTS: Of the 10 individuals diagnosed with epilepsy in the CHRNA4-776ins3 family, at least four had been in contact with psychiatric services. One individual had schizophrenia, while another family member had experienced at least two severe psychotic episodes, and had been taking antipsychotic medications for years. The third family member had been hospitalized at least three times for psychiatric problems. The fourth family member needs help with activities of daily living due to incapacitating apathy, although she does not have a psychiatric diagnosis. Such accumulation of psychiatric problems was not seen in the family with the Ser248Phe mutation. CONCLUSION: These findings suggest that there may be an association between the 776ins3 mutation and the psychiatric symptoms, a hypothesis that needs further testing.

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