A case report about focal status epilepticus as first presentation in Alzheimer’s disease: finding the culprit
Abstract Background Neuronal hyperexcitability has been proposed to play a key role in Alzheimer’s disease (AD). Understanding the relation between this enhanced excitability and AD pathology could provide a window for therapeutic interventions. However epileptiform activity is often subclinical, hi...
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BMC
2024-12-01
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| Series: | BMC Neurology |
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| Online Access: | https://doi.org/10.1186/s12883-024-03979-4 |
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| author | Astrid Devulder Greet Vanderlinden Evy Cleeren Valerie Goovaerts Tom Theys Koen Van Laere Wim Van Paesschen |
| author_facet | Astrid Devulder Greet Vanderlinden Evy Cleeren Valerie Goovaerts Tom Theys Koen Van Laere Wim Van Paesschen |
| author_sort | Astrid Devulder |
| collection | DOAJ |
| description | Abstract Background Neuronal hyperexcitability has been proposed to play a key role in Alzheimer’s disease (AD). Understanding the relation between this enhanced excitability and AD pathology could provide a window for therapeutic interventions. However epileptiform activity is often subclinical, hidden on scalp EEG and very challenging to assess with current diagnostic modalities. Case presentation A woman in her sixties presented with acute confusion. Despite a normal scalp electroencephalogram (EEG), magnetic resonance imaging (MRI) showed cytotoxic edema of the right mesial temporal lobe and hippocampal hypermetabolism was present on ([18F]-fluoro-2-deoxyglucose positron emission tomography (PET). Bilateral foramen ovale (FO) electrodes were placed to directly record mesial temporal activity and revealed continuous mesial temporal epileptic activity, while scalp EEG remained normal. After recovery, a new diagnosis of AD was established on cerebrospinal fluid. The lateralization of the epileptiform activity was congruent with the predominant side of tau pathology in the mesial temporal cortex on 18F-MK6240 PET. On follow-up MRI, two and five months later, the right hippocampus became atrophic. Conclusion This case highlights the significant role of neuronal hyperexcitability in early AD pathogenesis and how shared mechanisms between AD and epilepsy can complicate clinical management. |
| format | Article |
| id | doaj-art-65298b95016e4e008cfe1d666896eca4 |
| institution | OA Journals |
| issn | 1471-2377 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Neurology |
| spelling | doaj-art-65298b95016e4e008cfe1d666896eca42025-08-20T01:57:16ZengBMCBMC Neurology1471-23772024-12-012411510.1186/s12883-024-03979-4A case report about focal status epilepticus as first presentation in Alzheimer’s disease: finding the culpritAstrid Devulder0Greet Vanderlinden1Evy Cleeren2Valerie Goovaerts3Tom Theys4Koen Van Laere5Wim Van Paesschen6Laboratory for Epilepsy ResearchNuclear Medicine and Molecular Imaging, Department of Imaging and PathologyDepartment of Neurology, University Hospitals LeuvenDepartment of Neurology, University Hospitals LeuvenResearch Group Experimental Neurosurgery and NeuroanatomyNuclear Medicine and Molecular Imaging, Department of Imaging and PathologyLaboratory for Epilepsy ResearchAbstract Background Neuronal hyperexcitability has been proposed to play a key role in Alzheimer’s disease (AD). Understanding the relation between this enhanced excitability and AD pathology could provide a window for therapeutic interventions. However epileptiform activity is often subclinical, hidden on scalp EEG and very challenging to assess with current diagnostic modalities. Case presentation A woman in her sixties presented with acute confusion. Despite a normal scalp electroencephalogram (EEG), magnetic resonance imaging (MRI) showed cytotoxic edema of the right mesial temporal lobe and hippocampal hypermetabolism was present on ([18F]-fluoro-2-deoxyglucose positron emission tomography (PET). Bilateral foramen ovale (FO) electrodes were placed to directly record mesial temporal activity and revealed continuous mesial temporal epileptic activity, while scalp EEG remained normal. After recovery, a new diagnosis of AD was established on cerebrospinal fluid. The lateralization of the epileptiform activity was congruent with the predominant side of tau pathology in the mesial temporal cortex on 18F-MK6240 PET. On follow-up MRI, two and five months later, the right hippocampus became atrophic. Conclusion This case highlights the significant role of neuronal hyperexcitability in early AD pathogenesis and how shared mechanisms between AD and epilepsy can complicate clinical management.https://doi.org/10.1186/s12883-024-03979-4Alzheimer’s diseaseCase reportHippocampal atrophyTau pathologyTemporal lobe epilepsy |
| spellingShingle | Astrid Devulder Greet Vanderlinden Evy Cleeren Valerie Goovaerts Tom Theys Koen Van Laere Wim Van Paesschen A case report about focal status epilepticus as first presentation in Alzheimer’s disease: finding the culprit BMC Neurology Alzheimer’s disease Case report Hippocampal atrophy Tau pathology Temporal lobe epilepsy |
| title | A case report about focal status epilepticus as first presentation in Alzheimer’s disease: finding the culprit |
| title_full | A case report about focal status epilepticus as first presentation in Alzheimer’s disease: finding the culprit |
| title_fullStr | A case report about focal status epilepticus as first presentation in Alzheimer’s disease: finding the culprit |
| title_full_unstemmed | A case report about focal status epilepticus as first presentation in Alzheimer’s disease: finding the culprit |
| title_short | A case report about focal status epilepticus as first presentation in Alzheimer’s disease: finding the culprit |
| title_sort | case report about focal status epilepticus as first presentation in alzheimer s disease finding the culprit |
| topic | Alzheimer’s disease Case report Hippocampal atrophy Tau pathology Temporal lobe epilepsy |
| url | https://doi.org/10.1186/s12883-024-03979-4 |
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