András A. Horváth (Hungary)
National Institute of Mental Health, Neurology and Neurosurgery Neurocognitive Research CenterAuthor Of 1 Presentation
THE ROLE OF EPILEPTIC ACTIVITY IN THE PRODROMAL PHASE OF ALZHEIMER’S DISEASE
- András A. Horváth (Hungary)
Abstract
Background and Aims:
Growing body of evidence supports that patients with Alzheimer’s disease have a higher occurrence of epileptic seizures. Recent experiments also postulated that epileptiform discharges might contribute to the pathogenesis of cognitive decline. The aim of our study was to analyze the impact of epileptic activity on the cognitive performance and on the progression of cognitive decline in clinical and prodromal Alzheimer patients.
Methods:
We investigated 50 mild Alzheimer patients and 30 patients with mild cognitive impairment (MCI) with no history of epileptic seizures. All participants underwent a 24-hour electroencephalography, neurology, neuroimaging (structural and resting state functional MRI) and neuropsychology examination. Patients were enrolled in a 1-year follow-up study with repeated examination protocol.
Results:
Subclinical epileptiform discharges were recorded in 48% of Alzheimer and 33% of MCI patients. Epileptiform discharges were associated with lower performance scores in memory (p<0.001). Epileptic activity also associated with lower hippocampal volumes (p:0.012) and larger extent of disconnection between default mode network and temporal brain structures (p:0.034). Patients with spikes showed 1.3-times faster decline in global cognitive scores than patients without (p<0.001) and higher conversion rate into dementia by MCI patients (p<0.001).
Conclusions:
Epileptiform activity occurs in half of Alzheimer and third of MCI patients who have never suffered epileptic seizures. Epileptic activity associates with lower cognitive performance and impaired structural and functional organization of brain structures. Epileptic discharges accelerate the progression of cognitive decline. Our findings suggest the prominent role of epileptiform discharges in the pathomechanism of cognitive decline in Alzheimer pathology.
Presenter of 1 Presentation
THE ROLE OF EPILEPTIC ACTIVITY IN THE PRODROMAL PHASE OF ALZHEIMER’S DISEASE
- András A. Horváth (Hungary)
Abstract
Background and Aims:
Growing body of evidence supports that patients with Alzheimer’s disease have a higher occurrence of epileptic seizures. Recent experiments also postulated that epileptiform discharges might contribute to the pathogenesis of cognitive decline. The aim of our study was to analyze the impact of epileptic activity on the cognitive performance and on the progression of cognitive decline in clinical and prodromal Alzheimer patients.
Methods:
We investigated 50 mild Alzheimer patients and 30 patients with mild cognitive impairment (MCI) with no history of epileptic seizures. All participants underwent a 24-hour electroencephalography, neurology, neuroimaging (structural and resting state functional MRI) and neuropsychology examination. Patients were enrolled in a 1-year follow-up study with repeated examination protocol.
Results:
Subclinical epileptiform discharges were recorded in 48% of Alzheimer and 33% of MCI patients. Epileptiform discharges were associated with lower performance scores in memory (p<0.001). Epileptic activity also associated with lower hippocampal volumes (p:0.012) and larger extent of disconnection between default mode network and temporal brain structures (p:0.034). Patients with spikes showed 1.3-times faster decline in global cognitive scores than patients without (p<0.001) and higher conversion rate into dementia by MCI patients (p<0.001).
Conclusions:
Epileptiform activity occurs in half of Alzheimer and third of MCI patients who have never suffered epileptic seizures. Epileptic activity associates with lower cognitive performance and impaired structural and functional organization of brain structures. Epileptic discharges accelerate the progression of cognitive decline. Our findings suggest the prominent role of epileptiform discharges in the pathomechanism of cognitive decline in Alzheimer pathology.