Prevalence, Semiology, and Risk Factors of Epilepsy in Alzheimer’s Disease: An Ambulatory EEG Study

Horváth, András; Szücs, Anna; Hidasi, Zoltán; Csukly, Gábor; Barcs, Gábor; Kamondi, Anita

doi:10.3233/jad-170925

Cited by 59 publications

(80 citation statements)

References 54 publications

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“…Seizures are a common feature of AD in those with and without DS, occurring in a quarter of patients without DS with AD 22 and 40% of patients with DS and AD. 14 However, late-onset epilepsy was also noted in 7 people (4.8%) without a dementia diagnosis in our study, increasing mortality risk 10-fold.…”

Section: Discussionmentioning

confidence: 99%

Association of Dementia With Mortality Among Adults With Down Syndrome Older Than 35 Years

et al. 2019

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Key Points Question How does dementia status influence mortality in people with Down syndrome? Findings In a longitudinal study including 211 adults with Down syndrome 36 years and older, 27 people died during follow-up (mean, 28; range, 1-65 months), and dementia was the proximate cause of death in 70% of cases. Crude mortality rates were 5 times higher in those with dementia than those without. Meaning Nearly all older adults with Down syndrome now have dementia when they die, making this a vital population for researching disease progression, modifying factors, and potential treatments.

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Section: Discussionmentioning

confidence: 99%

Association of Dementia With Mortality Among Adults With Down Syndrome Older Than 35 Years

et al. 2019

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“…In two sleep EEG studies, IEA rate was 62% (Vossel et al, 2013) and 80% (Horváth et al, 2018b) in patients with clinical history of seizures. In these studies, IEA appeared mainly over the frontotemporal areas with a left-side dominance (Rao et al, 2009;Vossel et al, 2013;Cretin et al, 2016;Sarkis et al, 2016;Horváth et al, 2018b). Temporal occurrence of IEA was analyzed only in two studies: in the study of Vossel et al (2013), 10% of IEA was detected during wakefulness and 64% appeared exclusively in stage2 or deeper sleep, while in our previous report, 82% of IEA was associated with sleep and 55% was detected in deep sleep (Horváth et al, 2017b).…”

Section: Prevalence Of Sea and Iea In Cognitive Disorders Major Neuromentioning

confidence: 92%

“…IEA was analyzed in three studies with routine electroencephalogram (EEG) identifying interictal epileptiform activity in third of AD patients who presented with epileptic seizure (Rao et al, 2009;Cretin et al, 2016;Sarkis et al, 2016). In two sleep EEG studies, IEA rate was 62% (Vossel et al, 2013) and 80% (Horváth et al, 2018b) in patients with clinical history of seizures. In these studies, IEA appeared mainly over the frontotemporal areas with a left-side dominance (Rao et al, 2009;Vossel et al, 2013;Cretin et al, 2016;Sarkis et al, 2016;Horváth et al, 2018b).…”

Section: Prevalence Of Sea and Iea In Cognitive Disorders Major Neuromentioning

confidence: 99%

“…It should be noted that in Vossel's study from 2016, SEA was associated with faster deterioration of cognition determined by Mini-Mental Score Examination (Vossel et al, 2016). Moreover, studies also suggest that AD and mild cognitive impairment (MCI) patients with SEA have an earlier onset of cognitive decline being usually associated with more aggressive forms of AD that show faster progression (Vossel et al, 2016;Horváth et al, 2018b). Table 1 summarizes the AD studies on the prevalence of IEA and SEA.…”

Section: Prevalence Of Sea and Iea In Cognitive Disorders Major Neuromentioning

confidence: 99%

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Inhibiting Epileptiform Activity in Cognitive Disorders: Possibilities for a Novel Therapeutic Approach

et al. 2020

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Cognitive impairment is a common and seriously debilitating symptom of various mental and neurological disorders including autism, attention deficit hyperactivity disorder, multiple sclerosis, epilepsy, and neurodegenerative diseases, like Alzheimer's disease. In these conditions, high prevalence of epileptiform activity emerges as a common pathophysiological hallmark. Growing body of evidence suggests that this discrete but abnormal activity might have a long-term negative impact on cognitive performance due to neuronal circuitries' remodeling, altered sleep structure, pathological hippocampocortical coupling, and even progressive neuronal loss. In animal models, epileptiform activity was shown to enhance the formation of pathological amyloid and tau proteins that in turn trigger network hyperexcitability. Abolishing epileptiform discharges might slow down the cognitive deterioration. These findings might provide basis for therapeutic use of antiepileptic drugs in neurodegenerative cognitive disorders. The aim of our review is to describe the data on the prevalence of epileptiform activity in various cognitive disorders, to summarize the current knowledge of the mechanisms of epileptic activity in relation to cognitive impairment, and to explore the utility of antiepileptic drugs in the therapy of cognitive disorders. We also propose future directions for drug development and novel therapeutic interventions targeting epileptiform discharges in these disorders.

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“…During epileptogenesis, a wide spectrum of potentially pro‐epileptogenic neurodegenerative changes is seen in limbic structures including mossy fiber sprouting; neuronal reorganization‐synaptic remodeling; neurogenesis; blood‐brain barrier disruption, γ‐aminobutyric acid (GABA) receptor, and GABAergic neurons changes; alterations in peptide and brain‐derived neurotrophic factor (BDNF) expression; neuroinflammation; changes in ion channels; alterations in axonal transport, amyloid‐β peptide, tau, and PP2A pathology; and other cellular and functional changes . These neuropathological changes are not specific of epilepsy; however, they are similar to those of neurodegenerative disorders such as Alzheimer's disease, even when there is no clear history of epilepsy . Neurodegeneration is a progressive process that evolves during acquired epileptogenesis; however, some studies suggest that the neurodegeneration may not directly result in the epileptogenesis, but it may induce other processes that do .…”

Section: Neurodegenerative Mechanisms Relevant To Acquired Epilepsiesmentioning

confidence: 99%

Neurodegenerative pathways as targets for acquired epilepsy therapy development

2020

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There is a growing body of clinical and experimental evidence that neurodegenerative diseases and epileptogenesis after an acquired brain insult may share common etiological mechanisms. Acquired epilepsy commonly develops as a comorbid condition in patients with neurodegenerative diseases such as Alzheimer's disease, although it is likely much under diagnosed in practice. Progressive neurodegeneration has also been described after traumatic brain injury, stroke, and other forms of brain insults. Moreover, recent evidence has shown that acquired epilepsy is often a progressive disorder that is associated with the development of drug resistance, cognitive decline, and worsening of other neuropsychiatric comorbidities. Therefore, new pharmacological therapies that target neurobiological pathways that underpin neurodegenerative diseases have potential to have both an anti-epileptogenic and diseasemodifying effect on the seizures in patients with acquired epilepsy, and also mitigate the progressive neurocognitive and neuropsychiatric comorbidities. Here, we review the neurodegenerative pathways that are plausible targets for the development of novel therapies that could prevent the development or modify the progression of acquired epilepsy, and the supporting published experimental and clinical evidence. K E Y W O R D SAMPA, amyloid-β, glutamate, mTOR, neuroinflammation, tau

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Prevalence, Semiology, and Risk Factors of Epilepsy in Alzheimer’s Disease: An Ambulatory EEG Study

Cited by 59 publications

References 54 publications

Association of Dementia With Mortality Among Adults With Down Syndrome Older Than 35 Years

Association of Dementia With Mortality Among Adults With Down Syndrome Older Than 35 Years

Inhibiting Epileptiform Activity in Cognitive Disorders: Possibilities for a Novel Therapeutic Approach

Neurodegenerative pathways as targets for acquired epilepsy therapy development

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