Dementia with non-convulsive seizures: a case report

Chen, Yu-Shiue; Chen, Tsang-Shan; Huang, Chin-Wei

doi:10.1177/03000605211062453

Cited by 5 publications

(4 citation statements)

References 24 publications

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“…In a case study of an 89 year old woman with severe AD, intractable myoclonic epilepsy, and psychiatric symptoms of circadian rhythm disorder and irritability, perampanel improved both myoclonus and psychiatric symptoms (258). An additional case report demonstrated improved cognitive functioning in a patient with non-convulsive seizures and AD, supporting the case for early administration (259). In transgenic AD mice, inhibition of AMPA…”

Section: Ampa Receptor Antagonistsmentioning

confidence: 64%

Proposed mechanisms of tau: relationships to traumatic brain injury, Alzheimer’s disease, and epilepsy

Martin,

Leeman-Markowski

2024

Front. Neurol.

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Traumatic brain injury (TBI), Alzheimer’s disease (AD), and epilepsy share proposed mechanisms of injury, including neuronal excitotoxicity, cascade signaling, and activation of protein biomarkers such as tau. Although tau is typically present intracellularly, in tauopathies, phosphorylated (p-) and hyper-phosphorylated (hp-) tau are released extracellularly, the latter leading to decreased neuronal stability and neurofibrillary tangles (NFTs). Tau cleavage at particular sites increases susceptibility to hyper-phosphorylation, NFT formation, and eventual cell death. The relationship between tau and inflammation, however, is unknown. In this review, we present evidence for an imbalanced endoplasmic reticulum (ER) stress response and inflammatory signaling pathways resulting in atypical p-tau, hp-tau and NFT formation. Further, we propose tau as a biomarker for neuronal injury severity in TBI, AD, and epilepsy. We present a hypothesis of tau phosphorylation as an initial acute neuroprotective response to seizures/TBI. However, if the underlying seizure pathology or TBI recurrence is not effectively treated, and the pathway becomes chronically activated, we propose a “tipping point” hypothesis that identifies a transition of tau phosphorylation from neuroprotective to injurious. We outline the role of amyloid beta (Aβ) as a “last ditch effort” to revert the cell to programmed death signaling, that, when fails, transitions the mechanism from injurious to neurodegenerative. Lastly, we discuss targets along these pathways for therapeutic intervention in AD, TBI, and epilepsy.

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Section: Ampa Receptor Antagonistsmentioning

confidence: 64%

Proposed mechanisms of tau: relationships to traumatic brain injury, Alzheimer’s disease, and epilepsy

Martin,

Leeman-Markowski

2024

Front. Neurol.

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“…As suggested by initial findings, perampanel may effectively control seizures and contribute to improvement of cognitive function. 25 , 26 Consistent with published data, 25 the expert group suggests increasing the perampanel dose to 4 mg/day at an early stage, as long as it is tolerable in the patient and if the patient does not have comorbid psychiatric or behavioral disorders. It is also important to monitor for any behavior changes during the course of treatment.…”

Section: Best Practice Expert Recommendationsmentioning

confidence: 66%

“…A case report in Taiwan also supported the early administration of perampanel to improve cognitive performance in a patient with Alzheimer’s disease complicated with non-convulsive seizures. 26 …”

Section: Key Clinical and Real-world Evidence On Perampanelmentioning

confidence: 99%

Optimal Use of Perampanel in Elderly Asian Patients with Epilepsy: Expert Opinion

Huang¹,

Boonyapisit²,

Gunadharma³

et al. 2022

TCRM

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Managing epilepsy in the elderly remains complicated largely due to factors related to aging. In this population, management practices are increasingly shifting towards the use of newer-generation anti-seizure medications (ASMs) as they are generally associated with better tolerability and safety profiles than older ones. Perampanel is a new ASM with broad-spectrum efficacy and a favorable safety profile. However, because of the lack of information and experience in its use, the prescription of perampanel has not been optimized in the elderly in the real-world setting in Asia. A group of epilepsy experts across the region convened at a series of virtual meetings to share their experience and discuss recommendations on perampanel use in elderly patients, including dose optimization, considerations with treatment initiation, and strategies to manage adverse events and maximize tolerability. This article summarizes key clinical and real-world evidence for perampanel in the elderly and consolidates the experts’ opinions on optimizing perampanel use in elderly Asian patients with epilepsy, providing practical guidance for clinicians to address challenges related to treatment initiation and tolerance.

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“…The semiology of seizures varies among the different forms of AD. In sporadic AD the most frequent type are focal epileptic seizures presenting with altered level of consciousness without motor symptoms (55-70%) [10,14,41,51,[55][56][57]. Other symptoms include episodes of amnestic spells, déjà vu or jamais vu, speech arrest, staring spells and unexplained emotions or sensory phenomena.…”

Section: Comorbidities Increasing the Risk Of Epilepsymentioning

confidence: 99%

Mechanisms Involved in Epileptogenesis in Alzheimer’s Disease and Their Therapeutic Implications

Altuna¹,

Olmedo²,

Carmona‐Iragui³

et al. 2022

Preprint

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Epilepsy and Alzheimer's disease (AD) incidence increase with age. There are reciprocal relationships between epilepsy and AD. Epilepsy is a risk factor for AD and, in turn, AD is an independent risk factor for developing epilepsy in old age and abnormal AD biomarkers in PET and or CSF are frequently found in late onset epilepsies of unknown etiology. Accordingly, epilepsy and AD share pathophysiological processes including neuronal hyperexcitability and an early excitatory-inhibitory dysregulation leading to dysfunction in the inhibitory GABAergic and excitatory glutamatergic systems. Moreover, both β-amyloid and tau protein aggregates, the anatomopathological hallmarks of AD, have proepileptic effects. Finally, these aggregates have been found in the resection material of refractory temporal lobe epilepsies suggesting that epilepsy leads to amyloid and tau aggregates. Some epileptic syndromes, such as medial temporal lobe epilepsy share structural and functional neuroimaging findings with AD, leading to overlapping symptomatology such as episodic memory deficits and toxic synergistic effects. In this respect, the existence of epileptiform activity and electroclinical seizures in AD appears to accelerate progression of cognitive decline and the presence of cognitive decline is much more prevalent in epileptic patients than in elderly without epilepsy. Notwithstanding their clinical significance, the diagnosis of clinical seizures in AD is a challenge. Most are focal and manifest with altered level of consciousness without motor symptoms, and are often interpreted as cognitive fluctuations. Finally, despite the frequent association of epilepsy and AD dementia, there is a lack of clinical trials to guide the use of antiseizure medications (ASM). There is also a potential role for ASMs to be used as disease-modifying drugs in AD.

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Dementia with non-convulsive seizures: a case report

Cited by 5 publications

References 24 publications

Proposed mechanisms of tau: relationships to traumatic brain injury, Alzheimer’s disease, and epilepsy

Proposed mechanisms of tau: relationships to traumatic brain injury, Alzheimer’s disease, and epilepsy

Optimal Use of Perampanel in Elderly Asian Patients with Epilepsy: Expert Opinion

Mechanisms Involved in Epileptogenesis in Alzheimer’s Disease and Their Therapeutic Implications

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