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Can Epilepsy Lead To Alzheimer’s

Reasons Persons With Dementia Develop Seizures

Can seizures occur years before Alzheimers?

Individuals with dementia may experience seizures because of the structural changes that happen in the brain.

In some cases, they will occur after a brain infection like meningitis, head injury, or stroke.

As the cells in the brain begin to die, the size of the brain will shrink and this is something that can lead to seizures.

Some types of dementia like Alzheimers disease are a result of protein build-up in the brain that interferes with how cells in the brain communicate with each other.

This can result in nerve cells becoming hyper-excitable which implies that they will start to behave uncontrollably which can cause seizures.

Flashing Or Strobing Lights

One of the most famous seizure triggers is strobe lights. People with photosensitive epilepsy are affected by this trigger, and even everyday activities may cause seizures. The most common issues are watching television, playing video games, looking at contrasting light and dark patterns, and driving during daylight. Even blinking can lead to a seizure in certain individuals or situations. Despite this being a well-known trigger, this form of epilepsy accounts for just three percent of all cases. People with photosensitive epilepsy are often not aware of it until they have a seizure and may never have spontaneous seizures.

Clinical Characteristics Of Ncd People With Epilepsy

Among the study cohort, 40 people had epilepsy. Their characteristics are shown in Table 2. The median age at onset was 57.5 and 75.2% of people fulfilled the diagnostic criteria for young-onset NCDs with the age of onset < 65 years . Seven people developed epilepsy prior to cognitive decline and 33 after cognitive decline. The median duration between the onset of cognitive decline and the onset of epileptic seizures was 2 years , with 80% of people experiencing their first epileptic seizures within the time frame ranging from 2 years prior through to 6 years after the onset of cognitive decline .

Table 2. Clinical characteristics of people with epilepsy .

Figure 2. Onset of epilepsy in relation to the onset of cognitive decline. The yearly distribution of new-onset seizures relative to the year of onset of cognitive decline: the median duration between the onset of cognitive decline and the onset of epileptic seizures was 2 years , with 80% of people experiencing their first epileptic seizures within the time frame ranging from 2 years prior through to 6 years after the onset of cognitive decline.

Regarding the semiology of seizures, 2 people had FAS only, 13 had FIAS only, 14 had FBTCS , and 11 had GTCS. Eleven of the 13 people with FIAS has non-convulsive seizures without motor symptoms. Among the people who had seizures before dementia onset, most continued to have seizures during cognitive decline.

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Search Strategy And Selection Criteria

We selected references by reviewing the authors personal files and by searching PubMed for manuscripts published in English before Dec 1, 2016, with the term Alzheimers disease and assorted combinations of the following terms: epilepsy, seizures, epileptiform activity, network hyperexcitability, antiepileptic drugs, antiseizure drugs, anticonvulsants, Down syndrome, trisomy 21, dementia, neurodegenerative disease, early-onset, presenilin 1, presenilin 2, and amyloid precursor protein. We reviewed reference lists within original research and review articles for additional references. We finalised the reference list on the basis of originality and relevance to the scope of this Review. We focused on scientific literature of the past 8 years, but also included older publications of high merit or originality. Additional information about current clinical trials was obtained from

What Was Ultimately Wrong With The Patient

How infrequent seizures may lead to persistent memory loss ...

Temporal lobe seizures may transiently impair cognitive and memory function and result in fluctuating memory loss to reflect the ictal-post-ictal continuum. In Alzheimer’s disease, toxic accumulations of A-beta peptides underlies the memory disorder triggering synaptic degeneration, circuit remodeling, and abnormal synchronization within the same hippocampal networks to lead to progressive memory loss1. The neuronal hyperexcitability that is associated with seizures augments the synaptic release of A-beta and may further compound the cognitive deficits in compromised patients such as those with AD. While AD and epilepsy are felt to reflect independent disorders, progressive cognitive and memory deficits are known to occur in patients with TLS associated with hippocampal sclerosis. Furthermore, seizures are a common comorbidity in those with early onset AD. When seizures are subtle, nocturnal, or occur in seniors that expect memory loss, the diagnosis may be elusive. If memory loss fluctuates, subtle TLS without awareness should be considered. In our patient living alone, prolonged EEG had a greater yield than repeated EEG2.


  • Noebels J. A perfect storm: Converging paths of epilepsy and Alzheimer’s dementia intersect in the hippocampal formation. Epilepsia 2011 52:39-46.
  • Tatum WO IV, Ross J, Cole AJ. Epileptic pseudodementia. Neurology 1998 60:1137-1152.
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    Network Hyperexcitability In Alzheimers Disease

    In patients with mild cognitive impairment due to Alzheimers disease, task-based fMRI studies have shown increased hippocampal activation during memory encoding. Although this activation can be interpreted as the compensatory recruitment of neural reserves to meet cognitive demands within compromised brain regions, some evidence indicates that hyper activation of the hippocampus and multiple other cortical and subcortical brain regions during encoding is inefficient and might contribute to Alzheimers disease pathogenesis., The amount of hippocampal hyper activation in patients with mild cognitive impairment due to Alzheimers disease might predict future cognitive decline. Furthermore, in patients with amnestic mild cognitive impairment, suppressing hippocampal dentate gyrus and CA3 hyperactivation with levetiracetam improves their performance on a hippocampal-based pattern-separation task. Interestingly, 125 mg twice a day of levetiracetam was more effective than 250 mg twice a day at normalising fMRI changes and improving memory function in these patients. Since fMRI is an indirect measure of neuronal activity, the association between hippocampal hyperactivation detected by fMRI and epileptiform activity is poorly understood.

    Hypothetical model of the correlation between amyloid and tau deposition and network alterations in Alzheimers disease

    The Role Of Seizures In Alzheimers Disease Is Gaining Overdue Attention

    Evidence suggests that such abnormal electrical activity may occur much earlier than signs of memory loss

    Scientists who study Alzheimers disease have mostly ignored the role of seizures, but that is beginning to change, and new research suggests they may provide insight into the progression of the disease and pave the way for treatments.

    Its no surprise to neurologists that some people experience convulsive seizures in the later stages of the disease. In fact, the second patient ever to receive an Alzheimers diagnosis more than a century ago suffered from them. But because brain damage can cause seizures, they were long thought to be just one more casualty of a deteriorating brain.

    Now evidence is accumulating that such abnormal electrical activity is far more common and occurs much earlierand perhaps even precedes obvious signs of memory loss. This raises the possibility that seizures may be intimately tied up with the progression of the disease.

    Its been notoriously difficult to tease out the causes of Alzheimers, which is complex, progresses slowly, and may have many different triggers. Finding an association between seizures and dementia is by no means proof of causality, but the new studies excluded people with known risk factors for both epilepsy and Alzheimers, such as cerebrovascular disease and traumatic brain injury.

    Republished with permission from STAT. This article originally appeared on July 19, 2019

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    Evidence From Animal Models Of Alzheimers Disease

    Evidence from animal models helps us to better understand overlaps between AD and epilepsy.

    Experimental studies in the past years demonstrated that amyloid- and tau deposits might facilitate or even cause seizures at the same time there is evidence that seizures can increase brain deposits .

    Fig. 1

    In the figure, the key points of the mutual relationship between epilepsy and Alzheimers disease are displayed. The experimental evidence in animal models has clearly evidenced the potential presence of a vicious loop: A and tau deposits may be cause of seizures and seizures lead to increase in brain A deposits and tau phosphorylation . In the box on the right, the main findings supporting the association between temporal lobe epilepsy and AD in humans are summarized. A, amyloid- APP, amyloid- protein precursor NMDA, N-methyl-D-aspartate CSF, cerebrospinal fluid MCI, mild cognitive impairment LEV, Levetiracetam.

    Some limitations regarding the generalization of animal model findings to human brain pathology must be addressed. Most AD mice models come from genetic pedigrees, while in human population most cases of AD are sporadic . Moreover, mice models do not replicate perfectly the clinical features of human AD . Anyway, despite these limitations, molecular models provided new insights and interesting proofs of concept regarding the connections between epilepsy and AD.

    What Is The Link Between Seizures And Dementiablog

    Can alcohol consumption increase dementia risk? with Dr. Andrew Frank

    There are some symptoms of dementia that are more commonly known, such as memory loss. Seizures are a less common symptom of dementia that are not as understood. Hear from one of our dementia researchers who has been studying seizures in people with the condition.

    How common are epileptic seizures in dementia? Who is most at risk of having them? What do these seizures look like? What effect do they have on how someones memory changes over time?

    These are the questions that I have been researching since starting my PhD in 2016. I’m a student funded by Alzheimers Society as part of the University of Exeter doctoral training centre.

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    Repurposing New And Existing Drugs For Alzheimers

    Researchers at the University of British Columbia tested existing and experimental epilepsy drugs and concluded they could be effective in treating Alzheimers.

    Their new findings build on previous studies, in both mice and humans, that suggested the widely used anticonvulsant drug levetiracetam may slow the progression of Alzheimers, namely the damaging effects of memory loss.

    Levetiracetam, sold under the brand name Keppra, is an anticonvulsant drug that works against epilepsy by decreasing abnormal excitement in the brain.

    The Canadian research team tested levetiracetam and brivaracetam, an experimental epilepsy drug thats similar yet 10 times stronger than levetiracetam. In a Phase III randomized trial completed last year, 50 milligrams of brivaracetam resulted in significantly lower frequency of seizures compared with a group of participants taking a placebo.

    In the new study, researchers tested the effects of brivaracetam on mice with Alzheimers disease and found it completely reversed memory loss.

    The exact mechanism that causes this, however, remains a mystery to researchers.

    But researchers say their findings reinforce the theory that brain hyperexcitability or overreaction to stimuli plays an important role not only in epilepsy but also Alzheimers disease.

    An estimated 10 to 22 percent of patients with Alzheimers develop epilepsy. Some research suggests those who do are more likely to suffer serious memory impairments.

    Subclinical And Interictal Epileptiform Activity In Ad Patients

    When approaching the review of literature about AD and epileptiform activity, there are several limitations hindering comparison among studies: lack of definition of interictal epileptiform abnormalities , different electroencephalogram techniques used, methods of evaluation of IEAs by different researchers, etc. Criteria for IEAs definition were only recently validated . In particular, the IEAs are defined as paroxysmal sharp waveforms on EEG, lasting 20 to 200ms and followed by an associated slow after-wave, that disrupt background activity. Moreover, estimates of epileptiform activity in AD are limited by the use of non-invasive scalp recordings, a limitation that does not occur in animal models, in which subdural or depth electrodes are commonly used.

    Epileptiform activity is named interictal when detected in patients with seizures, and subclinical when detected in patients without known seizures.

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    Seizures And Alzheimers: Whats The Link

    Could epileptic seizures be a symptom of Alzheimers disease? A recent study has found that patients with dementia have an increased risk of having a seizure at a younger age, as compared to people without dementia.

    There appears to be a mechanism at work that puts people living with dementia at higher risk and recurrence of all types of seizures, said , Ph.D., chief science officer, Alzheimers Association. While we continue our push to find treatments and preventions for Alzheimers and other dementias, doctors should be aware of how common seizures are in this population to better monitor and treat these individuals.

    The study conducted by researchers at the University of Cincinnati analyzed a large U.S. national managed care database which included more than 2.8 million individuals with and without dementia, age 60 and older. Those who had dementia had a 6.5 percent increased risk for seizures where the origin could not be determined.

    Common Risk Factors For Epilepsy And Dementia

    Silent Seizures Associated with Alzheimer

    An important issue in dementia research is detection of disease at an early stage. The use of CSF and neuroimaging biomarkers to make the diagnosis of Alzheimers disease in the preclinical state is one strategy that has gained widespread currency . Similarly, the diagnosis of vascular dementia often rests on the presence of evidence of small vessel cerebrovascular change on MRI, while the clinical diagnosis of mixed Alzheimers disease/vascular dementia usually occurs when there are biomarkers suggesting the presence of both types of pathology . Precisely how individuals with epilepsy with preclinical dementia might present or be detected remains to be established . Indeed, it may well be that biomarkers for dementia in epilepsy might not be unique to people with epilepsy but rather reflect mixed pathologies, e.g. associated with Alzheimers disease and vascular dementia, as well as perhaps electrophysiological evidence of ongoing overt or covert abnormal electrical activity, e.g. IEDs.

    The intersections of Alzheimers disease, epilepsy and vascular disease. Several overlapping pathologies can contribute to development of late-onset epilepsy as well as the development of dementia. In particular, vascular risk factors are common in people with epilepsy. These may represent modifiable risk factors for both the development of dementia and of epileptogenesis.

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    Pathological Association Between Epilepsy And Alzheimers Disease

    In addition, other studies revealed the presence of tau pathology on cases of long-lasting chronic or drug-resistant epilepsy. In a postmortem study, chronic epilepsy was associated with increased tau neurofibrillary tangles at mid-Braak stages in patients aged 4065 years . Another clinicopathological study on resected temporal lobe tissues of 33 patients with drug-resistant TLE demonstrated the presence of hyperphosphorylated tau pathology in 94%of samples a positive correlation between post-operative cognitive decline and tau deposition was found in these patients. Moreover, an association between tau burden and history of secondary generalized seizures was identified, supporting the hypothesis of abnormal ictal activity contributing to an epilepsy-tau pathology in TLE. In this form of epilepsy, a high frequency of focal seizures gradually damages the hippocampal region of temporal lobe, leading to a significant memory loss. Synapse damage and synaptic protein loss are strongly related to the severity of dementia. Altered synaptic receptors endocytosis such as -amino-3-hydroxy-5-methyl-4-isoxazole propionic acid and N-methyl-D-aspartate has been reported to be crucial in the development of AD. Tau load could act as a promoting role in epilepsy development by enhancing excitotoxicity of NMDA receptors and increasing gamma-aminobutyric acid A receptors-mediated excitability .

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    Why Do People With Dementia Develop Seizures

    Ultimately, anything that changes the structure of the brain can cause seizures.

    This happens for some people after a stroke, a head injury, or with a brain infection like meningitis. A similar problem is happening in the brain in dementia. As cells in the brain die and the brain shrinks this can lead to epilepsy.

    In addition, we know that two proteins that build up in the brain of people with Alzheimers disease amyloid and tau affect how the brains nerve cells communicate with each other.

    Sometimes these nerve cells can become ‘hyper-excitable’, meaning they can behave uncontrollably, causing epileptic seizures.

    Frequency Of Seizures In Alzheimers Patients

    How Epilepsy Affects Memory?

    Data from over 20,000 people found the presence of active seizures were higher in persons with Alzheimers, according to another study that was conducted by the German Center for Neurodegenerative Diseases. The longer that individuals had been living with Alzheimers, the higher the risk for having a seizure and the earlier the seizures, the more severe memory problems, the study found.

    People with Alzheimers are at increased risk for seizures, in particular in more advanced stages of the disease, and they have an exceptionally high recurrence risk, said Jonathan Vöglein, M.D., Ludwig-Maximilian University of Munich. The high recurrence risk and potentially negative consequences of seizures suggest that individuals with Alzheimers should be treated with anti-epileptic drugs after their first seizure.

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    Progression Of Cognitive Deficits In Younger

    Several investigations have now also reported that there is progression of cognitive deficits over short periods of time , in younger adults with epilepsy . The most extensively studied group is patients with TLE in whom it is now apparent that there are widespread brain structural changes beyond the medial temporal lobes and that progression of cognitive impairment over time may occur in a significant proportion . While cognitive reserve indexed by baseline IQ, years of education or occupational complexitymay mitigate some of these effects, duration of epilepsy appears to be an important factor in determining progression of cognitive impairment .

    A recent study by Breuer and co-workers screened 287 adult patients for cognitive deterioration compared to expected premorbid IQ . A group of 27 individuals fulfilled the criteria . More than 77% of them had associated comorbidities . Analyses revealed that the most prominent factors that accounted for the variance in cognitive deterioration were those that might impact on cognitive reserve: low premorbid IQ and education level, later age of seizure onset and older age . These findings would be consistent with a double hit model in which pre-existing low brain reserve makes the brain more vulnerable to a second hit from the development of epilepsy.


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