Alzheimer’s disease (AD) is a progressive neurodegenerative condition primarily known for causing memory loss and cognitive decline. It is the most common form of dementia, affecting millions globally. AD is a complex brain disorder that can disrupt various neurological functions beyond cognition. Understanding the full spectrum of its effects, including the potential for altered electrical activity, is important for comprehensive patient care.
Establishing the Link Between Alzheimer’s and Seizures
There is a clear connection between Alzheimer’s disease and the development of seizures, confirming that AD significantly increases the risk of epilepsy. Individuals with Alzheimer’s are estimated to be five to ten times more likely to develop seizures compared to people without the disease in the same age group. This relationship is a serious comorbidity because seizures can accelerate cognitive decline and worsen the overall course of the disease.
The risk profile varies depending on the timing of disease onset. People with early-onset Alzheimer’s disease (EOAD), which begins before age 65, show a notably higher lifetime prevalence of seizures than those with late-onset AD (LOAD). Studies suggest that those with EOAD may be nearly twice as likely to experience seizures compared to those with LOAD.
The risk of having a seizure also increases with the duration and severity of the cognitive impairment. The overall prevalence of seizures in Alzheimer’s patients is estimated to be as high as 22% during the course of the disease, though many cases are likely missed due to subtle symptoms. The risk is particularly pronounced in genetically linked forms of AD, such as those associated with presenilin-1 mutations.
The Mechanisms Behind Neuronal Hyperexcitability
The underlying cause of seizure risk in Alzheimer’s disease is an unstable electrical state in the brain known as neuronal hyperexcitability. This means that brain networks become overactive and prone to synchronized, abnormal firing. The hallmark protein pathologies of AD—Amyloid-beta (Aβ) plaques and Tau tangles—directly interfere with normal communication between nerve cells.
Toxic forms of Amyloid-beta, particularly soluble oligomers, are major contributors to this electrical instability. These Aβ peptides disrupt the function of ion channels and alter neurotransmitter release, leading to an imbalance between excitatory and inhibitory signals. This shift results in a brain circuit that is excessively sensitive and easily triggered into a seizure state.
The accumulation of hyperphosphorylated tau protein, which forms neurofibrillary tangles, also contributes to the hyperexcitable state, particularly in the hippocampus. The hippocampus is a brain region central to memory formation and is highly vulnerable to AD pathology. The loss of neurons and the resulting unstable electrical circuits compound the problem, creating an environment where seizures can spontaneously occur.
This abnormal network activity can appear early in the disease process, potentially even before significant memory loss is clinically apparent.
Identifying Atypical Seizure Symptoms
A major challenge in Alzheimer’s care is that seizures often manifest in subtle, non-convulsive ways, easily mistaken for typical AD symptoms like confusion or agitation. The most common types of seizures seen in this population are focal seizures, which originate in a limited area of the brain. Unlike the dramatic, full-body convulsions associated with epilepsy, these focal events can be brief and difficult to recognize.
Subtle signs of a seizure may include staring spells, where the person appears unresponsive for a few seconds. Repetitive, involuntary movements, known as automatisms, are also common, such as lip-smacking, chewing motions, or fumbling with objects.
These episodes are often short-lived and resolve quickly, leading caregivers to dismiss them as a temporary lapse in attention or a sign of increasing confusion. Other atypical presentations involve brief periods of unexplained fear or euphoria, sudden interruptions in speech, or temporary memory lapses that seem worse than usual.
A sudden, unexplained fall or a transient, sharp decline in cognitive function that resolves after a period of confusion, known as a post-ictal state, should raise suspicion. These subtle manifestations highlight the need for careful observation, as recognizing these atypical symptoms is the first step toward a correct diagnosis.
Diagnosis and Management of Epilepsy in Alzheimer’s Patients
Diagnosing epilepsy in Alzheimer’s patients requires a high index of suspicion due to the subtle and overlapping nature of the symptoms. The primary diagnostic tool is Electroencephalography (EEG), which records the brain’s electrical activity. A standard, short-duration scalp EEG may not be sufficient to capture the fleeting electrical abnormalities in AD patients.
For a more accurate diagnosis, physicians often recommend extended or long-term video-EEG monitoring, sometimes lasting 24 hours or longer. This increases the chance of detecting abnormal electrical discharges.
This prolonged monitoring is important because some patients experience “subclinical” seizures or epileptiform activity that does not produce visible physical symptoms but can still contribute to cognitive decline. Identifying these subtle signs is a necessary step before beginning treatment.
The goal of treatment is to control seizures and prevent the accelerated cognitive decline that often accompanies them, typically using anti-epileptic drugs (AEDs). Selecting the appropriate AED is challenging due to the risk of drug interactions and potential side effects that can worsen dementia symptoms.
Newer-generation AEDs, such as levetiracetam, are often favored because they have a better side-effect profile and are less likely to interact with other medications. Careful monitoring and low-dose initiation are necessary to manage the patient’s epilepsy while minimizing any adverse impact on their cognitive function.