Alzheimer’s disease (AD) is a progressive disorder that destroys memory and thinking skills, ultimately affecting the ability to carry out simple tasks. Seizures are sudden, uncontrolled electrical disturbances in the brain that cause changes in behavior, movements, or consciousness. While not universal in AD, the risk of developing seizures is substantially elevated compared to the general population of the same age. This increased susceptibility introduces a serious complication, making recognition and management of seizures a growing focus in AD care.
Prevalence and Associated Risk Factors
AD patients face a significantly higher risk of seizures, up to 10 times more frequent than in age-matched individuals without dementia. The prevalence of active seizures is estimated to be around 1.5% at any given time, though a history of seizures is found in up to 6% of patients. The likelihood of developing seizures increases with the duration and severity of cognitive impairment.
Several specific characteristics further increase this risk. Patients with early-onset AD (before age 65) are particularly susceptible, sometimes showing nearly double the prevalence of late-onset AD. Specific genetic mutations linked to autosomal dominant AD, such as those in the PSEN1 gene, are strongly associated with seizures, sometimes presenting before cognitive symptoms begin. The risk also rises as the disease progresses, with active seizure frequency increasing from about 1.5% after five years of duration to over 5% after 11 years.
The Underlying Biological Connection
The relationship between AD and seizures stems from pathological changes that create neuronal hyperexcitability. The accumulation of abnormal proteins, specifically amyloid-beta plaques and tau tangles, disrupts the normal communication balance between brain cells. Amyloid-beta peptides directly interfere with synapse function, leading to unstable electrical activity and making neurons prone to firing uncontrollably.
The neurodegenerative process of AD also causes a loss of inhibitory neurons, which normally calm electrical signaling in the brain. This loss tips the scale toward excessive excitation, lowering the brain’s overall seizure threshold. This network dysfunction allows electrical signals to rapidly spread and synchronize abnormally, resulting in a seizure. The hippocampus, a brain region heavily affected by AD pathology, is a common site where this hyperexcitability begins.
Recognizing Seizure Manifestations
Seizures in AD patients are often subtle and easily overlooked or mistaken for typical dementia symptoms, such as confusion or behavioral changes. Unlike the dramatic, full-body convulsions often associated with seizures, those in AD patients are frequently non-convulsive. This subtlety makes careful observation by caregivers crucial for accurate identification.
A common type is the focal impaired awareness seizure, which may manifest as a brief staring spell, unresponsiveness, or a change in cognitive state. Repetitive, involuntary movements called automatisms are also highly suggestive of a seizure. These actions can include lip-smacking, chewing motions, hand wringing, or fiddling with clothing. Documenting the duration and characteristics of these unusual episodes is important for medical professionals to distinguish a seizure from other AD-related behaviors.
Management and Treatment Approaches
The management of seizures in a person with AD requires a careful approach due to the unique vulnerabilities of this population. Anti-Epileptic Drugs (AEDs) are the primary treatment, but physicians must consider the potential for adverse effects on compromised cognitive function. Many AEDs can cause sedation, dizziness, or confusion, which may worsen dementia symptoms and increase the risk of falls.
Treatment typically begins with a low dose of a well-tolerated AED and is slowly increased to find the minimum effective dose. Drug interactions are a significant concern, as AD patients are often on multiple medications for their dementia and other conditions. Careful selection of an AED is required to avoid complications. The goal of therapy is to control seizure frequency and reduce their impact on the patient’s quality of life without accelerating cognitive decline.