Alzheimer’s disease (AD) is a progressive neurological disorder that impairs memory and cognitive function. Seizures are sudden, uncontrolled episodes of abnormal electrical activity in the brain that cause changes in behavior or consciousness. A recognized connection exists between AD and an increased risk of developing seizures, although it is not traditionally considered a primary symptom. This co-occurrence complicates diagnosis and can accelerate cognitive decline, making awareness of this relationship important for patient care.
The Link Between Alzheimer’s and Seizure Risk
Patients with Alzheimer’s disease face a significantly higher risk of experiencing seizures compared to the age-matched general population. This risk is estimated to be between six and ten times greater in those with AD. Even lower estimates confirm the elevated risk, despite the wide range of prevalence reported across studies.
This increased vulnerability is not uniform across all patients. Individuals with early-onset AD (before age 65) show a particularly heightened susceptibility to seizures. The risk generally increases as the disease progresses into more advanced stages.
Studies tracking patients show that the risk of a first seizure can rise from approximately 1.5% in the early years to over 5% after a decade. Furthermore, once a seizure occurs, the likelihood of recurrence is exceptionally high, exceeding 70% within a relatively short period.
Biological Mechanisms Causing Hyperexcitability
The neuropathology of Alzheimer’s disease creates an environment abnormally sensitive to electrical overstimulation, known as hyperexcitability. The hallmark proteins of AD, amyloid-beta (\(\text{A}\beta\)) and hyperphosphorylated tau, disrupt the normal balance of neuronal signaling. Soluble \(\text{A}\beta\) forms, which cluster into small oligomers, are particularly disruptive to synaptic function.
These toxic aggregates interfere with both excitatory and inhibitory neural circuits. \(\text{A}\beta\) oligomers increase excitatory signaling while simultaneously weakening the brain’s natural inhibitory mechanisms. This imbalance results in a lower seizure threshold, making the brain more likely to generate uncontrolled electrical bursts.
Dysfunction of the neurotransmitter glutamate also contributes to this problem. Glutamate is the brain’s primary excitatory neurotransmitter, and in AD, its uptake by supportive astrocytes can be impaired. This failure allows glutamate to accumulate outside the neurons, leading to excessive stimulation and further hyperexcitability.
Neuroinflammation, a persistent immune response associated with AD, further destabilizes the neuronal environment. The loss of neurons and subsequent reorganization of neural networks also contribute to electrical instability. This combination of protein pathology, neurotransmitter imbalance, and inflammation sets the stage for aberrant electrical activity and seizure generation.
Recognizing Subtle Seizure Activity
Seizures in Alzheimer’s patients are often subtle and non-convulsive, making them challenging to distinguish from typical dementia-related behaviors. Unlike dramatic, full-body convulsions, these episodes frequently manifest as focal aware or focal impaired awareness seizures. They are sometimes referred to as “silent seizures” because they lack obvious motor symptoms.
Caregivers should watch for brief, recurring episodes that represent a sudden, temporary change from the person’s baseline. Subtle signs may include:
- Staring spells or an uncharacteristic blank look lasting only a few seconds or minutes.
- Sudden confusion, unexplained drowsiness, or brief periods of unresponsiveness.
- Repetitive, involuntary movements, known as automatisms.
- Cognitive or emotional fluctuations, such as sudden fear, euphoria, or a metallic taste sensation.
Automatisms can include simple actions like lip-smacking, chewing motions, fumbling with clothes, or repeated hand gestures. These subtle symptoms are often mistaken for the normal progression of cognitive decline or psychiatric symptoms, leading to underdiagnosis. A key distinction is that seizures typically begin suddenly, are stereotyped (happen the same way repeatedly), and are frequently followed by post-episode confusion or fatigue.
Diagnosis and Specialized Treatment Approaches
Diagnosing seizures in Alzheimer’s disease requires a high degree of suspicion, as the subtle nature of the symptoms complicates clinical observation. The most definitive diagnostic tool is the electroencephalogram (EEG), which measures the brain’s electrical activity. Since seizure activity can be infrequent, a standard short-term EEG may not capture an event.
Specialized techniques like extended or prolonged video-EEG monitoring are often necessary to detect intermittent or non-convulsive seizure activity. Extended monitoring increases the chance of recording an epileptiform discharge, which confirms the diagnosis.
Treatment involves the careful selection of anti-epileptic drugs (AEDs), a process complicated by existing cognitive impairment and potential drug interactions. The goal is to control seizures without worsening the patient’s cognitive function or behavior. Certain AEDs are avoided because they carry a higher risk of cognitive side effects in older patients.
Physicians often prefer AEDs with minimal impact on liver enzyme systems and low protein binding, reducing potential interactions with other medications. Levetiracetam and lamotrigine are frequently considered due to their favorable side-effect profiles and lower risk of cognitive impairment. Treatment must be initiated at a low dose and slowly adjusted to find the effective balance between seizure control and maintaining cognitive health.