"A New Type of Dementia—Called Seizures": When Temporal Lobe Epilepsy Hides Behind a Psychiatric Diagnosis

Why This Case Matters

Older adults frequently develop depression and cognitive decline, so clinicians reasonably reach for those explanations when a patient reports mood changes and memory loss.

Yet this case report shows that temporal lobe epilepsy (TLE)—a seizure disorder in which abnormal electrical activity arises in the brain’s temporal lobe and often disturbs memory and emotion—can imitate a primary psychiatric illness or a neurodegenerative disease, a disorder in which neurons progressively deteriorate and die.

A missed diagnosis carries real costs, because clinicians may prescribe medications that worsen the very problem they are trying to treat.

The authors describe a 75-year-old woman whose ‘depression’ and ‘Alzheimer’s-related cognitive decline’ turned out to be seizures, and her case gives clinicians a practical framework for deciding when to suspect epilepsy instead of—or alongside—a mood or memory disorder.

The Case

The patient came to the emergency department after she briefly lost consciousness, trembled, and made seizure-like movements for about 30 seconds. Earlier that day she had fallen out of bed and said only that she felt “very scared.”

Her history included depression, treated with escitalopram (a selective serotonin reuptake inhibitor antidepressant), and mild cognitive impairment (a measurable decline in memory or thinking that exceeds normal aging but does not yet disrupt daily life) that clinicians attributed to probable Alzheimer’s disease, the most common neurodegenerative dementia, for which she took donepezil.

She had never had a seizure or an electroencephalography (EEG) study, a test that records the brain’s electrical activity through scalp electrodes.

On arrival, her heart rate was slow at 49 beats per minute—a finding called bradycardia—and her initial workup, including a head CT scan and a carotid ultrasound, showed nothing abnormal.

Because of the new bradycardia, the team first attributed her collapse to medication-induced vasovagal syncope (fainting from a reflex that slows the heart and lowers blood pressure, also called neurally mediated syncope), while keeping cardiogenic syncope, fainting from a primary heart problem, on the differential.

The convulsive movements prompted the team to order an EEG to rule out seizures, and that single decision redirected the entire diagnosis.

A routine 30-minute EEG captured three focal seizures—seizures that begin in one localized region of the brain—arising in the left temporal lobe. Continuous EEG monitoring over 24 hours recorded 14 more, again localized to the left temporal region.

Magnetic resonance imaging (MRI), with and without gadolinium contrast, then revealed FLAIR hyperintensity —an abnormally bright signal —in the left mesial temporal lobe, a pattern consistent with mesial temporal sclerosis (MTS)—scarring and neuronal loss in the inner temporal lobe—which lobe that is the most common cause of TLE.

Reframing the “Psychiatric” History

Once seizures entered the picture, the family’s account of the patient’s symptoms took on new meaning. Her memory lapses had come as sudden, discrete episodes of confusion in which she repeated the same question, rather than the steady, progressive decline typical of Alzheimer’s disease.

Her mood changes arrived as sudden, unpredictable “waves of sadness” rather than the persistent low mood of major depressive disorder. The family had also overlooked her automatisms—repetitive, involuntary movements such as nose-wiping and picking at clothing, mostly on the left side—until the clinicians asked about them directly.

No single feature had raised concern on its own, but together, and once the EEG pointed the way, they formed a coherent picture of ictal and interictal phenomena—events during and between seizures—rather than two separate chronic diseases.

Seizure Treatment and Course

With a working diagnosis of TLE with MTS, the team stopped escitalopram and donepezil, both of which may have driven the bradycardia and the syncope that brought her in. They began antiseizure medication, starting with valproate, adding brivaracetam after further seizures, and then clobazam when seizures persisted on continuous EEG.

The hospital course brought complications that the authors treat as a lesson in themselves. Valproate raised her blood ammonia to a harmful level, a condition called hyperammonemia, so the team discontinued it.

A urinary tract infection contributed to delirium, an acute, fluctuating disturbance of attention, and the sedating antiseizure drugs added to her cognitive burden. That burden illustrates how easily polypharmacy—the use of many medications at once—harms older patients.

Once the team addressed these contributors and adjusted her regimen, she became seizure-free at discharge on brivaracetam (100 mg twice daily) and clobazam (5 mg once daily).”A follow-up EEG showed generalized and focal slowing, with no further seizures over two days of monitoring. The team did not repeat formal cognitive testing, yet her family reported that she had returned to her prior baseline.

Clinical Takeaways

The case yields several practical lessons.

1. An episodic course is the first red flag: steady decline points toward neurodegeneration, whereas sudden, discrete, recurring episodes of confusion or mood change should raise suspicion for a seizure disorder. Clinicians should also ask specifically about automatisms, because families dismiss behaviors like nose-wiping or clothing-picking as habit or agitation unless someone asks, and those movements can be a decisive clue.

2. A convulsive component to a fainting spell warrants an EEG; here, the team reached the right diagnosis only because it pursued an EEG despite a plausible cardiac and medication explanation for the collapse.

3. Clinicians should further recognize that psychiatric and cognitive symptoms can be reversible manifestations of seizures, because TLE with MTS drives depression and cognitive impairment directly through limbic system dysfunction—the limbic system being the network of temporal-lobe structures that governs emotion and memory—rather than acting only as a psychological reaction to chronic illness. Treating the seizures can therefore lift mood and sharpen cognition.

4. Epilepsy and neurodegenerative disease are not mutually exclusive, and the authors point to growing evidence of a two-way association between epilepsy and dementia, including Alzheimer’s disease.

This patient’s case supports a ‘dual pathology’ model, in which seizure activity acts as a superimposed and potentially modifiable contributor to cognitive and emotional symptoms rather than proof that Alzheimer’s disease was never present.

5. Clinicians must also watch for iatrogenic harm—harm caused by treatment itself—because even after the correct diagnosis, this patient developed valproate-induced hyperammonemic encephalopathy, which shows why close monitoring matters when a team starts antiseizure therapy in older adults.

The Bottom Line

This case illustrates a broader principle: episodic neuropsychiatric symptoms in older adults deserve a structured search for transient neurological events before anyone anchors the diagnosis to depression or dementia. The distinguishing features usually sit in the history—sudden versus gradual onset, episodic versus persistent course, and subtle automatisms—if clinicians know to ask.

Because epilepsy is a potentially reversible contributor to cognitive and emotional decline, a missed seizure disorder is more than a diagnostic curiosity; it can commit a patient to years of unnecessary psychiatric treatment, avoidable medication side effects, and preventable harm.

Glossary

Alzheimer’s disease: the most common neurodegenerative dementia, marked by progressive memory loss and cognitive decline.

antiseizure medication: a drug that reduces the frequency or severity of seizures by stabilizing electrical activity in the brain.

automatism: a repetitive, involuntary movement—such as lip-smacking, nose-wiping, or picking at clothing—performed without awareness during a focal seizure.

bradycardia: an abnormally slow heart rate, generally below 60 beats per minute.

brivaracetam: an antiseizure medication that dampens excessive neuronal firing by binding synaptic vesicle protein 2A.

cardiogenic syncope: fainting caused by a heart problem that briefly reduces blood flow to the brain.

carotid ultrasound: an imaging test that uses sound waves to check the carotid arteries in the neck for narrowing or blockage.

clobazam: a benzodiazepine antiseizure medication that enhances the inhibitory neurotransmitter GABA.

computed tomography (CT): an imaging test that combines X-rays into cross-sectional pictures of the body; a head CT images the brain.

continuous EEG monitoring: prolonged electroencephalography, often over 24 hours or more, that captures seizures a brief study can miss.

delirium: an acute, fluctuating disturbance of attention and awareness, often triggered by illness or medication.

donepezil: a cholinesterase inhibitor prescribed to ease cognitive symptoms in Alzheimer’s disease.

electroencephalography (EEG): a test that records the brain’s electrical activity through scalp electrodes and can detect seizures.

escitalopram: a selective serotonin reuptake inhibitor (SSRI) antidepressant.

FLAIR hyperintensity: a bright signal on a fluid-attenuated inversion recovery MRI sequence that indicates abnormal tissue.

focal seizure: a seizure that begins in one localized region of the brain.

gadolinium: a contrast agent injected during MRI to highlight abnormal tissue.

hyperammonemia: an excess of ammonia in the blood, which can impair brain function; when it causes confusion it is termed hyperammonemic encephalopathy.

iatrogenic: describing harm caused by medical treatment itself.

ictal: relating to the period during a seizure.

interictal: relating to the period between seizures.

limbic system: a network of interconnected brain structures, including the temporal-lobe hippocampus and amygdala, that governs emotion and memory.

magnetic resonance imaging (MRI): an imaging test that uses magnetic fields and radio waves to produce detailed pictures of soft tissue.

major depressive disorder: a psychiatric condition marked by persistent low mood and loss of interest lasting at least two weeks.

mesial temporal sclerosis (MTS): scarring and neuron loss in the inner temporal lobe, the most common cause of temporal lobe epilepsy.

mild cognitive impairment (MCI): a measurable decline in memory or thinking that exceeds normal aging but does not yet impair daily function.

neurodegenerative disease: a disorder in which neurons progressively deteriorate and die.

polypharmacy: the concurrent use of multiple medications, which raises the risk of drug interactions and side effects.

syncope: a temporary loss of consciousness caused by a brief drop in blood flow to the brain (fainting).

temporal lobe epilepsy (TLE): a form of epilepsy in which seizures originate in the temporal lobe, frequently affecting memory, emotion, and behavior.

urinary tract infection (UTI): an infection of the bladder, urethra, or kidneys.

valproate: a broad-spectrum antiseizure medication that can raise blood ammonia levels.

vasovagal syncope: fainting caused by a reflex that slows the heart and lowers blood pressure; also called neurally-mediated syncope.

Reference

Kunesh, J., Varkey, T., Meyyappan, A., Christianson, J., & Chrisman, C. (2026). “A new type of dementia—called seizures”: Temporal lobe epilepsy presenting as episodic neuropsychiatric symptoms. Academia Medicine and Health, 3. https://doi.org/10.20935/AcadMedHealth8284

About the Author

John S. Anderson, MA, LADC, BCB, BCN, QEEGD, is a veteran neurofeedback practitioner and educator with over five decades of experience in biofeedback and neurofeedback, beginning his work in 1974. He holds a master's degree in psychology and is certified by the Biofeedback Certification International Alliance (BCIA) and the International QEEG Certification Board. As the founder of the Minnesota Neuro-Training Institute, Anderson provides clinical services, mentorship, and professional training in neurotherapy. His clientele includes individuals with ADHD, learning disorders, chronic pain, and addiction. He is also a recognized instructor, offering BCIA-approved courses and QEEG certification programs, and contributes to educational initiatives such as Biosource Software's "Seminars Without Borders." Anderson integrates holistic healing practices with contemporary neurophysiological research to develop effective neurofeedback protocols.

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