Epilepsy is one of the most common neurological disorders in later life, with people over 65 years having the highest incidence (90–150 per 100,000). With current demographic trends, numbers are expected to rise, presenting a significant healthcare challenge. In addition to new‐onset cases, people diagnosed earlier now live longer. Premature mortality is two to three times higher than that of the general population. The increased risk of cognitive impairment, physical decline, and systemic comorbidities in older people presents specific diagnostic and treatment challenges.¹

CAUSES OF SEIZURES IN LATER LIFE

Infections, metabolic disturbances such as hyponatraemia, uraemia, and hepatic impairment may trigger acute symptomatic seizures (ASS). Head injury, alcohol, prescription medications, and intracranial vascular injury, particularly haemorrhages, may also trigger ASS and epilepsy. CNS infections are a significant risk factor in low‐ and middle‐income countries (LMIC) for ASS and epilepsy. Cerebrovascular disease is the most common risk factor in older people (~ 50%), along with tumours. Neurodegenerative disorders account for a third of cases. Rarer causes include autoimmune encephalitis. In up to a fifth of people, a clear cause is not established.^2–5 Some will have incipient dementia or lesions that are too subtle to visualise on imaging. In others, systemic factors, comorbidities, and polypharmacy may be contributory factors. Hypertension, diabetes, and smoking are associated with an elevated risk of late‐onset epilepsy. Conversely, higher physical activity and moderate alcohol intake have been associated with a lower risk, reflecting beneficial effects on brain health.⁶

Transient epileptic amnesia (TEA) is characterised by recurrent episodes of amnesia, typically lasting less than 30 minutes and occurring on awakening. The stereotyped nature and higher frequency differentiate it from transient global amnesia (TGA). There is a male preponderance, and the disorder can be associated with interictal memory disturbance, including autobiographic and topographical amnesia and accelerated long‐term forgetting. TEA is highly responsive to appropriate antiseizure medication (ASM).^7,8

An emerging paradigm suggests that epilepsy is a paroxysmal systemic disorder with a primary brain manifestation. This conceptualisation is perhaps most pertinent in the older population, where the ageing brain, mounting comorbidities, maladaptive changes in metabolism and physiology combine to increase seizure susceptibility.

DIAGNOSIS OF EPILEPSY

Diagnosis can be challenging because convulsive seizures, which are easy to identify, are rare, and focal seizures may present in atypical ways. Within the bounds of safety, it is helpful for carers and family members to video events for subsequent review by the clinician. Other reasons for a delay in diagnosis include a broader range of differential diagnoses, which may affect cognition, the presence of comorbidities, and polypharmacy. The absence of an eyewitness account due to less social interaction and living alone also plays a role. Recurrent stereotyped events, discrete episodes of motor or speech arrest or behavioural change, should always arouse suspicion. A sensorimotor presentation involving the ipsilateral limbs of an epileptic origin can mimic an acute stroke, as can post‐ictal paresis, which can persist from hours to days. Severe carotid stenosis can, at times, present with focal limb jerking.

The differential diagnosis includes syncope (vasovagal, cardiogenic, and orthostatic), delirium, transient ischaemic attack, and sleep disorders. Seizure mimics include TGA, migraine, and dissociative seizures.

As most seizures have a focal onset, intracranial imaging is essential for identifying a potential structural lesion. MRI is most appropriate due to its higher resolution, although X‐ray CT may offer a practical alternative in acute settings. Imaging often shows a burden of small vessel disease, but the relationship between this finding and seizures still requires elucidation. Screening blood tests are essential. These are more likely to suggest a trigger than in younger people; a full blood count, electrolytes, renal and liver function tests, thyroid function tests, and glucose levels are the minimum set. Autoantibody screening should be performed in cases with an explosive onset and if concurrent cognitive, psychiatric, or behavioural symptoms are present. A chest x‐ray and CSF examination should be considered in the appropriate clinical context.

An ECG, particularly if loss of consciousness was present, is mandatory. Further cardiac investigations may be appropriate to exclude cardiogenic syncope, which can lead to secondary anoxic seizures. This involves prolonged Holter monitoring, and if suspicion remains high, an implanted loop recorder may be used for further evaluation.

An EEG is less valuable in later life, when almost half of people will have nonspecific abnormalities.⁹ EEG is, however, an essential investigation in the setting of suspected non‐convulsive status epilepticus (NCSE) and is often diagnostic. Most episodes will be of focal onset, but generalised epilepsy may present, although rarely as newly onset epilepsy. Most commonly, with increasing life expectancy, people with generalised epilepsy that is in prolonged remission may relapse in old age, with a previous history of seizures not always being recalled. In contrast with a younger population, extra‐temporal seizures predominate in older people.¹⁰

Dissociative seizures do occur in later life, can potentially coexist with epilepsy, and often present a diagnostic challenge.^11,12 A misdiagnosis of epilepsy may lead to iatrogenic harm from medication, unnecessary investigations and admissions. An awareness of the possibility of dissociative seizures and the judicious use of video‐EEG telemetry should increase the diagnostic yield.¹³