“Epilepsy in older adults” is commonly referred to as epilepsy that begins after the age of 60 (or 65; [19]). This late-onset epilepsy is also referred to as “old-age epilepsy” or “new-onset epilepsy in older adults.” It needs to be distinguished from forms of epilepsy that already had their onset at a younger age and persist into older age (= “aged” epilepsy, [20]). Approximately one third of all cases of epilepsy begin after the age of 60 years [13]. The prevalence is 0.5–0.7% in the general population of industrialized countries, 1.5% in those over 75 years of age, and 2.5% in those over 85 years of age [13]. The increase in old-age epilepsy observed in recent decades is a consequence of increased life expectancy and probably more frequent survival from stroke and other cerebrovascular circulatory disorders, the main causes of initial onset in old age [17]. In addition to old-age epilepsy in the sense of a chronic disease, a distinction must be made between acute symptomatic epileptic seizures [14]. Status epilepticus (SE), especially nonconvulsive status, is more common in old than in middle-aged individuals; nonconvulsive seizures must always be included in the differential diagnosis of acutely confused older patients [21].

Symptoms of epileptic seizures in old age may differ from symptoms of epileptic seizures in childhood and mid-adulthood, and they may be overlooked [1]. A pilot study in nursing homes investigated the frequency with which such seizures are overlooked. Reported falls, loss of consciousness, and convulsions were the criteria for further diagnostic workup. In the total sample of 389 residents, 11 residents were identified with geriatric epilepsy (2.8%). Seven of these residents (1.8%) had known geriatric epilepsy, while four residents (1%) were newly diagnosed with epilepsy. Another five residents (1.3%) could not be conclusively diagnosed, meaning that other age-related forms of epilepsy may have existed. The authors suggest that geriatric epilepsy is underdiagnosed in nursing home residents [11].

Forms of seizure

The forms of epileptic seizures in older adults differ from those typically seen in younger people. Focal seizures predominate and are usually accompanied by impaired consciousness in older patients [1]. Approximately two thirds of patients with epilepsy in older age have focal epilepsy involving focal motor or non-motor seizures with preserved or even impaired consciousness, often with amnesia [21, 22]. A typical temporal aura is rarely described. This is due in no small part to the fact that most seizures in older patients begin in the frontal lobe [9]. Therefore, the precursors are often diffuse, described as a nonspecific vague sensation or dizziness, and are of little help in the differential diagnosis [22, 32]. Automatisms also occur less frequently. Thus, the entire seizure may be characterized by confusion, which can persist for a prolonged period following a seizure [29]. This may ultimately render it difficult or impossible to make a clear distinction between individual seizures. Bilateral tonic–clonic seizures (BTCS) occur and, when present as the first symptom of a seizure, are often used for intensive central nervous system (CNS) diagnosis to detect or exclude ischemia or a space-occupying lesion [10]. However, large epileptic seizures (BTCS) are also the type of seizures that cause the most anxiety in relatives and often make them feel that affected individuals may die. New cases of genetic generalized epilepsy are rare but occur with generalized tonic–clonic seizures (GTCS) as well as absences [5]. Absences usually occur as a first manifestation at this age in the form of a non-convulsive status [4]. However, it is also possible that absences or GTCS recur after a decades-long seizure-free interval since childhood or adolescence in the form of a recurrence of idiopathic generalized (genetic) epilepsy, which is then often no longer considered to be part of the “old disease” [32, 34]. If myoclonic seizures occur at this age, they are extremely rarely the first manifestation of generalized epilepsy in the sense of juvenile myoclonic epilepsy (Janz syndrome), although these late-onset epilepsies can also belong to the group of idiopathic (genetic) generalized epilepsies [5]. More often, they are a symptom in the setting of an underlying disease, such as Alzheimer’s disease, trisomy 21, or Creutzfeld–Jacob disease. Myoclonic seizures and coma are usually a sign of acute hypoxic brain injury and can also occur as a focal motor seizure with impaired consciousness [16].

Case study.

The case of a 60-year-old man with trisomy 21 was striking on the one hand by the fact that he was no longer co** well with everyday practical matters, often got lost and could no longer find his room in the living quarters, and also no longer immediately recognized all his caregivers. In addition to the symptoms indicating an incipient Alzheimer-type dementia (known to be frequent in Down’s syndrome), myoclonia and rarely also falls were noticeable, predominantly in the mornings. Diagnostic testing based on electroencephalography (EEG) quickly detected generalized epilepsy-type potentials, which were also recognizable between seizures, and valproate rapidly led to a reduction in myoclonia and falls [2].

Acute and subacute disorders of consciousness should always prompt suspicion of seizures or non-convulsive SE (NCSE; [16, 21]). This is clinically indistinguishable from other disorders of consciousness, psychosyndromes, or states of confusion or agitation and can be diagnosed most reliably by EEG. Non-convulsive SE with a confusional state and behavioral abnormalities often lasting longer than 30 min quickly leads to the diagnosis of a psychiatric disorder and admission to a psychiatric hospital [26, 28]. Signs that may be helpful in the differential diagnosis may be discrete myoclonia of the eyelids and hands or automatisms. Furthermore, NCSE may be of generalized or even focal etiology; EEG is important for differentiation but sometimes helpful only if one can record the onset of the status or if a focal deficit develops post seizure (paresis, aphasia; [30]). Particularly in the case of an initial manifestation, it is necessary to look for an acute or chronic inflammatory, cerebrovascular, or degenerative process, as well as traumatic brain injury or tumor [27]. Other causes may include psychotropic substances, as well as their discontinuation, in particular benzodiazepine withdrawal, or metabolic disorders [16]. In terms of treatment, parenteral administration of benzodiazepines (lorazepam 1–4 mg, clonazepam 1–2 mg, diazepam 10–20 mg) is usually rapidly successful, which can also play a diagnostic role. Buccal or nasal midazolam are newer, simpler options for home use.

Convulsive SE can occur in the context of a known epilepsy or as a symptom of an acute illness [21]. The risk of (convulsive) SE in old age is increased by a factor of 5–10 [16]. This is characterized by a seizure lasting longer than 30 min or rapid successive seizures without regaining consciousness. Disproportionately often, SE also represents the initial manifestation of senile epilepsy [9]. It is estimated that one in three symptomatic convulsive seizures in old age occurs primarily as SE. Both morbidity and mortality from SE in older adults are significantly increased [9]. According to recent studies, SE in adults occurring due to an underlying acute illness is etiologically due to cerebrovascular disease in 22%, antiepileptic drug depletion in 30%, and metabolic disorders in 15%—causes that, for various reasons, play a relevant role with increasing age [21]. Mortality is associated with etiology, time between status onset and adequate treatment initiation, and patient age. In this regard, mortality is significantly higher after the age of 60 years than in younger patients [7]. The incidence of causative acute illnesses that contribute to mortality is also increased in older age [8].

Seizures in people of higher age are often recognized late [23], and the rate of initial misdiagnosis is high [16]. One reason for this is the semiology, which differs from younger adults. In old age, seizures often occur as focal unconscious seizures with arrest, without classic symptoms such as automatisms or psychic phenomena [24, 26, 28], and BTCS are less common (26%) compared to young adults (65%; [29]). Auras are reported less frequently and often manifest nonspecifically as dizziness [32]. Symptoms such as pausing or postictal disorientation, which is often prolonged [12], can be misinterpreted as, for example, a state of confusion in the context of dementia. Patients themselves may not be able to make a detailed statement about their symptoms during the seizure partly due to cognitive impairments in the context of underlying diseases such as stroke or dementia [28]. In these cases, the diagnosis can be challenging, especially in the absence of a third-party history. Since people of higher age more often live alone and are less able to participate in social events, e.g., due to limited mobility, social isolation is another complicating factor in making a correct diagnosis [16]. The diagnosis of epilepsy presents a variety of psychosocial challenges to older people, as it may contribute to further limitations in independence and mobility, e.g., due to inability to drive or fear of falling during seizures. The risk of seizure-associated injuries from falls is high in people of older age [19], with fractures potentially leading to hospitalization, further immobilization, isolation, and long-term morbidity [34].

Differential diagnoses

One of the most important differential diagnoses of epileptic seizures in people of higher age is syncope, as in younger patients [23]. These can usually be differentiated from epileptic seizures by specific self-reported and third-party history with special attention to trigger factors (e.g., prolonged standing, physical exertion, heat, micturition, etc.), prodromal symptoms (undirected dizziness, cardiac arrhythmia, nausea, etc.), and duration. In addition to reflex syncope, which is the most common cause of syncope at any age, cardiogenic (arrhythmogenic or structural) genesis must be ruled out in people of higher age due to the frequent presence of cardiac comorbidities [23, 24]. Arrhythmogenic syncope, in particular, needs to be rapidly recognized and treated due to its unfavorable prognosis [31]. Electrocardiography (ECG) and, depending on the cardiovascular risk profile, medical history (palpitations, syncope on physical exertion, angina pectoris symptoms, etc.), clinical findings, echocardiography, and long-term ECG, preferably over several days, should be performed to clarify a passive loss of consciousness in old age [23, 31]. Syncope accompanied by motor discharges (convulsive syncope) is much more common than epilepsy in terms of lifetime prevalence [31], but may present a special challenge in terms of its differentiation from epileptic seizures [22, 26]. In contrast to the semiology in BTCS, there are often nonspecific prodromes followed by loss of consciousness with tonic extension of bilateral arms and subsequent irregular twitching, usually lasting for a shorter time (20–30 s) and accompanied by rapid reorientation [31]. The third-party history should specifically address lateralizing signs such as head-turning, unilateral motor discharges, and subsequent confusion [32, 34]. Urinary leakage is comparatively nonspecific and often also occurs in convulsive syncope, whereas lateral tongue biting is suggestive of an epileptic etiology [26]. The asystole seizure as a symptom of temporal epilepsy, which is not rare in old age, cannot be reliably distinguished clinically from syncope without EEG and ECG.

Case study.

A 65-year-old female patient at the author’s own clinic often experienced very bad falls, incurring numerous injuries and fractures in the course of seizures without prodromes until it was possible to detect the confirmatory asystolic seizure on video-EEG. In this seizure, a left temporal seizure pattern was followed by loss of consciousness for 15 s, and only then asystole for 30 s. It took more than 3 min until she was able to react, by which time the seizure pattern had spread bitemporally, ending after a good 2 min, and the patient remained briefly aphasic post seizure and was subsequently amnesic for the event.

Laboratory tests often show an increase in the concentration of creatine kinase (CK) after major epileptic seizures as a result of the pronounced motor activity during the seizure. If the half-life of CK is long, this value may still be elevated 3 days after the seizure. Prolactin has been shown to be a less specific parameter [10]. Other important differential diagnoses of epileptic seizures may be transient ischemic attacks, onset of dementia, and delirium of various causes in people of higher age due to the clinical presentation (speech disturbance, disorientation, inability to respond to stimuli in the absence of motor phenomena; [15, 22]). Basic laboratory tests including determination of blood glucose, electrolytes, renal and liver function parameters, as well as ammonia form the basis of diagnosis [10]. Electrolyte disturbances, such as hyponatremia, may present particularly in the setting of diuretic therapy or antidepressant medication with selective serotonin reuptake inhibitors (SSRIs; [32]). Hypoglycemia during antidiabetic therapy is common in older patients and manifests as fluctuating disorientation or vigilance [32]. Intoxications should also be ruled out in the acute diagnostic setting. Acute imaging is essential in the diagnosis of unclear episodes with impaired consciousness to exclude pathologies with a fluctuating course, such as subdural hematomas under oral anticoagulation, etc. [10].

Case study.

A 62-year-old man with mildly impaired intelligence presented to the author’s clinic with a very unusual combination of epilepsy with large seizures, movement disorder, and a highly pathologic EEG (Figs. 1 and 2). The hypothesis of late-onset idiopathic generalized epilepsy (IGE) was discarded when treatment with valproate was initiated without any effect, leading instead to an increase in seizures. He had never experienced absences or typical myoclonia, but on further questioning it was revealed that his movement abnormalities had started as early on as in childhood and that glucose was always very helpful. After a cerebrospinal fluid/serum glucose ratio of 40% (normal: 50–80%) was found, as well as decreased lactate of 1.5 mmol/l (1.7–2.6), a glucose transporter defect was clinically diagnosed. Genetic testing revealed a defect in exon 5 of the SLC2A1 gene, a clinically previously unclassified heterozygous alteration c.634C > G, leading to the incorporation of amino acid glycine instead of arginine in position 212. The patient could no longer be motivated to follow a ketogenic diet. With oxcarbazepine, which he tolerated well, he has remained seizure-free with respect to large seizures in the long term.

Fig. 1
figure 1

Interictal electroencephalography

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Fig. 2
figure 2

Ictal electroencephalography

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The diagnosis of epilepsy in older patients is more difficult than in younger patients for various reasons. Patients are often unable to provide precise information about their seizures, as in the case of the patient described above [4, 15]. On the one hand, this is due to the fact that epilepsy in old age is often associated with a low number of seizures (with or without disturbance of consciousness), which are not perceived as epileptic seizures as such by this group of people, who are often living alone (amnesia). On the other hand, focal forms are almost exclusively found as initial manifestations of epilepsy in older patients [22, 33]. The proportion of cases of generalized epilepsy is very low, and in individual cases it is probably not a true new case, but often a recurrence of absence that already existed in adolescence. Nevertheless, what is referred to as “late-onset IGE” exists and needs to be considered [5]. Seizure semiology in patients with old-onset epilepsy may differ significantly from seizures in younger patients [1, 22].

Case study.

A 72-year-old woman who had been treated by the author for many years reported twitching in the left facial region in the morning, as well as the problem of not being able to open her left eye, which recovered after about 30 min. She had well-controlled juvenile myoclonic epilepsy and, remembering myoclonia in young adulthood, now thought the epilepsy had “re-awakened” despite treatment with valproate 2 × 500 mg/day. Video-EEG monitoring then showed the presence of hemifacial spasm, while the EEG was completely normal, even during the “twitching.”

Large seizures (BTCS) are found in a high percentage [5] of younger patients and are usually recognized as epileptic seizures even by medical laypersons and are often preceded by prodromes or auras [22]. Affected individuals aged over 65 years were found [32, 34] to be less likely to self-report their seizures. In one study [22], BTCS was found in only 27% of elderly patients with epilepsy on video-EEG. In another study [29], a lower proportion of convulsive seizures was seen, but a higher proportion of events with clouding of consciousness and confusion. These seizures occur more frequently without typical automatisms [1, 22] and also as non-convulsive status, which can massively complicate the diagnosis. The initial manifestation of epilepsy as SE is associated with a significantly higher mortality rate compared to younger affected individuals [18]. The often atypical presentation of epileptic seizures not infrequently leads to misdiagnosis. For example, in the Veteran Affairs Cooperative Study of patients with an average age of 72 years, it was shown that primary-care physicians misdiagnosed and had not thought of epilepsy in approximately one quarter of cases [13, 25]. The most common misdiagnoses when multiple diagnoses were possible were unexplained change in consciousness (42%), confusion (38%), blackout (29%), impaired memory (17%), syncope (17%), dizziness (10%), and dementia (7%) [25]. In addition, patients may experience postictal phenomena such as paresis or aphasia, especially after convulsive seizures [1, 22]. These are then more easily noticeable than the preceding seizure, and the symptom is misrecognized as a stroke. Postictal paresis is found in just over 10% of seizures on video-EEG [12] and last longer than in younger patients [28]. Like these classic Todd’s phenomena, a postictal twilight state may be prolonged, which is suggestive of a dementia process [3, 4]. The occurrence of non-epileptic seizures is also little known in the group of people of higher age [6].

Case study.

A 68-year-old man presented in a state of high agitation with his two daughters during the author’s seizure consultation hours to report multiple seizures over a period of more than 3 months, but so far all diagnostics (magnetic resonance imaging, EEG, CSF) had been unremarkable. A video on the daughter’s cell phone brought clarity: One saw how the man slumped down in a highly stressful situation (an argument with his wife) and lay motionless on the floor in a type of playing-dead reflex for about 5 min. The association with the wife’s announcement that she wanted to leave him after 39 years of marriage soon became apparent. The narcissistic mortification of this man, among other things, had presumably been causative in this symptomatology. Even if non-epileptic seizures mostly occur in young adulthood, this man is by far not the only patient over 60 years of age to present with non-epileptic seizures—while known [6], this phenomenon is not very common.

Practical conclusion

  • Older people with epilepsy are seen much more often in acute centers or even at the general practitioner than in epilepsy centers or epilepsy outpatient departments.

  • General practitioners and neurologists should be aware of the often very mild semiology of seizures and encourage relatives to film unusual paroxysmal events, even with a cell phone.

  • It may also be useful to administer ex juvantibus 5–10 mg midazolam as a nasal spray or oral solution if frequent seizures cannot be recorded, the EEG remains mild between seizures, and the events are more widely spaced.

  • Untreated epilepsy in old age can lead to status epilepticus and be life-threatening, as can the sequelae of epileptic seizures, up to and including sudden unexpected death in epilepsy.

  • The diagnosis and differential diagnosis of seizures of all types in the elderly should be made in video-EEG monitoring.