ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Seizures and epilepsy in older adults: Etiology, clinical presentation, and diagnosis

Seizures and epilepsy in older adults: Etiology, clinical presentation, and diagnosis
Literature review current through: May 2024.
This topic last updated: Mar 13, 2023.

INTRODUCTION — Seizures and epilepsy are common in older adults. Nearly one-half of new-onset seizures occur in individuals over the age of 65 years [1,2]; however, recognizing seizures in this population is challenging because of the paroxysmal nature of the condition and the clinically subtle presentation of seizures in the majority of cases. Treatment decisions are also more complex; older patients are more susceptible to medication side effects and carry a greater burden of medical comorbidities.

Seizures are episodes of transient neurologic change due to hypersynchronous, hyperexcited neuronal activity. Seizures are divided into two categories: provoked and unprovoked. Provoked seizures, also known as acute symptomatic seizures, occur with an identifiable proximate cause and are not expected to recur in the absence of that particular cause or trigger (eg, hypoglycemia, alcohol withdrawal). Unprovoked seizures occur without an identifiable proximate cause, and epilepsy is defined as a condition of recurrent unprovoked seizures. In epilepsy, the seizures appear to occur spontaneously and are expected to recur in the absence of treatment. This topic will cover the clinical presentation, differential diagnosis, and etiology of seizures and epilepsy in older patients. The treatment of seizures and epilepsy in the older patients is discussed separately. (See "Seizures and epilepsy in older adults: Treatment and prognosis".)

EPIDEMIOLOGY — Acute symptomatic seizures are common in older patients. The incidence of acute symptomatic seizures in patients older than age 60 years is estimated at 0.55 to 1 per 1000, with linear increases every decade after age 30 years (figure 1) [3-5].

The incidence and prevalence of epilepsy (recurrent unprovoked seizures) also increase with age in adulthood and are highest in patients over 75 years of age [6-8]. In population-based studies, the incidence rate of new-onset epilepsy in older adults ranges from 1 to 3 per 1000 person-years [3,4,9-15] and is estimated to be two to six times higher than in younger adults [1]. The prevalence of epilepsy in older adults is approximately 2 to 5 percent [13,15], three to four times higher than in younger adults. Age has been shown to be an independent risk factor for developing seizures and epilepsy [9].

Among United States Medicare beneficiaries age 65 years and older, the average annual incidence of epilepsy for the years 2001 to 2005 was highest for Black beneficiaries (4.1 per 1000), intermediate for White beneficiaries (2.3 per 1000), and lowest for Asian and Native American beneficiaries (1.6 and 1.1 per 1000) [13]. This trend has been confirmed in other studies [15]. Additionally, older adults with epilepsy have mortality rates and health care expenditures that are approximately two times higher than older adults without epilepsy [16,17].

CAUSES AND RISK FACTORS — Both acute symptomatic seizures and epilepsy occur as a consequence of diseases and conditions that more commonly affect older adults [18].

Acute symptomatic seizures (provoked or triggered seizures) — Acute symptomatic seizures refers to seizures that occur at the time of a systemic illness or in close temporal association with a new brain insult, (eg, within one week of stroke, traumatic brain injury, anoxic encephalopathy, or intracranial surgery; at first identification of subdural hematoma; during the active phase of a central nervous system infection; or within 24 hours of a severe metabolic derangement) [19].

Causes of acute symptomatic seizures are wide-ranging; virtually any acute insult to the brain can cause a seizure (table 1).

Acute stroke — In older adults, acute stroke is the most common cause of acute symptomatic seizures, accounting for up to one-half of cases [3,5,20]. Seizures occur in 3 to 9 percent of acute cerebrovascular events; all stroke subtypes, including (rarely) transient ischemic attacks (TIAs), are associated with seizure [21-23].

Risk factors for acute poststroke seizures include hemorrhage, particularly lobar hemorrhage, large size of stroke, cortical involvement of ischemic stroke, and hyperglycemia [22-24]. Most acute seizures occur within 48 hours of ischemic stroke onset; in subarachnoid hemorrhage, seizures generally occur within hours [25,26]. Acute symptomatic seizures are also a risk factor for the eventual development of poststroke epilepsy. (See 'Epilepsy (unprovoked seizures)' below.)

Other acute intracranial lesions – Seizures may also be seen in association with subdural hematoma, hypoxic-ischemic brain injury, hypertensive encephalopathy, acute head trauma, and active intracranial infection. Trauma is the underlying cause of 4 to 17 percent of acute symptomatic seizures [3,5,20]. While older patients are susceptible to head trauma, they may be less likely to suffer acute seizures as a result than are younger patients [9,27]. Seizures associated with intracranial infections represent less than 3 percent of acute seizures in the older adult population [3,5,20].

Metabolic encephalopathy — Metabolic disturbances cause approximately 6 to 30 percent of acute symptomatic seizures in older adults [3,5,20]. Metabolic disturbances can precipitate seizures at any age, and older adults are at higher risk because of the increased prevalence of multiple medical conditions, polypharmacy, and complications. Hypoglycemia, hyperglycemia, hyponatremia, and uremic and hepatic encephalopathy are all causes of acute symptomatic seizures [28,29].

Drugs and alcohol — Drugs and drug withdrawal may be responsible for up to 10 percent of acute symptomatic seizures [3,5,20]. A number of medications have been implicated as a cause of acute seizures in late life (table 2) [30,31]. Older adults are likely to be particularly susceptible to seizures as a consequence of drugs because of a high prevalence of polypharmacy, impaired drug clearance, and a heightened sensitivity to the proconvulsant effects of medications [1]. Seizures can occur with alcohol, benzodiazepine, or barbiturate withdrawal [32].

Epilepsy (unprovoked seizures) — The causes of epilepsy are broadly categorized as genetic, structural, metabolic, immune, infectious, and unknown [33]. Major causes of epilepsy in older adults include cerebrovascular disease, neurodegenerative dementia, intracranial tumors, and trauma; a significant portion (one-third to one-half) are of unknown etiology (table 1) [3,4,10,20]. For all etiologies, the risk of developing epilepsy is highest in the initial one to two years after the onset of the precipitating factor [34].

Subacute and chronic stroke — Cerebrovascular disease is the most common known cause of epilepsy in older adults, responsible for one-third to one-half of cases of new-onset epilepsy in older patients [1,3,4,10,15,20,35,36]. Risk factors for poststroke epilepsy (hemorrhage, cortical involvement, stroke size) are similar to those for acute symptomatic seizures [24]. Acute symptomatic seizures and recurrent stroke are also risk factors for poststroke epilepsy [37]. Approximately 35 percent of individuals with acute symptomatic seizures at the time of stroke will develop poststroke epilepsy, compared with an overall 5 to 9 percent risk of poststroke epilepsy [37-39]. The risk of unprovoked seizures is highest in the first year after a stroke, but remains substantially elevated for at least seven years [40].

Neurodegenerative dementia — Alzheimer disease (AD) is a significant risk factor for epilepsy. Between 10 to 20 percent of patients with AD will develop seizures, a rate up to 10 times higher than expected [41-46]. A premorbid diagnosis of either AD or non-Alzheimer dementia are more common in patients presenting with a first unprovoked seizure compared with age-matched hospitalized controls (odds ratio [OR] 6 and 8, respectively) [47]. In prospective cohort studies, younger age at onset and more severe dementia have been identified as independent risk factors for incident epilepsy [43,47,48]. Likewise, comorbid epilepsy has been associated with earlier onset of cognitive decline in patients with amnestic mild cognitive impairment and AD [48,49].

Dementia is present in 9 to 17 percent of older adults with epilepsy [3,4,10,20]. In a population-based study that identified over 1000 older adults with incident epilepsy, dementia at baseline was much more likely compared with older adults without epilepsy (hazard ratio 7.39, 95% CI 5.21-10.50) [50]. Dementia may coexist and possibly interact with other causes of epilepsy. In a prospective study, preexisting dementia increased the risk of poststroke epilepsy [51]. In another retrospective case series, 40 percent of patients with dementia and seizures had another potential structural cause (usually stroke) for their seizures [52].

Other static or progressive intracranial lesions — Intracranial lesions including brain tumors, vascular malformations, and head trauma, also cause epilepsy in older adults. The tumors most frequently associated with epilepsy are gliomas, meningiomas, and metastases [36]. While these are more common in older than younger patients, seizures are less likely to be the presenting symptom in older adults [53].

Head trauma underlies 2 to 21 percent of epilepsy in the older adult population [3,10,20]. Older patients are particularly susceptible to head trauma, which may cause epilepsy as well as acute seizures [27,54].

Arteriovenous malformations usually manifest in younger adults; when first diagnosed in an older patient, seizures are much less likely to be the presenting symptom [55].

Psychiatric conditions — Emerging data suggest that preexisting psychiatric disorders are independently associated with new onset of epilepsy in older adults [56,57]. In a study of Medicare beneficiaries, prior history of substance abuse had the strongest significant association with new onset epilepsy in older adults (adjusted OR 2.5), followed by psychosis (adjusted OR 2.3), bipolar disorder (adjusted OR 2.0), schizophrenia (adjusted OR 1.7), and depression (adjusted OR 1.5) [57].

CLINICAL PRESENTATION

Seizure type and semiology — The clinical presentation of seizures in older adults is frequently different from that of younger adults, and seizures are often difficult to recognize. Older patients typically do not describe an aura or warning, and if they do, the symptoms may be nonspecific (dizziness or confusion). Seizures are also less likely to be convulsive or have motor features. In a randomized trial that enrolled nearly 600 older adults with new onset epilepsy, focal seizure with impairment of awareness was the most common seizure type, affecting 38 percent of patients [58].

Features that suggest seizure in older adults:

Confusion, behavioral change, or unresponsiveness

Sudden falls with no recall or warning

Recurrent events occurring in various positions or circumstances

Arousal from sleep with confusion or disorientation

Seizures in older adults are often difficult to recognize for the following reasons:

Lack of aura or preceding warning

Lack of motor features

Comorbid dementia

Misdiagnosis as delirium

Focal seizures in older adults are often featureless and lack automatic behaviors (eg, lip smacking, repetitive hand movements), which are frequently observed in younger patients with epilepsy. Family members or caregivers of older adults may describe episodic confusion, unresponsiveness, or sudden sleepiness, and these fluctuating symptoms may be difficult to distinguish from delirium [59,60]. Rarely, seizures in individuals with neurodegenerative conditions can present with clusters of myoclonus (brief lightning-like movements) and/or tonic seizures (brief stiffening of the muscles), which can be difficult to differentiate from movement disorders [41,61]. An under-recognized syndrome of late onset massive myoclonus with falls affects older patients with Down syndrome and is important to identify, particularly as survival with Down syndrome has improved [62]. (See "Down syndrome: Clinical features and diagnosis".)

Manifestations of the postictal period typically include confusion and suppressed alertness. Focal neurologic deficits may also be present, often referred to as Todd paralysis or postictal paresis. The postictal state may last from seconds to minutes to hours to days, depending upon several factors including location of seizure, the amount of cortex involved, the duration of the seizure, medications received, and age. Older patients with secondarily generalized seizures may have prolonged postictal confusion and sleepiness that persists for up to several days to a week, particularly if there is underlying brain dysfunction or neoplasm [63].

Convulsive and nonconvulsive status epilepticus — Status epilepticus (SE) is not infrequent in older patients; in one hospital-based study, 30 percent of first seizures in an older population presented as SE [34,64]. The incidence of SE in the older adult population (90 per 100,000) is almost twice that of the general population [65]. Stroke, either acute or remote, is the most frequent underlying etiology (in about one-third of patients) of convulsive SE [64]; other associated conditions include a history of epilepsy, dementia, and electrolyte imbalance [66]. Associated mortality is higher in older patients; in one cohort, 35 percent of patients over 60 with SE died as compared with 16 percent of older patients with similar conditions and seizures [64]. In a second cohort, approximately 65 percent of patients over 80 years with SE died [64,67]. Mortality is associated with the duration of the seizure activity, and also with the number of medical comorbidities [66].

Nonconvulsive status epilepticus (NCSE) is a challenging diagnosis, particularly in the older patient. It typically manifests as an altered mental status with confusion, psychosis, lethargy, or coma [68-72]. Occasionally, NCSE may present as a more focal cognitive disturbance with aphasia or a neglect syndrome, even in the absence of underlying structural pathology [68,70,73,74]. In a series of 236 patients of all ages (38 percent were age ≥60 years) without overt seizure activity who received an electroencephalography (EEG) as part of a coma evaluation, 8 percent had NCSE [75].

More than half of NCSE cases occur in the setting of acute medical conditions, such as organ failure, drug toxicity, alcohol and benzodiazepine withdrawal, and other metabolic disturbances [76-79]. Less commonly, NCSE complicates a known diagnosis of epilepsy or occurs as a first presentation of epilepsy [71,77,79,80]. Every cause of acute symptomatic seizures and epileptic seizures has been associated with NCSE.

In one series of NCSE in critically ill older patients, most patients had underlying brain pathology (defined by history or neuroimaging), but only 2 of 38 had a previous diagnosis of epilepsy [77]. Mortality is high (27 to 52 percent) in this setting [70,77,79,80]. Aggressive treatment of NCSE may actually play a role in morbidity and mortality through induced hypotension, cardiac arrhythmias, and prolonged sedation [70,77,81].

A more detailed discussion of the manifestations, diagnosis, and treatment of SE is presented elsewhere. (See "Convulsive status epilepticus in adults: Classification, clinical features, and diagnosis" and "Nonconvulsive status epilepticus: Classification, clinical features, and diagnosis".)

DIAGNOSTIC EVALUATION — The main purpose of the diagnostic evaluation is to establish whether the patient has had one or more provoked or unprovoked seizures and, if so, to determine the etiology of the seizures and/or epilepsy. For older adult patients with suspected seizures or epilepsy, the evaluation should include a detailed history of the event, electroencephalography (EEG) for select patients to identify epileptiform activity, a neuroimaging study for all patients to detect a structural brain lesion, and laboratory tests to look for metabolic causes.

Patient history — There is no diagnostic test that can substitute for a detailed history. The goals of the history taking are to characterize the events, rule out alternative diagnoses, determine whether similar events have happened in the past, and, if the events are convincing for seizures, evaluate for underlying etiology. Older adult patients often have comorbid cognitive impairment and may have difficulty giving an accurate history [82]. They can also be unaware of their seizures. Therefore, obtaining eyewitness reports is imperative. Patients should be evaluated with a screening test such as the Mini-Mental State Examination (MMSE) or the Montreal Cognitive Assessment (MoCA) if there is concern for cognitive impairment. (See "Evaluation of cognitive impairment and dementia".)

Description of the event – The most important part of the evaluation is the taking of the history and obtaining a reliable, detailed description of events from the patient, eye witnesses, and caregivers. This assessment should include a detailed description of the circumstances leading up to the seizure and the patient's behavior before, during, and after the event.

Medications and substances – Alcohol intoxication or withdrawal and drugs of abuse are also potential cause of seizure. A number of prescription or over-the-counter medications have also been associated with iatrogenic seizures (table 2). For most drugs, the magnitude of risk is likely low unless the drug is taken at supratherapeutic doses, or in combination with other drugs that inhibit its metabolism, or in the setting of underlying liver or renal dysfunction. Focal-onset seizures are less likely to be drug-induced compared with generalized tonic-clonic seizures.

Past medical history – Other risk factors for seizures should be addressed, including head injury, stroke, dementia, intracranial tumor or infection, immunosuppression, cancer, rheumatologic disorders, and hematologic disorders.

Electroencephalography — For older patients who are in the hospital for altered mental status of unclear etiology, EEG is a useful tool to exclude or identify seizure activity, especially NCSE, as a contributor to the encephalopathy. In contrast, a routine interictal EEG has limited diagnostic utility for older patients with unclear events when the history is more suggestive of syncope [82]. In the outpatient setting, if the clinical suspicion is high for seizures, a routine EEG can provide objective evidence to support a diagnosis of seizures and epilepsy; however, it is important not to interpret a negative EEG as evidence to disprove or exclude the diagnosis.

Elective video or ambulatory EEG monitoring can be invaluable in the evaluation of possible epilepsy in older adults, particularly when combined with ECG monitoring. However, video-EEG monitoring is not widely available outside of specialized centers. Several retrospective case series have found a high yield with events recorded in 55 to 83 percent of older patients who were selected for video-EEG monitoring, presumably because of clinical suspicion for seizures [83-86]. In one of the larger studies, 46 of 94 patients who had video-EEG monitoring had documented epileptic events and 27 documented nonepileptic events [83]. Nonepileptic diagnoses made in this setting include syncope, cerebrovascular events, obstructive sleep apnea and other sleep disorders, hypotension, and psychogenic events. (See "Video and ambulatory EEG monitoring in the diagnosis of seizures and epilepsy" and 'Differential diagnosis' below.).

Selection of appropriate patients for this test should be undertaken thoughtfully and should include an understanding of the frequency of events. Only individuals with events occurring at least weekly and who can tolerate hospital confinement should be considered. For individuals with rare events, continuous monitoring will likely be nondiagnostic because interictal (between seizure) EEG in the older person may be of limited utility, with relatively low sensitivity and specificity for the diagnosis of epilepsy (see "Electroencephalography (EEG) in the diagnosis of seizures and epilepsy"). Additionally, older patients are more susceptible to hospital complications such as deep venous thrombosis, deconditioning, delirium, and falls.

Nonspecific EEG abnormalities such as intermittent focal slowing are seen in 12 to 38 percent of older individuals without seizures [83,87]. Usually, these abnormalities make up a small portion (1 or 2 percent) of the tracing; more intrusive and more epileptiform abnormalities increase the likelihood of associated epilepsy [88].

A normal EEG does not rule out the possibility of seizures or epilepsy, and is seen in about two-thirds of patients with epilepsy [89,90]. Activation procedures (hyperventilation and photic stimulation) and repeated evaluations add little to the diagnostic yield of the test in this age group [90]. More frequent seizures and EEG recording within 24 hours of an event increase the likelihood of an abnormal interictal EEG [91].

Neuroimaging — A brain imaging study should be obtained in all older individuals with possible seizures or epilepsy, given the higher frequency with age of stroke and other structural disease as possible etiologies. In general, MRI of the brain is the preferred imaging modality because it is more sensitive than CT, especially if there are focal symptoms, abnormal neurologic exam findings, or abnormal EEG patterns. Contrast-enhanced imaging increases the ability to identify tumors, inflammatory disease, and abscesses, but is usually not required if these conditions are not specifically suspected. (See "Neuroimaging in the evaluation of seizures and epilepsy".)

In the Veterans Aging Cohort Study (VACS) of new-onset seizures in older patients (age ≥60 years), only 18 percent of patients were found to have normal CT scans [1]. Stroke was seen in 43 percent, encephalomalacia in 9 percent, and tumors in 2 percent. Other nonspecific abnormalities (atrophy, small vessel disease, hydrocephalus) were identified in the remaining and were probably incidental.

Laboratory evaluation — Because metabolic abnormalities can precipitate seizures in patients with and without epilepsy, patients with acute seizures should have blood analyzed for levels of electrolytes, blood urea nitrogen, creatinine, glucose, calcium, magnesium, and for liver function tests. Complete blood count, differential, and platelets should also be performed in anticipation of initiating antiseizure medications.

Because cerebrovascular disease is the most common identifiable etiology for seizures in older patients, laboratory evaluation for stroke risk factors (eg, fasting lipid panel) should be considered. (See "Overview of the evaluation of stroke".)

Lumbar puncture for cell count, protein, glucose, and stains with cultures should be performed whenever there is suspicion of meningitis or encephalitis.

Diagnostic pitfalls — Because of the "atypical" symptomatology, seizures in older patients are frequently misdiagnosed, or the diagnosis is delayed.

A hallmark of seizures is their paroxysmal and episodic presentation. Most seizures, whether focal or generalized, have a clear and abrupt clinical onset and rapid progression of symptoms over the course of seconds. The majority of seizures end spontaneously within two to three minutes. However, in the older adult, seizures can cause prolonged postseizure confusion and sleepiness. As a result, it can be challenging to ascertain if there is a paroxysmal and/or episodic quality to the events.

In the setting of severe medical illness, NCSE presents a particularly difficult diagnostic and treatment challenge. It manifests as an altered mental status with confusion, psychosis, lethargy, or coma. This nonspecific presentation can be associated with a delay to diagnosis, up to five days in one series [68]. A high index of suspicion for the diagnosis is required, as the underlying illness may often be deemed a sufficient explanation for altered sensorium.

In the large Veterans Affairs trial, 73 percent of patients ultimately diagnosed with epilepsy had a different referral diagnosis [1,58]. These included altered mental status, confusion, blackout spells, memory disturbance, syncope, dizziness, and dementia. In another series, transient ischemic attack (TIA), depression, and metabolic or psychiatric disorders were among the initial misdiagnoses [68]. Misdiagnosis is more common in patients with focal seizures than with generalized tonic-clonic seizures. Despite the known association of seizures and cerebrovascular disease, a history of stroke or TIA was associated with a 1.7-year delay to diagnosing seizures [92]. Similarly, comorbid dementia can obscure the recognition of seizures.

DIFFERENTIAL DIAGNOSIS — Differentiating seizures from other paroxysmal disorders can be challenging in the older adult for many of the same reasons that diagnosing seizures can be difficult. Older patients are more likely to have other medical conditions and take multiple medications; therefore, it is imperative to consider other paroxysmal conditions, including syncope due to cardiac arrhythmias or orthostatic hypotension, fluctuating behavioral disturbances and abnormal movements due to neurodegenerative conditions, metabolic disturbances, and transient ischemic attacks (TIAs).

Syncope — Cardiogenic syncope is common in the older population and associated with high morbidity and mortality. Cardiogenic syncope can occur when the patient is supine, be accompanied by incontinence, and result in a prolonged recovery period, particularly if the patient remains hypotensive, mimicking a postictal state. In addition, abnormal motor movements (brief jerky movements) may accompany syncope, further confusing the observer. Cardiogenic syncope can present as sudden falls without prodromal symptoms and result in serious self-injury. Orthostatic hypotension leading to syncope can also present as sudden falls because older patients may not recognize prodromal lightheadedness or dizziness due to cognitive impairment. (See "Nonepileptic paroxysmal disorders in adolescents and adults", section on 'Syncope' and "Syncope in adults: Epidemiology, pathogenesis, and etiologies" and "Syncope in adults: Clinical manifestations and initial diagnostic evaluation".)

Delirium and confusional states — Delirium and acute toxic-metabolic encephalopathy may be difficult to distinguish from focal seizures with impairment of consciousness or awareness and nonconvulsive status epilepticus (NCSE), particularly in a patient with baseline neurologic impairment [93]. Episodic, dramatic changes in mental status with a return to normal or baseline cognition strongly suggest seizures, but the presentation may be more subtle.

When present, stereotyped motor movements or automatisms suggest seizure. However, tremor, asterixis, and myoclonus are not uncommon in delirium. Hallucinations may be a feature of either condition. Causes of delirium (table 3) and seizures overlap, and delirium and seizures can coexist. Continuous video/electroencephalography (EEG) can identify or exclude seizures in this setting. (See "Diagnosis of delirium and confusional states".)

Transient ischemic attacks — TIAs may be mistaken for seizures, and in rare circumstances, they may also induce seizures (see 'Acute symptomatic seizures (provoked or triggered seizures)' above). The diagnosis of TIAs becomes much less likely if the history indicates multiple stereotyped episodes over an extended time period without permanent neurologic sequelae. It would be difficult to contemplate a circumstance of repeated ischemia to the same vascular territory without resulting in some neurologic deficits.

Typically, brain ischemia presents as "negative" symptoms such as hemiparesis or hemisensory loss. In contrast, seizures usually cause "positive" symptoms (involuntary shaking or movements) from neural hyperexcitability. One exception is the condition "limb-shaking" TIAs, which represent a source of diagnostic confusion. In this rare condition, cerebral ischemia occurring in the setting of high-grade carotid stenosis causes intermittent weakness in a single limb, which can mimic the clonic jerky movements of a focal motor seizure [94,95].

Certain symptoms, such as speech arrest or language dysfunction (aphasia), can occur in a TIA or a seizure. Sudden, isolated aphasia (sudden language dysfunction without other manifestations) is more likely to be a TIA but can occur with seizures. Evolving symptoms would be more suggestive of seizure. Associated confusion/disorientation and/or amnesia for the event would also favor the seizure diagnosis.

Transient global amnesia — Transient global amnesia (TGA) occurs in older individuals and is characterized by striking amnesia with preservation of other cognitive domains (patients remain awake, alert, and attentive). TGA episodes last much longer than most seizures (usually several hours) and are without lethargy or motor manifestations.

Episodes of amnesia that are epileptic in origin will typically be associated with diminished responsiveness, abnormal behaviors, and/or motor manifestations, features that are absent in TGA [96]. However, these symptoms may not be volunteered and should be specifically elicited. (See "Transient global amnesia".)

Sudden unexplained falls/drop attacks — These are events characterized by a sudden fall to the ground without warning. Although seizures can present in this fashion in older patients, cardiogenic syncope and vestibular pathologies are more likely potential causes. (See "Syncope in adults: Epidemiology, pathogenesis, and etiologies" and "Syncope in adults: Clinical manifestations and initial diagnostic evaluation" and "Evaluation of the patient with vertigo", section on 'Drop attacks'.)

Psychogenic spells and/or behavioral spells — It is a myth that late-onset psychogenic spells are rare; therefore, nonepileptic spells should be considered when evaluating the older adult with episodic changes in behavior. The clinical features of these nonepileptic events can be similar to spells seen in younger patients [97]. Nonepileptic spells in older patients can present with eye closure, staring, asynchronous limb movements, pelvic thrusting, and/or complex behaviors such as screaming or crying. Not all nonepileptic spells in older patients are psychogenic or somatoform in etiology. Episodic unresponsiveness or sudden episodes of decreased alertness can be seen in patients with Alzheimer disease and dementia with Lewy bodies and are not be epileptic in etiology.

The main difference between late-onset psychogenic nonepileptic attacks and psychogenic events in younger patients is the associated trauma; in older patients, health-related traumatic events are more likely, while in younger patients, antecedent sexual abuse is more likely [98]. (See "Psychogenic nonepileptic seizures: Etiology, clinical features, and diagnosis".)

Sleep disorders — Rapid eye movement (REM) sleep disorder can be mistaken for epilepsy. This is a parasomnia characterized by vivid dreams in REM sleep without the usual accompanying muscle atonia [34,37]. This causes individuals to "act out" their dreams, especially when they are vivid or frightening. Injuries to the patient and bed partner can result.

Patients are usually able to describe the dream, a feature that is helpful in distinguishing this from seizures. Episodes can recur during the night, and preferentially occur in the second half of sleep when there is the greatest preponderance of REM sleep.

While sometimes occurring as an isolated idiopathic condition in younger adults, REM sleep behavior disorder in older adults is most commonly associated with alpha-synuclein neurodegenerative disorders including dementia with Lewy bodies and Parkinson disease. It usually presents after the age of 50 years [36]. The diagnosis can be confirmed with polysomnography. (See "Rapid eye movement sleep behavior disorder".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Seizures (The Basics)")

Beyond the Basics topics (see "Patient education: Seizures in adults (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Acute symptomatic seizures are common in older adults, and the prevalence of epilepsy increases with age, being highest in patients >75 years of age. It is important to determine whether a first seizure is a provoked event that is not expected to recur in the absence of that trigger or if it is the first sign of new-onset epilepsy, a condition in which recurrent unprovoked seizures are expected in the absence of treatment. (See 'Epidemiology' above.)

In older adults, acute symptomatic seizures are most often seen in the setting of acute stroke and metabolic encephalopathy. Cerebrovascular disease and degenerative dementia are common causes of epilepsy in older patients, but one-third to one-half of cases are of unknown etiology. (See 'Causes and risk factors' above.)

The clinical presentation of seizures in the older population is often atypical and easily mistaken for other conditions such as delirium, transient ischemic attack, or syncope. Clinicians should maintain a high level of suspicion for possible seizures in older patients presenting with intermittent or fluctuating confusional states. (See 'Clinical presentation' above.)

A reliable history and description of the event from an eyewitness are invaluable and superior to testing in the diagnosis of epileptic seizures. Electroencephalography (EEG) monitoring, particularly video EEG monitoring, can be very helpful in the evaluation of patients with recurrent events. A brain imaging study should be obtained in all older patients with possible epilepsy due to the frequency of stroke or other structural disease as an etiology. Because metabolic abnormalities can precipitate seizures in patients with and without epilepsy, patients with acute seizures should have blood analyzed for electrolytes, blood urea nitrogen, creatinine, glucose, calcium, magnesium, and liver function tests. (See 'Diagnostic evaluation' above.)

Considerations in the differential diagnosis of seizures in older patients include syncope, delirium and confusional states, transient cerebral ischemia, and other disorders. (See 'Differential diagnosis' above.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Hyunmi Choi, MD, MS, and Anil Mendiratta, MD, who contributed to an earlier version of this topic review.

  1. Ramsay RE, Rowan AJ, Pryor FM. Special considerations in treating the elderly patient with epilepsy. Neurology 2004; 62:S24.
  2. Sander JW, Hart YM, Johnson AL, Shorvon SD. National General Practice Study of Epilepsy: newly diagnosed epileptic seizures in a general population. Lancet 1990; 336:1267.
  3. Loiseau J, Loiseau P, Duché B, et al. A survey of epileptic disorders in southwest France: seizures in elderly patients. Ann Neurol 1990; 27:232.
  4. Tchalla AE, Marin B, Mignard C, et al. Newly diagnosed epileptic seizures: focus on an elderly population on the French island of Réunion in the Southern Indian Ocean. Epilepsia 2011; 52:2203.
  5. Annegers JF, Hauser WA, Lee JR, Rocca WA. Incidence of acute symptomatic seizures in Rochester, Minnesota, 1935-1984. Epilepsia 1995; 36:327.
  6. Sen A, Jette N, Husain M, Sander JW. Epilepsy in older people. Lancet 2020; 395:735.
  7. GBD 2016 Epilepsy Collaborators. Global, regional, and national burden of epilepsy, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol 2019; 18:357.
  8. Beghi E, Giussani G, Costa C, et al. The epidemiology of epilepsy in older adults: A narrative review by the ILAE Task Force on Epilepsy in the Elderly. Epilepsia 2023; 64:586.
  9. Hauser WA. Seizure disorders: the changes with age. Epilepsia 1992; 33 Suppl 4:S6.
  10. Hauser WA, Annegers JF, Kurland LT. Incidence of epilepsy and unprovoked seizures in Rochester, Minnesota: 1935-1984. Epilepsia 1993; 34:453.
  11. Lühdorf K, Jensen LK, Plesner AM. Epilepsy in the elderly: incidence, social function, and disability. Epilepsia 1986; 27:135.
  12. Sillanpää M, Lastunen S, Helenius H, Schmidt D. Regional differences and secular trends in the incidence of epilepsy in Finland: a nationwide 23-year registry study. Epilepsia 2011; 52:1857.
  13. Faught E, Richman J, Martin R, et al. Incidence and prevalence of epilepsy among older U.S. Medicare beneficiaries. Neurology 2012; 78:448.
  14. Cossu P, Deriu MG, Casetta I, et al. Epilepsy in Sardinia, insular Italy: a population-based prevalence study. Neuroepidemiology 2012; 39:19.
  15. Choi H, Pack A, Elkind MS, et al. Predictors of incident epilepsy in older adults: The Cardiovascular Health Study. Neurology 2017; 88:870.
  16. Thurman DJ, Logroscino G, Beghi E, et al. The burden of premature mortality of epilepsy in high-income countries: A systematic review from the Mortality Task Force of the International League Against Epilepsy. Epilepsia 2017; 58:17.
  17. Lekoubou A, Bishu KG, Ovbiagele B. Health care expenditures among elderly patients with epilepsy in the United States. Epilepsia 2018; 59:1433.
  18. Li X, Breteler MM, de Bruyne MC, et al. Vascular determinants of epilepsy: the Rotterdam Study. Epilepsia 1997; 38:1216.
  19. Beghi E, Carpio A, Forsgren L, et al. Recommendation for a definition of acute symptomatic seizure. Epilepsia 2010; 51:671.
  20. Stephen LJ, Brodie MJ. Epilepsy in elderly people. Lancet 2000; 355:1441.
  21. Giroud M, Gras P, Fayolle H, et al. Early seizures after acute stroke: a study of 1,640 cases. Epilepsia 1994; 35:959.
  22. Bladin CF, Alexandrov AV, Bellavance A, et al. Seizures after stroke: a prospective multicenter study. Arch Neurol 2000; 57:1617.
  23. Procaccianti G, Zaniboni A, Rondelli F, et al. Seizures in acute stroke: incidence, risk factors and prognosis. Neuroepidemiology 2012; 39:45.
  24. Lancman ME, Golimstok A, Norscini J, Granillo R. Risk factors for developing seizures after a stroke. Epilepsia 1993; 34:141.
  25. Asconapé JJ, Penry JK. Poststroke seizures in the elderly. Clin Geriatr Med 1991; 7:483.
  26. Kilpatrick CJ, Davis SM, Tress BM, et al. Epileptic seizures in acute stroke. Arch Neurol 1990; 47:157.
  27. Bruns J Jr, Hauser WA. The epidemiology of traumatic brain injury: a review. Epilepsia 2003; 44 Suppl 10:2.
  28. Loiseau P. Pathologic processes in the elderly and their association with seizures.. In: Seizures and epilepsy in the elderly, Rowan AJ, Ramsay RE (Eds), Butterworth-Heinemann, Boston 1997. p.63.
  29. Malouf R, Brust JC. Hypoglycemia: causes, neurological manifestations, and outcome. Ann Neurol 1985; 17:421.
  30. Messing RO, Closson RG, Simon RP. Drug-induced seizures: a 10-year experience. Neurology 1984; 34:1582.
  31. Franson KL, Hay DP, Neppe V, et al. Drug-induced seizures in the elderly. Causative agents and optimal management. Drugs Aging 1995; 7:38.
  32. Hauser WA, Ng SK, Brust JC. Alcohol, seizures, and epilepsy. Epilepsia 1988; 29 Suppl 2:S66.
  33. Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology. Epilepsia 2017; 58:512.
  34. Hauser WA. Epidemiology of seizures and epilepsy in the elderly. In: Seizures and Epilepsy in the Elderly, Rowan AJ, Ramsay RE (Eds), Butterworth-Heinemann, Boston 1997. p.7.
  35. Hart YM, Sander JW, Johnson AL, Shorvon SD. National General Practice Study of Epilepsy: recurrence after a first seizure. Lancet 1990; 336:1271.
  36. Roberts MA, Godfrey JW, Caird FI. Epileptic seizures in the elderly: I. Aetiology and type of seizure. Age Ageing 1982; 11:24.
  37. So EL, Annegers JF, Hauser WA, et al. Population-based study of seizure disorders after cerebral infarction. Neurology 1996; 46:350.
  38. Sung CY, Chu NS. Epileptic seizures in thrombotic stroke. J Neurol 1990; 237:166.
  39. Merkler AE, Gialdini G, Lerario MP, et al. Population-Based Assessment of the Long-Term Risk of Seizures in Survivors of Stroke. Stroke 2018; 49:1319.
  40. Adelöw C, Andersson T, Ahlbom A, Tomson T. Prior hospitalization for stroke, diabetes, myocardial infarction, and subsequent risk of unprovoked seizures. Epilepsia 2011; 52:301.
  41. Hauser WA, Morris ML, Heston LL, Anderson VE. Seizures and myoclonus in patients with Alzheimer's disease. Neurology 1986; 36:1226.
  42. McAreavey MJ, Ballinger BR, Fenton GW. Epileptic seizures in elderly patients with dementia. Epilepsia 1992; 33:657.
  43. Romanelli MF, Morris JC, Ashkin K, Coben LA. Advanced Alzheimer's disease is a risk factor for late-onset seizures. Arch Neurol 1990; 47:847.
  44. Scarmeas N, Honig LS, Choi H, et al. Seizures in Alzheimer disease: Who, when, and how common? Arch Neurol 2009; 66:992.
  45. Imfeld P, Bodmer M, Schuerch M, et al. Seizures in patients with Alzheimer's disease or vascular dementia: a population-based nested case-control analysis. Epilepsia 2013; 54:700.
  46. Vossel KA, Tartaglia MC, Nygaard HB, et al. Epileptic activity in Alzheimer's disease: Causes and clinical relevance. Lancet Neurol 2017; 16:311.
  47. Hesdorffer DC, Hauser WA, Annegers JF, et al. Dementia and adult-onset unprovoked seizures. Neurology 1996; 46:727.
  48. Vossel KA, Beagle AJ, Rabinovici GD, et al. Seizures and epileptiform activity in the early stages of Alzheimer disease. JAMA Neurol 2013; 70:1158.
  49. Choi H, Thacker EL, Longstreth WT Jr, et al. Cognitive decline in older adults with epilepsy: The Cardiovascular Health Study. Epilepsia 2021; 62:85.
  50. Subota A, Jetté N, Josephson CB, et al. Risk factors for dementia development, frailty, and mortality in older adults with epilepsy - A population-based analysis. Epilepsy Behav 2021; 120:108006.
  51. Cordonnier C, Hénon H, Derambure P, et al. Influence of pre-existing dementia on the risk of post-stroke epileptic seizures. J Neurol Neurosurg Psychiatry 2005; 76:1649.
  52. Rao SC, Dove G, Cascino GD, Petersen RC. Recurrent seizures in patients with dementia: frequency, seizure types, and treatment outcome. Epilepsy Behav 2009; 14:118.
  53. Smith DF, Hutton JL, Sandemann D, et al. The prognosis of primary intracerebral tumours presenting with epilepsy: the outcome of medical and surgical management. J Neurol Neurosurg Psychiatry 1991; 54:915.
  54. Hiyoshi T, Yagi K. Epilepsy in the elderly. Epilepsia 2000; 41 Suppl 9:31.
  55. Hashimoto H, Iida J, Kawaguchi S, Sakaki T. Clinical features and management of brain arteriovenous malformations in elderly patients. Acta Neurochir (Wien) 2004; 146:1091.
  56. Ettinger AB, Copeland LA, Zeber JE, et al. Are psychiatric disorders independent risk factors for new-onset epilepsy in older individuals? Epilepsy Behav 2010; 17:70.
  57. Martin RC, Faught E, Richman J, et al. Psychiatric and neurologic risk factors for incident cases of new-onset epilepsy in older adults: data from U.S. Medicare beneficiaries. Epilepsia 2014; 55:1120.
  58. Rowan AJ, Ramsay RE, Collins JF, et al. New onset geriatric epilepsy: a randomized study of gabapentin, lamotrigine, and carbamazepine. Neurology 2005; 64:1868.
  59. Tinuper P, Provini F, Marini C, et al. Partial epilepsy of long duration: changing semiology with age. Epilepsia 1996; 37:162.
  60. Kellinghaus C, Loddenkemper T, Dinner DS, et al. Seizure semiology in the elderly: a video analysis. Epilepsia 2004; 45:263.
  61. Beagle AJ, Darwish SM, Ranasinghe KG, et al. Relative Incidence of Seizures and Myoclonus in Alzheimer's Disease, Dementia with Lewy Bodies, and Frontotemporal Dementia. J Alzheimers Dis 2017; 60:211.
  62. De Simone R, Puig XS, Gélisse P, et al. Senile myoclonic epilepsy: delineation of a common condition associated with Alzheimer's disease in Down syndrome. Seizure 2010; 19:383.
  63. Theodore WH. The postictal state: effects of age and underlying brain dysfunction. Epilepsy Behav 2010; 19:118.
  64. Sung CY, Chu NS. Status epilepticus in the elderly: etiology, seizure type and outcome. Acta Neurol Scand 1989; 80:51.
  65. Waterhouse EJ, DeLorenzo RJ. Status epilepticus in older patients: epidemiology and treatment options. Drugs Aging 2001; 18:133.
  66. Canouï-Poitrine F, Bastuji-Garin S, Alonso E, et al. Risk and prognostic factors of status epilepticus in the elderly: a case-control study. Epilepsia 2011; 52:1849.
  67. Towne AR, Pellock JM, Ko D, DeLorenzo RJ. Determinants of mortality in status epilepticus. Epilepsia 1994; 35:27.
  68. Sheth RD, Drazkowski JF, Sirven JI, et al. Protracted ictal confusion in elderly patients. Arch Neurol 2006; 63:529.
  69. Atefy R, Tettenborn B. Nonconvulsive status epilepticus on treatment with levetiracetam. Epilepsy Behav 2005; 6:613.
  70. Martin Y, Artaz MA, Bornand-Rousselot A. Nonconvulsive status epilepticus in the elderly. J Am Geriatr Soc 2004; 52:476.
  71. Fernández-Torre JL, Díaz-Castroverde AG. Non-convulsive status epilepticus in elderly individuals: report of four representative cases. Age Ageing 2004; 33:78.
  72. Piccenna L, O'Dwyer R, Leppik I, et al. Management of epilepsy in older adults: A critical review by the ILAE Task Force on Epilepsy in the elderly. Epilepsia 2023; 64:567.
  73. Chung PW, Seo DW, Kwon JC, et al. Nonconvulsive status epilepticus presenting as a subacute progressive aphasia. Seizure 2002; 11:449.
  74. Thomas P, Giraud K, Alchaar H, Chatel M. Ictal asomatognosia with hemiparesis. Neurology 1998; 51:280.
  75. Towne AR, Waterhouse EJ, Boggs JG, et al. Prevalence of nonconvulsive status epilepticus in comatose patients. Neurology 2000; 54:340.
  76. Olnes MJ, Golding A, Kaplan PW. Nonconvulsive status epilepticus resulting from benzodiazepine withdrawal. Ann Intern Med 2003; 139:956.
  77. Litt B, Wityk RJ, Hertz SH, et al. Nonconvulsive status epilepticus in the critically ill elderly. Epilepsia 1998; 39:1194.
  78. Martínez-Rodríguez JE, Barriga FJ, Santamaria J, et al. Nonconvulsive status epilepticus associated with cephalosporins in patients with renal failure. Am J Med 2001; 111:115.
  79. Bottaro FJ, Martinez OA, Pardal MM, et al. Nonconvulsive status epilepticus in the elderly: a case-control study. Epilepsia 2007; 48:966.
  80. Shneker BF, Fountain NB. Assessment of acute morbidity and mortality in nonconvulsive status epilepticus. Neurology 2003; 61:1066.
  81. Walker MC. Status epilepticus on the intensive care unit. J Neurol 2003; 250:401.
  82. Brodie MJ, Elder AT, Kwan P. Epilepsy in later life. Lancet Neurol 2009; 8:1019.
  83. McBride AE, Shih TT, Hirsch LJ. Video-EEG monitoring in the elderly: a review of 94 patients. Epilepsia 2002; 43:165.
  84. Kellinghaus C, Loddenkemper T, Dinner DS, et al. Non-epileptic seizures of the elderly. J Neurol 2004; 251:704.
  85. Drury I, Selwa LM, Schuh LA, et al. Value of inpatient diagnostic CCTV-EEG monitoring in the elderly. Epilepsia 1999; 40:1100.
  86. Lancman ME, O'Donovan C, Dinner D, et al. Usefulness of prolonged video-EEG monitoring in the elderly. J Neurol Sci 1996; 142:54.
  87. Drury I, Beydoun A. Seizures and epilepsy in the elderly revisited. Arch Intern Med 1998; 158:99.
  88. Normand MM, Wszolek ZK, Klass DW. Temporal intermittent rhythmic delta activity in electroencephalograms. J Clin Neurophysiol 1995; 12:280.
  89. Ramsay RE, Pryor F. Epilepsy in the elderly. Neurology 2000; 55:S9.
  90. Drury I, Beydoun A. Interictal epileptiform activity in elderly patients with epilepsy. Electroencephalogr Clin Neurophysiol 1998; 106:369.
  91. King MA, Newton MR, Jackson GD, et al. Epileptology of the first-seizure presentation: a clinical, electroencephalographic, and magnetic resonance imaging study of 300 consecutive patients. Lancet 1998; 352:1007.
  92. Spitz MC, Bainbridge JL, Ramsay RE, et al. Observations on the delay in diagnosis of seizures in the elderly: update 2 [abstract]. Epilepsia 2002; 43 Suppl 7:166.
  93. Veran O, Kahane P, Thomas P, et al. De novo epileptic confusion in the elderly: a 1-year prospective study. Epilepsia 2010; 51:1030.
  94. Ali S, Khan MA, Khealani B. Limb-shaking Transient Ischemic Attacks: case report and review of literature. BMC Neurol 2006; 6:5.
  95. Persoon S, Kappelle LJ, Klijn CJ. Limb-shaking transient ischaemic attacks in patients with internal carotid artery occlusion: a case-control study. Brain 2010; 133:915.
  96. Butler CR, Graham KS, Hodges JR, et al. The syndrome of transient epileptic amnesia. Ann Neurol 2007; 61:587.
  97. Behrouz R, Heriaud L, Benbadis SR. Late-onset psychogenic nonepileptic seizures. Epilepsy Behav 2006; 8:649.
  98. Duncan R, Oto M, Martin E, Pelosi A. Late onset psychogenic nonepileptic attacks. Neurology 2006; 66:1644.
Topic 2223 Version 38.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟