Seizures and Epilepsy in Older Adults - Etiology, Clinical Presentation, and Diagnosis - UpToDate PDF

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Seizures and epilepsy in older adults: Etiology, clinical

presentation, and diagnosis
Author: Tina Shih, MD
Section Editors: Steven C Schachter, MD, Kenneth E Schmader, MD
Deputy Editor: John F Dashe, MD, PhD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: May 2020. | This topic last updated: Nov 24, 2018.
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
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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 65 years of age. In population-based studies, the
incidence rate of new-onset epilepsy in older adults ranges from 1 to 3 per 1000 person-years [3,4,6-
12] 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 [10,12], three to four times higher than in
younger adults. Age has been shown to be an independent risk factor for developing seizures and
epilepsy [6].
Among United States Medicare beneficiaries age 65 years and older, average annual incident rates in
2001 to 2005 were highest in African Americans (4.1 per 1000) and lowest in Asian and Native
Americans (1.6 and 1.1 per 1000), in comparison to whites (2.3 per 1000) [10]. This trend has been
confirmed in other studies [12].
CAUSES AND RISK FACTORS
Both acute symptomatic seizures and epilepsy occur as a consequence of diseases and conditions
that more commonly affect older adults [13].
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) [14].
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 [3,5,15]. Seizures occur in 3 to 9 percent of
acute cerebrovascular events; all stroke subtypes, including (rarely) transient ischemic attacks
(TIAs), are associated with seizure [16-18].
Risk factors for acute poststroke seizures include hemorrhage, particularly lobar hemorrhage,
large size of stroke, cortical involvement of ischemic stroke, and hyperglycemia [17-19]. Most
acute seizures occur within 48 hours of ischemic stroke onset; in subarachnoid hemorrhage,
seizures generally occur within hours [20,21]. 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 [3,5,15]. While older patients are susceptible to head trauma, they may be
less likely to suffer acute seizures as a result than are younger patients [6,22]. Seizures
associated with intracranial infections represent less than 3 percent of acute seizures in the older
adult population [3,5,15].
● Metabolic encephalopathy — Metabolic disturbances cause approximately 6 to 30 percent of

acute symptomatic seizures in older adults [3,5,15]. 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 [23,24].
● Drugs and alcohol — Drugs and drug withdrawal may be responsible for up to 10 percent of
acute symptomatic seizures [3,5,15]. A number of medications have been implicated as a cause
of acute seizures in late life (table 2) [25,26]. 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 [27].
Epilepsy (unprovoked seizures) — The causes of epilepsy are broadly categorized as genetic,
structural, metabolic, immune, infectious, and unknown [28]. 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) [3,4,7,15]. For all
etiologies, the risk of developing epilepsy is highest in the initial one to two years after the onset of
the precipitating factor [29].
● 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 [1,3,4,7,15,30,31]. Risk factors for poststroke epilepsy (hemorrhage, cortical
involvement, stroke size) are similar to those for acute symptomatic seizures [19]. Acute
symptomatic seizures and recurrent stroke are also risk factors for poststroke epilepsy [32].
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
[32-34]. The risk of unprovoked seizures is highest in the first year after a stroke, but remains
substantially elevated for at least seven years [35].
● 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 [36-41]. 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) [42]. In prospective cohort studies,
younger age at onset and more severe dementia have been identified as independent risk
factors for incident epilepsy [38,42,43]. Likewise, comorbid epilepsy has been associated with
earlier onset of cognitive decline in patients with amnestic mild cognitive impairment and AD [43].
Dementia is present in 9 to 17 percent of older adults with epilepsy [3,4,7,15]. Dementia may
coexist and possibly interact with other causes of epilepsy. In a prospective study, preexisting
dementia increased the risk of poststroke epilepsy [44]. In another retrospective case series, 40
percent of patients with dementia and seizures had another potential structural cause (usually
stroke) for their seizures [45].
● 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 [31]. While these
are more common in older than younger patients, seizures are less likely to be the presenting
symptom in older adults [46].
Head trauma underlies 2 to 21 percent of epilepsy in the older adult population [3,7,15]. Older
patients are particularly susceptible to head trauma, which may cause epilepsy as well as acute
seizures [22,47].
Arteriovenous malformations usually manifest in younger adults; when first diagnosed in an older
patient, seizures are much less likely to be the presenting symptom [48].
● Psychiatric conditions — Emerging data suggest that preexisting psychiatric disorders are
independently associated with new onset of epilepsy in older adults [49,50]. 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) [50].
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 [51].
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
[52,53]. 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.
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 [54].
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 [29,55]. The incidence of SE in the older adult population (90 per 100,000) is almost
twice that of the general population [56]. Stroke, either acute or remote, is the most frequent
underlying etiology (in about one-third of patients) of convulsive SE [55]; other associated conditions
include a history of epilepsy, dementia, and electrolyte imbalance [57]. 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 [55]. In a second cohort, approximately
65 percent of patients over 80 years with SE died [55,58]. Mortality is associated with the duration of
the seizure activity, and also with the number of medical comorbidities [57].
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 [59-62].
Occasionally, NCSE may present as a more focal cognitive disturbance with aphasia or a neglect
syndrome, even in the absence of underlying structural pathology [59,61,63,64]. 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 [65].
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 [66-69]. Less
commonly, NCSE complicates a known diagnosis of epilepsy or occurs as a first presentation of
epilepsy [62,67,69,70]. 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 [67].
Mortality is high (27 to 52 percent) in this setting [61,67,69,70]. Aggressive treatment of NCSE may
actually play a role in morbidity and mortality through induced hypotension, cardiac arrhythmias, and
prolonged sedation [61,67,71].
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".)
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 [72]. 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 [72]. 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 [73-76]. In one of the larger studies,
46 of 94 patients who had video-EEG monitoring had documented epileptic events and 27
documented nonepileptic events [73]. 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 [73,77]. 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 [78].
A normal EEG does not rule out the possibility of seizures or epilepsy, and is seen in about two-thirds
of patients with epilepsy [79,80]. Activation procedures (hyperventilation and photic stimulation) and
repeated evaluations add little to the diagnostic yield of the test in this age group [80]. More frequent
seizures and EEG recording within 24 hours of an event increase the likelihood of an abnormal
interictal EEG [81].
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 drugs.
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
[59]. 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 [1,51]. 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 [59].
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 [82]. 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
[83]. 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
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carotid stenosis causes intermittent weakness in a single limb, which can mimic the clonic jerky
movements of a focal motor seizure [84,85]. (See "Pathophysiology of symptoms from carotid
atherosclerosis", section on 'Ischemic symptoms'.)
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
[86]. 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 [87]. 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 [88]. (See "Psychogenic
nonepileptic seizures".)
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 [29,32]. 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 [31]. 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 >65 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 editorial staff at UpToDate would like to acknowledge Hyunmi Choi,
MD, MS, and Anil Mendiratta, MD, who contributed to an earlier version of this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
Topic 2223 Version 33.0
GRAPHICS
Acute symptomatic seizures; rates by age, Rochester, Minnesota,

1975-1984
Data from: Annegers, JF, Hauser, WA, Lee, RJ, Rocca, WA. Incidence of acute symptomatic
seizures in Rochester, Minnesota, 1935-1984. Epilepsia 1995; 36:327.
Graphic 54496 Version 2.0
Causes of acute symptomatic seizures and epilepsy in older adults
Relative proportion (%)
Acute symptomatic seizures (provoked seizures)
Acute hemorrhagic and ischemic stroke 50%
Metabolic encephalopathy 6 to 30%
Drugs and alcohol 10%
Others (eg, recent head trauma, active intracranial infections) 5 to 20%
Epilepsy (unprovoked seizures)
Cerebrovascular disease (eg, prior stroke, vascular malformation) 30 to 50%
Dementia 9 to 17%
Others (eg, brain tumors, remote head trauma, prior intracranial 5 to 15%
infection)
Unknown 30 to 50%
Medications associated with seizures
Category Examples
Analgesics Opioids (eg, meperidine, tramadol)
Anticancer drugs ¶ Busulfan

Chlorambucil
Cytarabine
Doxorubicin
Etoposide
Fluorouracil
Interferon alfa
Methotrexate
Mitoxantrone
Nelarabine
Platinum-based drugs (eg, cisplatin)
Vinblastine
Vincristine
Antimicrobials Δ Carbapenems (eg, imipenem)

Cephalosporins (fourth generation
Fluoroquinolones (eg, ciprofloxacin)
Isoniazid ◊
Penicillins
Hypoglycemic agents Potentially any antidiabetic agent that can cause hypoglycemia
Immunosuppressants Azathioprine
Cyclosporine
Mycophenolate
Tacrolimus
Psychiatric Antipsychotics §
medications Atomoxetine
Bupropion
Buspirone
Lithium
Monoamine oxidase inhibitors ¥
Selective serotonin reuptake inhibitors ‡
Serotonin norepinephrine reuptake inhibitors ‡
Serotonin modulators
Tricyclic antidepressants (eg, amoxapine, clomipramine, maprotiline)
Pulmonary drugs Aminophylline

Theophylline
Stimulants Amphetamines
Methylphenidate
Sympathomimetics Anorexiants (eg, diethylpropion, phentermine, nonprescription diet aids)

and decongestants Phenylephrine
Pseudoephedrine
The magnitude of risk of seizure for various categories and individual agents is not well established. Factors that may
contribute to the risk of seizure with medications include overdose, alcohol abuse, organ dysfunction, drug
interactions, older age, and a history of seizures. Illicit drugs use, herbs/natural remedies (eg, guarana),
nonprescription supplements, and abrupt withdrawal from chronic alcohol use and certain prescription medicines (eg,
antiepileptic drugs, baclofen, benzodiazepines) are also associated with seizure.
This table is not all-inclusive. For detailed prescribing information, including reported adverse effects, readers should
refer to the individual drug information topics within UpToDate. Comprehensive information on drug interactions can
be determined using the Lexi-Interact tool included within UpToDate.
¶ For more details and additional anti-cancer drugs that have been associated with seizures, refer to UpToDate topic reviews
on the neurologic complications of anticancer therapies.
Δ Among antibiotics, evidence for an association is strongest for unsubstituted penicillins, fourth-generation cephalosporins,
imipenem, and ciprofloxacin in combination with renal dysfunction, brain lesions, and epilepsy [1].
◊ Seizures are a manifestation of pyridoxal-5-phosphate deficiency; they respond to pyridoxine and benzodiazepine
treatment. Refer to UpToDate topic review on isoniazid poisoning.
§ Clozapine has a higher risk of seizure than most other antipsychotics [2]; refer to UpToDate topic review on guidelines for
prescribing clozapine in schizophrenia for more information.
¥ Monoamine oxidase inhibitors include: furazolidone, isocarboxazid, linezolid, moclobemide, pargyline, phenelzine,
procarbazine, rasagiline, selegiline, tranylcypromine.
‡ Selective serotonin reuptake inhibitors and serotonin norepinephrine reuptake inhibitors do not increase seizure risk in
patients with epilepsy when used in therapeutic doses, but may be proconvulsant at toxic doses [3,4].
References:
1. Sutter S, Ruegg S, Tschudin-Sutter S, Seizures as adverse events of antibiotic drugs: A systematic review. Neurology
2015; 1332.
2. Hitchings AW, Drugs that lower the seizure threshold. Adverse Drug Reaction Bulletin 2016; 1151.
3. Kanner AM, Most antidepressant drugs are safe for patients with epilepsy at therapeutic doses: A review of the
evidence. Epilepsy Behav 2016;282.
4. Landmark CJ, Henning O, Johannessen SI. Proconvulsant effects of antidepressants - What is the current evidence?
Epilepsy Behav 2016;287.
Common causes of delirium and confusional states
Drugs and toxins

Prescription medications (eg, opioids, sedative-hypnotics, antipsychotics, lithium, skeletal muscle relaxers,
polypharmacy)
Nonprescription medications (eg, antihistamines)
Drugs of abuse (eg, ethanol, heroin, hallucinogens, nonmedicinal use of prescription medications)
Withdrawal states (eg, ethanol, benzodiazepines)
Medication side effects (eg, hyperammonemia from valproic acid, confusion from quinolones, serotonin syndrome)
Poisons:
Atypical alcohols (ethylene glycol, methanol)
Inhaled toxins (carbon monoxide, cyanide, hydrogen sulfide)
Plant-derived (eg, Jimson weed, Salvia)
Infections
Sepsis
Systemic infections; fever-related delirium
Metabolic derangements
Electrolyte disturbance (elevated or depressed): sodium, calcium, magnesium, phosphate
Endocrine disturbance (depressed or increased): thyroid, parathyroid, pancreas, pituitary, adrenal
Hypercarbia
Hyperglycemia and hypoglycemia
Hyperosmolar and hypoosmolar states
Hypoxemia
Inborn errors of metabolism: porphyria, Wilson disease, etc
Nutritional: Wernicke encephalopathy, vitamin B12 deficiency, possibly folate and niacin deficiencies
Brain disorders
CNS infections: encephalitis, meningitis, brain or epidural abscess
Epileptic seizures, especially nonconvulsive status epilepticus*
Head injury*
Hypertensive encephalopathy
Psychiatric disorders*
Systemic organ failure

Cardiac failure
Hematologic: thrombocytosis, hypereosinophilia, leukemic blast cell crisis, polycythemia
Liver failure: acute, chronic
Pulmonary disease, including hypercarbia and hypoxemia
Renal failure: acute, chronic
Physical disorders
Burns
Electrocution
Hyperthermia
Hypothermia
Trauma: with systemic inflammatory response syndrome, head injury*, fat embolism
CNS: central nervous system.

* Disorders that, while not truly systemic or "medical," may produce the clinical picture of delirium or confusional state in all
other aspects.

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7/6/2020 Seizures and epilepsy in older adults: Etiology, clinical presentation, and diagnosis - UpToDate

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Seizures and epilepsy in older adults: Etiology, clinical

Seizures are episodes of transient neurologic change due to hypersynchronous, hyperexcited

CAUSES AND RISK FACTORS

Acute symptomatic seizures (provoked or triggered seizures) — Acute symptomatic seizures

● Metabolic encephalopathy — Metabolic disturbances cause approximately 6 to 30 percent of

Features that suggest seizure in older adults:

● Confusion, behavioral change, or unresponsiveness

● Lack of aura or preceding warning

A more detailed discussion of the manifestations, diagnosis, and treatment of SE is presented

other paroxysmal conditions, including syncope due to cardiac arrhythmias or orthostatic

INFORMATION FOR PATIENTS

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

SUMMARY AND RECOMMENDATIONS

Use of UpToDate is subject to the Subscription and License Agreement.

Topic 2223 Version 33.0

Acute symptomatic seizures; rates by age, Rochester, Minnesota,

Graphic 54496 Version 2.0

Causes of acute symptomatic seizures and epilepsy in older adults

Relative proportion (%)

Acute symptomatic seizures (provoked seizures)

Acute hemorrhagic and ischemic stroke 50%

Metabolic encephalopathy 6 to 30%

Drugs and alcohol 10%

Others (eg, recent head trauma, active intracranial infections) 5 to 20%

Epilepsy (unprovoked seizures)

Cerebrovascular disease (eg, prior stroke, vascular malformation) 30 to 50%

Graphic 76342 Version 7.0

Medications associated with seizures

Analgesics Opioids (eg, meperidine, tramadol)

Anticancer drugs ¶ Busulfan

Antimicrobials Δ Carbapenems (eg, imipenem)

Pulmonary drugs Aminophylline

Sympathomimetics Anorexiants (eg, diethylpropion, phentermine, nonprescription diet aids)

Graphic 106961 Version 8.0

Common causes of delirium and confusional states

Drugs and toxins

Nonprescription medications (eg, antihistamines)

Withdrawal states (eg, ethanol, benzodiazepines)

Systemic infections; fever-related delirium

Endocrine disturbance (depressed or increased): thyroid, parathyroid, pancreas, pituitary, adrenal

Hyperglycemia and hypoglycemia

Hyperosmolar and hypoosmolar states

Inborn errors of metabolism: porphyria, Wilson disease, etc

Epileptic seizures, especially nonconvulsive status epilepticus*

Systemic organ failure

Hematologic: thrombocytosis, hypereosinophilia, leukemic blast cell crisis, polycythemia

Liver failure: acute, chronic

Pulmonary disease, including hypercarbia and hypoxemia

Renal failure: acute, chronic

CNS: central nervous system.

Graphic 59893 Version 5.0

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