Possible seizures in stroke patients
The differential diagnosis of transient neurologic dysfunction is broad, and the elderly population that is at highest risk of stroke and transient ischemic attack (TIA) is also at risk of many conditions that can mimic seizures.3
may not be in this population. Causes include92:
Upright posture at onset and a typical warning of lightheadedness, nausea, warmth, and fading vision and hearing are common but not universal, and stroke patients may have difficulty reporting these sensations. Cardiac arrhythmias, some potentially fatal, may lead to sudden loss of , even in the supine position. In these patients, palpitations may be noted if onset is not sudden or at other times.
A few myoclonic jerks commonly accompany syncope, and tonic stiffening (as well as more complex movements) may also occur, especially if the head is kept upright. The pathophysiology of such is release of brain stem activity from cortical influence rather than an electrocortical seizure.
In addition, syncope can rarely occur as a vertebrobasilar TIA, especially when flow through one or both carotids is severely compromised.
The episodic headache and other symptoms of sometimes are preceded by an , 5 to 60 minutes of cortical or brain stem dysfunction.93 Migraine auras are distinguished from seizures by their more gradual, often visual, warning and longer duration. Associated symptoms include nausea or vomiting, photophobia, and phonophobia. Headache usually, but not always, follows. “Migraine equivalents” without headache are more common in the elderly and are occasional causes of TIA-like symptoms or of actual TIAs.15 Loss of consciousness is rare but may occur with so-called basilar migraine.
It must be recognized that migraine and epilepsy can coexist, that headaches often follow epileptic seizures, and that a migraine attack can, rarely, precipitate a seizure.93
Migraine is discussed more fully in Migraine and epilepsy.
Transient ischemic attacks (TIAs)
TIAs themselves can be confused with seizures, although they have characteristic symptoms and (if prolonged enough to persist to the time of evaluation) signs consistent with known vascular territories. They typically evolve over minutes and last minutes to hours.
Jackson was first to point out that seizures generally manifest “positive” symptoms, such as stiffening or shaking in the motor system or hallucinations in the special modalities, whereas ischemic symptoms are usually “negative” (e.g., weakness, sensory loss). Exceptions to this rule include ischemic paresthesias, rare motor seizures,94 and “limb-shaking” TIAs.95
"Limb-shaking TIAs" are rare manifestations of severe carotid stenosis. They can be distinguished from motor seizures mainly by
On the other hand, rare seizure types, such as amaurosis (total or hemianopic, not monocular) or aphasic ,96 require to be distinguished from TIAs.
Patients with cerebral amyloid angiopathy have been noted to have transient events for which the underlying pathophysiology has not been established; no evidence of microscopic bleeding, transient ischemia, or epilepsy has been discovered. The duration is more similar to that of TIAs than of the other potential etiologies.22
Movement disorders can usually be readily distinguished from seizures because they are typically long-lasting and associated with preserved consciousness. Although usually bilateral, they may be unilateral after infarction, particularly infarction of the basal ganglia, thalamus, or subthalamus.
In patients with depressed mental status, toxic or metabolic processes may at times produce movement disorders, such as extrapyramidal reactions to neuroleptics or multifocal myoclonus in uremia. Although the multifocality is not typical of seizures, and the movements are not time-locked to discharges on EEG, such discharges are often present and imply “cortical irritability” that may later be manifest as clear-cut seizures.
Asterixis, an abrupt, repetitive loss of during maintenance of certain postures, often occurs in patients with depressed mental status due to hepatic or other encephalopathies. After cerebral or brain stem stroke, it can occur unilaterally, contralateral to the lesion. Its positional nature usually distinguishes it from motor seizures, although rare cases of epileptic asterixis have been reported.
Antiepileptic drugs, especially at toxic levels, also can produce involuntary movements, such as dystonia with phenytoin or tremor with valproate.
Sleep disorders may result in microsleeps or more prolonged sleep attacks due to any cause of hypersomnolence. The most common cause is disrupted sleep from obstructive sleep apnea, a condition which (like stroke) is common among patients with hypertension, atherosclerosis, and obesity. Furthermore, many thrombotic strokes, in particular, occur during sleep and are characterized by patients’ awakening with a new .
The second most common medical reason for sleep deprivation leading to sleep attacks is the movement disorder termed periodic limb movements in sleep.97 These movements usually involve one or both lower limbs, with dorsiflexion of the ankle and flexion of the knee and hip, and are sustained for 1 to 2 seconds and repeated approximately every one-half minute. This condition is associated with restless legs , a need to walk around or otherwise move the legs, often in response to a crawling sensation felt when lying in bed or otherwise at rest.
is a more dramatic but much less common cause of hypersomnolence, usually associated with symptoms of hypnagogic or hypnopompic hallucinations, sleep paralysis, and especially cataplexy.97 Onset is rare after early adulthood, although cases related to brain stem , demyelination, and, rarely, infarction have been reported. Although microsleeps may occur without warning, more prolonged sleep attacks are usually preceded by a subjective feeling of sleepiness. Unlike in complex partial seizures, the eyes are usually closed, and the patient may be awakened with stimulation.
Parasomnias can be difficult to distinguish from nocturnal seizures. The classic parasomnias of slow-wave sleep, sleepwalking, and night terrors are conditions of childhood, although the former sometimes persists into adulthood. They are not associated with stroke. In the population at risk for stroke, nocturnal wandering is more likely to occur after a , and patients usually return to normal awareness rapidly, if stimulated.
A parasomnia of rapid eye movement (REM) sleep, REM behavior disorder, by contrast, typically begins late in life and may be associated with extrapyramidal syndromes such as Parkinson’s disease. Cases in patients with stroke may be coincidental, given the typical ages for both disorders. These attacks consist of partial arousals from REM with a loss of the usual muscle atonia, resulting in “acting out” of dreams, often in a violent manner that may reflect defensive behavior prompted by a frightening dream.97 The timing of the spells later in the night, when REM periods are longer, can be a useful clue. Polysomnography with additional EEG electrodes may be necessary to distinguish this disorder from nocturnal partial seizures.
Sleep disorders are discussed more fully in Sleep disorders and epilepsy.
Altered behavior due to toxic-metabolic disturbances usually lasts much longer than changes due to seizures. The possibility of certain causes of encephalopathy (e.g., hyperglycemia, hypoglycemia, hyponatremia, hypocalcemia, hypomagnesemia) precipitating acute symptomatic seizures can further confuse the picture.
The EEG, although typically showing diffuse , can, at times, display multifocal sharp waves or the triphasic wave pattern, which may be difficult to distinguish from the generalized sharp-slow complexes of nonconvulsive generalized SE.
These disturbances are discussed more fully in Metabolic disorders and seizures.
Psychogenic nonepileptic seizures
Distinguishing psychogenic nonepileptic seizures (NESs), also known as pseudoseizures or psychogenic seizures, from epileptic seizures is a major undertaking of epilepsy monitoring units. Evidence suggests that this phenomenon is most common in young adults, especially women, but there are few data on the frequency and manifestations in elderly patients, and it may be underdiagnosed.
Patients with a previous psychiatric history are likely to be at higher risk, as may be those with depression or other psychiatric complications of stroke, but data are unavailable.
In general, compared to epileptic seizures, psychogenic NESs display less stereotypy, longer duration, a more waxing and waning nature, and nonphysiologic progression.98 Eyes tend much more often to be closed during unresponsive periods. Environmental precipitants are more likely and injuries less likely, although there are many exceptions. Unlike epileptic seizures, NES do not arise from sleep, although they may arise from “pseudosleep,” and may be required.
Increased intracranial pressure
Transient increases in intracranial pressure can result in temporary alteration in awareness or, less often, focal neurologic dysfunction. The classic situations are a posterior fossa mass or intermittent obstruction of ventricular flow by a third ventricular tumor, but acute can occur in patients after subarachnoid hemorrhage99 or after ischemic or hemorrhagic stroke in the cerebellum.
Patients with cerebral edema as a result of hemispheric infarction are likely to show catastrophic focal deficits followed by progressive obtundation.
Headache is common in all of these scenarios, if the patient is alert and articulate enough to report it.
Adapted from: Bromfield, EB, and Henderson GV. Seizures and cerebrovascular disease. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;269–289.
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