Evaluation of the first seizure in adults
Steven C Schachter, MD
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INTRODUCTION — A seizure is a sudden change in behavior that is the consequence of brain dysfunction. Epileptic seizures result from electrical hypersynchronization of neuronal networks in the cerebral cortex. Epilepsy is characterized by recurrent epileptic seizures due to a genetically determined or acquired brain disorder [1]. Approximately 0.5 to 1 percent of the population has epilepsy. Nonepileptic seizures (NES), are sudden changes in behavior that resemble epileptic seizures but are not associated with the typical neurophysiological changes that characterize epileptic seizures [2-4].
NES are subdivided into two major types: physiological and psychogenic. Physiological NES are caused by a sudden alteration of neuronal function due to metabolic derangement or hypoxemia. Causes of physiological NES include cardiac arrhythmias, syncope, and severe hypoglycemia. Psychogenic NES are thought to result from stressful psychological conflicts or major emotional trauma and are more challenging to recognize and diagnose than physiological NES, but rarely occur de novo in patients without a significant psychiatric history.
The pharmacological treatment of epileptic seizures is directed at restoring neuronal function to normal, while the treatment of NES is specific to the disorder that triggered the seizure. Thus, the primary goal in evaluating a patient's first seizure is to resolve whether the seizure resulted from a treatable systemic process or intrinsic dysfunction of the central nervous system and, if the latter, the nature of the underlying brain pathology. This evaluation will determine the likelihood that a patient will have additional seizures and assist in the decision whether to begin anticonvulsant therapy [5,6].
The differential diagnosis and clinical features of seizures and the diagnostic evaluation of the first seizure in adults are reviewed here. While convulsive and nonconvulsive status epilepticus may be the initial presentation of epilepsy, they are not specifically discussed because clinical recognition is straightforward [7]. (See "Status epilepticus in adults"). The treatment of chronic epilepsy is reviewed separately. (See "Overview of the management of epilepsy in adults").
ETIOLOGY
Epileptic seizures — Less than one-half of epilepsy cases have an identifiable cause. It is presumed that epilepsy in most, if not all, of these other patients is genetically determined. In the remainder of patients in whom an etiology can be determined, the causes of epileptic seizures include congenital brain malformations, inborn errors of metabolism, high fevers, head trauma, brain tumors, stroke, intracranial infection, cerebral degeneration, withdrawal states, and iatrogenic drug reactions [8]. (See "Post-traumatic seizures and epilepsy"). In the elderly, vascular, degenerative, and neoplastic etiologies are more common than in younger adults and children [9]. A higher proportion of epilepsy in children is due to congenital brain malformations than in other age groups. (See "Epilepsy syndromes in children").
These general principles were illustrated in a population-based cohort study of 1195 patients with newly diagnosed or suspected epileptic seizures, 564 of whom had definite epileptic seizures [10]. The proportions of males and females were similar, 25 percent were under the age of 15, and 24 percent were 60 years or older. The majority (62 percent) of epileptic seizures were idiopathic. In the remainder, the cause was vascular disease in 15 percent and tumor in 6 percent. The proportion with an identifiable cause was much higher in older patients; 49 percent were due to vascular disease and 11 percent to tumor.
Onset of seizures in late life may be a risk factor for stroke, possibly because covert cerebrovascular disease can often be the mechanism of new onset epilepsy in older patients. This point is illustrated by a study of 4,709 people with idiopathic epilepsy beginning at or after the age of 60 years, but no history of stroke [11]. Subjects were matched to the same number of controls with no history of epilepsy or stroke. In longitudinal follow-up, the epilepsy group had a significantly higher risk of stroke at any time point compared with controls (hazard ratio 2.9, 95% CI 2.45-3.41). This finding suggests that new onset of seizures in older patients should prompt evaluation and treatment for stroke risk factors.
Head injury accounts for a relatively small proportion of epilepsy overall. The risk to an individual who suffers head trauma varies widely from minimal risk in people who have a concussive head injury in which the loss of consciousness or amnesia is less than 30 minutes, to at least a 12-fold increased risk over 10 years in people who suffer trauma-induced prolonged amnesia, subdural hematoma, or brain contusion [12]. Antiepileptic drugs prevent seizures in the first week after head injury, but do not prevent the development of epilepsy [13]. (See "Post-traumatic seizures and epilepsy").
Physiological nonepileptic seizures — A number of medical disorders are known to cause physiological NES (show table 1). Hyperthyroidism can cause seizures and can exacerbate seizures in patients with epilepsy. Hypoglycemic seizures are most common in diabetic patients who take excessive amounts of insulin or oral hypoglycemics; islet cell tumors are much less common, but seizures may be the initial presentation. Prodromal symptoms of hypoglycemic seizures include diaphoresis, tachycardia, anxiety, and confusion. Nonketotic hyperglycemia most commonly occurs in elderly diabetics and can cause focal motor seizures. Precipitous falls in serum sodium concentrations can trigger generalized tonic-clonic seizures (see "Generalized seizures" below), usually in association with a prodrome of confusion and depressed level of consciousness. These convulsions are associated with a high risk of mortality and must be treated urgently. (See "Manifestations of hyponatremia and hypernatremia"). Hypocalcemia is a rare cause of seizures and most often occurs in neonates. In adults, hypocalcemia may occur after thyroid or parathyroid surgery or in association with renal failure, hypoparathyroidism, or pancreatitis. Typical prodromic symptoms and signs are mental status changes and tetany. Magnesium levels below 0.8 mEq/L may result in irritability, agitation, confusion, myoclonus, tetany, and convulsions, and may be accompanied by hypocalcemia. (See "Clinical manifestations of hypocalcemia"). Renal failure and uremia are often associated with seizures, particularly myoclonic seizures (see "Generalized seizures" below). Generalized tonic-clonic seizures occur in approximately 10 percent of patients with chronic renal failure, usually late in the course. Seizures may also occur in patients undergoing dialysis as part of the dialysis disequilibrium syndrome; associated symptoms are headache, nausea, muscle cramps, irritability, confusion, and depressed level of consciousness. (See "Seizures in patients undergoing hemodialysis"). Disorders of porphyrin metabolism may cause seizures. Acute intermittent porphyria (AIP) is due to a partial deficiency of porphobilinogen deaminase, which results in excess delta-aminolevulinic acid and porphobilinogen in the urine. Seizures occur in approximately 15 percent of AIP attacks and are usually generalized tonic-clonic seizures, although partial seizures may occur (see "Auras (simple partial seizures)" below and see "Complex partial seizures" below). Other symptoms of AIP include abdominal pain and behavioral changes. (See "Acute intermittent porphyria"). Cerebral anoxia as a complication of cardiac or respiratory arrest, carbon monoxide poisoning, drowning, or anesthetic complication can cause myoclonic and generalized tonic-clonic seizures. Cerebral anoxia due to syncope can result in very brief tonic and/or clonic movements without a prolonged postictal state, which is why syncope frequently results in an evaluation for seizures. (See "Evaluation of the patient with syncope", section on Distinction of syncope from seizures).
DIFFERENTIAL DIAGNOSIS — Several conditions must be differentiated from epileptic seizures.
Sleep disorders — Some patients have seizures that predominantly or exclusively occur during sleep; these must be distinguished from parasomnias and sleep-related movement disorders [14].
REM behavior disorder is a parasomnia that consists of sudden arousals from REM sleep immediately followed by complicated, often aggressive, behaviors for which the patient is amnestic. Diagnosis is clarified by overnight sleep testing (polysomnography). (See "Clinical features and diagnosis of dementia with Lewy bodies", section on REM sleep disorder). Other parasomnias that can be confused with epilepsy are sleepwalking or sleep terrors. (See "Classification of sleep disorders", section on Parasomnias.)
Specific features of the events (eg, duration, clustering, age at onset, timing, stereotypy, recall, vocalizations) can help distinguish nocturnal seizures from sleep disorders (show table 2), but individually these are neither specific nor sensitive [15]. A questionnaire that includes these features and scores their presence or absence according to likelihood of epileptic seizures has been developed and validated in a sample of 62 patients with paroxysmal nocturnal events [15]. In this study, this Frontal Lobe Epilepsy and Parasomnias (FLEP) Scale (show table 2) had a sensitivity of 100 percent and a specificity of 90 percent when compared with video-electroencephalogram monitoring, but additional validation studies are required. Recording episodes on video-EEG monitoring remains necessary when the diagnosis is unclear [16].
Transient ischemic attack — Transient ischemic attack — Transient ischemic attacks (TIAs) may last seconds to minutes. They are generally characterized by "negative" symptoms and signs (such as weakness or visual loss) rather than the "positive" symptoms and signs (eg, jerking movements, stiffening, or visual illusions or hallucinations) that generally accompany seizures. However, positive symptoms can occur in a TIA. As an example, so-called "limb-shaking TIAs" are a well described phenomenon associated with preocclusive disease in the contralateral internal carotid or middle cerebral artery.
Also, the postictal state after seizure may include lateralizing "negative" symptoms such as weakness, a phenomenon referred to as Todd's paralysis. If ictal symptoms were unobserved, the chief complaint may be one of primarily negative symptoms. Rarely, the seizure ictus itself is manifest as weakness, even paralysis of a limb or by speech arrest [17]. (See "Differential diagnosis of brain ischemia").
Transient global amnesia — Transient global amnesia (TGA) is a syndrome characterized by the acute onset of severe anterograde amnesia accompanied by retrograde amnesia, without other cognitive or focal neurologic impairment. The amnesia resolves within 24 hours. Most patients are middle aged or older adults. Episodes are usually not recurrent, but some patients have infrequent attacks that recur over several years.
The etiology of TGA is uncertain [18]. Most TGA episodes are probably related to vasoconstriction or migraine, but some may be caused by transient ischemia or complex partial seizures. TGA can be associated with small focal abnormalities on diffusion-weighted MRI [19-23], but the significance of these remains unclear.
Migraine — Migraine auras such as visual illusions and basilar migraine symptoms, including altered consciousness, can mimic complex partial seizures. Furthermore, the headache that follows complex partial and generalized tonic-clonic seizures is migrainous in quality and duration. (See "Complex partial seizures" below and see "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults").
CLINICAL FEATURES — The diagnostic evaluation of a first seizure begins with the history. An accurate description of the seizure may be difficult to obtain from the patient and witnesses; it is usually necessary to ask pointed questions about the circumstances leading up to the seizure, the ictal behaviors, and the postictal state. It is also worthwhile to inquire specifically whether the patient has had prior seizures, including febrile seizures in infancy, or other episodes that were not evaluated by a physician or that were labeled as something other than seizures.
Seizure precipitants or triggers — A key element in the history is whether a particular environmental or physiological precipitant or trigger immediately preceded the seizure. Some patients with epilepsy tend to have seizures under particular conditions, and their first seizure may provide a clue to their so-called seizure trigger. Triggers include (but are not limited to) strong emotions, intense exercise, loud music, and flashing lights. (See "Photic-induced seizures" below). These triggers are often experienced immediately before the seizure.
Other physiological conditions such as fever, the menstrual period, lack of sleep, and stress can also precipitate seizures, probably by lowering seizure threshold rather than directly causing a seizure. As a result, the temporal relationship to the presenting seizure is often less clear. Triggers may also precipitate physiological nonepileptic seizures (NES); a cough, for example, can bring on a syncopal seizure.
However, the majority of patients with epilepsy have no identifiable or consistent trigger to their seizures. In addition, triggers are the sole cause of epileptic seizures in only a very small percentage of patients.
**Photic-induced seizures — Photosensitivity has received considerable attention as a seizure trigger. The light stimulation may come from a natural or artificial source, in particular television shows and video games. The most famous incident occurred in relation to a Pokémon cartoon aired in 1997 in Japan in which 685 children (from an estimated 7 million viewers) sought medical attention for neurologic symptoms; most (about 80 percent) were felt to be seizures [24,25]. Three-fourths of the children had not experienced seizures previously.
A review of photic-induced seizures made the following epidemiologic observations [25]: Children are more susceptible to photic-induced seizures and photoparoxysmal electroencephalogram (EEG) changes than adults; and photosensitivity may decline in individuals with photic-induced seizures. A tendency for photic-induced seizures may be inherited. Photoconvulsive seizures are usually generalized, but they may be partial. Individuals may be sensitive to certain light triggers but not others. Women appear more susceptible, but males dominate in reports of video game-induced seizures, probably because they play them more.
The stimuli that are most likely to induce seizures appear to be identifiable. Guidelines for restricting use of specific signals on television broadcasts exist in Japan and Great Britain, and a working group has developed draft consensus guidelines in the United States [26].
While photosensitivity suggests seizures, it may not be specific to epilepsy. In one case report, a child with presumed photosensitive epilepsy was found to have visually-induced syncope with bradycardia followed by cardiac arrest, documented by EKG and normal EEG activity during the event [27].
Seizure symptoms and signs — The next step in the history is to identify the symptoms and signs (observed behaviors) that occurred throughout the seizure.
**Auras (simple partial seizures) — The symptoms that a patient experiences at the beginning of the seizure are referred to as the warning or aura. Auras are seizures that affect enough of the brain to cause symptoms, but not enough to interfere with consciousness. In the seizure classification system established by the International League Against Epilepsy, auras are called simple partial seizures (show table 3); "simple" means that consciousness is not impaired and "partial" means that only part of the cortex is disrupted by the seizure [28].
The symptoms of simple partial seizures vary from one patient to another and depend entirely on where the seizure originates in the brain, that is, the part of the cortex that is disrupted at the onset of the seizure. A seizure that begins in the occipital cortex may result in flashing lights, while a seizure that affects the motor cortex will result in rhythmic jerking movements of the face, arm, or leg on the side of the body opposite to the involved cortex (Jacksonian seizure).
Auras that commonly occur in patients with epilepsy are shown in the table (show table 4). These symptoms can also be experienced under other circumstances, but do not typically precede physiological NES. Thus, the occurrence of an aura supports the diagnosis of an epileptic seizure.
When a patient's first seizure was not preceded by a simple partial seizure, it is more difficult to distinguish whether it was an epileptic seizure or a NES. Many epileptic patients do not have a warning when their seizures start. Instead, they abruptly lose consciousness, which they may describe as blacking out, when the part of the cortex that controls memory is disrupted by the seizure. However, this process is not specific for epileptic seizures and therefore does not allow differentiation from NES.
**Complex partial seizures — The classification system for epileptic seizures includes several seizure types that are characterized by an abrupt loss of consciousness: complex partial seizures ("complex" means that consciousness and awareness of the surroundings are lost), absence seizures, and generalized tonic-clonic seizures (also known as convulsions; "tonic" refers to muscle stiffening and "clonic" refers to muscle jerking) (show table 3).
Complex partial seizures (previously called temporal lobe seizures or psychomotor seizures) are the most common type of seizure in epileptic adults. During the seizure patients appear to be awake but are not in contact with others in their environment and do not respond normally to instructions or questions. They often seem to stare into space and either remain motionless or engage in repetitive behaviors, called automatisms, such as facial grimacing, gesturing, chewing, lip smacking, snapping fingers, repeating words or phrases, walking, running, or undressing. Patients may become hostile or aggressive if physically restrained during complex partial seizures.
Complex partial seizures typically last less than three minutes and may be immediately preceded by a simple partial seizure. Afterward, the patient enters the postictal phase, often characterized by somnolence, confusion, and headache for up to several hours (show table 5). The patient has no memory of what took place during the seizure other than, perhaps, the aura.
The behaviors that typify complex partial seizures are not specific for epileptic seizures and may be observed in association with NES.
**Generalized seizures — In contrast to partial seizures, generalized seizures originate virtually in all the regions of the cortex. Absence seizures and generalized tonic-clonic seizures are types of generalized seizures. Other subtypes of generalized seizures are clonic, myoclonic, tonic, and atonic seizures. Absence seizures usually occur during childhood and typically last between 5 and 10 seconds. They frequently occur in clusters and may take place dozens or even hundreds of times a day. Absence seizures cause sudden staring with impaired consciousness. If an absence seizure lasts for 10 seconds or more, there may also be eye blinking and lip smacking. Absence seizures are discussed in greater detail separately. (See "Epilepsy syndromes in children", section on Absence seizures). A generalized tonic-clonic seizure (also called grand mal seizure, major motor seizure, or convulsion) is the most dramatic type of seizure (show table 6). It begins with an abrupt loss of consciousness, often in association with a scream or shriek. All of the muscles of the arms and legs as well as the chest and back then become stiff. The patient may begin to appear cyanotic during this tonic phase. After approximately one minute, the muscles begin to jerk and twitch for an additional one to two minutes. During this clonic phase the tongue can be bitten, and frothy and bloody sputum may be seen coming out of the mouth. The postictal phase begins once the twitching movements end. The patient is initially in a deep sleep, breathing deeply, and then gradually wakes up, often complaining of a headache. Clonic seizures cause rhythmical jerking muscle contractions that usually involve the arms, neck, and face. Myoclonic seizures consist of sudden, brief muscle contractions that may occur singly or in clusters and that can affect any group of muscles, although typically the arms are affected. Consciousness is usually not impaired. Tonic seizures cause sudden muscle stiffening, often associated with impaired consciousness and falling to the ground. Atonic seizures (also known as drop seizures or drop attacks) produce the opposite effect of tonic seizures — a sudden loss of control of the muscles, particularly of the legs, that results in collapsing to the ground and possible injuries.
The behaviors that typify absence seizures and generalized tonic-clonic seizures are not specific for epileptic seizures and may be observed in association with NES.
Other aspects of the patient history
**Medication history — There are a number of medications that have been associated with iatrogenic seizures [8,29]. Partial-onset seizures are less likely to be drug-induced than generalized tonic-clonic seizures.
**Past medical history — There are a number of risk factors for epileptic seizures that should be addressed, including head injury, stroke, Alzheimer's disease, history of intracranial infection, and alcohol or drug abuse.
**Family history — A positive family history of seizures is highly suggestive that the patient has epilepsy. In particular, absence seizures and myoclonic seizures may be inherited. Occasionally, a family member does not have seizures but has an abnormal electroencephalogram.
Physical and neurologic examination — The physical examination is generally unrevealing in patients with epileptic seizures, but is important when central nervous system infection or hemorrhage are diagnostic possibilities. The neurologic examination should evaluate for lateralizing abnormalities, such as weakness, hyperreflexia, or a positive Babinski sign, that may point to a contralateral structural brain lesion.
DIAGNOSTIC STUDIES
Laboratory screening — Laboratory evaluations that are appropriate for the evaluation of a first seizure include glucose, calcium, magnesium, hematology studies, renal function tests, and toxicology screens. Tests for porphyria may be considered under appropriate clinical circumstances. Some laboratory abnormalities such as metabolic acidosis and leukocytosis may occur as a result of the seizure; thus, abnormal test results detected immediately after the seizure has occurred should be repeated.
**Prolactin — Serum prolactin assessment has limited utility as a diagnostic test for epileptic seizures [30]. The serum prolactin concentration may rise shortly after generalized tonic-clonic seizures and some partial seizures. Typically, a level is drawn 10 to 20 minutes after the event and compared with a baseline level drawn six hours later. Criteria for abnormality are not well established; many investigators use twice the baseline level.
A systematic review made the following conclusions regarding prolactin as a diagnostic test for epileptic seizures [31]: Pooled sensitivity was higher for generalized tonic-clonic seizures than for partial complex seizures (60 versus 46 percent). An elevated serum prolactin level can be useful in differentiating generalized tonic-clonic and partial complex seizures from psychogenic seizures in adults and older children. The positive predictive value is greater than 93 percent, if the pretest probability is 50 percent or higher. Because of low sensitivity, a normal prolactin level is insufficient to exclude epileptic seizures or support a psychogenic diagnosis. Some studies suggest that prolactin rises after syncope. Prolactin levels cannot be used to differentiate seizure from syncope. Insufficient data preclude conclusions regarding the utility of prolactin levels after simple partial seizures, repetitive seizures, status epilepticus, and in neonates.
Lumbar puncture — A lumbar puncture is essential if the clinical presentation is suggestive of an acute infectious process that involves the central nervous system or the patient has a history of cancer that is known to metastasize to the meninges. In other circumstances the test is not likely to be helpful and may be misleading since a prolonged seizure itself can cause cerebrospinal fluid pleocytosis. Lumbar puncture should only be performed after a space occupying brain lesion has been excluded by appropriate neuroimaging studies.
Electroencephalography — The electroencephalogram (EEG) is an essential study in the diagnostic evaluation of epileptic seizures. If abnormal, the EEG may aid in confirming the diagnosis of epileptic seizures and also indicate whether a patient has generalized or partial seizures. Use of sleep deprivation and provocative measures during the test, such as hyperventilation and intermittent photic stimulation, increase the yield [32,33]. In one study of 85 individuals, sleep deprivation resulted in a higher rate of focal discharges than routine EEG (13 versus 7 percent) [33]. An abnormal EEG that confirms the clinical diagnosis of epilepsy substantially increases the likelihood that the patient will experience a second seizure over the next two years [34].
However, a normal EEG does not rule out epilepsy, and many EEG abnormalities are nonspecific. As an example, both generalized and focal slowing are common in patients with migraine headaches. Diffuse slowing may also occur with a wide variety of encephalopathies or in association with some medications, especially at high dosages. Epileptiform abnormalities are usually more informative than less specific changes.
Neuroimaging — A neuroimaging study should be done to exclude a structural brain abnormality if the patient's first seizure was clearly not a physiological NES. Brain magnetic resonance imaging (MRI) is preferred over computed tomography (CT) to identify specific lesions such as cortical dysplasias, infarcts, or tumors. Nevertheless, a brain CT scan is suitable to exclude a mass lesion, hemorrhage, or large stroke under emergency situations or if an MRI is unavailable or contraindicated (eg, in patients with pacemakers, non-compatible aneurysm clips, or severe claustrophobia).
The value of neuroimaging in the evaluation of adults with a first seizure was demonstrated in a retrospective review of CTs in 148 patients studied within 30 days of the seizure [35]. The cause of seizure was established in 71 patients (48 percent); a structural lesion was identified by CT in 55, 16 had metabolic seizures, and the remainder were idiopathic. CT findings agreed with the results of neurologic and EEG examination in 82 percent of cases. However, structural lesions (including three tumors) were found by CT in an additional 14 patients (15 percent) with nonfocal findings.
Structural abnormalities on brain MRI or CT usually suggest a symptomatic, focal-onset epilepsy syndrome, but these findings should not be interpreted in isolation. In two case series, 22 to 24 percent of patients with idiopathic generalized epilepsy had structural neuroimaging abnormalities [35,36]. Most of these findings, however, were nonspecific (eg, white matter and basal ganglia abnormalities, cortical atrophy).
In young to middle-aged adults, common MRI findings are mesial temporal sclerosis, sequelae of head injury, congenital anomalies, brain tumors, and vascular lesions. In the elderly, MRIs often reveal strokes, cerebral degeneration, or neoplasms. However, up to 50 percent of patients, regardless of age, have normal neuroimaging studies. The utility of brain MRI in children presenting with a seizure is discussed separately. (See "Clinical and laboratory diagnosis of seizures in infants and children", section on Neuroimaging).
WHEN TO START ANTIEPILEPTIC THERAPY — The decision to initiate therapy with antiepileptic drugs is often difficult. This topic is discussed separately. (See "Overview of the management of epilepsy in adults", section Antiepileptic drug therapy).
PSYCHOSOCIAL CONSIDERATIONS — Newly diagnosed patients with epilepsy may suffer a number of losses, including loss of independence, employment, insurance, ability to drive, and self-esteem. As the treatment plan is formulated, these psychosocial issues should be explored with patients so that appropriate referrals for additional help and counseling can be initiated.
Driving — States vary widely in driver licensing requirements for patients with epilepsy [37]. This topic is discussed in more detail elsewhere. (See "Driving restrictions for patients with seizures and epilepsy").
HOSPITALIZATION — Hospitalization may be required for patients who have a first seizure associated with a prolonged postictal state or incomplete recovery. Other indications for hospitalization include status epilepticus, the presence of a systemic illness that may require treatment, a history of head trauma, or questions regarding compliance.
REFERRAL — Many primary care physicians do not feel comfortable with the initial evaluation and management of patients with seizures and refer them to neurologists. All patients in whom the diagnosis is in question should be referred to a neurologist. Other indications for referral include focal findings on the neurologic examination or EEG, or a history suggestive of a focal seizure. Some experts believe that all patients with suspected seizures should be referred to a specialist [38].
CONCLUSIONS — The primary objectives of the medical evaluation of the first seizure are to establish whether it resulted from a correctable systemic process, and if not, whether the patient is at risk for developing further unprovoked seizures. A careful history, physical and neurologic examinations, and laboratory evaluation are usually helpful in achieving these objectives and determining the appropriate therapeutic approach. Referral to a specialist is indicated for most persons suspected of having a seizure, especially if focal features are present on examination or testing.
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