Key Concepts
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Lifetime seizure incidence reaches up to 10% in the US population and depends upon multiple factors including age, history of epilepsy, structural brain or neurodegenerative disease, genetic predisposition, acuity and severity of metabolic derangements.
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Seizures are the result of an imbalance in the excitation and inhibitory neuronal synapses in the cerebral cortex or limbic system.
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Epilepsy is a condition associated with a lower seizure threshold and an inherently higher risk of recurrent seizures in a lifetime.
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Acute symptomatic seizures occur at, or in close temporal relationship with, a distinct provoked event, and may occur with any toxic or metabolic, structural, ischemic, inflammatory, or infectious insult.
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The initial evaluation of seizure includes the identification of seizure characteristics, duration, and etiology of possible inciting events. Recognizing the occurrence of similar events in the past is key in determining triggers and distinguishing the management priorities between patients with epilepsy or with acute symptomatic seizures.
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The majority of seizures will cease spontaneously within 5 minutes; however, when physiologic seizure termination pathways are overwhelmed resulting in status epilepticus, characterized by the persistent and exponential refractory response to abortive seizure therapies. The magnitude of treatment refractoriness is time dependent; therefore a prompt stepwise escalation of therapies aiming at seizure termination is warranted.
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Prompt identification and, whenever possible, reversal of seizure triggers are priorities. In particular, assessing for and correcting hypoglycemia should occur as early as possible.
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Initial nonpharmacologic interventions include ensuring physical safety of patients with seizures to prevent traumatic injuries and aspiration. During convulsions, focusing on lateral decubitus positioning and suctioning of oral cavity are important to prevent aspiration; the use of intraoral devices may lead to trauma without additional benefit.
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Pharmacologic interventions center on the timely and dose-appropriate administration of parenteral benzodiazepines, which are first-line therapy (i.e., lorazepam intravenous [IV] up to 0.1 mg/kg in divided doses, or midazolam IV/intramuscular [IM]/intranasal [IN] 5 to 10 mg).
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In pregnant patients, eclampsia should be considered the underlying etiology of de novo seizures after 20 weeks of gestational age and up to 8 weeks postpartum. Clinical evaluation should focus on evaluating for associated symptoms (e.g., headache, visual abnormalities and confusion), as well as focal neurologic deficits. Neuroimaging should be considered if neurologic deficits persist, prolonged loss of consciousness or encephalopathy. IV magnesium 4 to 6 g is first-line therapy in the pregnant patient experiencing new-onset seizures.
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During the postictal state, key priorities in management include ensuring airway patency with optimal positioning in those with alteration of consciousness, evaluation for nonconvulsive seizures and acute brain injuries or inciting factors that warrant further definitive treatment.
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Nonconvulsive status epilepticus can only be diagnosed with electroencephalography (EEG) monitoring and should be considered in any patient with prolonged, unexplained altered mental status. Patients at higher risk include those with poorly controlled epilepsy, acute brain injury, sepsis, and intoxication.
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A patient with new-onset seizures with a normal neurologic examination who returns to baseline mental status and does not have comorbid disease does not require diagnostic testing beyond, serum glucose and sodium levels, a pregnancy test (in women), and a noncontrast head computed tomography (CT); a toxicologic screen is considered in select patients.
Foundations
Epidemiology
Seizures represent distressful and physically traumatic events that have the potential for lifelong social consequences and challenges to quality of life. The risk for an unprovoked or acute symptomatic seizure is approximately 8% to 10%; however, only 3%, or 1 in 26 Americans, will ultimately be diagnosed with epilepsy at some point in their lifetime. Up to one in four seizures evaluated in the emergency department (ED) represent first-time seizures.
The incidence and risk of seizures are influenced by many factors, including age; history and type of epilepsy, structural brain disease, neurodegenerative diseases; presence of renal or hepatic disease; metabolic derangements; and exposure to triggers. Patients presenting to the ED with seizures have a bimodal distribution in terms of age, with the highest incidence among infants and individuals older than 75 years old. This is explained by the high prevalence of febrile seizures in infants and structural brain damage in elders.
Up to 45% of adults presenting with a first unprovoked seizure will experience another within 2 years, most occurring in the first year. The risk is higher with known brain lesions, neuroimaging or electroencephalography (EEG) abnormalities, or nocturnal seizures ; the latter are associated with epilepsy syndromes. Up to 50% of patients with epilepsy have recurrent seizures despite initiation of therapy. Human immunodeficiency virus (HIV)-positive patients have an increased risk of seizures, and two-thirds of those who present with new-onset seizures experience recurrence.
Etiologies underlying seizure events are diverse; importantly, the etiology plays a role in the risk for seizure recurrence and the progression to status epilepticus. For a comprehensive list of etiologies of seizures and status epilepticus according to type of insult and neurologic process refer to Chapter 88 (Box 88.1), and for pediatric considerations, refer to Chapter 169.
Pathophysiology
Seizures are the clinical manifestation of increased excitation or impaired inhibition of neurons that result in the abnormal firing and synchronization of neighboring neurons. This recruitment is complex and follows neural networks that may be deep and cross the midline of the brain. Marked alteration of consciousness ensues when seizures propagate diffusely to the bilateral cortex or diencephalon or to deeper structures involving the reticular activating system in the brainstem. Increased inhibition, effect of medications, and neuronal exhaustion mediate postictal states, which reflect transient neurologic deficits that may include alteration of consciousness, language, sensory, motor deficits (Todd paralysis), and/or abnormal emotional states. The duration of a postictal state ranges from minutes to a few hours, with the majority lasting less than 1 hour. Longer postictal states are associated with generalized convulsive seizures, duration of the seizure, and older age.
Seizures are typically self-limited. A combination of mechanisms ultimately leads to their termination including reflex inhibition, neuronal exhaustion, or alteration of the local balance of neurotransmitters between the excitatory acetylcholine and glutamate with the inhibitory γ-aminobutyric acid (GABA). However, when these mechanisms fail, progression to status epilepticus ensues, leading to a cascade of changes within the brain: a decrease in GABA A receptor subunits as these migrate inside cells and a parallel increase in the excitatory N -methyl- d -aspartic acid (NMDA) receptors occur; these events are time sensitive and underscore the pathophysiology of treatment refractoriness and benzodiazepine resistance (GABA A mediated). The International League Against Epilepsy put forth operational time definitions of status epilepticus according to different seizure types that reflect: (1) likelihood of continued seizure activity due to failure of abortive mechanisms and (2) likelihood of secondary long-term sequelae ( Table 14.1 ). This time distinction originated from the notion that different seizure types may have different consequences and distinct pathophysiologic mechanisms. The understanding that seizure types may have different presentations and associated sequelae lays the foundation for individualized therapeutic algorithms according to the type of status epilepticus. For example, the clinical threshold for escalating antiseizure therapies should be lower in seizure patterns associated with high morbidity: much lower in convulsive generalized status epilepticus than in focal nonconvulsive status epilepticus.
TABLE 14.1
Classification of Status Epilepticus According to Time Domains.
| Type of Status Epilepticus | Duration of Time (Further Seizure Activity Likely) | Duration of Time (Long-term Sequelae Likely) |
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| Tonic-clonic | 5 min | 30 min |
| Focal with impaired awareness | 10 min | >60 min |
| Absence | 10–15 min | Unknown |
Diagnostic Approach
Pivotal Findings
History and physical findings assist in differentiating seizure from other acute medical conditions. They help identify triggers, which will heavily influence decisions on the need for secondary prophylaxis and guide the selection of antiseizure drug according to the specific seizure type.
Clinical manifestations of seizures vary widely depending upon the region of the brain affected; they may range from subtle cognitive and/or mental status changes to coma, apneic spells, sensory and motor manifestations, and dysautonomia. Seizures can be classified according to their semiology into types, duration, refractoriness to treatment, and etiology. The classification of seizure types has therapeutic implications and facilitate communication between providers.
A revised classification of seizure types by the International League Against Epilepsy provides an operational framework that relies on the clinical manifestations of seizures ( Fig. 14.1 ). The first classification branch underscores the importance of the seizure onset: focal which include those with secondary generalization (i.e., focal to bilateral tonic-clonic), generalized, or unknown; the latter is reserved for cases when the onset is not witnessed. The terms “complex seizures” or “focal dyscognitive seizures” traditionally used to reflect impairment of consciousness have been replaced by the term “focal seizures with impaired awareness.” Note that patients may be immobile during a focal aware seizure, so long as they retain awareness of self and the environment. Further specification of motor onset or nonmotor onset centers on the descriptive assessment of the first prominent sign or symptom in the seizure. Automatisms usually include oral or finger stereotypic movements such as lip smacking, yawning, repetitive vocalizations, or picking at sheets or clothing; these automatisms can be complex and often arise from a frontal seizure focus. Seizures impairing distinct cognitive domains such as language (e.g., aphasia) or abnormal thoughts and perceptions (e.g., dèjá vu, hallucinations, illusions, or perceptual distortions)—often referred to as “auras”―are now termed “cognitive seizures.” These cognitive seizures commonly arise from the orbital frontal region manifesting as olfactory hallucinations, or from the temporal lobe, which classically manifests as epigastric rising sensation, auditory hallucinations, and increased fear or impending doom.
Classification of Seizure Types (Extended Version).
The time criteria for status epilepticus are based on duration of seizures and depend on seizure type (see Table 14.1 ). Other classifications of status epilepticus, which include several different categorizations according to semiology, etiology, age, and EEG correlates, are reported in Chapter 88 (Table 88.1 and Box 88.2).
History Taking and Physical Exam
The ramifications of a seizure diagnosis have important direct consequences for patients, which include restriction of certain activities (e.g., driving, swimming unsupervised, and operation of heavy machinery) and therapeutic implications. The first diagnostic task in the ED is to determine whether the patient has actually experienced an epileptic event and if similar events have occurred in the past. Obtaining a detailed description of the sequence of events leading to the seizure-like activity and the semiology of the episode is paramount.
In general, ictal events have five properties:
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Abrupt onset. Identify immediate preceding events and whether auras, which are focal seizures, were present (e.g., perception alterations: visual, smell, tactile, auditory, gastric heave, impending doom, anxiety, and irrational fear). Check for immediate triggers, such as sleep deprivation, missed medications, new medications, alcohol or substance use, infections, or other inciting events.
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Brief duration. Seizures rarely last longer than 60 to 120 seconds (except in status epilepticus), although bystanders may overestimate their duration.
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Alteration of consciousness. Generalized seizures are characterized by loss of consciousness, whereas focal seizures may be accompanied by an alteration in consciousness.
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Purposeless, stereotypic, and nonsuppressible. Automatisms and undirected tonic-clonic movements are common in ictal events; if witnessed, a gentle attempt to suppress clonic activity (i.e., brief careful restraint of a convulsing limb in an attempt to extinguish movement) helps differentiate tremors and other nonepileptic convulsive events from seizures. Tonic-clonic movements are often rhythmic and if involving other body parts, synchronous. Dystonic posturing in tonic seizures is also common; they are usually asymmetric when bilateral and distinct from extensor or flexor posturing associated with neurologic emergencies.
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A postictal state of variable duration, which correlates with the duration of the preceding seizure. The transient neurologic deficit may be sensory, motor, visual, cognitive, emotional, or related to consciousness. In general, the postictal state occurs with all seizure types, except absence. Postictal periods following seizures are typically transient (length-dependent according to seizure duration); the acute encephalopathic state may include lethargy, confusion, and impaired recollection of events.
Seizures may also be accompanied by transient cardinal systemic signs of sympathetic stimulation, such as tachycardia, hypertension, or tachypnea. Autonomic discharges and bulbar muscle involvement may result in urinary or fecal incontinence, vomiting (with aspiration risk), lateral tongue biting, and airway compromise in the peri-ictal period. All of these signs are helpful discriminators in the differential evaluation of seizure-like episodes, although the presence or absence of these findings neither confirms nor excludes seizure occurrence. Evidence of physical injury should be thoroughly investigated because these may be occult in the altered patient.
Once a seizure is suspected, determining the underlying trigger is imperative. This should be followed by an inquiry regarding prior seizure history. New-onset seizures or a change in seizure patterns in those with known epilepsy may be the primary manifestation of serious underlying diseases and should prompt a thorough evaluation. If there is a documented history of seizures, ED evaluation may be limited to identifying precipitants and obtaining an antiseizure drug level, when applicable/available as the most common etiology is poor compliance or adjustment in regimen leading to subtherapeutic levels. The history should focus on clinical factors known to decrease the seizure threshold, such as recent illness or trauma, drug or alcohol use, sleep deprivation, potential adverse drug-drug interactions with antiseizure drugs, medication noncompliance, recent change in dosing regimens, or change in ictal pattern or characteristics. In women of reproductive age with epilepsy, catamenial exacerbation of seizures is extremely common. Furthermore, pregnancy can affect clearance of antiseizure drugs, leading to subtherapeutic levels. In pregnant women with and without a history of epilepsy, eclampsia must be considered.
After the seizure activity has ceased, resting vital signs are evaluated. Fever and underlying infection can cause seizures, although there may be a low-grade temperature elevation immediately after a generalized convulsive seizure. Tachypnea, tachycardia, fever, or an abnormal blood pressure that persists beyond the immediate postictal period may indicate toxic exposure, hypoxia, infection, or an acute central nervous system lesion. Pertinent physical findings may include nuchal rigidity, stigmata of substance abuse, lymphadenopathy suggestive of HIV disease or malignancy, dysmorphic features, or skin lesions. The examination should also focus on potential adverse sequelae of convulsive seizures, such as head trauma, oral and tongue injury, posterior shoulder dislocation, or back pain. (See Table 88.3.)
Finally, a complete neurologic examination is performed. A persistent focal deficit after a seizure (e.g., Todd paralysis) often indicates the focal origin of the event but also may suggest underlying structural injury, such as ischemic or hemorrhagic strokes. Approximately half of patients with convulsive generalized status epilepticus have subsequent nonconvulsive seizures when placed on continuous EEG monitoring, and more than 15% will be in nonconvulsive status epilepticus. The patient with persistent altered consciousness should be carefully examined for signs of ongoing subtle convulsive or nonconvulsive seizures, such as abnormal eye movements and facial myoclonus. The higher-risk population for ongoing nonconvulsive status epilepticus include those with acute or remote brain injury (including prior violations of the intracranial cavity with craniotomies), toxic exposure, sepsis, or renal or liver failure.
Ancillary Testing
Laboratory Testing
Women of reproductive age should be tested for pregnancy.
The serum glucose level should be determined in every seizing or postictal patient because hypoglycemia is a common metabolic cause of provoked seizures. Ictal activity of any semiology can occur at a plasma glucose level less than 45 mg/dL, although some patients may have a seizure at higher levels. Prolonged seizures can also cause hypoglycemia. Seizures that do not cease after correction of low blood glucose deserve further evaluation and treatment for alternative causes.
Patients with prolonged generalized convulsions (e.g., >2 minutes) should have creatine kinase and lactic acid tested to assess for rhabdomyolysis and acute metabolic acidosis, respectively; prolonged convulsions or tonic posturing without increased lactic acid are less likely to be epileptic in nature. Presence of a lactic acidosis that resolves on subsequent ED testing supports a seizure diagnosis. In epilepsy patients with unexplained increase in seizure frequency and a stable antiseizure regimen, infections such as common viral illness should be considered as precipitating events. Patients with a dramatic increase in the severity of seizures or those with an abnormal neurologic examination should undergo a more thorough laboratory assessment.
In patients with advanced age or comorbidities or who are ill in appearance, the diagnostic evaluation should be expanded to include a basic or comprehensive metabolic panel to assess metabolic derangements that may trigger seizures. Sodium, calcium, and magnesium are all associated with cell membrane stabilization; most commonly, hyponatremia and hypocalcemia are triggers of seizures. Because magnesium helps stabilize the neuronal cell membrane, hypomagnesemia is a common finding in adult and children presenting with seizures in several settings. Keep in mind that total body magnesium levels may not be reflected by serum levels. Hypomagnesemia must be considered and may warrant empiric treatment in cases of malnutrition or chronic alcoholism, for example. Patients with lower serum bicarbonate on basic metabolic panel may benefit from blood gas analysis and lactic acid testing. Anion gap metabolic acidosis is commonly secondary to lactic acidosis in convulsive seizures; acidosis is typically transient with lactic acid levels declining within the first hour after convulsions cease. Patients with prolonged nonepileptic convulsions often have normal lactic acid levels and white blood cell count. Persistent lactic acidosis or other anion gap acidosis suggests an underlying process, including sepsis, ketosis (alcoholic or diabetic), or poisoning (methanol, iron, isoniazid, ethylene glycol, salicylates, carbon monoxide, or cyanide). Liver enzyme (i.e., AST and ALT) abnormalities may indicate the presence of chronic disease or underlying hepatic-mediated metabolic derangements. Patients with known or suspected history of liver disease or those that take valproic acid should have ammonia tested given the heightened risk for hyperammonemia, which further increases the risk for seizures and will impact therapeutic decisions on antiseizure regimen. Routine testing of prolactin is not indicated given its relative lack of sensitivity and specificity for seizures.
Proposed cutoff laboratory values for acute symptomatic seizures and those values that can be interpreted as thresholds of metabolic derangements for lowering the seizure threshold can be found in Chapter 88 (Box 88.3).
Patients with or without history of epilepsy who are on antiseizure medications for any indication (i.e., seizure prophylaxis, mood stabilization, anxiety, and/or adjunctive psychiatric treatment) should have levels obtained, as available. The turnaround time for antiseizure drug level results varies widely; phenytoin, phenobarbital, valproic acid, and carbamazepine are the most commonly available levels with the fastest turnaround times and well-established therapeutic ranges. Lamotrigine, topiramate, and oxcarbazepine have therapeutic ranges established, but prolonged turnaround times reaching several days makes their assessment impractical in the emergent setting. Levetiracetam level has a broad therapeutic range with unclear ideal targets and variable turnaround times based on institution but may still prove instrumental in confirming compliance, particularly when patients have repeated visits to the ED with similar presentations who report not missing doses. Free levels of antiseizure drugs that are highly protein bound (e.g., valproic acid and phenytoin) are more accurate, and widely available online calculators provide a correction of total levels according to albumin.
Patients who are on medications that have epileptogenic potential (e.g., lithium) should have the levels of these drugs tested, whenever available. Directed toxicology screens with blood or urine samples should be performed if substance abuse (particularly cocaine, amphetamines, and other sympathomimetic agents) or overdose of aspirin or acetaminophen is suspected. However, many drugs of abuse (e.g., synthetic marijuana) and medications (e.g., baclofen, bupropion) that may be implicated in the etiology of seizures do not have a widely available testing method, and so, negative routine toxicology screens should be interpreted with caution. Furthermore, positive urine toxicologic screen for sympathomimetic agents are not confirmatory of the etiology of seizures in all cases because these substances can be detected in specimens for several days to weeks after the exposure. However, the screen may suggest a possible etiology and may help with future medical and psychiatric disposition.
Reactive leukocytosis of varying magnitude is very common after convulsive seizures; there are no thresholds of elevated white blood cell count that may definitively suggest a concomitant infectious process. Febrile patients should be evaluated for the source of the fever, including consideration of lumbar puncture and respiratory viral testing (i.e., influenza, respiratory syncytial virus). Lumbar puncture should also be considered in immunocompromised patients and in those presenting with acute headache concerning for subarachnoid hemorrhage, meningismus, or persistent altered mental status. Pleocytosis in cerebrospinal fluid may indicate infectious or autoimmune etiologies.
Imaging Studies
Neuroimaging is recommended by the American Academy of Neurology in adults presenting with new-onset seizures; it can be performed in the ED or at a follow-up in those who are back to a normal neurologic baseline and do not have headache. Most patients with a history of epilepsy, particularly in those who return to baseline, do not require neuroimaging. Box 14.1 summarizes characteristics of patients presenting with seizures that should prompt consideration for neuroimaging.
BOX 14.1
Characteristics Prompting Consideration of Neuroimaging in a Patient With Seizures
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Age >40 years
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Coma
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Immunocompromised state
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Clot disorder (hypercoagulability or hypocoagulability)
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History of intracranial hemorrhage
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History of malignancy
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Severe, thunderclap headache
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Status epilepticus, convulsive and nonconvulsive, of unclear etiology
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Stigmata of neurocutaneous syndromes
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Suspected trauma
Headache is occasionally a postictal symptom. There are no specific characteristics pertaining to the quality of postictal headaches. Severe headache, thunderclap nature (reaching maximum severity from onset within seconds), associated neurologic deficits, altered mental status, meningismus, and/or fever should prompt additional evaluation with computed tomography (CT) of head. If there is clinical suspicion for meningoencephalitis or subarachnoid hemorrhage, after a nondiagnostic CT, lumbar puncture must be considered as part of the diagnostic management. Patients with a history of malignancy, immunosuppression, use of systemic anticoagulation, or history of prior intracranial hemorrhage; who are older than 40 years; or in whom trauma is suspected should have consideration for CT in the ED.
CT perfusion, a contrast-enhanced modality with arterial phase and postsignal processing of imaging, can be particularly helpful in the evaluation of transient neurologic deficits consistent with Todd paralysis; in these cases, acute ischemic stroke is high in the differential and can be reliably detected by this modality. However, there are no specific CT perfusion findings in seizure patients because their perfusion status is dependent on the temporal relationship of seizure and time of imaging acquisition. If magnetic resonance imaging (MRI) is readily available, it can be used instead of CT in most patients as long as the patient is stable to lay flat for a prolonged period: It has increased sensitivity for subtle structural lesions and adds to the diagnostic yield in patients with recurrent seizures and in those with focal abnormal EEG. When MRI is obtained in the work-up of seizures, the addition of gadolinium, T2 thin coronal views through hippocampus and limbic structures increases its diagnostic yield. Reversible cortical restricted diffusion is the typical signature of prolonged seizures on MRI (see Chapter 88 , Fig. 88.1). For pediatric considerations, refer to Chapter 169); in brief, emergent neuroimaging in children presenting with seizures is indicated in the setting of an abnormal neurologic exam or medical or surgical comorbidities and in those younger than 3 years with focal or prolonged seizures.
Electroencephalography
EEG is useful to diagnose nonconvulsive status epilepticus, monitor seizure activity, guide third-line therapies after intubation and neuromuscular blockade, and help differentiate seizures from other nonepileptic presentations. ED-based EEG may assist with the prompt diagnosis of epilepsy in patients with new-onset seizures and decision making on the initiation of secondary seizure prophylaxis; however, studies demonstrating its cost-effectiveness are lacking. New devices with limited montage or assembly that can be performed at the point of care in select cases may be of value and expedite EEG in the emergent setting but are not routinely recommended.
Cardiac Monitoring
Patients with a history of cardiac disease, with preceding or ongoing cardiac symptoms, and who continue to seize may benefit from cardiac monitoring. The same is true of patients suspected of overdose. An electrocardiogram (ECG) is also an early screen for drug toxicity. Tricyclic cardiotoxicity may manifest as a QRS complex lasting more than 0.1 second or a rightward shift of the terminal 40 ms of the frontal plane QRS complex (a prominent R wave in lead aV R ). The ECG can also identify a prolonged QT, a delta wave, Brugada pattern, or heart block, which might contribute further clues to the seizure etiology. Electrocardiographic changes are common in the peri-ictal period and range from sinus tachycardia to more concerning features such as ST segment depression and T wave inversion. Prolongation of intervals on ECG is common in the peri-ictal period, which may challenge differentiating seizures from a primary cardiac related etiology of syncope.
Differential diagnoses
The differential diagnoses to consider when evaluating for seizure are listed in Box 14.2 . In all of these conditions, clarification of associated signs and symptoms (e.g., loss of sphincter control, postictal state, tongue biting, inability to suppress movements), exam (e.g., nystagmus, delayed pupillary response, hyperreflexia, abnormal plantar reflex), and the circumstances of the event (i.e., when and where the event occurred, the precipitating events, positioning, type of movements) are instrumental in discerning whether the event is epileptic or not in nature. In addition, several of these conditions may overlap with seizures because they are associated with seizure triggers, or even represent precipitating events themselves. Transient cerebral ischemia (focal or global) can be associated with nonepileptic convulsive symptoms such as convulsive syncope or limb-shaking transient ischemic attacks. A variety of movement disorders, including those that are transient and associated with toxins, can lead to tonic, myoclonic, or clonic symptoms that may be hard to differentiate from seizures. Migraine with an aura can be confused with nonconvulsive seizures given the positive visual phenomenon. However, migraine has a gradual or protracted temporal evolution prior to developing a peak of symptoms over several minutes followed by gradual resolution; these are key distinctive features from occipital seizures, in which such evolution is much faster in the order of seconds to a few minutes. Furthermore, these patients will almost always have a history of migraine, often with similar presentation.
BOX 14.2
Differential Diagnoses for Seizures
The following are diagnoses with presentations that can be difficult to differentiate from seizure activity.
