Seizures and Status Epilepticus
Elaine Rabin
CLINICAL CHALLENGE
Seizures are the clinical manifestations of abnormal, increased, synchronized electrical activity in the brain. An estimated 10% of the population experience at least one seizure in their lifetime, and of those, 3% develop epilepsy, which is a condition of recurrent unprovoked seizures.
Seizures may occur as a result of an acute underlying condition or insult—termed a provoked or acute symptomatic seizure. A seizure that occurs in the absence of such a condition is termed unprovoked. One of the goals in emergency practice is to identify those causative conditions that may lead to further harm and address them if possible (Table 17.1). Seizures can also be due to sequelae of a prior intracranial insult such as stroke, trauma, or anoxia, in which case it is referred to as a remote symptomatic seizure.
Ictus is often used to refer to the period during which a seizure occurs. Currently used classification systems are summarized in Table 17.2 and Figure 17.1.1 Seizures can be either convulsive or nonconvulsive; in the latter case, motor activity is not a key component of the presentation. Seizures may also be classified as focal or generalized. Focal or partial seizures occur when the abnormal electrical activity is limited to one area of the brain. These may manifest as motor, sensory, autonomic, or behavioral depending on their location. Signs and symptoms can be nonspecific, ranging from jerking of one limb or muscle group, to a strange taste or smell, or a sense of déjà vu or hyper spirituality. In some cases, focal electrical activity can spread to other areas and to the contralateral hemisphere. The symptoms progress in kind until the whole brain and whole body are involved, resulting in a generalized seizure.
Generalized seizures involve both hemispheres of the brain and may also be convulsive (commonly tonic-clonic) or nonconvulsive. Some seizures may be preceded by an aura, which is itself actually a focal seizure that may help identify the location of an epileptic focus, for example déjà vu points to the temporal lobe. Status epilepticus (SE) is a subset of generalized seizures characterized by a single prolonged ictal period or multiple recurrent seizures without return to baseline. This is a true neurologic emergency that is associated with high rates of neurologic injury as well as nonneurologic morbidity and mortality. SE may be convulsive status epilepticus (CSE) or nonconvulsive status epilepticus (NCSE) at the outset. CSE that is undertreated or untreated may progress to NCSE. Historically, SE was defined as a seizure lasting longer than 30 minutes, but current guidelines recommend beginning treatment after only 5 minutes of convulsive activity.2
TABLE 17.1 Differential Diagnosis of Provoked Seizures | ||
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TABLE 17.2 Seizure Classification | ||||||||
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 Figure 17.1: International League Against Epilepsy (ILAE) epilepsy classification. EEG, electroencephalogram. Based on Fisher RS, Cross JH, D’Souza CD, et al. Epilepsia2017 instruction manual for 2017 ILEA seizure definitions.pdf. Epilepsia. 2017;58(4):531-542. |
TABLE 17.3 Differential Diagnosis of Patient of Altered Mental Status After a Seizure | ||
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Most seizures last under 5 minutes, although they may be followed by a period of confusion or altered mental status termed the postictal period. This is a normal, benign condition that rarely lasts > 1 hour. A prolonged episode of altered mental status following a seizure should prompt investigation of other causes (Table 17.3).
The key to seizure diagnosis and management in the emergency department (ED) is gathering as much supporting history as possible and performing a careful neurologic examination to uncover evidence that a seizure took place or is still ongoing. The diagnosis of seizures may not be straightforward; 17% of patients referred to specialty epilepsy centers for “refractory seizures” do not actually have a seizure disorder and may be exposed to unnecessary medications or driving restrictions.3 More recently, 10% of patients enrolled in a large multicenter study of SE were determined to have been having psychogenic convulsions.4 Compounding diagnostic error is the failure to consider and or recognize nonconvulsive seizures in patients with altered behavior or are in coma: In one report, 12% of comatose patients in intensive care units (ICUs) were found to be in NCSE.5
PATHOPHYSIOLOGY
Brain function requires communication among organized networks of neurons. This communication is driven by electrical activity created by changes in sodium and potassium gradients across neuronal membranes. Neurotransmitters such as glutamate cause excitatory states in nearby neurons, leading to increased electrical activity. Other neurotransmitters, such as gamma aminobutyric acid (GABA) are inhibitory, suppressing electrical activity.
Under normal circumstances, equilibrium between excitation and inhibition keeps electrical activity at normal levels; seizures are initiated when excitatory activity is abnormally high and organized in rhythmic pulses. In generalized seizures, this activity is thought to start in the cortex, and then recruits subcortical structures, with the rhythmic activity possibly coordinated by the thalamus. Perpetuation of the excitatory activity occurs when the high levels of potassium exiting the cells interfere with the usual inhibitory mechanisms of the neuronal networks. Abnormal electrical activity usually terminates spontaneously, possibly due to depletion of excitatory substances or reflex activation of inhibitory substances. GABA-mediated inhibition among certain neuronal networks may contribute to both initiation and cessation of seizures.6,7
Genetic abnormalities that regulate neurotransmitters, and control the sodium-potassium pump, have been associated with epilepsy. Brain tissue may become “epileptogenic” after an insult, for example, trauma, stroke, or infection; a process termed epileptogenesis. Identification and removal of epileptogenic foci is the basis of some epilepsy surgeries. In addition, a seizure may be incited by a change in the neuronal homeostatic environment because of a wide variety of pathologies including drug toxicity, withdrawal, infection, and electrolyte abnormalities.
Pathophysiologic consequences of a seizure may include a period of transient apnea and hypoxia. There may be autonomic dysfunction, with fluctuations in blood pressure. Serum lactate and serum glucose levels may increase, and there is often an increase in the white blood cell (WBC) count (but with no increase in bands). Body temperature is frequently elevated after a generalized convulsion. Acidosis due to elevated lactate occurs within 60 seconds of a convulsive event, but
should normalize within 1 hour of ictus. A transient cerebrospinal fluid (CSF) pleocytosis of up to 20 WBCs/mm3 has been reported to occur in 2% to 23% of patients with seizures.
should normalize within 1 hour of ictus. A transient cerebrospinal fluid (CSF) pleocytosis of up to 20 WBCs/mm3 has been reported to occur in 2% to 23% of patients with seizures.
After 30 minutes of seizure activity, many of the body’s homeostatic regulating mechanisms fail. Cerebral blood flow autoregulation may be lost and, combined with alterations in blood pressure, cerebral perfusion may be compromised; combined, these factors contribute to the high mortality seen in CSE. The addition of increased neuronal metabolism to this picture may result in neuronal damage. Even if systemic factors such as acidosis and hypoxia are controlled, prolonged SE results in neuronal damage secondary to the release of neurotoxic excitatory amino acids and influx of calcium into cells.
PREHOSPITAL CONSIDERATIONS
Seizures are a common reason patients activate emergency medical services (EMS). Although most patients evaluated by prehospital providers will have stopped seizing by the time of first contact, a small but important minority will have persistent convulsions and should generally be presumed to be in SE. Multiple trials have demonstrated that treatment of seizures by prehospital providers is safe, efficacious, and results in improved patient outcome.6 EMS protocols for managing prehospital SE vary by region, but must take into account the feasibility of drug storage and challenges to parenteral administration in the prehospital environment. Management begins with a blood glucose determination, whereas intramuscular (IM) midazolam or intravenous (IV) lorazepam are recommended first-line abortive therapies. Rectal diazepam is not first line because absorption and onset are variable. Other commonly performed interventions include provision of supplemental oxygen and continuous monitoring of SpO2 and end-tidal CO2.
For patients who have had a witnessed seizure but are not actively seizing, no specific therapy is indicated. Routine supportive care should be provided, and the patient should be placed in a position of comfort to facilitate maintenance of a patent airway and to prevent hypoxia. Routine IV placement may be considered, but is not mandatory. Precautions should be taken to prevent patient and provider injury in the case of recurrent seizure.
APPROACH/THE FOCUSED EXAMINATION
Approach to the patient who has had a seizure requires a careful history to characterize circumstances surrounding the event and to identify potential precipitants. Patients who are actively seizing or postictal may present challenges to obtaining a history, and the focus is on stabilization and treatment. All patients with a seizure history are at risk for another event, and at all times need to be in a safe environment, that is, guard rails up on the stretcher and never allowed to ambulate or go into the bathroom alone. Figure 17.2 outlines a possible approach to the patient with suspected seizure.
History
In the case of a patient who is actively seizing, assessment and stabilization must occur simultaneously. EMS should be queried as to the circumstances under which the patient was found, and specific questions should be asked regarding evidence of trauma or paraphernalia suggestive of alcohol or drug use, as well as any medications found. Family or friends, if available, should be asked about preceding events, especially trauma, or any recent complaints such as headache, fever, confusion, or other systemic signs. They should be asked to supply known past medical and surgical history with particular attention to any history of seizure disorder or current use of antiepileptic drugs (AEDs). Additional sources of collateral history should be sought, including seeking out the patient’s primary or specialist physicians and additional bystanders not present in the ED.
If the patient is not actively convulsing, has returned to baseline, and has a known history of seizures, the provider should determine whether the event was a typical seizure for them and whether it fits within the usual pattern of recurrence. An atypical episode should not automatically be presumed to have been a seizure, and other etiologies must be considered. History of specific triggers for a seizure should be investigated including sleep deprivation, medication nonadherence,
new medications, or trauma. A history of drug or alcohol use, or sudden abstinence thereof, and any signs or symptoms of a systemic insult such as infection or ischemia should be sought.
new medications, or trauma. A history of drug or alcohol use, or sudden abstinence thereof, and any signs or symptoms of a systemic insult such as infection or ischemia should be sought.
 Figure 17.2: Approach to the patient with a suspected seizure. AED, antiepileptic drug; PNES, psychogenic nonepileptic seizure. |
For the patient who has no history of prior seizure, the emergency clinician’s first goal must be to determine whether this is, in fact, the diagnosis. Typically, the challenge is to differentiate between seizure and other causes of transient loss of consciousness such as syncope, and psychogenic events. The provider should enquire into the circumstances surrounding the event such as the presence of an aura, palpitations, light-headedness, blurred vision, or chest pain. Obtaining a history from witnesses can often provide the key to the diagnosis. Witnesses are better at recalling some aspects of the event such as muscle tone or eye deviation. Medical and social history should be obtained, with specific attention to risk factors for seizure such as prior intracranial injury, lesion, or surgery; current medication use that might lower the seizure threshold such as bupropion; and recent drug and alcohol use. Risk factors for syncope such as prior cardiac disease, personal or family history of dysrhythmias, and family history of sudden cardiac death should also be sought. Specific historic factors that may assist in distinguishing between seizure and syncope are discussed in the Evidence section.
Many patients who present with an apparent first-time seizure will, on careful questioning, have had prior seizures that were either unrecognized or for which medical attention was not sought. Open-ended questioning about prior “spells” or episodes may prompt recall. Enquiring about signs of nocturnal seizures such as waking to find a bitten tongue, enuresis, or other injuries, and evidence of nonconvulsive seizures such as spells of unresponsiveness, myoclonic jerking, or sensory experiences suggestive of an aura, may also stimulate recollection of prior events. Identification of these prior episodes allows for a better determination of the risk of seizure recurrence and can inform decisions regarding therapy.
The Focused Examination
The examination should begin with an accurate and complete set of vital signs. Tachycardia, hypertension, and transient hypoxia may be encountered during active convulsions, but generally recover rapidly following their termination. Etiologies of persistent vital sign abnormalities should be investigated. If the patient is actively convulsing at the time of examination, specific note should be made of the body parts involved and the type of movements. Note should be made of abnormalities in tone such as head turning and gaze deviation. If the onset of the episode is witnessed, attention should be paid to the order in which differing body parts become involved.
In the patient who has had a seizure but has returned to baseline, a more thorough examination can be obtained with the patient’s cooperation. A general physical examination should be undertaken to evaluate for complications of seizures such as aspiration or trauma; tongue injury may be noted. Posterior shoulder dislocations are rare, but possible.
The neurologic examination should begin with assessment of the patient’s level of consciousness, attention, and orientation. Comparison to baseline should be made. Altered behavior including subtle changes only appreciated by the family may be the result of an NCSE. A full examination of the cranial nerves and extremity strength and sensation will reveal focal motor or sensory deficits, if present. Signs of upper motor neuron lesions such as hyperreflexia and abnormal Babinski reflex should be sought; these are often present in the postictal period and resolve quickly. Gait testing should be performed, and assessment of balance and coordination made. Specific testing for cerebellar function such as finger-to-nose, heel-to-shin, and rapid alternating movements should be performed as well. Visual fields should be assessed. Funduscopic examination may reveal evidence of papilledema if there is increased intracranial pressure from a mass lesion or edema.
Diagnostic Testing
Laboratory Studies
For patients presenting after a first-time seizure who are alert, oriented, and have no clinical findings, appropriate laboratory studies include a serum glucose level, electrolytes, and a pregnancy test in women of child-bearing age. A drug-of-abuse screen should be considered. Other tests are of very low yield in this group of patients. Those who are on dialysis, malnourished, taking diuretics, or who have underlying significant medical disorders usually require more extensive testing including a complete blood count (CBC), blood urea nitrogen (BUN), creatinine, calcium, phosphate, and magnesium, as well as a urinalysis.
Rhabdomyolysis is a rare consequence of a seizure and is diagnosed if the urine tests positive for blood in the absence of red blood cells on the microscopic examination. Serum creatine phosphokinase (CPK) levels are not useful in differentiating seizures from other causes of loss of consciousness.
Patients with a known seizure disorder who have a “typical” event but who are asymptomatic, alert, and oriented in the ED do not routinely require serum chemistries aside from an AED level, if available. Those with other underlying disease such as diabetes that could result in a metabolic derangement may warrant more extensive evaluation. It is important to consider potential precipitants such as infections or new medications that might have contributed to the event.
Patients in CSE, and patients who are not actively convulsing but are persistently altered, require comprehensive diagnostic testing, which may include serum glucose, electrolytes, urea nitrogen, creatinine, magnesium, phosphate, calcium, CBC, pregnancy test in women of child-bearing age, AED levels, liver function tests, and a drug-of-abuse screen. An arterial blood gas (ABG) analysis obtained in a convulsing patient will show an anion gap metabolic acidosis that is usually secondary to lactic acidosis. The anion gap acidosis should resolve within 1 hour of the seizure ending; persistence after 1 hour suggests the presence of one of the other causes of an anion gap acidosis.
Lumbar Puncture
In the immunocompetent patient, Lumbar puncture should strongly be considered in the immune-competent patient with SE of unknown etiology, a prolonged post-ictal period or persistently-altered mental status, or with signs or symptoms of meningitis such as fever, headache, or neck stiffness. Prospective data do not support routine LP in other immunocompetent patients
with a first-time seizure.8 Patients with human immunodeficiency virus (HIV) and new-onset seizure have historically demonstrated a high prevalence of central nervous system (CNS) infection— in particular, cryptococcal meningitis—with some manifesting no additional signs of infection. LP in the absence of other signs of infection may be considered in this population.
with a first-time seizure.8 Patients with human immunodeficiency virus (HIV) and new-onset seizure have historically demonstrated a high prevalence of central nervous system (CNS) infection— in particular, cryptococcal meningitis—with some manifesting no additional signs of infection. LP in the absence of other signs of infection may be considered in this population.
Neuroimaging
Up to 40% of patients with a first-time seizure have an abnormal head computed tomography (CT).9 An estimated 20% of patients with a first-time seizure and an abnormal CT have a normal neurologic examination. A head CT should be performed in the ED whenever a patient with seizure has a suspected acute intracranial process, a history of acute head trauma, malignancy, immunocompromised state, fever, persistent headache, anticoagulation, or a new focal neurologic examination10: In those cases where the patient has a normal neurologic examination, has returned to a normal baseline, and has no concerning comorbidities, a neuroimaging study can be deferred if the patient has access to timely follow-up. In these cases, a magnetic resonance imaging (MRI) would be the preferred imaging.
Electroencephalography
An electroencephalogram (EEG) in the ED may be useful for those patients with persistently altered mental status in whom subtle CSE or NCSE is suspected (see subsequent text). An EEG may also be useful when a patient’s motor activity has been suppressed by either paralysis or barbiturate coma and there is a need to assess ongoing seizure activity.
MANAGEMENT
Management priorities will vary depending on whether the patient is suspected to be in SE or has returned to baseline. The presence or absence of a history of prior seizures and risk factors such as immune compromise and drug or alcohol use will also influence decision-making.
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