A seizure is an episode of abnormal neurologic function caused by inappropriate electrical discharge of brain neurons. Neuronal electrical discharge, in its most simple form, can be thought of as the homeostasis of glutaminergic (excitatory) and γ-aminobutyric acid (inhibitory) activity. The seizure is the clinical attack experienced by the patient in the setting of inappropriate excitatory activity. Some patients with “epileptic” electroencephalographic (EEG) discharges may not experience any overt clinical symptoms. Some seizure-like episodes may be due to causes other than abnormal brain electrical activity, but such attacks are not true seizures.

Epilepsy is a clinical condition in which an individual is subject to recurrent seizures. It implies a fixed, more excitatory condition of the brain with a lower seizure threshold. The term epileptic does not refer to an individual with recurrent seizures caused by reversible conditions such as alcohol withdrawal, toxins, hypoglycemia, or other metabolic derangements.

Primary, or idiopathic, seizures are those in which no evident cause can be identified. Secondary, or symptomatic, seizures are a consequence of an identifiable neurologic condition, such as a mass lesion, previous head injury, or stroke. Electrical stimulation of the brain, convulsant potentiating drugs, profound metabolic disturbances, or a sharp blow to the head all may cause reactive seizures in otherwise normal individuals. Reactive seizures are generally self-limited, and a reactive seizure is not considered to be a seizure disorder or epilepsy.

There are further definitions of seizures based on clinical factors: a provoked seizure has an acute precipitating event within 7 days of the insult; an unprovoked seizure has no acute precipitating factor or may result from a very remote incident; status epilepticus is seizure activity for ≥5 minutes or two or more seizures without regaining consciousness between seizures¹; and refractory status epilepticus is persistent seizure activity despite the IV administration of adequate amounts of two antiepileptic agents.

SEIZURE CLASSIFICATION

The International League Against Epilepsy recommends dividing seizures into two major groups: generalized seizures and partial seizures (Table 171-1). When there are inadequate data to categorize the seizure, the seizure is considered unclassified.

GENERALIZED SEIZURES

Generalized seizures are thought to be caused by a nearly simultaneous activation of the entire cerebral cortex, perhaps caused by an electrical discharge originating deep in the brain and spreading outward. The attacks begin with abrupt loss of consciousness. Loss of consciousness may be the only clinical manifestation of the seizure (as in absence attacks), or there may be a variety of motor manifestations (e.g., tonic posturing, clonic jerking of the body and extremities).

Generalized tonic-clonic seizures (grand mal) are the most familiar and dramatic of the generalized seizures. In a typical attack, the patient suddenly becomes rigid (tonic phase), trunk and extremities are extended, and the patient falls to the ground. As the tonic phase subsides, there is increasing coarse trembling that evolves into a symmetric, rhythmic (clonic) jerking of the trunk and extremities. Patients are often apneic during this period and may be cyanotic. They often urinate and may vomit. As the attack ends, the patient is left flaccid and unconscious, often with deep, rapid breathing. Typical attacks last from 60 to 90 seconds; bystanders generally overestimate the duration of the seizure. Consciousness returns gradually, and postictal confusion, myalgias, and fatigue may persist for several hours or more.

Absence seizures (petit mal) are very brief, generally lasting only a few seconds. Patients suddenly develop altered consciousness but no change in postural tone. They appear confused, detached, or withdrawn, and current activity ceases. They may stare or have twitching of the eyelids. They may not respond to voice or to other stimulation and may exhibit involuntary movements or lose continence. The attack ceases abruptly, and the patients typically resume previous activity without postictal symptoms. Patients and witnesses may be unaware that anything has happened. Classic absence seizures occur in school-age children and are often attributed by parents or teachers to daydreaming or inattention. The attacks can occur as frequently as 100 or more times daily and may result in poor school performance. They usually resolve as the child matures. Similar attacks in adults are more likely to be minor complex partial seizures and should not be termed absence. The distinction is important because the causes and treatment of the two seizures are different.

PARTIAL (FOCAL) SEIZURES

Partial seizures are due to electrical discharges beginning in a localized region of the cerebral cortex. The discharge may remain localized or may spread to involve nearby cortical regions or the entire cortex. Focal seizures are more likely to be secondary to a localized structural lesion of the brain.

In simple partial focal seizures, the seizure remains localized, and consciousness and mentation are not affected. It is possible to deduce the likely location of the initial cortical discharge from the clinical features at the onset of the attack. For example, unilateral tonic or clonic movements limited to one extremity suggest a focus in the motor cortex, whereas visual symptoms suggest an occipital focus. Bizarre olfactory or gustatory hallucinations suggest a focus in the medial temporal lobe. Such sensory phenomena, known as auras, are often the initial symptoms of attacks that then become more widespread, termed secondary generalization.

Complex partial seizures are focal seizures in which consciousness or mentation is affected. They are often caused by a focal discharge originating in the temporal lobe and are sometimes referred to as temporal lobe seizures. Complex partial seizures are commonly misdiagnosed as psychiatric problems because symptoms can be so bizarre. Symptoms may include automatisms, visceral symptoms, hallucinations, memory disturbances, distorted perception, and affective disorders. Common automatisms include lip smacking, fiddling with clothing or buttons, or repeating short phrases. Visceral symptoms often consist of a sensation of “butterflies” rising up from the epigastrium. Hallucinations may be olfactory, gustatory, visual, or auditory. There may be complex distortions of visual perception, time, and memory. Affective symptoms may include intense sensations of fear, paranoia, depression, elation, or ecstasy. Because such seizures result in alterations of thinking and behavior, they were previously referred to as psychomotor seizures, but to avoid any confusion with psychiatric illness, the term complex partial seizure is preferred.

As noted, a focal seizure may spread to involve both hemispheres, mimicking a typical generalized seizure. For the purpose of classification, diagnosis, and treatment, such attacks are still regarded as focal seizures. In some patients, the discharge may spread so rapidly that no focal symptoms are evident, and the correct diagnosis may depend entirely on demonstration of the focal discharge on an EEG recording.

HISTORY

When a patient presents after the event, the first step is to determine whether the episode was truly a seizure. Obtain a careful history of the details of the attack from the patient and any bystanders who witnessed the attack. Inquire about the physical description of the attack, because witnesses may mislabel the activity and mistake nonseizure activity as a seizure.

Important avenues of inquiry include the presence of a preceding aura, abrupt or gradual onset, progression of motor activity, loss of bowel or bladder control, presence of oral injury, and whether the activity was localized or generalized and symmetric or unilateral. Ask about the duration of the episode and determine the presence of postictal confusion or lethargy.

Next, determine the clinical context of the episode. If the patient is a known epileptic, clarify the baseline seizure pattern. If the attack is consistent with the previous seizure pattern, identify precipitating factors of the current seizure. Common precipitating factors include missed doses of antiepileptic medications; recent alterations in medication, including dosage change or conversion from brand name; sleep deprivation; increased strenuous activity; infection; electrolyte disturbances; and alcohol or substance use or withdrawal.

If there is no previous history of seizures, a more detailed inquiry is needed. Symptoms such as unexplained injuries, nocturnal tongue biting, or enuresis suggest previous unwitnessed or unrecognized seizures. Ask about a history of recent or remote head injury. Ask about any previous similar episodes that may be suspect as seizures. Persistent, severe, or sudden headache suggests intracranial pathology. Pregnancy or recent delivery raises the possibility of eclampsia. A history of metabolic or electrolyte abnormalities, hypoxia, systemic illness (especially cancer), coagulopathy or anticoagulation, exposure to industrial or environmental toxins, drug ingestion or withdrawal, and alcohol use may point to predisposing factors (Table 171-2).

PHYSICAL EXAMINATION

Immediately obtain a complete set of vital signs and a point-of-care glucose determination. In the post-seizure setting, focus the initial exam on checking for injuries, especially to the head or spine, as a result of the seizure itself. A posterior shoulder dislocation is an injury that is easy to overlook. Lacerations of the tongue and mouth, dental fracture, and pulmonary aspiration are also frequent sequelae.

Perform a directed, complete neurologic examination and subsequent serial examinations. Follow the patient’s level of consciousness and mentation closely to avoid missing nonconvulsant status epilepticus (see below). A transient focal deficit (usually unilateral) following a simple or complex focal seizure is referred to as Todd’s paralysis and should resolve within 48 hours.

Clinical features that help to distinguish seizures from other, nonseizure attacks include:

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  Abrupt onset and termination. Some focal seizures are preceded by auras that can last 20 to 30 seconds, but most attacks begin abruptly. Attacks reported to develop over several minutes or longer should be regarded with suspicion. Most seizures last only 1 or 2 minutes, unless the patient is in status epilepticus.

  
  
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  Lack of recall. Except for simple partial seizures, patients usually cannot recall the details of an attack.

  
  
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  Purposeless movements or behavior during the attack.

  
  
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  Most seizures, except for simple absence attacks or simple partial seizures, are followed by a period of postictal confusion and lethargy.

DIFFERENTIAL DIAGNOSIS

Many episodic disturbances of neurologic function may be mistaken for seizures (seizure mimics). A complete review of these conditions is too lengthy for inclusion here, but several important entities are mentioned (Table 171-3).

Syncope usually presents with prodromal symptoms, such as lightheadedness, diaphoresis, nausea, and “tunnel vision.” However, cardiac syncope may occur suddenly without any prodromal warning. Syncope may be associated with injury, incontinence, or even brief tonic-clonic activity. Recovery is usually rapid, with no postictal-like symptoms. For further discussion see chapter 52, “Syncope.”

Pseudoseizures can be extremely difficult to distinguish from true seizures and may occur in a patient who also has a documented seizure disorder. Pseudoseizures are psychogenic in origin and are often associated with a conversion disorder, panic disorder, psychosis, impulse control disorder, Munchausen syndrome, or malingering. Suspect the diagnosis of pseudoseizures when seizures occur in response to emotional upset or only occur with witnesses present. These attacks are often bizarre and highly variable. Patients often are able to protect themselves from noxious stimuli during the attack. Characteristic movements include side-to-side head thrashing, rhythmic pelvic thrusting, and clonic extremity motions that are alternating rather than symmetric. Incontinence and injury are uncommon, and there is usually no postictal confusion. Patients will often stop the seizure-like activity on command. Accurate diagnosis of pseudoseizures may require prolonged EEG or video monitoring to demonstrate normal EEG activity during an attack. The lack of a lactic acidosis or elevated prolactin level drawn within 10 to 15 minutes of the cessation of seizure-like activity makes true seizures much less likely.

Hyperventilation syndrome can be misdiagnosed as a seizure disorder. A careful history will reveal the gradual onset of the attacks with shortness of breath, anxiety, and perioral numbness. Such attacks may progress to involuntary spasm (especially carpopedal) of the extremities and even loss of consciousness, although postictal symptoms are rare. Asking the patient to hyperventilate often reproduces the episodes.

Movement disorders, such as dystonia, chorea, myoclonic jerks, tremors, or tics, may occur in a variety of neurologic conditions. Consciousness is always preserved during these movements, and the patient can often temporarily suppress the movements.

Migraine headaches may be preceded by an aura similar to that seen in some partial seizures. The most common migraine aura is the scintillating scotoma. Migraine headaches may also be accompanied by focal neurologic symptoms, such as homonymous hemianopsia or hemiparesis. However, active movement disorders are inconsistent with migraine.

LABORATORY TESTING

Individualize the use of laboratory studies. In a patient with a well-documented seizure disorder who has had a single unprovoked seizure, the only tests that may be needed are a glucose level and pertinent anticonvulsant medication levels.

In the case of an adult with a first seizure or unclear seizure history, more extensive studies are usually needed and depend on the clinical context. Obtain serum glucose, basic metabolic panel, lactate, calcium, magnesium, a pregnancy test, and toxicology studies. Consider assays for anticonvulsant drug levels. A seizure may result in a lactate-driven, wide anion gap metabolic acidosis.²

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