is estimated that between 1% and 2% of emergency department (ED) visits are for seizure‐related complaints, with many of these patients using EMS systems. Most receive advanced level care [1]. In one study, seizures accounted for almost 12% of pediatric EMS transports [2]. Seizures are a common cause of repeated ambulance use [3]. Every community has a cadre of patients with poorly controlled seizures or alcohol‐related seizures who use EMS frequently. This group of frequent users may lead to a casual indifference to all patients with seizures. EMS clinicians must recall that seizures at some level are the symptom of some central nervous system (CNS) dysfunction and initiate appropriate diagnostic and management steps to terminate seizures to lessen morbidity.
Pathophysiology
The concept of a seizure threshold suggests that everyone has the capacity to experience seizures at some level of individual physiological stress. The precipitating events may be electrolyte abnormalities, medications, medication withdrawal, toxins, hypoxia, CNS infections, systemic infections, trauma, or even sleep deprivation. A fundamental distinction in management is to determine whether a seizure results from some identifiable cause or if it is unprovoked. When seizures are secondary to some other condition, they are symptomatic seizures or provoked seizures. Unprovoked seizures occur without an identifiable cause. Again, epilepsy is defined by episodes of unprovoked seizures.
At a cellular level, seizures are thought to originate in the cerebral cortex or thalamus. Lesions of the brainstem, deep white matter, and cerebellum are not epileptogenic. Seizures result from excitation of susceptible groups of cerebral neurons, with progressively larger groups of neurons developing synchronous discharges. Clinical signs and symptoms follow when a critical mass of neurons is reached [4]. At a biochemical level, there is a disturbance in the balance of cellular excitation and inhibition. Glutamate is the most common excitatory neurotransmitter and acts at the n‐methyl‐D‐asparate (NMDA) receptor. Current theory is that failure of inhibition mediated by the neurotransmitter gamma‐aminobutyric acid (GABA) system leads to prolongation of many seizures. The neurotransmitter receptor sites are thought to be the sites of action of the antiepileptic drugs. With frequent or persistent seizure activity, physiological changes of hypoxia, acidosis, hyperthermia, hypotension, and reduced cerebral perfusion may occur. At one time, these were thought to be the cause of neuronal injury. However, many different avenues of investigation have suggested that injury follows prolonged excessive neuronal discharges even if systemic pathophysiological factors are controlled [4]. Some experimental evidence suggests that neurotransmitter receptors may change in sensitivity or quantity with prolonged seizures; the potential effectiveness of medications might change as seizure duration persists [5, 6].
Differential diagnosis
There is a differential diagnosis for seizures since a number of clinical conditions may simulate generalized convulsions (Box 17.1). Syncope is a frequent consideration in the differential diagnosis. Loss of consciousness is abrupt in syncope and occasionally the brief myoclonic jerks that accompany the faint are a source of confusion. “Convulsive syncope” results from the cerebral hypoperfusion during the syncopal event. Investigations and treatments should be directed toward the cause of syncope [7].
Box 17.1 Differential diagnosis of seizures in adults
1 Seizures: from abnormal, excessive neuronal dischargesUnprovoked seizuresSymptomatic or secondary seizures
2 Nonepileptic seizures: appear to be seizures but do not result from abnormal excessive neuronal dischargesPsychogenic seizures (sometimes the term nonepileptic seizures is used synonymously with psychogenic seizures)Repetitive abnormal posturingInvoluntary movement disordersSyncope/convulsive syncopeConcussion/convulsive concussionSleep disorders
A person experiencing a blow to the head may have a brief episode of extremity stiffening at the time of impact that understandably may be confused with seizure activity. These events clinically resemble brief abnormal extensor posturing, though myoclonic and tonic‐clonic movements are also described. Return to consciousness following these events is usually prompt. These “convulsive concussions” are not associated with injury or neurologic sequelae and do not predict future seizures [8, 9]. Posttraumatic epilepsy may occur after head trauma but is associated with more severe head injuries. These late‐presenting seizures are typical in appearance and associated with a postictal confusional state.
In any series of stroke patients, seizures and postictal states are a significant source of diagnostic confusion [10, 11]. Seizure patients may have postictal weakness or confusion that mimics some stroke symptoms. Subarachnoid hemorrhage may cause fragmentary or repetitive extensor posturing that at times is confused with seizures [12, 13].
Nonepileptic seizures, also known as pseudoseizures, psychogenic, or hysterical seizures, often result in diagnostic uncertainty. Simply stated, the patient appears to be having a seizure, but subsequent observations prove that the apparent convulsion does not follow from the excessive neuronal discharges that characterize epileptic seizures. The usual descriptions of nonepileptic seizures include side‐to‐side head movements, out‐of‐phase limb movements, and pelvic thrusting [14]. Other reports indicate that simple unresponsiveness without motor movements is a frequent presentation [15].
Classification of seizure types
In theory, almost any behavior or experience may result from the abnormal synchronous discharges of groups of neurons. Motor movements, sensory experiences, or abnormal behaviors may all represent seizures [16]. Patterns are seen that allow a categorization of seizures (Box 17.2) [17]. Modern classification schemes are based on video electroencephalogram (EEG) correlations, but at times seizure‐type classification may be made from direct patient observation.
Box 17.2 Classification of seizure types
Focal Onset
Aware | Impaired
Awareness
Motor Onset
automatisms
atonic
clonic
epileptic spasms
hyperkinetic
myoclonic
tonic
Nonmotor Onset
autonomic
behavior arrest
cognitive
emotional
sensory
Focal to bilateral
tonic‐clonic
Generalized Onset Motor
tonic‐clonic
clonic
myoclonic
myoclonic‐tonic‐clonic
