eMedicine Specialties > Emergency Medicine > Neurology

Status Epilepticus

Author: J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
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Updated: Aug 24, 2009

Introduction

Background

The term status epilepticus may be used to describe any continuing type of seizure. This discussion focuses on generalized convulsive status epilepticus (GCSE). Generalized refers to abnormal excessive cortical electrical activity, while convulsive refers to the motor activity of a seizure.

Recently, the concept of subtle status epilepticus has emerged. Subtle status epilepticus consists of electrical seizure activity that endures when the associated movements are fragmentary or even absent. The terminology is confusing since this is sometimes designated a type of nonconvulsive status epilepticus. Subtle status epilepticus, epileptic encephalopathy, and even ICU status are all terms used to refer to this clinical condition of dissociated cortical epileptiform activity from convulsive motor movements. Nonconvulsive status epilepticus includes conditions such as absence status epilepticus, complex partial status epilepticus, and other epileptic twilight states and is not discussed in this section.

Traditionally, generalized convulsive status epilepticus was defined as 30 minutes of continuous seizure activity or a series of seizures without return to full consciousness between the seizures. Many believe that a shorter period of seizure activity causes neuronal injury and that seizure self-termination is unlikely after 5 minutes; some suggest times as brief as 5 minutes to define status epilepticus.¹ For purposes of this review, a duration of 5 minutes of continuous generalized convulsive activity is used arbitrarily as part of the definition of GCSE, as well as recurrent seizures without a return to consciousness between seizures.

Pathophysiology

Significant physiologic changes accompany generalized convulsive status epilepticus (GCSE). Many of these systemic responses are thought to result from the catecholamine surge that accompanies the seizures. Hypertension, tachycardia, cardiac arrhythmias, and hyperglycemia are examples of these systemic effects. Body temperature may increase in patients following the vigorous muscle activity that accompanies GCSE (but, of course, infectious etiologies also must be considered in febrile patients). Lactic acidosis is common after a single generalized motor seizure and resolves with termination of the seizure.

Cerebral metabolic demand increases greatly with GCSE; however, cerebral blood flow and oxygenation are thought to be preserved or even elevated early in the course of GCSE. Research with paralyzed and artificially ventilated animals concluded that neuronal loss after focal or generalized status epilepticus is linked to the abnormal neuronal discharges and not simply to the systemic effects of GCSE. The hippocampus seems especially vulnerable to damage by this mechanism.

On a neurochemical level, seizures are sustained by an imbalance of excess excitation and reduced inhibition. Glutamate is the most common excitatory neurotransmitter and the NMDA (N-methyl-D-aspartate) receptor subtype is involved. Gamma-aminobutyric acid (GABA) is the most common inhibitory neurotransmitter. Failure of inhibitory processes is increasingly thought to be the major mechanism leading to status epilepticus.

Most seizures terminate spontaneously. Which processes are involved in seizure termination and why or how these processes fail in status epilepticus are active areas of inquiry.

Frequency

United States

Approximately 50,000-200,000 cases of status epilepticus occur per year (using traditional epidemiologic definitions).²

Mortality/Morbidity

• The overall mortality rate is about 20%; death most often is related to an underlying cause of brain injury.³
• The mortality rate is highest in elderly patients with hypoxic or ischemic central nervous system (CNS) insults.

Sex

Males and females are affected equally.

Age

• Status epilepticus occurs in all age groups but more frequently at the extremes of age.
• In the neonatal group, status epilepticus may be related to perinatal hypoxic insults or metabolic disorders.
• At the other extreme of age, elderly persons have an increased incidence of status epilepticus secondary to ischemic CNS insults.

Clinical

History

• A history of epilepsy frequently is elicited.
• A history of systemic or CNS neoplasms, infections, metabolic disorders, toxic ingestions, alcohol cessation, and many other conditions may give clues to the precipitating cause of seizures.
• In roughly one third of cases, status epilepticus is the initial presentation of a seizure disorder.
• Noncompliance with medications is the rule rather than the exception.
• The history may suggest associated injuries, such as a fall or involvement in a motor vehicle accident.

Physical

• Generalized convulsive status epilepticus (GCSE) often is recognizable to the clinician at the bedside when typical rhythmic tonic-clonic activity is present.
• Consciousness is impaired.
• Rarely, status epilepticus may present as a persistent tonic seizure.
• Psychogenic seizures may be, at times, indistinguishable from GCSE based on appearance alone.
  • One study noted that when confronted by pseudoseizures, physicians immediately assumed that a neurologic emergency was present and embarked on an aggressive course of pharmacotherapy, neglecting physical examination and historical information. In this study, unresponsiveness without movement was the most common presentation.⁴
  • Other reviews of psychogenic status epilepticus note other frequently seen presentations, including asynchronous extremity movement, forward pelvic thrusting, and geotropic eye movements (a physical finding that indicates the eyes deviating toward the ground in a nonphysiologic manner whether the head is turned left or right).⁵
• Rapid repeated extensor or flexor posturing may be confused with convulsive activity by a casual observer.
• Repetitive myoclonus in a comatose patient following diffuse hypoxic brain injury may simulate generalized seizures.
  • The physiologic origin of the myoclonic jerks may not be cortical.
  • The myoclonus usually is limited in duration to several hours.
• Suspect subtle status epilepticus in any patient who does not regain consciousness within 20-30 minutes of cessation of generalized seizure activity.
  • The motor expression of the abnormal cortical electrical activity may change so that a flicker of an eyelid or twitch of an extremity is the only sign of the ongoing generalized electrical discharges.
  • Motor activity may be absent even in the presence of ongoing electrical status epilepticus.
• Associated injuries that may be present in patients with seizures include tongue lacerations (typically lateral), shoulder dislocations, head trauma, and facial trauma.

Causes

The causes of status epilepticus represent an imperfect division into 3 groups.

• In roughly one third of cases, an exacerbation of an idiopathic seizure disorder is thought to be the cause (this is a diagnosis of exclusion).
• In another one third of cases, the episode of status epilepticus represents the first onset of a seizure disorder (a diagnosis of exclusion).
• A myriad of other conditions may precipitate status epilepticus, including toxic or metabolic causes and anything that might cause cortical structural damage.
  • Stroke (remote or acute)
  • Hypoxic injury
  • Tumor
  • Subarachnoid hemorrhage
  • Trauma
  • Toxicologic etiology (eg, cocaine, theophylline, isoniazid, alcohol withdrawal)
  • Electrolyte abnormalities (eg, hyponatremia, hypernatremia, hypercalcemia, hepatic encephalopathy)
  • Infectious etiology (eg, meningitis, brain abscess, encephalitis)
  • A variety of toxins, notably sympathomimetics, may precipitate status epilepticus
  • Isoniazid (INH) may cause seizures and is unique in having a specific antidote, pyridoxine (B-6).

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