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Status Epilepticus Clinical Presentation

  • Author: Julie L Roth, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
 
Updated: Feb 19, 2016
 

History

Generalized convulsive status epilepticus (SE) is usually easy to diagnose, but an understanding of its evolution from overt convulsions through subtle SE is important. Patients may present with an undramatic clinical picture if they have subtle SE at the time of presentation.

Treiman and coworkers[45, 46, 47] described the clinical and electroencephalographic (EEG) changes accompanying generalized convulsive SE. The event usually begins with a series of generalized tonic, clonic, or tonic-clonic seizures that often are dramatic. Each seizure is discrete; the motor activity stops abruptly, coincident with the end of the electrographic seizure. Each convulsion is followed by gradual recovery, and then the next seizure occurs.

If the condition is not treated or is treated inadequately, SE persists, and the motor manifestations become less dramatic than before. Eventually, only subtle movements (eg, nystagmoid jerks of the eyes or twitching of the shoulder) may be seen—that is, subtle SE. If SE continues, all motor activity may stop, though EEG seizures persist (ie, electrical generalized convulsive SE).

The paradoxical evolution of apparent clinical improvement is important to understand. The clinician unfamiliar with this phenomenon may stop treatment because of the apparent improvement. Treatment should be continued until the EEG seizure activity has resolved completely.

In some patients, the underlying encephalopathic insult is so severe that only a few (or no) generalized convulsions occur before subtle convulsive activity develops. Finally, as the patient evolves from generalized tonic-clonic SE into subtle and then electrical generalized tonic-clonic SE, the manifestations become less intermittent and more continuous than before.

Persons accompanying the patient may be able to provide important information. A history of epilepsy frequently is elicited. Among patients with established epilepsy, noncompliance with medications is the rule rather than the exception. In roughly one third of cases, status epilepticus is the initial presentation of a seizure disorder.

In those without epilepsy, the history may suggest associated injuries, such as a fall or involvement in a motor vehicle accident. 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.

Nonmotor simple partial status epilepticus

By clinical history, nonmotor simple partial SE involves subjective sensory disturbances, including the following:

  • Focal or unilateral paresthesias or numbness
  • Focal visual changes, usually characterized by flashing lights
  • Focal visual obscuration or focal colorful hallucinations
  • Olfactory or gustatory hallucinations
  • Atypical rising abdominal sensations

These focal phenomena with preserved consciousness are not uncommon as self-limited seizures, and they most often occur as auras associated with complex partial and secondarily generalized seizures. However, in rare cases, they persist in an ongoing or recurrent fashion that fulfills the criteria for focal SE.

Because these particular forms of SE involve sensory disturbances with preserved consciousness, no helpful clinical signs are associated with them. The gradual evolution of nonmotor simple partial SE into overt complex partial or generalized SE helps provide clinically apparent confirmation of these rare forms of FSE.

In rare instances, a focal or generalized seizure may precede such an episode of SE. However, long-lasting focal sensory disturbances after convulsive seizures often represent a transient postictal phenomenon rather than focal SE. EEG often helps in making this clinical distinction.

Epilepsy partialis continua

Focal SE of the motor cortex, known as epilepsy partialis continua, may occur in various contexts. Some authors subdivide epilepsy partialis continua into type I (nonprogressive) and type II (progressive).

Type I epilepsy partialis continua features intermittent, semirhythmic, and involuntary twitching involving a discrete subset of muscles. Although any group of muscles may exhibit these features, it is observed most commonly in the face and ipsilateral distal hand musculature. Myoclonus of this variety may evolve into a partial or generalized convulsion.

Many other attendant historical symptoms may be present, depending on the nature of the focal insult. These symptoms heavily influence the ultimate clinical outcome in this setting.

Type I classically occurs after acute insults to the sensorimotor cortex. These insults may be infectious (eg, Russian spring-summer encephalitis), neoplastic, immune mediated, structural, traumatic, metabolic, or vascular.

Nonketotic hyperglycemic diabetes, particularly in association with hyponatremia, occasionally causes epilepsy partialis continua, often in patients with a preexisting focal CNS lesion (eg, stroke). Epilepsy partialis continua may be a feature of mitochondrial disorders such as mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes (MELAS) and myoclonic epilepsy with ragged-red fiber disease (MERRF).[48]

The syndrome of childhood epilepsy with rolandic spikes (ie, benign rolandic epilepsy) may occasionally involve epilepsy partialis continua. Patients have prolonged speech arrest, facial twitching, and sialorrhea, in episodes that are clinically similar to those of the syndrome, though more prolonged than usual.

Type II epilepsy partialis continua, the progressive form, is usually linked with Rasmussen encephalitis, a unique and rare epilepsy syndrome that predominantly affects children. Children with Rasmussen encephalitis historically had a variety of seizures, including simple and complex partial seizures with occasional secondary generalization; epilepsy partialis continua is yet another seizure type these patients have.

In addition to seizures, patients have gradual loss of unilateral function, and in parallel, imaging studies show focal or unilateral hemispheric atrophy. The typical age of onset is 5-10 years, though the range is broad, and rare cases are reported in adults.

Intellectual skills may become impaired to various degrees, and language skills may be affected, depending on the age of onset and the laterality of the process. Pathologic findings include cortical atrophy, reactive gliosis including microglial nodules, and some perivascular lymphocytosis, occasionally with necrotic features.

Although the subject of intense scrutiny, the etiology of Rasmussen encephalitis remains unknown. Numerous attempts to identify a consistent viral pathogen have failed. An autoimmune hypothesis based on a glutamate receptor subtype has been suggested, but this remains unproven in humans.

Complex partial status epilepticus

Complex partial SE often begins with a history of recurrent or prolonged simple partial seizures, or it may follow or precede a generalized convulsive seizure. Patients are often confused and have variable responsiveness. Memory of the event is usually impaired. Behavior may fluctuate or be bizarre.

Many patients have clinical automatisms, as with typical complex partial seizures, including repetitive lip-smacking, fumbling, or swallowing movements. Subtle nystagmus may be observed.

The range of confusion can be great, with some patients having mildly diminished responsiveness and with others in frank stupor or in a catatonic state. Aphasia and other localizing signs and symptoms (eg, focal weakness) may accompany complex partial SE.

Type I complex partial SE refers to recurrent, recognizable complex partial seizures without recovery between seizures. Type II represents continuous, ongoing complex partial seizure activity. Clinical cycling may be most indicative of type I, though this clinical inference may not be highly reliable.

Clinically distinguishing complex partial SE from absence (generalized) nonconvulsive SE may be problematic; an EEG showing focal or lateralized features may be helpful. EEG is a particularly valuable tool in this setting because treatment options may partly depend on this distinction. Knowledge of the patient's interictal EEG and clinical syndrome, when possible, may also help make this important clinical distinction.

As in generalized SE, patients with focal SE often have an established history of epilepsy, and subtherapeutic anticonvulsant levels or other new metabolic or systemic stressors may be implicated in the expression of FSE. Alternatively, acute or chronic focal cerebral injuries of various kinds (especially, vascular insults) may provide the substrate for new-onset focal seizures and SE.

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Physical Examination

Generalized convulsive status epilepticus 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.

A number of features on physical examination may provide information about the underlying cause of SE. Needle track marks might suggest SE secondary to the use of illicit, or street, drugs. Features on neurologic examination can also be helpful.

Papilledema, a sign of increased intracranial pressure, suggests a possible mass lesion or brain infection. Lateralized neurologic features, such as increased tone, asymmetric reflexes, or lateralized features of the movement during SE itself, are suggestive of the seizures beginning in a localized region of the brain, and they may suggest a structural brain abnormality.

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 or transformed status epilepticus in any patient who does not have improving level of 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.

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Complications

Complications of status epilepticus are many. Systemic complications include the following:

  • Hyperthermia
  • Acidosis
  • Hypotension
  • Respiratory failure
  • Rhabdomyolysis
  • Aspiration
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Contributor Information and Disclosures
Author

Julie L Roth, MD Neurologist, Epilepsy and General Neurology, Comprehensive Epilepsy Program, Rhode Island Hospital; Assistant Professor, Department of Neurology, The Warren Alpert Medical School of Brown University

Julie L Roth, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society

Disclosure: Nothing to disclose.

Coauthor(s)

Andrew S Blum, MD, PhD Director, Adult Epilepsy and EEG Laboratory, Comprehensive Epilepsy Program, Rhode Island Hospital; Associate Professor of Neurology, The Warren Alpert Medical School of Brown University

Andrew S Blum, MD, PhD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Massachusetts Medical Society

Disclosure: Received royalty from Springer Publishing for editor of text, the clinical neurophysiology primer.

Chief Editor

Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine

Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, Phi Beta Kappa

Disclosure: Nothing to disclose.

Acknowledgements

Norberto Alvarez, MD Assistant Professor, Department of Neurology, Harvard Medical School; Consulting Staff, Department of Neurology, Boston Children's Hospital; Medical Director, Wrentham Developmental Center

Norberto Alvarez, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, and Child Neurology Society

Disclosure: Nothing to disclose.

Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Jose E Cavazos, MD, PhD, FAAN Associate Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, Program Director of the Clinical Neurophysiology Fellowship, University of Texas School of Medicine at San Antonio; Co-Director, South Texas Comprehensive Epilepsy Center, University Hospital System; Director of the San Antonio Veterans Affairs Epilepsy Center of Excellence and Neurodiagnostic Centers, Audie L Murphy Veterans Affairs Medical Center

Jose E Cavazos, MD, PhD, FAAN is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, and American Neurological Association

Disclosure: GXC Global, Inc. Intellectual property rights Medical Director - company is to develop a seizure detecting device. No conflict with any of the Medscape Reference articles that I wrote or edited.

Daniel J Dire, MD, FACEP, FAAP, FAAEM Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Rick Kulkarni, MD Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

Edward H Maa, MD Chief of Comprehensive Epilepsy Program, Department of Neurology, Denver Health and Hospitals; Assistant Professor, Department of Neurology, University of Colorado School of Medicine and Veterans Affairs Medical Center

Edward H Maa, MD is a member of the following medical societies: American Academy of Neurology and American Epilepsy Society

Disclosure: UCB Pharma Honoraria Speaking and teaching

Erasmo A Passaro, MD, FAAN Director, Comprehensive Epilepsy Program/Clinical Neurophysiology Lab, Bayfront Medical Center, Florida Center for Neurology

Erasmo A Passaro, MD, FAAN is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Association, and American Society of Neuroimaging

Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Forest Honoraria Speaking and teaching

Mark Spitz, MD Professor, Department of Neurology, University of Colorado Health Sciences Center

Mark Spitz, MD is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society

Disclosure: pfizer Honoraria Speaking and teaching; ucb Honoraria Speaking and teaching; lumdbeck Honoraria Consulting

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Treatment algorithms for convulsive status epilepticus.
Focal status epilepticus. Electroencephalograph (EEG) in a patient with epilepsia partialis continua caused by Rasmussen encephalitis before hemispherectomy. The patient had long-standing, intractable partial epilepsy since the first decade of life. Seizures included complex partial with occasional secondary generalization and repetitive myoclonus involving the left side of the body. Note the frequent epileptiform discharges at 1-2 Hz involving the right frontocentral channels. These were evident on many of the patient's routine EEGs. Clinical myoclonus is often correlated with high-voltage bursts of such activity.
Focal status epilepticus. Electroencephalograph (EEG) in a 35-year-old patient with a history of intractable partial epilepsy, in complex partial status epilepticus. The patient underwent a rapid antiepileptic drug taper as an inpatient for long-term video/EEG monitoring as a presurgical candidate. On clinical observation, the patient abruptly stopped and stared, exhibiting automatisms. This first of 2 EEG fragments covers approximately 30 seconds and illustrates the start and evolution of a seizure in the right temporal lobe. The onset appears to be at Sp2 and T4. Note the time of the event, 18:35 on May 9.
Focal status epilepticus. This electroencephalographic (EEG) fragment was obtained at approximately 12:39 on May 10, 18 hours after the onset of complex partial status epilepticus originating in the right temporal lobe, in a 35-year-old patient with a history of intractable partial epilepsy. Other EEG acquisitions over the interval were identical. On clinical observation, the patient was lethargic, sluggish, and vague, with variable responsivity to examiners. Note the persistent epileptiform discharges at 1.5-2.5 Hz with phase reversal mainly at Sp2 though infrequently shifting to Sp1 and F7. The bulk of the discharges are maximal at Sp2, reflecting their mesial temporal origin, with rare, subtle, and low-amplitude reflection from lateral neocortical channels (F8). Background activities are slow with admixed beta frequencies. This finding corresponds to complex partial status epilepticus.
 
 
 
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