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Status Epilepticus
Status Epilepticus
Author: Julie L Roth, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA more... Updated: May 26, 2011
Background
Status epilepticus (SE) is a common, life-threatening neurologic disorder. It is essentially an acute, prolonged epileptic crisis. Etiologically, SE can be imperfectly divided into 3 groups. SE can represent an exacerbation of a pre-existing seizure disorder, the initial manifestation of a seizure disorder, or an insult other than a seizure disorder (see Etiology). In patients with known epilepsy, the most common cause is a change in medication. Recognition of SE may be easy or difficult. SE in the patient with sequential, generalized major motor convulsions is obvious; the patient with nonconvulsive or subtle SE presents a diagnostic dilemma (see Differentials). Aggressive treatment is necessary. Maintenance of vital signs, including respiratory function, is of major importance. Early treatment measures are performed in concert with diagnostic studies (see Treatment). In April 2007, a major symposium convened in London to discuss and summarize current diagnosis, treatment, and research efforts in status epilepticus. The proceedings were published as a supplement of the journal Epilepsia.[1] The introduction of the proceedings provides a good summary.[2] Treatment guidelines were also proposed.[3] Go to Epilepsy and Seizures for an overview of this topic. Also see Pediatric Status Epilepticus.
Historical aspects
The first description of SE in the medical literature was in a Babylonian text from the first millennium BC. The author recognized the severity of the condition: "If an epilepsy demon falls many times upon him on a given day, he seven times punishes him and possesses him, his life will be spared. If he falls upon him eight times, his life may not be spared."[4] Wolf et al described a case of probable 3-day absence stupor documented in Austria in 1501.[5] Several descendants of the affected person in this historical case have been shown to have a primary idiopathic epileptic syndrome.
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Although subtle SE is, by definition, nonconvulsive, it should be distinguished from other NCSE. Subtle SE is considered the most severe clinical stage of generalized convulsive SE and patients with subtle SE, in contrast to that of those with NCSE, have a dismal prognosis.
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Complex partial SE is rare. Although many cases of prolonged complex partial SE without long-term neurologic sequelae have been described, negative outcomes can occur. No criteria for differentiating the cases associated with a poor outcome are known. Complex partial SE that arises in the limbic cortex (eg, mesial temporal lobe) causes signs and symptoms such as staring, unresponsiveness, automatisms, atypical anxiety, rising abdominal symptoms, dj vu, or more profound stupor. Complex partial SE of frontal-lobe origin may produce clinical symptoms indistinguishable from cases of temporal-lobe origin. While isolated complex partial seizures usually originate in the temporal lobe, complex partial SE usually has an extratemporal focus. Shorvon believes that at least 15% of patients with complex partial epilepsy have a history of nonconvulsive SE.[17]
Pathophysiology
On a neurochemical level, seizures are sustained by 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. Significant physiologic changes accompany generalized convulsive SE. Many of these systemic responses (eg, tachycardia, cardiac arrhythmias, hyperglycemia) are thought to result from the catecholamine surge that accompanies the seizures. In the early stages of SE, prominent elevation in systemic arterial pressure is seen. In a study of 21 patients, White et al found a mean elevation of systolic pressure of 85 mm Hg and an elevation of diastolic pressure of 42
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mm Hg.[18] As SE continues, blood pressures may decrease to levels below their former baseline. Body temperature may increase in patients, as a result of the vigorous muscle activity and central sympathetic drive that accompany generalized convulsive SE (but, of course, infectious etiologies also must be considered in febrile patients). In a study by Aminoff and Simon, 75 of 90 patients with SE had hyperthermia, with temperatures reaching 42C.[19] Hyperthermia has been correlated with poor neurologic outcomes and should be treated aggressively. Marked acidosis usually occurs. In a study of 70 spontaneously ventilating patients with SE, 23 had a pH of less than 7.0.[19] The acidosis has both a respiratory and a metabolic component. The acidosis usually should not be treated; it does not correlate with the degree of neuronal injury, and acidosis is known to have an anticonvulsant effect. The acidosis resolves with termination of the seizure. A mild leukocytosis (primarily due to demargination) is common in both blood and cerebrospinal fluid (CSF). In a study of 80 patients, 50 without evidence of infection had WBC count elevations from 12.7-28.8 X 109 /L (12,70028,800 cells/L). Bands should not be seen. CSF pleocytosis is common but the cell-count elevations are usually modest. In one study, only 4 of 65 patients had greater than 30 cells in the CSF.[19] Convulsive SE affects not only the mechanical aspects of breathing but also causes pulmonary edema. Many of the medications used to treat SE (specifically, benzodiazepines and barbiturates) inhibit respiratory drive both individually and synergistically when given in combination. A patient with convulsive SE who has already received a full loading dose of benzodiazepines should be electively intubated before being given. Cerebral metabolic demand increases greatly with generalize convulsive SE. However, cerebral blood flow and oxygenation are thought to be preserved or even elevated early in the course. Research with paralyzed and artificially ventilated animals concluded that neuronal loss after focal or generalized SE is linked to the abnormal neuronal discharges and not simply to the systemic effects of the seizures. For example, Meldrum and Horton demonstrated that prolonged seizure activity results in pathologic changes after 30 minutes; after 60 minutes, neurons begin to die.[20] The hippocampus seems especially vulnerable to damage by this mechanism. These observations parallel findings in human clinical studies, which have shown that the duration of SE correlates directly with morbidity and mortality rates. The longer the SE persists, the more likely that neurons will be damaged by excitatory neurotransmitters. Sustained seizure activity also progressively reduces GABA inhibition. On a receptor level, GABAergic mechanisms fail and seizures become pharmacoresistent.[21] Neuronal death probably results from the inability to handle large increases in intracellular calcium brought about by prolonged exposure to excitatory neurotransmitters. However, changes in gene expression that are induced by SE result in alterations in the number or subunit composition of ion channels, receptors, cell metabolism, and neuronal connectivity.[2, 22] The observation that prior history of epilepsy is associated with a better prognosis might be related to the fact that brief seizures might result in upregulation of neuroprotective mechanisms. This may serve as a form of adaptive tolerance.[2] Alterations in the availability of existing receptors during SE might occur relatively quickly. This might contribute to responsiveness to benzodiazepines.[23] SE in the developing brain seems to have lesser consequences despite a greater susceptibility to seizures.[24] This might be due to better adaptive mechanisms to cope with excitotoxicity.
Etiology
Etiologically, SE can be imperfectly divided into 3 groups. SE can represent an exacerbation of a pre-existing seizure disorder, the initial manifestation of a seizure disorder, or an insult other than a seizure disorder. In patients with known epilepsy, the most common cause is a change in medication; the change may be directed
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by physician (eg, placing the patient on nothing-by-mouth [NPO] status before surgery) or may be due to abrupt cessation on the patients part, whether intentional or unintentional. A myriad of other conditions may precipitate SE, including toxic or metabolic causes and anything that might produce cortical structural damage, as follows: Stroke (remote or acute) Hypoxic injury Tumor Subarachnoid hemorrhage Head trauma Drugs (eg, cocaine, theophylline); isoniazid (INH) may cause seizures and is unique in having a specific antidote, pyridoxine (vitamin B-6) Alcohol withdrawal Electrolyte abnormalities (eg, hyponatremia, hypernatremia, hypercalcemia, hepatic encephalopathy) Neoplasms CNS infections (eg, meningitis, brain abscess, encephalitis) Toxins, notably sympathomimetics In more recent series of SE, HIV infection and use of illicit drugs were reported with increased frequency. Causes of SE vary significantly with age. DeLorenzo et al reported that in patients younger than 16 years, the most common cause was fever and/or infection (36%); in contrast, this accounted for only 5% of SE in adults.[25] In adults, the most common precipitant was cerebrovascular disease (25%), whereas this factor caused only 3% of pediatric cases. In a more refined study that focused on children, Shinnar et al found that in children younger than 2 years with SE, more than 80% of cases were of febrile or acute symptomatic origin.[26] In contrast, cryptogenic and remote symptomatic causes were more common in older children than in younger children.
Epidemiology
Extrapolating from a population-based study in Richmond, VA, DeLorenzo et al estimated that 50,000-200,000 cases of SE occur annually in the United States.[27] In 1994, Shorvon estimated that cases of nonconvulsive SE occurred at an annual rate of 15-20 per 100,000 population, of which only 3-4 were clearly instances of complex partial SE.[28] This finding is in accordance with Celesia's early estimates in 1976.[13] True absence status (ie, generalized, ongoing, 3-Hz spike-and-wave activity) may account for fewer patients with nonconvulsive SE than previously believed. Nonconvulsive SE, and by extension focal SE, is believed to be frequently overlooked. Epilepsy partialis continua is rare by comparison, even in pediatric epilepsy referral centers, though it is overwhelmingly a syndrome of children. In the author's series of 41 patients with focal SE who were referred from a tertiary referral center that treated adults over 15 years, only 3 had epilepsy partialis continua.
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the author's study of adults with focal SE, the age range was 15-91 years with a mean age of 62 years. Most available studies are retrospective; prospective data on the age-related incidence of focal SE are still lacking.
Prognosis
Prognosis is related most strongly to the underlying process causing SE. For example, if meningitis is the etiology, the course of that disease dictates outcome. Patients with SE from anticonvulsant irregularity or those with alcohol-related seizures generally have a favorable prognosis if treatment is commenced rapidly and complications are prevented. A multivariate analysis by Drislane et al identified presentation in coma and SE caused by anoxia/hypoxia as indicators of a poor prognosis.[30] However, in a small case series of cardiac arrest patients who developed postanoxic SE, predictors of a favorable outcome included preserved brainstem reactions, cortical somatosensory evoked potentials, and EEG reactivity.[31] These patients were treated with therapeutic hypothermia. The more advanced the stage of SE, the less favorable the response to treatment. In the Veterans Affairs Status Epilepticus Cooperative study, 56% of patients who were first seen with overt, generalized convulsive SE responded to initial treatment. Only 15% of the individuals with subtle, generalized convulsive SE responded to initial treatment.[32] Treating nonconvulsive SE is urgent because longer duration of this condition correlates with a worse prognosis.[33]
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injury, though rare instances may occur. However, nonconvulsive SE appears so often in the company of serious neurologic or medical injury that clinically significant morbidity and mortality are common. Patients with focal motor SE (ie, epilepsy partialis continua) have a particularly poor prognosis if they are untreated in the setting of Rasmussen encephalitis. In the author's series of patients with focal SE, patients with new neurologic insults (eg, acute stroke) or those whose SE occurred postoperatively had a mortality rate of 67%. Those with a history of epilepsy did well overall. In this group, SE was usually precipitated by a new toxic and/or metabolic or other medical aggravator and had little to no lasting neurologic aftereffects. The author compared patients with recurrent seizures with those who had ongoing, continuous seizure activity. No difference in outcome was observed between the subgroups of focal SE.
Patient Education
Reinforcement of compliance with prescribed medications at routine clinical encounters may be helpful in preventing SE. For patient education information, see the Brain and Nervous System Center, as well as Seizures Emergencies and Epilepsy.
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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. J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. 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 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 Specialty Editor Board 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 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 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
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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 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, and Phi Beta Kappa Disclosure: Nothing to disclose.
References
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