Author: Julie L Roth, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA more... Updated: May 26, 2011
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. The introduction of the proceedings provides a good summary. Treatment guidelines were also proposed. Go to Epilepsy and Seizures for an overview of this topic. Also see Pediatric Status Epilepticus.
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." Wolf et al described a case of probable 3-day absence stupor documented in Austria in 1501. Several descendants of the affected person in this historical case have been shown to have a primary idiopathic epileptic syndrome.
Definition of status epilepticus
In early studies, SE was defined by its duration—that is, as continuous seizures occurring for longer than 1 hour. Clinical and animal experiences later showed that pathologic changes and prognostic implications occurred when SE persisted for 30 minutes. Therefore, the time for the definition was shortened. The working group on SE of the Epilepsy Foundation (formerly the Epilepsy Foundation of America) formulated the current definition: "More than 30 minutes of continuous seizure activity or two or more sequential seizures without full recovery of consciousness between seizures." Many believe that a shorter period of seizure activity causes neuronal injury and that seizure self-termination is unlikely after 5 minutes. Consequently, Lowenstein and others have suggested a duration of longer than 5 minutes as part of the a criterion for SE, if the seizure type is one in which typical generalized convulsive seizures resolve spontaneously after 3-5 minutes. The Epilepsy Foundation working group recommended that emergency department physicians treat seizures as SE if seizure activity has continued for more than 10 minutes.
Classification of status epilepticus
The term status epilepticus may be used to describe continuing seizure of any type. The predominant type of seizure further refines the definition of SE, and several classification schemes have been proposed. Categorization of SE cases is no simple matter because they often exhibit characteristics of both focal and generalized processes. Considerable literature has been devoted to this question over the last 30 years, beginning with Geier et al in 1976, Ellis and Lee in 1978, and Niedermeyer et al in 1979. Several investigators have suggested that the bulk of these indeterminate examples are instances of focal onset episodes of status that have secondarily generalized, in the same manner as many focal onset seizures. EEGs of patients with these conditions fail to capture the onset of status; therefore, this critical element is lost. Some of these instances are characterized by diffuse, slow (< 3 Hz) spike-and-wave activity, albeit with focal predominance. In many instances, interictal recordings demonstrate focal discharges that further implicate a focal process. Whether such cases are best grouped with focal status remains controversial. Luders and Rona have suggested a detailed semiologic classification along 3 axes: (1) the type of brain function predominantly compromised, (2) the body part involved, and (3) The evolution over time. Celesia and Treiman proposed simpler schemes, which are more useful than other systems for emergency treatment decisions. The Treiman classification is as follows: Generalized convulsive SE Subtle SE Nonconvulsive SE (including absence SE and complex partial SE) Simple partial SE
Generalized convulsive status epilepticus
Generalized convulsive SE is the most frequent and potentially dangerous type of SE. Generalized refers to the abnormal excessive cortical electrical activity, while convulsive refers to the motor activity of a seizure.
Subtle status epilepticus
Subtle SE consists of electrical seizure activity in the brain that endures when the associated motor responses are fragmentary or even absent. The terminology is confusing, since subtle SE is sometimes designated a type of nonconvulsive SE (NCSE).
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.
Nonconvulsive status epilepticus
Nonconvulsive SE is divided into 2 categories: absence SE and complex partial SE. Differentiating these subtypes is important, since they indicate major differences in treatment, etiology, and prognosis. In one review, NCSE has been further subdivided according to the age of occurrence, as follows: Neonatal and infantile Only in childhood In both childhood and adult life In late adult life Several epileptic syndromes, such as electrical status epilepticus in slow-wave sleep (ESES), would be classified under the "NCSE only in childhood" category.
Absence status epilepticus
On clinical presentation, a clear change in the level of consciousness is observed in patients with absence SE. Most patients are not comatose but are lethargic and confused, with decreased spontaneity and slow speech. Absence SE is also known as absence stupor because of the apparent state of low alertness. The ictal electroencephalograph (EEG) during typical absence SE demonstrates generalized spike and wave discharges. The frequency may be slower than 3 Hz, and the waveforms (though bilaterally synchronous) are often irregular, poorly formed, and discontinuous, especially in the late stages. In adults and in some children, the apparently bisynchronous EEG discharges may represent complex partial SE as opposed to true absence SE. About 2.6% of patients with absence seizures have had an episode of absence SE earlier in their lives. Approximately 10% of adults with childhood-onset absence seizures experience absence SE. About 75% of all cases of absence SE occur before the age of 20 years. When it occurs in adults, the patients are often elderly. The mean age of onset of absence SE in adults is 51 years. Typical absence SE that occurs in children or adolescents who have primary or idiopathic generalized epilepsy (which includes absence seizures) readily responds to treatment. In contrast, absence SE in the symptomatic, primary generalized epilepsies (eg, Lennox-Gastaut syndrome) is often more difficult to control. Four issues should be considered in the differential diagnoses of absence SE. First, complex partial SE usually manifests with recurring cycles of 2 separate phases: ictal and interictal. In contrast, absence SE usually occurs as 1 continuous episode of variable intensity. Second, stereotyped automatisms can be seen in both complex partial and absence SE, though they tend to be richer in complex partial SE than in absence SE. Anxiety, aggression, fear, and irritability may be most common in complex partial SE, but they can be seen in both types. Third, EEG is the best way to differentiate absence SE from complex partial SE. Fourth, other possibilities include a postictal state and encephalopathies from toxic-metabolic causes, drugs, trauma, or infection. Psychiatric causes should be considered. No deaths or long-term morbidity due to typical absence SE have been reported. Whether absence SE in children with developmental dementia and myoclonic/astatic epilepsy is injurious to the brain is controversial. Differentiating absence SE from other causes is important because many mimics of absence SE can lead to irreversible neuronal damage if they are not aggressively treated.
Complex partial status epilepticus
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, déjà 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.
Simple partial status epilepticus
By definition, simple partial SE consists of seizures that are localized to a discrete area of cerebral cortex and produce no alteration in consciousness. Because this form of epilepsy is rare, no good studies have been done to determine its incidence. Focal SE can arise in any region of the cortex. When motor cortex is affected, the condition is termed epilepsia partialis continua (EPC), which characteristically involves repetitive, often rhythmic, unilateral focal twitching of the limbs and/or face, usually with preservation of consciousness. This sparing of consciousness subcategorizes EPC as a form of simple partial SE. Other regions of cortex similarly may generate focal SE. These cases are characterized by predictable phenotypes depending on the function of the particular region involved. For example, episodes of focal SE involving primary sensory cortex are expected to be associated with focal sensory symptoms, and occipital focal SE causes focal visual symptoms (eg, flashing spots of light, colorful visual hallucinations). Focal SE of language cortex typically causes aphasia, termed ictal aphasia. Diagnosis is primarily based on clinical findings. Because of the relatively small area of cerebral cortical involvement, results of conventional scalp EEG are frequently uncharacteristic of the clinical ictal activity, or they may be normal. In contrast to convulsive SE, simple partial SE is not associated with high rates of morbidity or mortality. Outcomes seem to be related to the underlying etiology, the duration of the SE, the age of the patient, and the medical complications, as in convulsive SE. Treatment involves the same drugs and general pharmacologic principles as those used for convulsive SE. However, the relatively low morbidity and mortality rates suggest that aggressive treatment might not be needed. For example, if first-line drugs are ineffective, the clinician may elect not to use a general anesthetic agent to stop simple partial SE.
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
mm Hg. 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 42°C. 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. 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/µL). 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. 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. 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. 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. Alterations in the availability of existing receptors during SE might occur relatively quickly. This might contribute to responsiveness to benzodiazepines. SE in the developing brain seems to have lesser consequences despite a greater susceptibility to seizures. This might be due to better adaptive mechanisms to cope with excitotoxicity.
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
by physician (eg, placing the patient on nothing-by-mouth [NPO] status before surgery) or may be due to abrupt cessation on the patient’s 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. 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. In contrast, cryptogenic and remote symptomatic causes were more common in older children than in younger children.
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. 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. This finding is in accordance with Celesia's early estimates in 1976. 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.
Sex and race in status epilepticus
SE affects males and females equally. SE is not believed to have a predilection for any particular racial or ethnic group.
Age-related differences in incidence
The age frequency of SE probably follows the same curve as that of the incidence of seizures generally. This J shaped curve reflects the high frequency in the young and the increasing incidence with advancing age. Up to 70% of SE cases occur in children. However, the incidence of SE is highest in the population older than 60 years, at 83 cases per 100,000 population. Focal status epilepticus probably obeys a similar age relationship, though the data are understandably limited. In
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 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. 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. 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. Treating nonconvulsive SE is urgent because longer duration of this condition correlates with a worse prognosis.
Mortality from status epilepticus
Mortality rates related to SE have decreased over the last 60 years, probably in relation to faster diagnosis and more aggressive treatment. The probability of death is closely correlated with age. In prospective population-based studies, DeLorenzo et al found mortality rates of 13% for young adults, 38% for the elderly, and >50% for those older than 80 years. In 1998, the Veterans Affairs Status Epilepticus Cooperative Study Group reported mortality rates of 27% for overt generalized convulsive SE and 65% for subtle generalized convulsive SE. DeLorenzo et al reported a mortality rate of 21% in patients with generalized SE, defining mortality as death occurring within 30 days. Aicardi and Chevrie examined 239 children with generalized convulsive SE that lasted longer than an hour; 26 died, and 88 had permanent neurologic damage (47 of whom had been neurologically intact before the episode). Death most often is related to an underlying cause of brain injury. According to Hauser, no more than 2% of patients die directly from SE. In a prospective study of 24 SE patients who died, 10 had a gradual decrease in mean arterial pressure and/or heart rate. The remaining 14 had no cardiac changes until the time of death. About 90% of patients with cardiac decompensation had a history of many risk factors for atherosclerotic cardiovascular disease, whereas only 30% of those without acute cardiac decompensation had clinically significant risk factors.
Prognosis in nonconvulsive status epilepticus
Models of partial epilepsy have demonstrated profound and long-lasting neurologic changes after experimental SE. In human studies, occasional patients have reportedly had profound memory and behavioral changes after episodes of complex partial SE. In some reports, the duration of the status was linked with these lasting memory deficits. However, most cohorts of patients with nonconvulsive did not undergo prestatus and poststatus neuropsychologic testing to permit direct comparison. Krumholz and colleagues described 7 cases of serious morbidity and 3 deaths in patients with complex partial SE. The study has been criticized because many of the patients had severe neurologic or medical insults in addition to status, which may have been pivotal in the genesis of their residual neurologic deficits. Nonetheless, 3 patients had prolonged memory and/or other cognitive deficits, possibly provoked by their SE. Data from available studies suggest that nonconvulsive SE alone usually does not cause irreversible neurologic
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.
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.
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 and 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, and Massachusetts Medical Society Disclosure: Nothing to disclose. 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 eMedicine 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. 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
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.
1. Proceedings and abstracts of the First London Colloquium on Status Epilepticus, University College London, April 12-15, 2007. Epilepsia. 2007;48 Suppl 8:1-109. [Medline]. 2. Shorvon SD, Trinka E, Walker MC. The proceedings of the First London Colloquium on Status Epilepticus--University College London, April 12-15, 2007. Introduction. Epilepsia. 2007;48 Suppl 8:1-3. [Medline]. 3. Kälviäinen R. Status epilepticus treatment guidelines. Epilepsia. 2007;48 Suppl 8:99-102. [Medline]. 4. Wilson JV, Reynolds EH. Texts and documents. Translation and analysis of a cuneiform text forming part of a Babylonian treatise on epilepsy. Med Hist. Apr 1990;34(2):185-98. [Medline]. 5. Wolf P, Trinka E, Bauer G. Absence status epilepticus: the first documented case?. Epilepsia. 2007;48 Suppl 8:4-5. [Medline]. 6. Epilepsy Foundation of America. Treatment of convulsive status epilepticus. Recommendations of the Epilepsy Foundation of America's Working Group on Status Epilepticus. JAMA. Aug 18 1993;270(7):8549. [Medline]. 7. Lowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status epilepticus. Epilepsia. Jan 1999;40(1):120-2. [Medline]. 8. Lowenstein DH, Cloyd J. Out-of-hospital treatment of status epilepticus and prolonged seizures. Epilepsia. 2007;48 Suppl 8:96-8. [Medline]. 9. Geier S, Bancaud J, Bonis A, Enjelvin M. [Tele-E.E.G. recordings of three epileptic attacks classified as episodes of PM status (author's transl)]. Rev Electroencephalogr Neurophysiol Clin. Apr-Jun 1977;7(2):201-2. [Medline]. 10. Ellis JM, Lee SI. Acute prolonged confusion in later life as an ictal state. Epilepsia. Apr 1978;19(2):11928. [Medline]. 11. Niedermeyer E, Fineyre F, Riley T, Uematsu S. Absence status (petit mal status) with focal characteristics. Arch Neurol. Jul 1979;36(7):417-21. [Medline]. 12. LÃ¼ders HO, Rona S, Rosenow F, et al. A semiological classification of status epilepticus. Epileptic Disord. Jun 2005;7(2):149-50. [Medline]. 13. Celesia GG. Modern concepts of status epilepticus. JAMA. Apr 12 1976;235(15):1571-4. [Medline]. 14. Treiman DM. Generalized convulsive, nonconvulsive, and focal status epilepticus. In: Feldman E, ed.
Current Diagnosis in Neurology. St. Louis: Mosby-Year Book;1994:11-8. 15. Lennox W, Lennow MA. Epilepsy and Related Disorders. Boston, MA: Little Brown;. 1960. 16. Cascino GD. Nonconvulsive status epilepticus in adults and children. Epilepsia. 1993;34 Suppl 1:S21-8. [Medline]. 17. Shorvon S. The outcome of tonic-clonic status epilepticus. Curr Opin Neurol. Apr 1994;7(2):93-5. [Medline]. 18. White PT, Grant P, Mosier J, Craig A. Changes in cerebral dynamics associated with seizures. Neurology. Apr 1961;11(4)Pt 1:354-61. [Medline]. 19. Aminoff MJ, Simon RP. Status epilepticus. Causes, clinical features and consequences in 98 patients. Am J Med. Nov 1980;69(5):657-66. [Medline]. 20. Meldrum BS, Horton RW. Physiology of status epilepticus in primates. Arch Neurol. Jan 1973;28(1):1-9. [Medline]. 21. Naylor DE, Liu H, Wasterlain CG. Trafficking of GABA(A) receptors, loss of inhibition, and a mechanism for pharmacoresistance in status epilepticus. J Neurosci. Aug 24 2005;25(34):7724-33. [Medline]. 22. Sloviter RS, Zappone CA, Bumanglag AV, Norwood BA, Kudrimoti H. On the relevance of prolonged convulsive status epilepticus in animals to the etiology and neurobiology of human temporal lobe epilepsy. Epilepsia. 2007;48 Suppl 8:6-10. [Medline]. 23. Goodkin HP, Sun C, Yeh JL, Mangan PS, Kapur J. GABA(A) receptor internalization during seizures. Epilepsia. 2007;48 Suppl 5:109-13. [Medline]. 24. Holmes GL. Influence of brain development on status epilepticus. Epilepsia. 2007;48 Suppl 8:19-20. [Medline]. 25. DeLorenzo RJ, Pellock JM, Towne AR, Boggs JG. Epidemiology of status epilepticus. J Clin Neurophysiol. Jul 1995;12(4):316-25. [Medline]. 26. Shinnar S, Pellock JM, Moshe SL, et al. In whom does status epilepticus occur: age-related differences in children. Epilepsia. Aug 1997;38(8):907-14. [Medline]. 27. DeLorenzo RJ, Hauser WA, Towne AR, et al. A prospective, population-based epidemiologic study of status epilepticus in Richmond, Virginia. Neurology. Apr 1996;46(4):1029-35. [Medline]. 28. Shorvon S. Definition, classification and frequency of status epilepticus. In: Shorvon S, ed. Epilepticus: Its Clinical Features and Treatment in Children and Adults. Cambridge: Cambridge University Press; 1994:21-33. 29. Waterhouse EJ, DeLorenzo RJ. Status epilepticus in older patients: epidemiology and treatment options. Drugs Aging. 2001;18(2):133-42. [Medline]. 30. Drislane FW, Blum AS, Lopez MR, Gautam S, Schomer DL. Duration of refractory status epilepticus and outcome: Loss of prognostic utility after several hours. Epilepsia. Jan 19 2009;[Medline]. 31. Rossetti AO, Oddo M, Liaudet L, Kaplan PW. Predictors of awakening from postanoxic status epilepticus after therapeutic hypothermia. Neurology. Feb 24 2009;72(8):744-9. [Medline]. 32. Treiman DM, Meyers PD, Walton NY, et al. A comparison of four treatments for generalized convulsive status epilepticus. Veterans Affairs Status Epilepticus Cooperative Study Group. N Engl J Med. Sep 17 1998;339(12):792-8. [Medline]. 33. Thomas P. How urgent is the treatment of nonconvulsive status epilepticus?. Epilepsia. 2007;48 Suppl 8:44-5. [Medline]. 34. Aicardi J, Chevrie JJ. Convulsive status epilepticus in infants and children. A study of 239 cases.
Epilepsia. Jun 1970;11(2):187-97. [Medline]. 35. Lowenstein DH, Alldredge BK. Status epilepticus. N Engl J Med. Apr 2 1998;338(14):970-6. [Medline]. 36. Hauser WA. Status epilepticus: epidemiologic considerations. Neurology. May 1990;40(5 Suppl 2):9-13. [Medline]. 37. Boggs JG, Marmarou A, Agnew JP, et al. Hemodynamic monitoring prior to and at the time of death in status epilepticus. Epilepsy Res. Aug 1998;31(3):199-209. [Medline]. 38. Krumholz A, Sung GY, Fisher RS, Barry E, Bergey GK, Grattan LM. Complex partial status epilepticus accompanied by serious morbidity and mortality. Neurology. Aug 1995;45(8):1499-504. [Medline]. 39. Treiman DM, Walton NY, Kendrick C. A progressive sequence of electroencephalographic changes during generalized convulsive status epilepticus. Epilepsy Res. Jan-Feb 1990;5(1):49-60. [Medline]. 40. Treiman DM, Meyers PD, Walton NY. DVA Status Epilepticus Cooperative Study Group. Duration of generalized convulsive status epilepticus: relationship to clinical symptomatology and response to treatment. Epilepsia. 1992;33(Suppl 3):66. 41. Treiman DM. Electroclinical features of status epilepticus. J Clin Neurophysiol. Jul 1995;12(4):343-62. [Medline]. 42. Bien CG, Elger CE. Epilepsia partialis continua: semiology and differential diagnoses. Epileptic Disord. Mar 2008;10(1):3-7. [Medline]. 43. Leis AA, Ross MA, Summers AK. Psychogenic seizures: ictal characteristics and diagnostic pitfalls. Neurology. Jan 1992;42(1):95-9. [Medline]. 44. Jagoda A, Richey-Klein V, Riggio S. Psychogenic status epilepticus. J Emerg Med. Jan-Feb 1995;13(1):31-5. [Medline]. 45. Holtkamp M, Othman J, Buchheim K, Meierkord H. Diagnosis of psychogenic nonepileptic status epilepticus in the emergency setting. Neurology. Jun 13 2006;66(11):1727-9. [Medline]. 46. Kutluay E, Beattie J, Passaro EA, Edwards JC, Minecan D, Milling C, et al. Diagnostic and localizing value of ictal SPECT in patients with nonconvulsive status epilepticus. Epilepsy Behav. Mar 2005;6(2):212-7. [Medline]. 47. Assal F, Papazyan JP, Slosman DO, Jallon P, Goerres GW. SPECT in periodic lateralized epileptiform discharges (PLEDs): a form of partial status epilepticus?. Seizure. Jun 2001;10(4):260-5. [Medline]. 48. Karlov VA. Complex partial status epilepticus. Epilepsia. Sep 2007;48(9):1815. [Medline]. 49. Brenner RP. EEG in convulsive and nonconvulsive status epilepticus. J Clin Neurophysiol. Sep-Oct 2004;21(5):319-31. [Medline]. 50. Kaplan PW. The EEG of status epilepticus. J Clin Neurophysiol. Jun 2006;23(3):221-9. [Medline]. 51. DeLorenzo RJ, Waterhouse EJ, Towne AR, et al. Persistent nonconvulsive status epilepticus after the control of convulsive status epilepticus. Epilepsia. Aug 1998;39(8):833-40. [Medline]. 52. Szabo K, Poepel A, Pohlmann-Eden B, Hirsch J, Back T, Sedlaczek O, et al. Diffusion-weighted and perfusion MRI demonstrates parenchymal changes in complex partial status epilepticus. Brain. Jun 2005;128:1369-76. [Medline]. 53. Rossetti AO. Which anesthetic should be used in the treatment of refractory status epilepticus?. Epilepsia. 2007;48 Suppl 8:52-5. [Medline]. 54. Arif H, Hirsch LJ. Treatment of status epilepticus. Semin Neurol. Jul 2008;28(3):342-54. [Medline]. 55. Parviainen I, Uusaro A, Kalviainen R, et al. Propofol in the treatment of refractory status epilepticus.