Focal unaware status epilepticus …

Fernando Cendes MD PhD

Epilepsy & Seizures

Updated 03.05.2024
Released 04.26.2001
Expires For CME 03.05.2027

Focal unaware status epilepticus

Author: Fernando Cendes MD PhD

See Contributor Disclosures

Editor: Jerome Engel Jr MD PhD

Focal unaware status epilepticus

In This Article

Quick Link

Introduction

Overview

The most recent classification of seizure types by the International League Against Epilepsy (ILAE) proposed to eliminate the terms dyscognitive, simple partial, complex partial, psychic, and secondarily generalized seizures (89). The term focal seizures with impaired awareness substituted that of complex partial seizures (89). However, this position paper of the ILAE commission for classification and terminology did not consider “dyscognitive” as a synonym for “complex partial” (89).

The term dyscognitive seizures was described by Lüders and colleagues as seizures causing “interference of high cognitive functions essential for fully intact consciousness, including alterations of praxis (apraxia), language (aphasia), and the patient's ability to form memories (amnesia). These alterations of consciousness do not affect the arousal system or postural muscle tone, and the patient remains partially aware of the external and internal environment, even if the alterations of cognition may interfere somewhat with its perception. Dyscognitive seizures are best identified by listing the specific cognitive disturbance (apraxic seizures, aphasic seizures, amnestic seizures, and so on)” (182). Thus, dyscognitive seizures could be translated as focal seizures with impaired awareness that do not affect the arousal system or postural muscle tone. However, most of the studies discussed herein do not differentiate dyscognitive status from focal status epilepticus with impaired awareness that affect the arousal system or postural muscle tone. In keeping with the most recent ILAE proposal, we will use here the term focal seizures with impaired awareness or focal unaware seizures instead of dyscognitive seizures (89).

Focal unaware status represents a most intriguing epileptic condition. Variable confusion and responsiveness, impaired memory of the event, fluctuating and often bizarre behavior—including automatisms—and sometimes lateralizing signs, such as aphasia, are usually present. However, if focal unaware status presents only with subtle signs and symptoms of cognitive and autonomic impairment, it might be difficult to recognize and differentiate from psychiatric conditions. EEG remains essential to diagnose focal unaware status epilepticus and to differentiate it from generalized nonconvulsive status epilepticus (absence status). Causes of focal unaware status epilepticus include acute and chronic focal cerebral injuries, including ischemic stroke, intracranial hemorrhage, abscess, meningoencephalitis, neoplasias, malformations, and a history of epilepsy. Medications and other metabolic and systemic stressors (eg, infections, hypoxemia) may be implicated or superimposed. The list of differential diagnosis includes toxic or metabolic encephalopathy, delirium, psychiatric conditions, limbic encephalitis, and transient global amnesia. Of particular importance are the more recently described syndromes associated with antibodies against synaptic proteins that may occur with or without cancer, including limbic encephalitis with antibodies directed towards the antigens of the voltage-gated potassium channel complex (LGI1, CASPR2, Contactin-2), as well as other antibodies (to NMDA receptors [NMDARs], AMPA receptors [AMPARs], and GABA type B receptors [GABABRs]). In this updated article, the author discusses evidence about diagnosis and treatment of focal unaware status epilepticus.

Key points

	• Focal unaware seizures produce impairment in cognition, including perception, attention, emotion, memory, or the ability to perform complex executive functions. The clinical presentation may not be recognized as a seizure manifestation, and EEG is crucial for diagnosis and management of dyscognitive status epilepticus.
	• Focal unaware epilepticus, as in other types of status epilepticus, is defined as focal unaware seizures lasting 10 minutes or longer. However, a clinical operational definition of 5 minutes of continuous seizure provides an appropriate indication for initiating treatment.
	• Focal unaware and other forms of nonconvulsive status epilepticus are often misdiagnosed. A high index of suspicion is necessary in patients who received treatment for convulsive status epilepticus and do not recover, in critically ill patients with acute encephalopathy, and in patients with focal epilepsy with inappropriate behavior of confusional state.
	• The treatment of status epilepticus has potential risks, and aggressive treatment with sedation and intubation may not be appropriate for some patients with focal unaware status epilepticus, in particular for older patients with serious comorbidities. In these situations, treatment with less sedative antiepileptic drugs should be considered.

Historical note and terminology

Status epilepticus was infrequently recorded up to the dissertation of Louis Calmeil, where the expression “etat de mal” is first found, but still in the notion of generalized convulsive status epilepticus only (33). The proceedings of the 10th Marseilles Colloquium of 1962 represent the first book on this subject (99). At the Marseilles Colloquia 1962 and 1964, definitions and classifications of seizures and of status epilepticus were proposed with the obvious notion that there are as many types of status as types of seizures.

Trousseau was probably the first who observed that petit mal seizures might, as with grand mal, occur in such frequency "that one seizure would become confused with the next, simulating a continuous seizure that might persist for 2 or 3 days" (288). But, although Trousseau identified petit mal status, his was not the first description of nonconvulsive status epilepticus. In 1822, Prichard described cases of epileptic fugue and furor as well as "epileptic ecstasy" (221). Bright, as well as Charcot, described fugue states, and Hughlings Jackson described such a condition in temporal lobe epilepsy (28; 39; 272).

In 1954, Penfield and Jasper identified recurrent sensory phenomena (simple partial status epilepticus; aura continua) and found them to be "at least as common as continuing circumscribed movements" (213). In 1945 and 1960, Lennox and Lennox used the term petit mal status for psychiatric conditions associated with continuous bifrontal spike-wave activity and with a duration of hours to days (172; 173).

The questions of whether psychomotor seizures (referred to the temporal lobe) also could occur as a status epilepticus and whether such status activity could be the underlying cause for prolonged twilight states were, however, for a long time controversially discussed (166; 97).

The most important early literature dealing with psychomotor status epilepticus has been focused on the phenomenological description of this condition, distinguishing the discontinuous form, characterized by the occurrence of psychomotor attacks that follow each other at 2- to 10-minute intervals, from the continuous form (133; 328).

Major reviews on status epilepticus were the Santa Monica, California Conference (114) and the Seventeenth Annual Merritt-Putnam in Boston, which was published as a supplement to Epilepsia (62; 183). In the same year, five position papers on nonconvulsive status epilepticus were published in the Journal of Clinical Neurophysiology (141). Comprehensive reviews on the behavioral manifestations, presentation, evaluation, and treatment followed (71; 142; 152).

The London Innsbruck Colloquia on Status Epilepticus have discussed and reviewed current advances on molecular and basic science, as well as clinical and therapeutic aspects of status epilepticus (250; 250), and a new proposal for definition and classification of status epilepticus was proposed by a ILAE task force (282).

Definition and problems with definition

Status epilepticus. The term status was used "whenever a seizure persists for sufficient length of time (subsequently defined as at least 30 to 60 minutes) or is repeated frequently enough to produce a fixed or enduring epileptic condition.” This definition is enshrined into the World Health Organization dictionary of epilepsy as well as the Handbook of clinical neurology and Handbook of electroencephalography and clinical neurophysiology (96; 232; 100). A widely accepted operational definition of status epilepticus was that of a condition in which epileptic activity persists for 30 minutes or more (268). The ILAE Task Force on Classification of Status Epilepticus proposed a new definition of status epilepticus to account for the heterogeneous etiology, phenomenology, and prognosis of nonconvulsive status epilepticus (282). This definition incorporates elements of time (termed T1 and T2) and four additional axes (semiology, etiology, EEG correlate, and age). T1 indicates when seizures need to be acutely treated (eg, 10 minutes for focal status epilepticus with impaired awareness and 10 to 15 minutes for absence status epilepticus). T2 indicates the time at which the likelihood of permanent neuronal injury increases, and more aggressive therapy may be justified (more than 60 minutes for focal status epilepticus with impaired awareness and unknown for absence status epilepticus) (282).

It is estimated that there are between 65,000 and 150,000 cases of status epilepticus in the United States each year, and that approximately 25% are nonconvulsive (34; 132; 278; 147). At least 10% of patients with epilepsy suffer a status epilepticus during the course of their disease, and 50% of status epilepticus appears in patients with no known history of epilepsy (240). Status epilepticus is more frequent in developmental and epileptic encephalopathies and epilepsies with structural etiologies, particularly those arising from trauma, tumor, or infection involving the frontal lobe. Both acute and remote cerebral insults can cause status epilepticus, as can severe systemic disease that causes status epilepticus secondary to a toxic-metabolic encephalopathy. Status epilepticus is present in nearly all types and syndromes. Tonic-clonic status epilepticus is the best-known type, and its diagnosis is simple, but focal status epilepticus presents a diagnostic challenge. Particularly difficult clinically is the differential diagnosis of dyscognitive focal status epilepticus, absence status epilepticus, and above all, the form termed "late-onset de novo absence status epilepticus,” which may present as confusional syndrome in the elderly (240; 26; 153; 246).

Nonconvulsive confusional status epilepticus. Nonconvulsive confusional status epilepticus has been categorized into groups having focal or generalized EEG epileptic activity and by etiology and level of consciousness, which predict outcome (143; 251). Based on ictal EEG, a classical separation is: (1) absence status and (2) focal unaware status epilepticus. The differential diagnosis is difficult on the basis of clinical semiology alone. Absence status can complicate many epileptic syndromes; it is characterized by confusion of varying intensity and is associated in 50% of cases with bilateral myoclonia (274). The EEG shows ictal generalized paroxysmal activity; normalization is obtained after benzodiazepine injection.

The search for a new classification scheme for status is justified by the fact that there are types of status in which no overt "seizure" occurs, including epileptic confusional states. Moreover, there are other borderline or boundary conditions as, for example, lateralized periodic discharges (LPDs) or periodic lateralized epileptiform discharges (PLEDs) in the EEG (40; 203; 174). LPDs are a matter of controversy, and many authors believe that this EEG pattern reflects severe cerebral dysfunction rather than epileptic activity (130; 285; 174). However, when LPDs occur in a comatose patient after a generalized tonic-clonic status epilepticus, the diagnosis of nonconvulsive status epilepticus should be considered. By contrast, LPDs or continuous EEG abnormalities in the context of acute cerebral damage, such as stroke or anoxic or traumatic brain damage, are more difficult to interpret (266; 130; 174). However, ictal EEG patterns with a typical spatiotemporal evolution faster than 2.5 Hz in a comatose patient reflect nonconvulsive seizures or nonconvulsive status epilepticus and should be treated (285).

The 2006 proposal of the ILAE Classification Core Group (77), an attempt to complete the earlier work of the Task Force on Classification and Terminology, differentiates "self-limited epileptic seizure types" from "Status epilepticus". Under "Status epilepticus," this report lists nine headings: (I) epilepsia partialis continua of Kojevnikov, (II) supplementary motor area (SMA) status epilepticus, (III) aura continua, (IV) dyscognitive focal (psychomotor, complex partial) status epilepticus, (V) tonic-clonic status epilepticus, (VI) absence status epilepticus, (VII) myoclonic status epilepticus, (VIII) tonic status epilepticus, and (IX) subtle status epilepticus.

The category (IV) focal unaware (dyscognitive focal, psychomotor, complex partial) is divided into (A) mesial temporal and (B) neocortical. The explanatory text for these two subtypes is as follows: "Mesial temporal: Focal status epilepticus, predominantly involving mesial limbic structures, consists of serial focal unaware ictal events without return of clear consciousness in between. Onset can be limited to one side, or can alternate between hemispheres,” and "Neocortical: Focal status epilepticus originating in various neocortical regions can present with a wide variety of unpredictable clinical patterns. Status epilepticus from some frontal foci can resemble absence status or generalized tonic-clonic status. It can present as repetitive discrete behavioral seizures. To some extent, this type of status epilepticus can reflect the neocortical region of origin. For example, occipital status epilepticus might present with unexplained blindness, whereas dysphasia or aphasia could represent focal status in language cortex" (77).

The 2015 report of the ILAE Task Force on Classification of Status Epilepticus proposes the following four axes for defining subtypes of status epilepticus: (1) semiology; (2) etiology; (3) EEG correlates; and (4) age (282). Ideally, every patient should be categorized according to each of these four axes; however, they acknowledge that this will not always be possible. Axis 1 (semiology) refers to the clinical presentation and is, therefore, the backbone of this classification. The two main taxonomic criteria are the presence or absence of prominent motor symptoms and the degree (qualitative or quantitative) of impaired consciousness. Those forms with prominent motor symptoms and impairment of consciousness may be summarized as convulsive as opposed to the nonconvulsive forms of status epilepticus (282).

Clinical manifestations

Presentation and course

Focal unaware status epilepticus often begins with a history of recurrent or prolonged focal seizures, or it may follow or precede a generalized convulsive seizure. Patients with mesial temporal status often are confused and exhibit variable responsiveness. Memory of the event usually is impaired. Behavior may fluctuate or be bizarre. Often, patients exhibit clinical automatisms as with typical focal seizures with impaired awareness, including repetitive lip-smacking, fumbling, or swallowing movements. Subtle nystagmus may be observed. The range of confusion can be great. Some patients present with mildly diminished responsiveness and others with frank stupor or a catatonic state. Aphasia and other localizing signs and symptoms (eg, dystonic hand posturing) may accompany mesial temporal dyscognitive focal status.

Table 1. Criteria for the Diagnosis of Focal Unaware Status Epilepticus

	• Recurrent focal unaware seizures without full recovery of consciousness between seizures, or a continuous "epileptic twilight state" with cycling between unresponsiveness and partially responsive phases (lasting greater than 10 minutes). However, a clinical operational definition of 5 minutes of continuous seizure provides an appropriate indication for initiating treatment.
	• Ictal EEG with recurrent epileptiform patterns like those seen in isolated focal unaware seizures.
	• With exceptions, an observable effect of IV antiepileptic drug on both ictal EEG and clinical manifestations of the status
	• Interictal EEG with a consistent epileptiform focus, usually in one or both temporal lobes
With modifications adapted from (279; 158; 282)

For the purpose of this article, we would like to suggest the following operational definition (Table 1): focal unaware status epilepticus is an epileptic condition (defined by clinical and electroencephalographic signs and symptoms) of at least 10 minutes or more in duration, with a large spectrum of clinical manifestations and encompassing subtle clinical signs as well as some behavioral disturbances and psychosis-like states, in particular complex (polymodal) hallucinations with at least a temporary alteration of consciousness. Furthermore, we ask for additional first-order-plausibility criteria that set the level in the sense that (1) observed symptoms should fit with the known functional anatomy and, thus, with localization of the EEG-discharge; and (2) (in the case of more diffuse and difficult-to-describe personality and behavioral changes) that there is a clear-cut relationship in time between particular subtle signs and symptoms and the epileptic EEG activity.

Nonconvulsive status epilepticus refers to focal seizures without impaired awareness (aura continua), focal unaware status, and absence status epilepticus. Focal unaware status epilepticus and absence status epilepticus exhibit an epileptic twilight state of altered contact with the environment. In focal status epilepticus without impaired awareness (aura continua), no impairment of consciousness occurs, and the behavior changes reflect focal ictal discharges confined to a circumscript area of the cortex.

Onset can be sudden or insidious. In the best documented cases, the focal unaware status condition evolved gradually with minor symptoms (aura continua) in the beginning. The type of the aura continua depended on the initially circumscribed discharge localization reflecting the functional anatomy of the brain. In those circumstances where the onset zone was located in the neocortex, the hallucinations often were unimodal at the beginning (ie, visual if the EEG discharge was in the visual and acoustic if the discharge was in the acoustic cortex). With progressive spread of the ongoing epileptic discharges into mesial temporolimbic core structures, the quality of the hallucinations became more complex, and polymodal complex hallucinations, autonomous-vegetative signs, and signs and symptoms in the emotional and affective sphere prevailed. On the other hand, a recognizable seizure event might be at the beginning, and the focal unaware status manifests itself as ictal twilight state with ongoing discharges in some (usually temporolimbic) structures.

The typical overall gestalt of a focal unaware mesial temporal (or limbic) status epilepticus is that of a fluctuating, waxing-waning condition with alterations of restless, sometimes fearful, and agitated behavior with memory flashbacks, experiential hallucinations, delusions, and hallucinations. Automatisms can be present. This contrasts with the more monotonous three per second spike slow-wave absence status (spike wave stupor) with clouded consciousness and slowed and impaired thinking. Nowack and Shaikh suggest that focal unaware status epilepticus can progress through stages (defined by EEG) analogous to those described by Treiman in generalized convulsive status epilepticus (278; 205).

Some authors have designated subtypes of focal nonconvulsive status epilepticus according to the prevailing signs and symptoms (193; 98; 318). In focal unaware status, the following categories of signs and symptoms can prevail: somatosensory signs and symptoms with dysesthesia as well as visual, acoustic, olfactory, gustatory, and autonomic phenomena.

The predominance of dysphasic or aphasic signs and symptoms is far less frequent but well documented as the sole manifestation of focal status epilepticus (295; 97; 112; 67; 223; 309; 200; 108; 66; 291; 45; 287; 216; 113). Kirshner and colleagues describe aphasia secondary to focal status epilepticus of the basal temporal language area (146). Ozkaya and colleagues describe aphasic status epilepticus with periodic lateralized epileptiform discharges in a bilingual patient with a clinical course, which supports the belief that a second language area for a second language learned in later stages of life is located in an area of the brain different from that for the native language (207). Cases where aphasia is the sole ictal symptom or long-lasting aphasia of epileptic origin, as in aphasic status epilepticus, could present a challenging diagnosis (227; 134; 139).

Landau-Kleffner syndrome (syndrome of acquired epileptic aphasia) must also be mentioned here. This childhood disorder, in which persisting aphasia develops in association with severe focal EEG abnormalities, was described in 1957 by Landau and Kleffner and in 1971 by Worster-Drought (165; 329; 164). Billard and colleagues describe four cases with acquired aphasia with electrical subclinical status epilepticus and acquired aphasia in epileptic children (21). Although more than 200 cases have been reported, the etiology, pathogenesis, and pathophysiology are still widely unknown (249).

Halasz and colleagues presented a unifying concept of the syndromes of self-limited focal childhood epilepsies, Landau-Kleffner syndrome, and electrical status epilepticus in sleep, treating them as a spectrum of disorders with a common transient, age-dependent, nonlesional, genetically based epileptogenic abnormality (110).

Symptoms and signs observed in focal unaware status epilepticus of the neocortical subtype usually reflect the functional specialization of the neocortical area of origin.

It is well known that autonomic symptoms can be the leading ictal feature (317). Rabending and Fischer describe nonconvulsive status epilepticus with ictal bradycardia and asystolia (228). Umbilical sensations in children and long-lasting borborygmi, widened pupils, pilomotor phenomena, goose-flesh or periodically shivering, and so on have been described (30; 292; 312; 324; 314; 315; 316; 324; 106; 264). In Panayiotopoulos syndrome, Panayiotopoulos and Koutroumanidis document recurrent autonomic status epilepticus with emesis (209; 210; 155; 273; 86). Autonomic status epilepticus is often accompanied by certain peculiarities of personality and behavior; therefore, we describe autonomic phenomena in the context of limbic dyscontrol syndrome (102; 314). Common overt or subtle behavioral changes are irritability, fear, panic, and sometimes existential emptiness or some other form of pathological self-perception. Particularly rare ictal or status symptoms, however, are aggression (62) or fear (121; 193).

Limbic encephalitis may present with similar autonomic features and other typical semiology of mesial temporal lobe seizures. Autonomic symptoms occur in 50% or more of patients with autoimmune encephalitis associated with leucine-rich glioma-inactivated protein 1 (LGI1) and glutamic acid decarboxylase (GAD) antibodies (138). Déjà-vu and other ictal experiential phenomena occur in patients with GAD and less frequently in N-methyl-D-aspartate receptor (NMDAR) antibodies (138). New onset focal status with experiential symptoms and acute memory complaints are more frequent in NMDAR encephalitis (138). Wieser and colleagues describe a pilomotor status epilepticus in nonparaneoplastic limbic encephalitis with antibodies to voltage-gated potassium channels (299; 326).

Evidence that long-lasting pain is a special form of focal status epilepticus is scant, but this possibility should not be completely discarded (311; 327; 241; 332; 95; 253; 245).

Prognosis and complications

Sequelae associated with status epilepticus are best documented with convulsive status epilepticus, but might also be associated with certain types of nonconvulsive status epilepticus (158). The morbidity of nonconvulsive status epilepticus that follows a nonconvulsive status is high (42; 73). One study in patients with status showed that older age, long duration, and nonconvulsive status epilepticus in coma were associated with new neurologic deficits, which were predictors of long-term mortality (230).

There is experimental as well as clinical evidence that generalized convulsive status epilepticus produces lasting neuropathological damage in the hippocampus, neocortex, and cerebellum due to associated metabolic failure. Cerebellar (Purkinje and basket cell) damage was related particularly to hyperpyrexia and hypotension, and was prevented by control of the systemic metabolic derangements (ie, hyperpyrexia, hypotension, hypoxia, acidosis, and hypoglycemia) (195; 60).

Morbidity and mortality in relation to etiology. The previous notion that nonconvulsive status epilepticus is a relatively benign entity is not true (195; 255; 73). Treiman and colleagues found higher mortality rates in nonconvulsive status epilepticus compared to generalized convulsive epilepticus, 65% and 27% respectively (280). The outcome of nonconvulsive status epilepticus is worse in patients without previous history of epilepsy than in patients with epilepsy (220).

Etiology is the main factor determining outcome (286). Other factors influencing outcomes for both convulsive and nonconvulsive status epilepticus are (1) duration, and (2) treatment of the status epilepticus, as well as (3) age of the patient (73; 230). Mortality and morbidity are lower in children compared to adults: death (10% to 35%), intellectual and other neurologic morbidity (10% to 35%), chronic epilepsy (30% of children first presenting with status), and recurrent status epilepticus (15% to 20%) (248).

Nonconvulsive status epilepticus (and focal motor seizures) at onset have been identified as risk factors for refractory convulsive status epilepticus (190).

Absence status epilepticus appears to cause no lasting effects (Niedermeyer and Khalife 1965; 07; 275; 103).

Because classical focal unaware status epilepticus usually occurs in patients with known epilepsy, it is difficult to determine its risks and complications. The theoretical basis for neuronal injury resulting from focal unaware status epilepticus may be identical to that from generalized convulsive. Although most reported cases of the disorder have returned to baseline neurologic function, several patients have had prolonged memory deficits (78; 191; 279; 47). Varon and colleagues reported on a transient Kluver-Bucy syndrome following complex partial status epilepticus (293).

It is difficult to dissect out that portion of the long-term harm done by epileptiform discharges or nonconvulsive status epilepticus from that related to the underlying illness (225; 226; 258; 333). In general, when nonconvulsive status epilepticus has been reported concurrent with acute brain injury, poor outcomes have been attributed to the acute brain injury. Nonconvulsive status epilepticus in such a constellation has been seen as an epiphenomenon, not necessarily as a contributing cause of brain damage (140; 04). However, evidence suggests that nonconvulsive status epilepticus might significantly increase the vulnerability of the brain to permanent damage by mechanisms of secondary injury (296; 230). Biochemical evidence supports this deleterious synergy. DeGiorgio and colleagues found the highest levels of serum neuronal enolase (a marker of neuronal injury) in patients with combined status epilepticus and acute brain injury (59).

For focal unaware status epilepticus, several studies indicate that prolonged memory deficits can occur (78; 279; 159; 230).

Clinical vignette

A 43-year-old man is brought to the emergency room by paramedics because he was seen in a shopping mall “confused,” exhibiting inappropriate behavior, and unable to speak clearly. The attending physician prescribed haloperidol, which worsened his confusion and made him fluctuate between agitation and somnolence. Later on a family member arrived at the hospital and informed that the patient had temporal lobe epilepsy and may have forgotten to take his medications. A neurologist was called for consultation and ordered an EEG that showed diffuse slow waves and frequent rhythmic sharp waves in the temporal lobes, as well as repetitive ictal discharges over the left temporal lobe region. He was given intravenous diazepam with improvement of the EEG seizure activity. After receiving a loading dose of intravenous phenytoin, he gradually improved his cognition and was back to normal 12 hours later.

Focal unaware status epilepticus is pleomorphic and often misdiagnosed. This diagnosis should always be considered in patients with focal epilepsies with abrupt inappropriate behavior of confusional state, as well as in patients who received treatment for convulsive status epilepticus and do not recover, and in critically ill patients with acute brain damage.

Biological basis

Localization

It is obvious that focal unaware status epilepticus of the mesial temporal subtype involves the limbic system, with the hippocampal formations and nuclei amygdalae as its core structures.

The hippocampal formation has been shown to be able to discharge in a status-like manner during depth recordings (320). Discharge-associated signs and symptoms might be subtle (electrical status epilepticus with minor symptoms) but consistent with hemisphere-specific deficits in tachistoscopic lexical recognition tasks and face matching tasks respectively (320). This is in line with H2O positron emission tomography data attributing associative functions (ie, associative binding) to the hippocampal formation (117; 120; 119; 118).

The nuclei amygdalae are candidates for explaining the rich and multifaceted signs and symptoms observed in limbic seizures and limbic status epilepticus. This is because nearly all cortical areas of the temporal lobe, major parts of the frontal lobe, and the insular cortex project to the amygdala (18). Some amygdaloid nuclei receive several cortical sensory projections with substantial convergence of cortical input. It is well documented that visual, auditory, olfactory, and, to some extent, taste information reaches the amygdala. Somatosensory input is less clear, but there is reason to believe that all five modalities have some convergence in the dorsomedial part of the lateral nucleus. For example, the dorsomedial part of the lateral nucleus receives projections from the orbitofrontal area, which responds to olfactory stimulation; this part is also the major amygdaloid projection zone of the cortical taste area. In addition, there are posterior insular cortex projections to this area carrying visceral, and probably other, somatic information. Moreover, auditory input from the temporal polar cortex projects powerfully to this region. Visual projections are directed primarily to the dorsolateral part of the lateral nucleus (319).

Dyscognitive focal status epilepticus of the neocortical subtype usually reflects the functional specialization of the neocortical area of origin, ie, it is associated with a rather specific pattern of signs and symptoms.

The role of the insular cortex in dyscognitive focal status epilepticus is not well established. Insular cortex has not been a favorite target for depth recording because of the increased risk of bleeding following insertion of depth electrodes. Some magnetoencephalographic studies in Landau-Kleffner syndrome, however, have localized the spike generator in this syndrome into the intrasylvian cortex (208).

Pathophysiology

In humans, the underlying pathophysiology of the various subtypes of nonconvulsive status epilepticus remains largely undetermined. Because the prolonged epileptic discharges are the hallmark of a status epilepticus, the impairment of seizure terminating mechanisms in local networks may be the common denominator. The absence status, and probably some borderline forms resembling dyscognitive status epilepticus, may result from excessive recurrent inhibition through thalamocortical circuits, and, thus, would not be mediated by excitotoxic effects of NMDA activation (93; 129). Therefore, some forms of nonconvulsive status epilepticus may be more benign than others. There is some evidence of neuronal injury in focal unaware status epilepticus (116) and nonconvulsive status epilepticus associated with severe brain injury (159; 137; 334). DeGiorgio and colleagues found elevated neuro-specific enolase in cerebrospinal fluid and serum during focal unaware and myoclonic nonconvulsive status epilepticus (58; 59).

With the wide availability of magnetic resonance imaging and positron emission tomography, a large amount of peri- and post-ictal changes on both anatomic and functional imaging examinations has been recognized (50; 70; 128; 269; 13).

A rat model of nonconvulsive limbic status for 12 to 24 hours results from a 90-minute period of continuous electrical stimulation of the hippocampus (180). With a latency of approximately 1.5 months, the rats developed spontaneous recurrent seizures and pathological changes identical to human mesial temporal sclerosis (19). Nairismagi and colleagues reported similar findings demonstrating progressive neurodegeneration in amygdala and hippocampus after status epilepticus induced in rats by electrical stimulation of the amygdala (201).

These models, centered on the limbic system, provide good experimental basis for suggesting that focal status epilepticus with impaired awareness may induce long-term sequelae (201). Similar conclusions may be drawn from a study of pilocarpine-induced time-limited nonconvulsive status epilepticus in rats by Krsek and colleagues (157). Sloviter and Olney and colleagues found comparable results by stimulating the perforant path (206; 257). With these and similar experiments, they concluded that neuronal damage was directly related to the duration and intensity of electrographic seizure activity, in particular high-frequency (about 10 Hz) discharges lasting over 20 minutes. Spike and sharp-wave discharges with a frequency less than 1 Hz produced no damage (181).

Gorter and colleagues found that in their rat model for mesial temporal lobe epilepsy, neuronal cell death was induced by the initial status epilepticus and not by later repeated spontaneous seizures (104).

Wasterlain and colleagues list evidence that self-sustaining status epilepticus might be a condition maintained by potentiation of glutamate receptors and by plastic changes in substance P and other peptide neuromodulators (305). Coulter and DeLorenzo stressed the fact that status epilepticus is difficult to produce in vitro in normal extracellular medium, suggesting that seizure-terminating mechanisms are normally robust (54). To produce long-duration, self-sustained epileptic discharges in vitro, they have found it necessary to include reciprocally connected entorhinal cortex with hippocampal slices. They conclude that reentrant activation from distant sites may be necessary for maintenance of status epilepticus-like activity of long duration.

Acute consequences of experimental limbic status epilepticus are alterations in membrane potential and membrane properties of hippocampal pyramidal cells accompanied by alterations in neurotransmitter-activated conductances and receptor expression. Some of these acute alterations in receptor and transmembrane ion-gradient may be critically involved in the development of drug resistance during the late stages of status epilepticus. Indeed, the multidrug transporter P-glycoprotein (PGP) is overexpressed in several regions of the temporal lobe including endothelial cells of the dentate gyrus and parenchymal cells of the CA1 and CA3 sectors of the hippocampus and the amygdala (244). In the study of Seegers and colleagues, kainate was administered at a dose that produced a generalized convulsive status epilepticus, which was limited to a duration of 90 minutes by diazepam (244). However, most P-glycoprotein increases seen 24 hours after status epilepticus were only transient: 10 days after the kainate-induced status epilepticus, no significant differences to controls were determined except for an increase in parenchymal P-glycoprotein expression in the dentate hilus and CA1 sector.

Suopanki and colleagues showed that kainic acid-induced status epilepticus produces changes in the expression and localization of endogenous palmitoyl-protein thioesterase 1, the deficiency of which causes drastic neurodegeneration (265). Immunological stainings showed that status epilepticus in adult rats led to a progressive and remarkable increase of palmitoyl-protein thioesterase 1 in limbic areas of the brain. Within 1 week, the maximal expression was observed in CA3 and CA1 pyramidal neurons of the hippocampus. In the surviving pyramidal neurons, palmitoyl-protein thioesterase 1 localized in vesicular structures in cell soma and neuritic extensions. After seizures, colocalization of palmitoyl-protein thioesterase 1 with synaptic membrane marker (NMDAR2B) was enhanced. Further, synaptic fractionation revealed that after seizures palmitoyl-protein thioesterase 1 was readily observed on the presynaptic side of synaptic junction. These data suggest that palmitoyl-protein thioesterase 1 may protect neurons from excitotoxicity.

Rogawski and colleagues summarized the evidence that GluR5 (GLU(K5)) kainate receptors, a type of ionotropic glutamate receptor, play a role in the amygdala's vulnerability to seizures and epileptogenesis (231). Topiramate at low concentrations causes slow inhibition of GluR5 kainate receptor-mediated synaptic currents in the basolateral amygdala, indicating that it may protect against seizures, at least in part, through suppression of GluR5 kainate receptor responses. The use of topiramate in human refractory status epilepticus has been discussed and showed good efficacy (277; 24).

Thus, experimental evidence suggests that the brain reorganizes itself in response to excess neural activation. Contributing factors to this reorganization include activation of glutamate receptors, second messengers, immediate early genes, transcription factors, neurotrophic factors, axon guidance molecules, protein synthesis, neurogenesis, and synaptogenesis. Some of the resulting changes contribute to seizure susceptibility. Neuronal loss as a consequence of limbic status activity contributes to circuit restructuring. Loss of selective types of interneurons, alteration of GABA receptor configuration, or decrease in dendritic inhibition contribute to the development of spontaneous seizures (92; 197; 198; 08; 192). Conversely, development of an epileptic condition enhances the susceptibility of the limbic system to trigger status epilepticus discharges. An episode of status epilepticus that involves the limbic system clearly elicits brain damage, at least among adult animals. Furthermore, evidence exists that some effects of status epilepticus in rats, such as the one on hippocampal GABA-A receptors, are age-dependent (336).

Thus, from experimental evidence it might be concluded that long-term consequences of status epilepticus in the limbic system include alterations in patterns of expression of neurotransmitter receptors and in the function of excitatory and inhibitory synapses, cell loss, and circuit rearrangements within the limbic system. An episode of status epilepticus that involves the limbic system clearly elicits brain damage, at least among adult animals. This brain damage can contribute to the development of epilepsy. Conversely, development of an epileptic condition enhances the susceptibility of the limbic system to trigger status epilepticus discharges.

Differential diagnosis

Confusing conditions

The clinical characteristics of nonconvulsive status epilepticus may be highly variable. By including (arguably incorrectly) any state with altered mental status that also has epileptiform features on the EEG in the category of nonconvulsive status epilepticus, the literature encompasses a wide spectrum of clinical concomitants: from focal neurologic deficits to Wernicke aphasia, neuropsychiatric manifestations, confusion, and learning difficulties in children and adolescents (262; 123; 161; 274; 291; 152).

Classification is difficult and presently might be best accomplished along several axes (Table 2). Focal unaware status should certainly be distinguished from absence status. The classical absence status primary criteria have been established (Table 3), but in reality, many cases are borderline or atypical (122). Rona and colleagues present a semiological classification of status epilepticus focusing on the main clinical manifestations and the evolution of the status episode (233). The clinical manifestations are subdivided into semiological components and classified along three axes: the type of brain function predominantly compromised by the seizure activity, the body part involved, and its evolution over time. Each axis contains several subcategories, so that many different levels of accuracy are possible.

Table 2. Classification of Status Epilepticus Along the Axes (1) Convulsive - Nonconvulsive, and (2) Generalized - Focal

	Convulsive	Nonconvulsive
Generalized	Tonic-clonic Tonic Myoclonic	Absence
Focal	Focal motor	Dyscognitive (focal non-motor with impaired awareness) Focal nonmotor without impaired awareness (aura continua)
• Other related epileptiform encephalopathies • Electro-encephalographic status epilepticus • Subtle status epilepticus
Note: The third axis would be continuous - intermittent (discontinuous). The fourth could describe whether status appears de novo, in people with epilepsy, or in severely ill patients; the fifth axis could list whether status epilepticus appears in wakefulness or different forms of sleep, particularly slow wave sleep, or both (158).

Table 3. Criteria for absence status epilepticus

	• Prolonged change of consciousness or behavioral function (greater than 15 min)
	• Generalized epileptic EEG abnormality (in classical cases 3/sec spike slow-waves) that is definitively changed from the preictal state
	• A prompt observable effect of IV antiepileptic drug on both ictal EEG and clinical manifestations of the status
Adapted from (219; 158; 282)

In nonconvulsive status epilepticus, the level of consciousness may range from a barely discernible (if any) decrease in level of consciousness or alteration in cognition to comatose states in the face of severe anoxia. The term “nonconvulsive status epilepticus” is unsatisfactory because the original use of it, which referred to "the wandering confused" (Charcot patient), has now evolved to include the comatose, gravely ill patient in the intensive care unit (27). Most of these patients have myriad medical and metabolic problems (303).

Behavioral changes may be difficult to identify as being ictal in nature. The gold standard is continuous EEG monitoring (285; 65). Seshia and McLachlan argue that symptom abolition after surgery might be sufficient to prove the epileptic nature (245).

With nonconvulsive status epilepticus, affect and mood alteration may vary widely, alternating between a state of delirium or mania-like episodes with inappropriate laughter to depression. Patients will act strangely or have speech problems that range from the inappropriate “word salad” to mutism. Echolalia-palilalia as the sole manifestation of nonconvulsive status epilepticus and global developmental delay as the main manifestation of nonconvulsive status epilepticus in a toddler have been described (176; 247).

Differential diagnosis of the Landau-Kleffner syndrome and other conditions in the spectrum of epileptic encephalopathies with spike-and-wave activation in sleep (SWAS), also known as electrical status epilepticus in sleep, should observe several facts. SWAS are characterized by various combinations of cognitive, language, behavioral, and motor regression associated with marked spike-and-wave activation in sleep (270; 247; 68; 260). Landau–Kleffner syndrome (LKS) is a specific subtype of epileptic encephalopathy with spike-and-wave activation in sleep, where regression affects mainly language, with an acquired auditory agnosia (260) Family history is usually negative, and children have previously developed normally.

Focal status epilepticus with the expression of emotional/affective and subtle vegetative-autonomous symptoms only. Status-like recurrent pilomotor seizures are rare but well documented in relation to temporal lobe pathology, usually gliomas (06; 236; 326). For many, the so-called interictal personality and behavioral syndrome as well as other described personality peculiarities are also intimately linked with an active temporal lobe epilepsy (308; 314). Focal status epilepticus with the expression of emotional/affective and subtle vegetative-autonomous symptoms exist (320). However, the causal relationship usually remains a guess because very localized ongoing epileptic discharges in deep-brain regions cannot be picked up in the routine scalp EEG. Pontius has reported on motiveless fire-setting and implicated focal limbic seizure kindling by revived memories of fires in what she called "limbic psychotic trigger reaction" (218).

Differentiating epileptic psychoses from focal unaware status epilepticus. Epileptic behavioral disturbances and psychoses might be due to prolonged nonconvulsive seizure activity. The idea that some abnormal mental states in epilepsy might be a form of partial status epilepticus is intriguing. Usually, epileptic psychosis is divided broadly into ictal, postictal, and interictal categories, each with distinctive features (281). Although the postictal psychosis is usually associated with delirium, altered consciousness, and amnesia, the interictal psychosis is characterized by clear consciousness, retained memory, and less severe behavioral disturbances. The ictal psychosis in focal status epilepticus with impaired awareness and with fluctuating or frequently recurring focal electrographic epileptic discharges, arising in temporal or extratemporal regions, presents itself as a confusional state with variable clinical state. It is said that extratemporal, frontal focal status has less cycling symptomatology, and that severe confusion is less pronounced in comparison to temporal lobe status epilepticus. Fronto-orbital polar status epilepticus is said to be particularly poor in clinical symptoms.

Various diseases, drugs, and other factors have been associated with nonconvulsive status epilepticus and must be considered in the list of differential diagnoses. Causes of focal unaware status epilepticus are acute and chronic focal cerebral injuries, including ischemic stroke, intracranial hemorrhage, abscess, meningoencephalitis, neoplasias, malformations, and a history of epilepsy. Medications (eg, cyclosporin and lithium), other metabolic (eg, hyponatremia, hypo- and hypercalcemia, hypoglycemia) and systemic stressors (eg, infections, hypoxemia) may be implicated or superimposed. The list of differential diagnoses includes toxic or metabolic encephalopathy, delirium, psychiatric conditions, and transient global amnesia. Furthermore, limbic encephalitis [both paraneoplastic (79; 145) and nonparaneoplastic], and herpes simplex encephalitis can be challenging differential diagnoses (298; 234; 337). Creutzfeldt-Jakob disease can present with focal or regional EEG abnormalities that might mimic nonconvulsive status epilepticus (49; 85; 323). Also, psychogenic status epilepticus has to be considered (211; 74), as well as metastatic CNS disease (22). In a review of nonconvulsive status epilepticus in children, acute hypoxic-ischemic injury was the most frequent etiology (5 of 19; 26%), followed by exacerbation of underlying metabolic disease (21%), acute infection (16%), and change in antiepileptic drug regimen (16%) (271).

Associated and underlying disorders

In a retrospective review of all pediatric patients who were admitted or transferred to the PICU with an unexplained decrease in level of consciousness, no overt clinical seizures, and EEG recordings performed within 24 hours of onset of an altered state of consciousness, 23 of 141 patients who met criteria for inclusion in the study were found to have nonconvulsive status epilepticus. The largest group of patients (43%) had no preexisting neurologic condition prior to the onset of nonconvulsive status epilepticus. In the remainder, the etiology of nonconvulsive status epilepticus included acute structural brain lesion (48%), acute nonstructural brain lesion (22%), epilepsy-related seizure (13%), and others (17%) (239). Nonconvulsive status epilepticus is common in children with acute encephalopathy, and features may be misleading; therefore, a high index of suspicion and EEG are mandatory in these situations (01; 107).

Factors associated with nonconvulsive status epilepticus have been described in a wide variety of diseases such as organ failure, electrolyte imbalance, peritoneal dialysis, hypersensitive encephalopathy, and epileptic encephalopathy (43; 237). It also has been reported in the following cases:

• Stroke (02)
• Hashimoto encephalopathy (289)
• Subarachnoid hemorrhage (64; 177)
• Malignant tumor (37) and brain metastases (23)
• Cortical dysplasia (199; 202; 330)
• Ring chromosome 20 syndrome (214; 11; 178)
• Pituitary apoplexy (55)
• Lafora body disease (52; 179)
• Multiple sclerosis
• Hypocalcemia (147)
• Hypercalcemia (161)
• HIV infection (168)
• Mycoplasma pneumoniae infection complications (135)
• Neurosyphilis and Jarisch-Herxheimer reaction in patients with neurosyphilis (150; 185; 109)
• Systemic lupus erythematosus (84; 290)
• MELAS (81; 51)
• Nonketotic hyperglycemia (304)
• Acute porphyria (310)
• In mentally retarded adults induced by recurrent rectal diazepam overadministration (29)

Afsar and colleagues identified 30 patients (out of 121 = 25%) with poststroke status epilepticus (02). Two thirds were early-onset and one third late-onset status epilepticus. Only ischemic stroke was found in the late-onset group. Nonconvulsive status epilepticus was more frequent in the early-onset group.

Medication and medication withdrawal (189) have been repeatedly reported as inducers of nonconvulsive status epilepticus (61). Examples are:

• Microvascular endothelial cell chemotherapy of urothelial cancer (194)
• Cyclosporine treatment (63)
• Ifosfamide (222)
• Cephalosporins (69; 188; 03; 41; 224)
• Lithium and neuroleptics (163; 17)
• Intrathecal fluorescein injection (48)

Nonconvulsive status epilepticus was described as a complication of electroconvulsive therapy (229; 259; 261; 212; 111) and induced by various drugs, mainly psychotropic agents (331) such as antidepressants (196), neuroleptics, ketamine (which has anticonvulsive and proconvulsive actions) (160), morphine (20), and antiepileptics such as tiagabine (242; 127; 148; 12; 90; 56; 131; 184; 256; 149; 300; 136). In most instances, tiagabine-induced nonconvulsive status epilepticus is absence status (148). Abrupt withdrawal of hypnotic-sedative drugs, benzodiazepines in particular, may provoke nonconvulsive status epilepticus (75; 331; 83). Nonconvulsive status epilepticus has also been reported as a result of acute carbon monoxide poisoning (31), in association with valproate-induced hyperammonemic encephalopathy (294), after replacement of valproate with lamotrigine (283), and precipitated by carbamazepine (187) and levetiracetam (10). Star fruit ingestion was also described (36) as a cause in a dialysis patient.

Diagnostic workup

To diagnose nonconvulsive status epilepticus, two principal requirements have to be fulfilled: (1) some clinically evident alteration in mental status or behavior from baseline and (2) seizure activity on the EEG. Many difficulties exist in defining baseline behavioral change, and persons at risk for nonconvulsive status epilepticus are also those whose behavioral changes might often be ascribed to other conditions. For example, patients with mental retardation have clear cognitive abnormalities. Correlating behavioral change from baseline with EEG evidence of ongoing epileptic activity is essential to diagnose nonconvulsive status epilepticus (286).

The Salzburg criteria for nonconvulsive status epilepticus and the American Clinical Neurophysiology Society Standardized Critical Care EEG Terminology 2021 include a trial with intravenous antiseizure medications to assess EEG and clinical response as a diagnostic criterion for definite nonconvulsive status epilepticus and possible nonconvulsive status epilepticus (170; 125).

Either intravenous benzodiazepines or non-benzodiazepines antiseizure medications can be used for a diagnostic trial. However, non-benzodiazepines should be prioritized in patients who already have impaired alertness or are at risk of respiratory depression. Levetiracetam, valproate, lacosamide, brivaracetam, fosphenytoin, or phenobarbital are all considered appropriate choices for a diagnostic intravenous trial (171).

Essential clinical features. The diagnosis of focal unaware status epilepticus should be made only if clinical signs and symptoms, which last for more than 10 minutes, are accompanied by clear-cut localized EEG epileptiform discharge patterns. These patterns include rhythmical discharges in the corresponding brain region, which is most often the temporal area. However, one has to consider that scalp EEG might miss the ongoing discharges in deep limbic structures or reflect them incompletely or distortedly. Clinical symptoms and signs are manifold and can combine, although often they consist of plurimodal complex experiential hallucinations and twilight states (101; 76; 57). A dyscognitive status epilepticus requires video-documentation of the behavior together with the EEG. Polygraphic recording of heart rate, respiration, and galvanic skin reflex may be useful. The so-called hairline EEG as a screening tool for nonconvulsive status epilepticus has a low sensitivity and is no longer recommended (151). Continuous video-EEG monitoring in ICU significantly improves detection of seizures and status epilepticus and is the only way to detect subclinical seizures and some forms of nonconvulsive status in comatose or confused patients (09).

EEG evidence of ictal activity. A wide spectrum of EEG ictal morphologies may be seen with nonconvulsive status epilepticus (141). Putting aside EEG changes that have doubtful clinical significance such as midtemporal theta of drowsiness, wicket spikes, or subclinical rhythmic epileptiform discharges of adults, problems of interpretation may frequently be encountered with rhythmic EEG morphologies that have sharp contours or waxing and waning progressions.

Triphasic waves, when exceeding one per second and suppressed by diazepam, often straddle the borders of encephalopathy and epilepsy, particularly when they exhibit spiky morphologies and wax and wane. Triphasic waves are supposed to increase with arousal. Triphasic waves in lithium or other acute intoxication may exhibit a prominent and distinctive first phase resembling spike-slow-wave complexes; triphasic waves may decrease in the setting of hyperammonemia after IV diazepam. Periodic or "pseudoperiodic" lateralized epileptiform discharges pose a similar problem when associated with neurologic deficits (130; 174).

The EEG in focal unaware or limbic status epilepticus may exhibit localized high-frequency tonic discharges restricted to limbic structures, along with fast clonic, slow clonic, or mixed pattern if invasive intracranial EEG recording techniques such as depth electrodes, foramen ovale electrodes, and subdural strips and grids are available (320). Scalp EEG has its limitations and may not pick up localized discharges in EEG of mesial temporal lobe structures. In the scalp EEG, only propagated and morphologically altered patterns might be seen. The scalp EEG discharges most often consist of rhythmic theta or theta/delta, but other frequencies such as alpha have also been described in generalized nonconvulsive status epilepticus, which might be viewed as a borderline form (15).

Waxing and waning as well as paroxysmal pattern changes can occur (215; 317). Waxing and waning may be seen in terms of time (ie, appearance and disappearance of epileptiform patterns), but also in terms of enlargement and diminution of the epileptogenic area (ie, volume). Both phenomena might be interrelated and most probably are a function of the specific properties of the neuronal population pathologically recruited into the epileptiform discharges. Commonly, specific seizure suppressing maneuvers exert a recognizable effect on the formal aspects of the EEG discharges (313; 321).

Granner and Lee analyzed EEG characteristics comprehensively in a large series (85 ictal episodes in 78 patients) of nonconvulsive status epilepticus cases (105). The ictal discharges were generalized in 59 episodes (69%), diffuse with focal predominance in 15 (18%), and focal in 11 (13%). The morphologies and patterns of persistence varied greatly. Frequency of ictal discharge was also variable and was almost always less than 3 Hz. Several findings suggested possible focal onset with secondary generalization even in so-called "generalized cases.” This study (105), as well as a systematic review (266), demonstrate that nonconvulsive status epilepticus is a highly heterogeneous epileptic state electrographically.

Ictal SPECT. Ictal SPECT may be helpful for localizing the discharging brain area and indeed can be easily accomplished in a status condition (199).

1H-MRS, T2-weighted fluid attenuated inversion recovery (T2-FLAIR), and diffusion-weighted (DWI) MRI. 1H-MRS, T2-FLAIR, and diffusion-weighted MRI might show changes associated with the discharging epileptic focus (91; 44). Increased signal of the cerebral cortex and subcortical structures, including hippocampus, thalamus, claustrum, caudate and splenium, on T2-FLAIR and DWI are the most common ictal MRI changes in convulsive and nonconvulsive status. These changes may be reversible, appearing within hours of seizure onset and resolving within days or weeks (186). Seizure-related MRI changes during status were associated with a higher risk of neurologic deterioration, duration of status, and worse prognosis (53).

Villalobos-Chavez and colleagues related sequential MRI changes to vasogenic and cytotoxic oedema secondary to the status with disrupture of the blood-brain barrier (297). Corresponding to the clinical evolution, reversible and irreversible focally abnormal metabolism can be determined with 1H-MRS, reflecting both increased neuronal activity and neuronal damage (167; 44). 1H-MRS during or shortly after focal seizures shows abnormally high lactate levels in the area of seizure onset, but during absence seizures, or absence status, the lactate levels are normal (35).

Prolactin, luteinizing hormone, creatine-phosphokinase, neurone-specific enolase, and indicators of adenosine triphosphate depletion. Concentrations of prolactin and luteinizing hormone as well as creatine-phosphokinase in blood were reported to show a good correlation with seizure frequency, and it has been suggested that an increase of prolactin would be helpful for diagnosis of epileptic seizures, with a view towards differentiating, in particular, epileptic from nonepileptic events (169). Although prolactin concentrations exceeding 700 µU/mL might significantly indicate an epileptic seizure, the absence of elevated prolactin levels does not exclude status epilepticus (not even a grand-mal status) and certainly not nonconvulsive focal status or absence status (276; 162; 14; 87; 88). Moreover, prolactin was found to be elevated after nonepileptic seizures (217). In addition, it should not be forgotten that endocrine and neuroendocrine changes can occur as a result of antiepileptic drug therapy, making a comparison with concentrations of persons not treated with antiepileptic drugs rather difficult, even if circadian fluctuations are taken into consideration (175; 156). In conclusion, prolactin and creatine-phosphokinase might be elevated after severe epileptic seizures, but their value for differential diagnosis of epileptic versus nonepileptic seizures is limited, and it is unlikely that they contribute much to the diagnosis of focal unaware status.

Response to treatment. In general, response to high-dosed antiseizure medications can be used in the differential diagnosis, but there are exceptions. There are patients in whom classical antiseizure medications of first choice, such as intravenous diazepam, did not completely suppress the localized discharges associated with focal status epilepticus (313). Nevertheless, intravenous diazepam may serve as a valuable diagnostic tool in differentiating generalized from focal onset nonconvulsive status epilepticus.

However, rhythmic sharp waves resulting from metabolic encephalopathy also can be abolished by benzodiazepines, similar to nonconvulsive status epilepticus, without improvement in mental status (94). Periodic lateralized epileptiform discharges in severe vascular brain damage are known to respond only moderately, if at all, to antiseizure medication (266).

Management

As discussed above, focal unaware status epilepticus may induce long-term sequelae and might need more aggressive treatment to prevent further brain damage. However, the treatment of status epilepticus has potential risks, and aggressive treatment with sedation and intubation may not be appropriate for some patients with focal unaware status epilepticus, in particular for older patients with serious comorbidities. In these situations, treatment with less sedative antiseizure medications should be considered (306; 250). Aggressive treatment of status epilepticus with anesthetic drugs (thiopental, midazolam, propofol, and high-dose phenobarbital) can provide rapid seizure control, but it might lead to serious medical complications and worse outcomes (267; 05; 73).

It is widely accepted that concurrent acute brain injury and status epilepticus are synergistically deleterious (25; 307; 137). Waterhouse and colleagues found that when status epilepticus complicates acute stroke, mortality is three times higher than in stroke alone (307). Therefore, for nonconvulsive status epilepticus in association with acute brain injury, early and intensive intervention might be necessary (137). The danger that patients might suffer iatrogenically from aggressive treatment makes it necessary to find a balance between the potential neurologic morbidity of nonconvulsive status epilepticus and the possible morbidity of intravenous antiepileptic drugs (141; 152; 302; 286). Hypotension and respiratory depression are among the most common unwarranted side effects of intravenous antiseizure medications.

Focal status epilepticus is reported to be controlled by diazepam in 88% of 67 patients (249). Therefore, for the treatment of typical absence status epilepticus and uncomplicated complex partial status epilepticus, oral benzodiazepines are recommended (301).

Rapid-acting anesthetic agents, such as midazolam and propofol, are being used more often for refractory status epilepticus (16; 38; 124; 115). The role of propofol, which has barbiturate- and benzodiazepine-like effects at the GABA-A receptor and has a potent anticonvulsant action at clinical doses, has been reviewed by Stecker and colleagues and Brown and Levin (32; 263). Propofol-associated fatal myocardial failure and rhabdomyolysis has been reported by Zarovnaya and associates (335). Therefore, propofol infusion for the treatment of status epilepticus should be carefully weighted against its risk to develop propofol infusion syndrome. Prolonged propofol infusion at high doses for the treatment of status epilepticus should be used with caution, and in all cases careful monitoring for rhabdomyolysis and acidosis must be performed.

Midazolam (MDZ) is considered an antiepileptic drug of first choice because it is short acting and, therefore, can be well titrated on prolonged infusion. The recommended regimen is for one or two bolus injections of 0.1 to 0.3 mg/kg, to be followed by an infusion of 0.05 to 0.4 mg/kg per hour. It is metabolized in the liver. The elimination half life of 1.5 to 3.5 hours is prolonged to up to 10 hours in the elderly. Chronic renal failure does not strongly affect pharmacokinetics. However, severe hepatic disease might slow elimination. Usually, mild bradycardia and slight fall of arterial blood pressure may occur at conventional doses. Apnea has not been reported in status, but this is clearly a potential risk (72).

Several authors have reported on the usefulness of midazolam treatment, which can be administered intravenously, intramuscular (IM), or intranasal (46; 154; 284). Claassen and associates have studied the efficacy of continuous intravenous midazolam for refractory nonconvulsive status epilepticus reviewing 33 episodes of refractory nonconvulsive status epilepticus in their neurologic intensive care unit over 6 years (46). All patients were monitored with continuous EEG. Midazolam infusion rates were titrated to eliminate clinical and EEG seizure activity; continuous intravenous midazolam was discontinued once patients were seizure free for 24 hours. The mean duration of status epilepticus before treatment was 3.9 days (range 0 to 17 days). In addition to benzodiazepines, 94% of patients had received at least two antiepileptic drugs before starting continuous intravenous midazolam. The mean loading dose was 0.19 mg/kg, the mean maximal infusion rate was 0.22 mg/kg per hour, and the mean duration of continuous intravenous midazolam therapy was 4.2 days (range 1 to 14 days). Acute treatment failure (seizures 1 to 6 hours after starting continuous intravenous midazolam) occurred in 18% of episodes, breakthrough seizures (after 6 hours of therapy) in 56%, posttreatment seizures (within 48 hours of discontinuing therapy) in 68%, and ultimate treatment failure (frequent seizures that led to treatment with pentobarbital or propofol) in 18%. Breakthrough seizures were clinically subtle or purely electrographic in 89% of cases and were associated with an increased risk of developing posttreatment seizures. The authors concluded that, although most patients with refractory status epilepticus initially responded to continuous intravenous midazolam, over half developed subsequent breakthrough seizures, which were predictive of posttreatment seizures and were often detectable only with continuous EEG. A double-blind, randomized, noninferiority trial compared the efficacy of intramuscular midazolam with that of intravenous lorazepam for children and adults and concluded that intramuscular midazolam is as safe and effective as intravenous lorazepam for prehospital seizure cessation (254).

Topiramate may be useful in refractory focal status epilepticus. High efficacy of rapidly titrated topiramate via nasogastric tube in two young children has also been reported (24). Intravenous levetiracetam might be useful in elderly patients, in particular in those with multiple medications (80; 238; 243). Intravenous sodium valproate and levetiracetam appear to be an alternative in patients with focal unaware status epilepticus, as well as in patients with liver disease, or to avoid intubation (235; 306).

The use of intravenous lacosamide as an alternative treatment in status epilepticus has been reported in retrospective case series (class IV evidence) (144; 126).

As mentioned above, the situation is different in those epileptiform encephalopathies in which EEG spikes and sharp waves may not impair clinical function but merely reflect damage from severe brain injuries. In disorders like anoxic encephalopathy or in some patients with periodic epileptiform discharges, very aggressive treatment is perhaps not indicated. Furthermore, the presence or absence of periodic discharges does not predict the timing of the first seizure or status in critical care patients (65). Abolition of sharp waves by benzodiazepines might help to decide on treatment, but it is known that rhythmic sharp waves resulting from metabolic encephalopathy can be abolished by benzodiazepines, similar to nonconvulsive status epilepticus, without improvement in mental status, suggesting that definitive electrographic diagnosis of primary nonconvulsive status epilepticus should not be based entirely on abolition of sharp waves by benzodiazepines (94). Clearly, more work needs to be done regarding the significance of certain EEG patterns (particularly periodic discharges) and when and how to treat them (124; 82).

References

01: Abend NS, Gutierrez-Colina AM, Topjian AA, et al. Nonconvulsive seizures are common in critically ill children. Neurology 2011;76(12):1071-7. PMID 21307352
02: Afsar N, Kaya D, Aktan S, Sykut-Bingol C. Stroke and status epilepticus: stroke type, type of status epilepticus, and prognosis. Seizure 2003;12:23-7. PMID 12495645
03: Alpay H, Altun O, Biyikli NK. Cefepime-induced non-convulsive status epilepticus in a peritoneal dialysis patient. Pediatr Nephrol 2004;19:445-7. PMID 14986079
04: Aminoff MJ. Do nonconvulsive seizures damage the brain. - No. Arch Neurol 1998;55:119-21. PMID 9443719
05: Amorim E, McGraw CM, Westover MB. A theoretical paradigm for evaluating risk-benefit of status epilepticus treatment. J Clin Neurophysiol 2020;37:385-92. PMID 32890059
06: Andermann F, Gloor P. Pilomotor seizures. Neurology 1984;34:1623. PMID 6504342
07: Andermann F, Robb JP. Absence status: a reappraisal following review of thirty-eight patients. Epilepsia 1972;13:177-87. PMID 4501885
08: Arabadzisz D, Antal K, Parpan F, Emri Z, Fritschy JM. Epileptogenesis and chronic seizures in a mouse model of temporal lobe epilepsy are associated with distinct EEG patterns and selective neurochemical alterations in the contralateral hippocampus. Exp Neurol 2005;194:76-90. PMID 15899245
09: Arndt DH, Lerner JT, Matsumoto JH, et al. Subclinical early posttraumatic seizures detected by continuous EEG monitoring in a consecutive pediatric cohort. Epilepsia 2013;54(10):1780-8. PMID 24032982
10: Atefy R, Tettenborn B. Nonconvulsive status epilepticus on treatment with levetiracetam. Epilepsy Behav 2005;6:613-6. PMID 15876554
11: Augustijn PB, Parra J, Wouters CH, Joosten P, Lindhout D, van Emde Boas W. Ring chromosome 20 epilepsy syndrome in children: electroclinical features. Neurology 2001;57:1108-11. PMID 11571346
12: Balslev T, Uldall P, Buchholt J. Provocation of non-convulsive status epilepticus by tiagabine in three adolescent patients. Europ J Paed Neurology 2000;4:169-70. PMID 11008259
13: Bauer G, Gotwald T, Dobesberger J, et al. Transient and permanent magnetic resonance imaging abnormalities after complex partial status epilepticus. Epilepsy Behav 2006;8:666-71. PMID 16503204
14: Bauer J, Landgraf S, Schrell U, et al. Anstieg der serum-prolactinkonzentration nach frontallappenanfällen. Dtsch Med Wschr 1991;16:1824-7. PMID 1959486
15: Bauer J, Neumann M, Kolmel HW, Elger CE. Clinical correspondence: ictal generalized rhythmic alpha activity during non-convulsive status epilepticus. Eur J Neurol 2000;7:735-40. PMID 11136366
16: Begemann M, Rowan AJ, Tuhrim S. Treatment of refractory complex-partial status epilepticus with propofol: case report. Epilepsia 2000;41:105-9. PMID 10643932
17: Bellesi M, Passamonti L, Silvestrini M, Bartolini M, Provinciali L. Non-convulsive status epilepticus during lithium treatment at therapeutic doses. Neurol Sci 2006;26:444-6. PMID 16601939
18: Ben-Ari Y, editor. The amygdaloid complex (INSERM symposium 20). Amsterdam: Elsevier/North-Holland, Biomedical Press, 1981:516.
19: Bertram EH, Lenn NJ, Lothman EW. The hippocampus in experimental chronic epilepsy: a morphometric analysis. Ann Neurol 1990;27:38-43. PMID 2301927
20: Bertran F, Denise P, Letellier P. Nonconvulsive status epilepticus: the role of morphine and its antagonist. Neurophysiol Clin 2000;30:109-12. PMID 10812579
21: Billard C, Autret A, Laffont F, et al. Aquired aphasia in epileptic children – four cases with electrical infraclinic status epilepticus during sleep. Rev Electroencephalogr Neurophysiol Clin 1981;11:457-67. PMID 6808603
22: Blitshteyn S, Jaeckle KA. Nonconvulsive status epilepticus in metastatic CNS disease. Neurology 2006;66:1261-3. PMID 16636249
23: Blitshteyn S, Jaeckle KA. Status epilepticus in patients with CNS metastases. Arch Neurol 2007;64(6):916; author reply 916-7. PMID 17562948
24: Blumkin L, Lerman-Sagie T, Houri T, et al. Pediatric refractory partial status epilepticus responsive to topiramate. J Child Neurol 2005;20:239-41. PMID 15832617
25: Bogousslavski J, Martin R, Regli F, Despland PA, Bolyn S. Persistent worsening of stroke sequela after delayed seizures. Ann Neurol 1992;49:385-8. PMID 1558520
26: Bottaro FJ, Martinez OA, Pardal MM, Bruetman JE, Reisin RC. Nonconvulsive status epilepticus in the elderly: a case-control study. Epilepsia 2007;48(5):966-72. PMID 17381437
27: Brenner RP. Is it status. Epilepsia 2002;43(Suppl 3):103-13. PMID 12060012
28: Bright R. Reports of medical cases, selected with a view of illustrating the symptoms and cure of diseases by a reference to morbid anatomy. Vol 2. London: Taylor, 1831.
29: Brodtkorb E, Sand T, Kristiansen A, Torbergsen T. Non-convulsive status epilepticus in the adult mentally retarded. Classification and role of benzodiazepines. Seizure 1993;2:115-23. PMID 7909489
30: Brody JA, Odom GL, Kunkle EC. Pilomotor seizures: report of a case associated with a central glioma. Neurology 1960;10:993-7.
31: Brown KL, Wilson RF, White MT. Carbon monoxide-induced status epilepticus in an adult. J Burn Care Res 2007;28(3):533-6. PMID 17438487
32: Brown LA, Levin GM. Role of propofol in refractory status epilepticus. Ann Pharmacother 1998;32:1053-9. PMID 9793598
33: Calmeil LF. De l'épilepsie, étudiée sous le rapport de son siège et de son influence sur la production de l'aliénation mentale. Paris: Thèse de l'Université de Paris, 1824.
34: Cascino GD. Nonconvulsive status epilepticus in adults and children. Epilepsia 1993;34(Suppl 1):21-8. PMID 8462490
35: Cendes F, Stanley JA, Dubeau F, Andermann F, Arnold DL. Proton magnetic resonance spectroscopic imaging for discrimination of absence and complex partial seizures. Ann Neurol 1997;41(1):74-81. PMID 9005868
36: Chang CH, Yeh JH. Non-convulsive status epilepticus and consciousness disturbance after star fruit (Averrhoa carambola) ingestion in a dialysis patient. Nephrology (Carlton) 2004;9:362-5. PMID 15663637
37: Chang JW, Chang JH, Park SC, Kim TS, Park YG, Chung SS. Radiologically confirmed de novo glioblastoma multiforme and hippocampal sclerosis associated with the first onset of nonconvulsive simple partial status epilepticus. Acta Neurochir (Wien) 2001;143:297-300; discussion 300-1. PMID 11460918
38: Chapman MG, Smith M, Hirsch NP. Status epilepticus. Anaesthesia 2001;56:648-59. PMID 11437765
39: Charcot JM. Clinical lectures on the diseases of the nervous system. Savill T, translator. London: New Sydenham Society, 1889.
40: Chatrian G, Shaw CM, Leffman H. The significance of periodic lateralized epileptiform discharges. Electroencephalogr Clin Neurophysiol 1964;17:177-93. PMID 14204927
41: Chedrawi AK, Gharaybeh SI, Al-Ghwery SA, Al-Mohaimeed SA, Alshahwan SA. Cephalosporin-induced nonconvulsive status epilepticus in a uremic child. Pediatr Neurol 2004;30:135-9. PMID 14984909
42: Chen J, Xie L, Hu Y, et al. Nonconvulsive status epilepticus after cessation of convulsive status epilepticus in pediatric intensive care unit patients. Epilepsy Behav 2018;82:68-73. PMID 29587188
43: Chow KM, Wang AY, Hui AC, Wong TY, Szeto CC, Li PK. Nonconvulsive status epilepticus in peritoneal dialysis patients. Am J Kidney Dis 2001;38:400-5. PMID 11479169
44: Chu K, Kang DW, Kim JY, Chang KH, Lee SK. Diffusion-weighted magnetic resonance imaging in nonconvulsive status epilepticus. Arch Neurol 2001;58:993-8. PMID 11405815
45: Chung PW, Seo DW, Kwon JC, Kim H, Na DL. Nonconvulsive status epilepticus presenting as a subacute progressive aphasia. Seizure 2002;11:449-54. PMID 12237073
46: Claassen J, Hirsch LJ, Emerson RG, Bates JE, Thompson TB, Mayer SA. Continuous EEG monitoring and midazolam infusion for refractory nonconvulsive status epilepticus. Neurology 2001;57:1036-42. PMID 11571331
47: Cockerell OC, Walker MC, Sander JW, Shorvon SD. Complex partial status epilepticus: a recurrent problem. J Neurol Neurosurg Psychiatry 1994;57:835-7. PMID 8021671
48: Coeytaux A, Reverdin A, Jallon P, Nahory A. Non convulsive status epilepticus following intrathecal fluorescein injection. Acta Neurol Scand 1999;100:278-80. PMID 10510691
49: Cohen D, Kutluay E, Edwards J, Peltier A, Beydoun A. Sporadic Creutzfeldt-Jakob disease presenting with nonconvulsive status epilepticus. Epilepsy Behav 2004;5:792-6. PMID 15380138
50: Cole AJ. Status epilepticus and periictal imaging. Epilepsia 2004;45 (Suppl 4):72-7. PMID 15281962
51: Corda D, Rosati G, Deiana GA, Sechi G. "Erratic" complex partial status epilepticus as a presenting feature of MELAS. Epilepsy Behav 2006;8:655-8. PMID 16473046
52: Corkill RG, Hardie RJ. An unusual case of Lafora body disease. Eur J Neurol 1999;6:245-7. PMID 10053240
53: Cornwall CD, Dahl SM, Nguyen N, et al. Association of ictal imaging changes in status epilepticus and neurological deterioration. Epilepsia 2022;63(11):2970-80. PMID 36054260
54: Coulter DA, DeLorenzo RJ. Basic mechanisms of status epilepticus. Adv Neurol 1999;79:725-33. PMID 10514858
55: Craig JJ, Gibson JM. Non-convulsive status epilepticus: a treatable cause of confusion in pituitary apoplexy. Br J Neurosurg 2000;14:141-3. PMID 10889889
56: de Borchgrave V, Lienard F, Willemart T, van Rijckevorsel K. Clinical and EEG findings in six patients with altered mental status receiving tiagabine therapy. Epilepsy Behav 2003;4:326-37. PMID 12791336
57: Degen R. Besondere manifestationen epileptischer anfälle. In: Fröscher W, Vassella F, editors. Die epilepsien. Berlin: W de Gruyter, 1994:475-86.
58: DeGiorgio CM, Gott PS, Rabinowicz AL, Heck CN, Smith T, Correale J. Neuron-specific enolase, a marker of acute neuronal injury, is increased in complex partial status epilepticus. Epilepsia 1996;37:606-9. PMID 8681891
59: DeGiorgio CM, Heck CN, Rabinowicz AL, Gott PS, Smith T, Correale J. Serum neuron-specific enolase in the major subtypes of status epilepticus. Neurology 1999;52:746-9. PMID 10078721
60: DeGiorgio CM, Tomiyasu U, Gott PS, Treiman DM. Hippocampal pyramidal cell loss in human status epilepticus. Epilepsia 1992;33:23-7. PMID 1733757
61: Delanty N, Vaughan CJ, French JA. Medical causes of seizures. Lancet 1998;352:383-90. PMID 9717943
62: Delgado-Escueta AV, Wasterlain CG, Treimann DM, Porter RJ, editors. Status epilepticus. Advances in neurology. Vol. 34. New York: Raven Press, 1983:15-35.
63: Delpont E, Thomas P, Gugenheim J, et al. Prolonged confusion syndrome in the course of cyclosporine treatment: a state of confusion. Neurophysiol Clin 1990;20:207-15. PMID 2233652
64: Dennis LJ, Claassen J, Hirsch LJ, Emerson RG, Connolly ES, Mayer SA. Nonconvulsive status epilepticus after subarachnoid hemorrhage. Neurosurgery 2002;51:1136-44. PMID 12383358
65: Dericioglu N, Arsava EM, Topcuoglu MA. Time to detection of the first seizure in patients with nonconvulsive status epilepticus in the neurological intensive care unit. Clin EEG Neurosci 2020;51:70-3. PMID 31533458
66: DeToledo JC, Minagar A, Lowe MR. Persisting aphasia as the sole manifestation of partial status epilepticus. Clin Neurol Neurosurg 2000;102:144-8. PMID 10996712
67: Dinner DS, Lueders H, Lederman R, Gretter TE. Aphasic status epilepticus: a case report. Neurology 1981;31:888-91. PMID 6165933
68: Dirik E, Yis U, Hudaoglu O, Kurul S. Nonconvulsive status epilepticus and neurodevelopmental delay. Pediatr Neurol 2006;35:209-12. PMID 16939862
69: Dixit S, Kurle P, Buyan-Dent L, Sheth RD. Status epilepticus associated with cefepime. Neurology 2000;54:2153-5. PMID 10851381
70: Doherty CP, Cole AJ, Grant PE, et al. Multimodal longitudinal imaging of focal status epilepticus. Can J Neurol Sci 2004;31:276-81. PMID 15198460
71: Drislane FW. Presentation, evaluation, and treatment of nonconvulsive status epilepticus. Epilepsy Behav 2000;1:301-14. PMID 12609161
72: Dundee JW, Halliday NJ, Harper KW, Brogden RN. Midazolam: a review of its pharmacological properties and therapeutic use. Drugs 1984;28:519-43. PMID 6394264
73: Dupont S, Kinugawa K. Nonconvulsive status epilepticus in the elderly. Rev Neurol (Paris) 2020;176:701-9. PMID 32169326
74: Dworetzky BA, Mortati KA, Rossetti AO, Vaccaro B, Nelson A, Bromfield EB. Clinical characteristics of psychogenic nonepileptic seizure status in the long-term monitoring unit. Epilepsy Behav 2006;9:335-8. PMID 16872909
75: Emre M, Walser H, Baumgartner G. Non-convulsive status epilepticus after abrupt withdrawal of hypnotic-sedative drugs. Eur Arch Psychiatry Neurol Sci 1985;235:21-5. PMID 2864252
76: Engel J Jr. Seizures and epilepsy. Contemporary neurology series. Vol. 31. Philadelphia: FA Davis Company, 1989.
77: Engel J Jr. Report of the ILAE classification core group. Epilepsia 2006;47:1558-68. PMID 16981873
78: Engel J Jr, Ludwig BJ, Feteli M. Prolonged partial complex status epilepticus: EEG and behavioral observations. Neurology 1978;28:863-9. PMID 567760
79: Espay AJ, Kumar V, Sarpel G. Anti-Hu-associated paraneoplastic limbic encephalitis presenting as rapidly progressive non-convulsive status epilepticus. J Neurol Sci 2006;246:149-52. PMID 16631204
80: Farooq MU, Naravetla B, Majid A, Gupta R, Pysh JJ, Kassab MY. IV levetiracetam in the management of non-convulsive status epilepticus. Neurocrit Care 2007;7(1):36-9. PMID 17657655
81: Feddersen B, Bender A, Arnold S, Klopstock T, Noachtar S. Aggressive confusional state as a clinical manifestation of status epilepticus in MELAS. Neurology 2003;61:1149-50. PMID 14581687
82: Ferlisi M, Shorvon S. The outcome of therapies in refractory and super-refractory convulsive status epilepticus and recommendations for therapy. Brain 2012;135(Pt 8):2314-28. PMID 22577217
83: Fernandez-Torre JL. De novo absence status of late onset following withdrawal of lorazepam: a case report. Seizure 2001;10:433-7. PMID 11700998
84: Fernandez-Torre JL, Sanchez JM, Gonzalez C, Fernandez-Guinea O. Complex partial status epilepticus of extratemporal origin in a patient with systemic lupus erythematosus. Seizure 2003;12:245-8. PMID 12763474
85: Fernandez-Torre JL, Solar DM, Astudillo A, Cereceda R, Acebes A, Calatayud MT. Creutzfeldt-Jakob disease and non-convulsive status epilepticus: a clinical and electroencephalographic follow-up study. Clin Neurophysiol 2004;115:316-9. PMID 14744571
86: Ferrie CD, Caraballo R, Covanis A, et al. Autonomic status epilepticus in Panayiotopoulos syndrome and other childhood and adult epilepsies: a consensus view. Epilepsia 2007;48(6):1165-72. PMID 17442005
87: Fichsel H. Spezielle laboruntersuchungen zur anfallsdiagnostik: CPK, prolaktin. Labordiagnostik zur therapieüberwachung und zur anfallsdiagnostik. In: Fröscher W, Vassella F, editors. Aspekte der epilepsie-diagnostik. Berlin: Blackwell Wissenschaft, 1991:24-36.
88: Fichsel H. Spezielle laboruntersuchungen zur anfallsdiagnostik: CPK, prolaktin. In: Fröscher W, Vasella F, editors. Die epilepsien. Berlin: W de Gruyter, 1994:439-40.
89: Fisher RS, Cross JH, French JA, et al. Operational classification of seizure types by the International League Against Epilepsy: Position Paper of the ILAE Commission for Classification and Terminology. Epilepsia 2017;58(4):522-30. PMID 28276060
90: Fitzek S, Hegemann S, Sauner D, Bonsch D, Fitzek C. Drug-induced nonconvulsive status epilepticus with low dose of tiagabine. Epileptic Disord 2001;3:147-50. PMID 11679307
91: Flacke S, Wullner U, Keller E, Hamzei F, Urbach H. Reversible changes in echo planar perfusion- and diffusion-weighted MRI in status epilepticus. Neuroradiology 2000;42:92-5. PMID 10663481
92: Foster JA, Puchowicz MJ, McIntyre DC, Herkenham M. Activin mRNA induced during amygdala kindling shows a spatiotemporal progression that tracks the spread of seizures. J Comp Neurol 2004;476:91-102. PMID 15236469
93: Fountain NB, Lothman EW. Pathophysiology of status epilepticus. J Clin Neurophysiol 1995;12:326-42. PMID 7560021
94: Fountain NB, Waldman WA. Effects of benzodiazepines on triphasic waves: implications for nonconvulsive status epilepticus. J Clin Neurophysiol 2001;18:345-52. PMID 11673700
95: Fromm GH, Faingold C, Browning RA, Burnham WM, editors. Epilepsy and the reticular formation. Neurology and neurobiology. Vol. 27. New York: Alan R Liss Inc, 1987.
96: Gastaut H. Dictionary of epilepsy. Geneva: World Health Organization, 1973.
97: Gastaut H. Aphasia: the sole manifestation of focal status epilepticus. Neurology 1979;29:1638. PMID 116143
98: Gastaut H. Classification of status epilepticus. In: Delgado-Escueta AV, Wasterlain CG, Treimann DM, Porter RJ, editors. Status epilepticus. Advances in neurology. Vol. 34. New York: Raven Press, 1983:15-35.
99: Gastaut H, Roger J, Lob H, editors. Les états de mal épileptique: compte rendu de la réunion européenne d'information électroencephalographique, Xth Colloque de Marseille 1962. Paris: Masson, 1967.
100: Gastaut H, Tassinari C. Status epilepticus. In: Remond A, editor. Handbook of electroencephalography and clinical neurophysiology. Vol 13A. Amsterdam: Elsevier, 1975:39-45.
101: Gibbs FA, Stamps FW. Epilepsy handbook. Springfield: Thomas, 1958.
102: Girgis M, Kiloh LG, editors. Limbic epilepsy and the dyscontrol syndrome. Developments in Psychiatry. Vol. 4. Amsterdam: Elsevier/North-Holland Biomed Press, 1980.
103: Gokyigit A, Caliskan A. Diffuse spike-wave status of 9-year duration without behavioural change or intellectual decline. Epilepsia 1995;36:210-3. PMID 25192295
104: Gorter JA, Goncalves Pereira PM, van Vliet EA, Aronica E, Lopes da Silva FH, Lucassen PJ. Neuronal cell death in a rat model for mesial temporal lobe epilepsy is induced by the initial status epilepticus and not by later repeated spontaneous seizures. Epilepsia 2003;44:647-58. PMID 12752463
105: Granner MA, Lee SI. Nonconvulsive status epilepticus: EEG analysis in a large series. Epilepsia 1994;35:42-7. PMID 8112256
106: Green JB. Pilomotor seizures. Neurology 1984;34:837-9. PMID 6539452
107: Greiner HM, Holland K, Leach JL, Horn PS, Hershey AD, Rose DF. Nonconvulsive status epilepticus: the encephalopathic pediatric patient. Pediatrics 2012;129(3):e748-55. PMID 22331332
108: Grimes DA, Guberman A. De novo aphasic status epilepticus as a complication from electroconvulsive therapy. Epilepsia 1997;38:945-9. PMID 9579898
109: Gurses C, Kurtuncu M, Jirsch J, et al. Neurosyphilis presenting with status epilepticus. Epileptic Disord 2007;9(1):51-6. PMID 17307712
110: Halasz P, Kelemen A, Clemens B, et al. The perisylvian epileptic network. A unifying concept. Ideggyogy Sz 2005;58:21-31. PMID 15884395
111: Hallikainen H, Mervaala E. Complex partial status epilepticus as a complication from electroconvulsive therapy [in Finnish]. Duodecim 2004;120:74-7. PMID 14976811
112: Hamilton NG, Matthews T. Aphasia: the sole manifestation of focal status epilepticus. Neurology 1979;29:745-8. PMID 108612
113: Hasegawa T, Shiga Y, Narikawa K, et al. Periodic episodes of aphasia as an unusual manifestation of partial status epilepticus. J Clin Neurosci 2005;12:820-2. PMID 16153849
114: Hauser WA. Epidemiology, morbidity and mortality of status epilepticus. Presented at the International Symposium on Status Epilepticus. Santa Monica, California: 1980.
115: Hayashi K, Osawa M, Aihara M, et al. Efficacy of intravenous midazolam for status epilepticus in childhood. Pediatr Neurol 2007;36(6):366-72. PMID 17560497
116: Heinrich A, Runge U, Kirsch M, Khaw AV. A case of hippocampal laminar necrosis following complex partial status epilepticus. Acta Neurol Scand 2007;115(6):425-8. PMID 17511853
117: Henke K, Buck A, Weber B, Wieser HG. Human hippocampus establishes associations in memory. Hippocampus 1997;7:249-56. PMID 9228523
118: Henke K, Treyer V, Weber B, et al. Functional neuroimaging predicts individual memory outcome after amygdalohippocampectomy. Neuroreport 2003;14:1197-202. PMID 12824759
119: Henke K, Weber B, Kneifel S, Wieser HG, Buck A. Human hippocampus associates information in memory. Proc Nat Acad Sci U S A 1999b;96:5884-9. PMID 10318979
120: Henke K, Weber B, Schwedler K, et al. PET studies of memory. Schweiz Arch Neurol Psych 1999a;150:89-96.
121: Henriksen GF. Status epilepticus partialis with fear as clinical expression. Report of a case and ictal EEG-findings. Epilepsia 1973;14:39-46. PMID 4517635
122: Hess R, Scollo-Lavizzari G, Wyss FE. Borderline cases of petit mal status. Eur Neurol 1971;5:137-54. PMID 5000720
123: Hilkens PH, de Weerd AW. Non-convulsive status epilepticus as cause for focal neurological deficit. Acta Neurol Scand 1995;92:193-7. PMID 7484071
124: Hirsch LJ, Claassen J. The current state of treatment of status epilepticus. Curr Neurol Neurosci Rep 2002;2:345-56. PMID 12044254
125: Hirsch LJ, Fong MWK, Leitinger M, et al. American Clinical Neurophysiology Society's Standardized Critical Care EEG Terminology: 2021 Version. J Clin Neurophysiol 2021;38(1):1-29. PMID 33475321
126: Hofler J, Trinka E. Lacosamide as a new treatment option in status epilepticus. Epilepsia 2013;54(3):393-404. PMID 23293881
127: Holtkamp M, Pfeiffer M, Buchheim K, Meierkord H. Tiagabine and non-convulsive status epilepticus. Nervenarzt 1999;70:1104-6. PMID 10637817
128: Hong KS, Cho YJ, Lee SK, Jeong SW, Kim WK, Oh EJ. Diffusion changes suggesting predominant vasogenic oedema during partial status epilepticus. Seizure 2004;13:317-21. PMID 15158702
129: Hosford DA. Animal models of nonconvulsive status epilepticus. J Clin Neurophysiol 1999;16:306-13. PMID 10478703
130: Hughes JR. Periodic lateralized epileptiform discharges: do they represent an ictal pattern requiring treatment? Epilepsy Behav 2010;18:162-5. PMID 20554251
131: Imperiale D, Pignatta P, Cerrato P, Montalenti E, Ravetti C, Benna P. Nonconvulsive status epilepticus due to a de novo contralateral focus during tiagabine adjunctive therapy. Seizure 2003;12:319-22. PMID 12810347
132: Jagoda A. Nonconvulsive seizures. Emerg Med Clin North Am 1994;12:963-71. PMID 7956893
133: Janz D. Die Epilepsien. Stuttgart: Thieme, 1969.
134: Jaraba Armas S, Sala-Padró J, Veciana M, et al. New-onset non-lesional aphasic status epilepticus. Clinical description, diagnostic clues, and treatment algorithm. Acta Neurol Scand 2022;145(5):579-89. PMID 35130366
135: Jeffery KJ, Ellis SJ, Fink CG. Non-convulsive status epilepticus as a complication of Mycoplasma pneumoniae infection. Br J Clin Pract 1995;49:155-6. PMID 7779670
136: Jette N, Cappell J, Vanpassel L, Akman CI. Tiagabine-induced nonconvulsive status epilepticus in an adolescent without epilepsy. Neurology 2006;67:1514-5. PMID 17060592
137: Jordan KG. Nonconvulsive status epilepticus in acute brain injury. J Clin Neurophysiol 1999;16:306-13. PMID 10478706
138: Kaaden T, Madlener M, Angstwurm K, et al. Seizure semiology in antibody-associated autoimmune encephalitis. Neurol Neuroimmunol Neuroinflamm 2022;9(6):e200034. PMID 36266054
139: Kantzeli A, Brandt C, Tomka-Hoffmeister M, Woermann F, Bien CG. De novo aphasic status epilepticus: Finally making the diagnosis by long-term EEG. Epilepsy Behav Rep 2022;17:100513. PMID 35005597
140: Kaplan PW. Nonconvulsive status epilepticus in the emergency room. Epilepsia 1996;37:643-50. PMID 8681896
141: Kaplan PW. Nonconvulsive status epilepticus. J Clin Neurophysiol 1999;16:323-60. PMID 10478707
142: Kaplan PW. Behavioral manifestations of nonconvulsive status epilepticus. Epilepsy Behav 2002;3:122-39. PMID 12609414
143: Kaplan PW. The clinical features, diagnosis, and prognosis of nonconvulsive status epilepticus. Neurologist 2005;11:348-61. PMID 16286878
144: Kellinghaus C, Berning S, Immisch I, et al. Intravenous lacosamide for treatment of status epilepticus. Acta Neurol Scand 2011;123(2):137-41. PMID 20868429
145: Kile SJ, Kim JC, Seyal M. Complex partial status epilepticus in paraneoplastic limbic encephalitis. Clin EEG Neurosci 2007;38(3):172-4. PMID 17844948
146: Kirshner HS, Hughes T, Fakhoury T, Abou-Khalil B. Aphasia secondary to partial status epilepticus of the basal temporal language area. Neurology 1995;45:1616-8. PMID 7644064
147: Kline CA, Esekogwu VI, Henderson SO, Newton KI. Non-convulsive status epilepticus in a patient with hypocalcemia. J Emerg Med 1998;16:715-8. PMID 9752943
148: Knake S, Hamer HM, Schomburg U, Oertel WH, Rosenow F. Tiagabine-induced absence status in idiopathic generalized epilepsy. Seizure 1999;8:314-7. PMID 10486298
149: Koepp MJ, Edwards M, Collins J, Farrel F, Smith S. Status epilepticus and tiagabine therapy revisited. Epilepsia 2005;46:1625-32. PMID 16190934
150: Kojan S, Van Ness PC, Diaz-Arrastia R. Nonconvulsive status epilepticus resulting from Jarisch-Herxheimer reaction in a patient with neurosyphilis. Clin Electroencephalogr 2000;31:138-40. PMID 10923200
151: Kolls BJ, Husain AM. Assessment of hairline EEG as a screening tool for nonconvulsive status epilepticus. Epilepsia 2007;48(5):959-65. PMID 17433054
152: Korff CM, Nordli DR Jr. Diagnosis and management of nonconvulsive status epilepticus in children. Nat Clin Pract Neurol 2007;3(9):505-16. PMID 17805245
153: Korn-Lubetzki I, Steiner-Birmanns B, Galperin I, Benasouli Y, Steiner I. Nonconvulsive status epilepticus in older people: a diagnostic challenge and a treatable condition. J Am Geriatr Soc 2007;55(9):1475-6. PMID 17767694
154: Koul R, Chacko A, Javed H, Al Riyami K. Eight-year study of childhood status epilepticus: midazolam infusion in management and outcome. J Child Neurol 2002;17:908-10. PMID 12593465
155: Koutroumanidis M, Rowlinson S, Sanders S. Recurrent autonomic status epilepticus in Panayiotopoulos syndrome: video/EEG studies. Epilepsy Behav 2005;7:543-7. PMID 16105750
156: Krause KH. Nebenwirkungen der antiepileptika. In: Fröscher W, Vasella F, editors. Die Epilepsien. Berlin: W de Gruyter, 1993:660-98.
157: Krsek P, Mikulecka A, Druga R, Hlinak Z, Kubova H, Mares P. An animal model of nonconvulsive status epilepticus: a contribution to clinical controversies. Epilepsia 2001;42:171-80. PMID 11240586
158: Krumholz A. Epidemiology and evidence for morbidity of nonconvulsive status epilepticus. J Clin Neurophysiol 1999;16:314-22. PMID 10478704
159: Krumholz A, Sung G, Fisher RS, Barry E, Bergey GK, Grattan LM. Complex partial status epilepticus accompanied by serious morbidity and mortality. Neurology 1995;45:1499-504. PMID 7644048
160: Kugler J, Doenicke A. Ketamine-anticonvulsive and proconvulsive actions. Anaesthesist 1994;43(Suppl 2):2-7. PMID 7840410
161: Kumpfel T, Lechner C, Auer D, Kraft E, Lydtin H, Trenkwalder C. Non-convulsive status epilepticus with marked neuropsychiatric manifestations and MRI changes after treatment of hypercalcaemia. Acta Neurol Scand 2000;102:337-9. PMID 11083513
162: Kurlemann G, Heyen P, Menges EM, et al. Prolaktin und wachstumshormon im serum nach zerebralen Krampfanfällen im kindes- und jugendalter. Epilepsie-Blätter 1990;3(Suppl):16.
163: Lambreva E, Vecellio M, Wieser HG, Buddeberg C. Neurotoxic encephalopathy caused by neuroleptics and lithium [in German]. Nervenarzt 2005;76:756-9. PMID 15959751
164: Landau WM. Landau-Kleffner syndrome: an eponymic badge of ignorance. Arch Neurol 1992;49:353-9. PMID 1558513
165: Landau WM, Kleffner F. Syndrome of acquired aphasia with convulsive disorder in children. Neurology 1957;7:523-30. PMID 13451887
166: Landolt H. Die dämmer- und verstimmungszustände bei epilepsie und ihre elektroenzephalographie. Z Gesamte Inn Med 1963;185:411-30.
167: Lazeyras F, Blanke O, Zimine I, Delavelle J, Perrig SH, Seeck M. MRI, (1)H-MRS, and functional MRI during and after prolonged nonconvulsive seizure activity. Neurology 2000;55:1677-82. PMID 11113222
168: Lechner C, Auer D, Kumpfel T, Hesse J, Fuchs HH. Prolonged non-convulsive status epilepticus as an early clinical manifestation of epilepsy in connection with HIV infection-case report with EEG and MRI follow-up. Fortschr Neurol Psychiatr 1998;66:326-30. PMID 9697007
169: Leiderman DB, Csernansky JG, Moses JA. Neuroendocrinology and limbic epilepsy: relationships to psychopathology, seizure variables, and neuropsychological function. Epilepsia 1990;31:270-4. PMID 2344844
170: Leitinger M, Beniczky S, Rohracher A, et al. Salzburg Consensus Criteria for non-convulsive status epilepticus--approach to clinical application. Epilepsy Behav 2015;49:158-63. PMID 26092326
171: Leitinger M, Gaspard N, Hirsch LJ, et al. Diagnosing nonconvulsive status epilepticus: Defining electroencephalographic and clinical response to diagnostic intravenous antiseizure medication trials. Epilepsia 2023;64(9):2351-60. PMID 37350392
172: Lennox WG. The petit mal epilepsies - their treatment with tridione. JAMA 1945;129:1069-74.
173: Lennox WG, Lennox MA. Epilepsy and related disorders. Boston/Toronto: Little, Brown Comp, 1960.
174: Lin L, Drislane FW. Lateralized periodic discharges: a literature review. J Clin Neurophysiol 2018;35:189-98. PMID 29718828
175: Lindbom U, Tomson T, Nilsson BY, Andersson DE. Serum prolactin response to metoclopramide during status epilepticus. J Neurol Neurosurg Psychiatry 1992;55:685-867. PMID 1527538
176: Linetsky E, Planer D, Ben-Hur T. Echolalia-palilalia as the sole manifestation of nonconvulsive status epilepticus. Neurology 2000;55:733-4. PMID 10980752
177: Little AS, Kerrigan JF, McDougall CG, et al. Nonconvulsive status epilepticus in patients suffering spontaneous subarachnoid hemorrhage. J Neurosurg 2007;106(5):805-11. PMID 17542523
178: Locharernkul C, Ebner A, Promchainant C. Ring chromosome 20 with nonconvulsive status epilepticus: electroclinical correlation of a rare epileptic syndrome. Clin EEG Neurosic 2005;36:151-60. PMID 16128150
179: Lopez-Meza EG, Cerda-Tellez F, Alanis Gueyara IM, Fernandez Gonzalez-Aragon MC, Ruano-Calderon LA. Non-convulsive epileptic status associated with Lafora disease: two case reports [in Spanish]. Rev Neurol 2003;37:945-7. PMID 14634925
180: Lothman EW, Bertram EH, Bekenstein JW, Perlin JB. Self-sustaining limbic status epilepticus induced by "continuous" hippocampal stimulation: electrographic and behavioral characteristics. Epilepsy Res 1989;3:107-19. PMID 2707248
181: Lowenstein DH, Shimosaka S, So YT, Simon RP. The relationship between electrographic seizure activity and neuronal injury. Epilepsy Res 1991;10:49-54. PMID 1790772
182: Lüders H, Amina S, Bailey C, et al. Proposal: different types of alteration and loss of consciousness in epilepsy. Epilepsia 2014;55:1140-4. PMID 24981417
183: Macdonald RL, editor. Status epilepticus in adults and children: new developments in pathogenesis and treatment. Epilepsia 1999;40(Suppl 1):1-66.
184: Mangano S, Cusumano L, Fontana A. Non-convulsive status epilepticus associated with tiagabine in a pediatric patient. Brain Dev 2003;25:518-21. PMID 13129597
185: Marano E, Briganti F, Tortora F, et al. Neurosyphilis with complex partial status epilepticus and mesiotemporal MRI abnormalities mimicking herpes simplex encephalitis. J Neurol Neurosurg Psychiatry 2004;75:833. PMID 15145994
186: Mariajoseph FP, Sagar P, Muthusamy S, Amukotuwa S, Seneviratne U. Seizure-induced reversible MRI abnormalities in status epilepticus: A systematic review. Seizure 2021;92:166-73. PMID 34525432
187: Marini C, Parmeggiani L, Masi G, D'Arcangelo G, Guerrini R. Nonconvulsive status epilepticus precipitated by carbamazepine presenting as dissociative and affective disorders in adolescents. J Child Neurol 2005;20(8):693-6. PMID 16225818
188: Martinez-Rodriguez JE, Barriga FJ, Santamaria J, et al. Nonconvulsive status epilepticus associated with cephalosporins in patients with renal failure. Am J Med 2001;111:115-9. PMID 11498064
189: Matsuda N, Nakamura K, Watanabe A, Endo K, Yamamoto T. [Non-convulsive status epilepticus due to discontinuation of taking a benzodiazepine]. Nippon Naika Gakkai Zasshi 2006;95(11):2292-4. PMID 17168405
190: Mayer SA, Claassen J, Lokin J, Mendelsohn F, Dennis LJ, Fitzsimmons BF. Refractory status epilepticus: frequency, risk factors, and impact on outcome. Arch Neurol 2002;59:205-10. PMID 11843690
191: Mayeux R, Lueders H. Complex partial status epilepticus: case report and proposal for diagnostic criteria. Neurology 1978;28:957-61. PMID 99691
192: Mazarati A, Lu X. Regulation of limbic status epilepticus by hippocampal galanin type 1 and type 2 receptors. Neuropeptides 2005;39:277-80. PMID 15944022
193: McLachlan RS, Blume WT. Isolated fear and complex partial status epilepticus. Ann Neurol 1980;8:639-41. PMID 7212655
194: Meessen S, Riedel RR, Bruhl P. Status epilepticus in MVEC chemotherapy of urothelial cancer. Urologe A 1990;29:348-9. PMID 2291262
195: Meldrum BS, Vigouroux RA, Brierley JB. Systemic factors and epileptic brain damage. Arch Neurol 1973;29:82-7. PMID 4197956
196: Miyata H, Kubota F, Shibata N, Kifune A. Non-convulsive status epilepticus induced by antidepressants. Seizure 1997;6:405-7. PMID 9663805
197: Mohapel P, Ekdahl CT, Lindvall O. Status epilepticus severity influences the long-term outcome of neurogenesis in the adult dentate gyrus. Neurobiol Dis 2004;15:196-205. PMID 15006689
198: Morimoto K, Fahnestock M, Racine RJ. Kindling and status epilepticus models of epilepsy: rewiring the brain. Progr Neurobiol 2004;73:1-60. PMID 15193778
199: Mueller SG, Trabesinger AH, Buck F, Kollias SS, Boesiger P, Wieser HG. Proton magnetic resonance spectroscopy characteristics of a focal cortical dysgenesis during status epilepticus and in the interictal state. Seizure 2001;10(7):518-24. PMID 11749111
200: Murchison JT, Sellar RJ, Steers AJ. Status epilepticus presenting as progressive dysphasia. Neuroradiology 1995;37:438-9. PMID 7477849
201: Nairismagi J, Grohn OH, Kettunen MI, Nissinen J, Kauppinen RA, Pitkanen A. Progression of brain damage after status epilepticus and its association with epileptogenesis: a quantitative MRI study in a rat model of temporal lobe epilepsy. Epilepsia 2004;45:1024-34. PMID 15329065
202: Ng YT, Kim HL, Wheless JW. Successful neurosurgical treatment of childhood complex partial status epilepticus with focal resection. Epilepsia 2003;44:468-71. PMID 12614407
203: Niedermeyer E. Epileptic seizure disorders. In: Niedermeyer E, Lopes da Silva F, editors. Electroencephalography. 3rd ed. Baltimore: Williams and Wilkins, 1993:461-564.
204: Niedermeyer E, Khalifeh R. Petit mal status ("spike-wave-stupor"): an electro-clinical appraisal. Epilepsia 1965;6:250-62. PMID 4953776
205: Nowack WJ, Shaikh IA. Progression of electroclinical changes in complex partial status epilepticus: filling in the blanks. Clin Electroenephalogr 1999;30:5-8. PMID 9891184
206: Olney JW, de Gubareff T, Sloviter RS. "Epileptic" brain damage in rats induced by sustained electrical stimulation of the perforant path. II. Ultrastructural analysis of acute hippocampal pathology. Brain Res Bull 1983;10:699-712. PMID 6871738
207: Ozkaya G, Kurne A, Unal S, Oguz KK, Karabudak R, Saygi S. Aphasic status epilepticus with periodic lateralized epileptiform discharges in a bilingual patient as a presenting sign of "AIDS-toxoplasmosis complex". Epilepsy Behav 2006;9:193-6. PMID 16697709
208: Paetau R, Granstrom ML, Blomstedt G, Jousmaki V, Korkman M, Liukkonen E. Magnetoencephalography in presurgical evaluation of children with the Landau-Kleffner syndrome. Epilepsia 1999;40:326-35. PMID 10080514
209: Panayiotopoulos CP. Panayiotopoulos syndrome: a common and benign childhood epileptic syndrome. London: John Libbey, 2002.
210: Panayiotopoulos CP. Autonomic seizures and autonomic status epilepticus peculiar to childhood: diagnosis and management. Epilepsy Behav 2004;5:286-95. PMID 15145296
211: Papavasiliou A, Vassilaki N, Paraskevoulakos E, Kotsalis CH, Bazigou H, Bardani I. Psychogenic status epilepticus in children. Epilepsy Behav 2004;5:539-46. PMID 15256192
212: Parker V, Nobler MS, Pedley TA, Sackeim HA. A unilateral, prolonged, nonconvulsive seizure in a patient treated with bilateral ECT. J ECT 2001;17:292-3. PMID 11417926
213: Penfield W, Jasper HH. Epilepsy and functional anatomy of the human brain. Boston: Little Brown, 1954.
214: Petit J, Roubertie A, Inoue Y, Genton P. Non-convulsive status in the ring chromosome 20 syndrome: a video illustration of 3 cases. Epileptic Disord 1999;1:237-41. PMID 10937160
215: Petsche H, Rappelsberger P, Lapins R, Vollmer R. Rhythmicity in seizure patterns-topographical aspects. In: Speckmann EJ, Caspers H, editors. Origin of cerebral field potentials. Stuttgart: Thieme, 1979:60-79.
216: Pinol-Ripoll G, Perez-Lazaro C, Beltran-Marin I, Lopez del Val LJ, Pascual-Millan LF, Mostacero-Miguel E. Aphasia as the sole symptom of partial status epilepticus [in Spanish]. Rev Neurol 2004;39:1096-7. PMID 15597276
217: Pohlmann-Eden B, Wellhausser H, Stefanou A, Schmidt R. Correlation of serum prolactin and cortisol values with paroxysmal disorders of epileptic and non-epileptic origin and their clinical value. Fortschr Neurol Psychiatr 1993;61:363-8. PMID 8270226
218: Pontius AA. Motiveless firesetting: implicating partial limbic seizure kindling by revived memories of fires in "Limbic Psychotic Trigger Reaction". Percept Mot Skills 1999;88:970-82. PMID 10407907
219: Porter RJ, Penry JK. Petit mal status. In: Delgado-Escueta AV, Wasterlain CG, Treiman DM, Porter RJ, editors. Status epilepticus. Advances in neurology. New York: Raven Press, 1983:34:61-7.
220: Power KN, Gramstad A, Gilhus NE, Engelsen BA. Adult nonconvulsive status epilepticus in a clinical setting: semiology, aetiology, treatment and outcome. Seizure 2015;24:102-6. PMID 25458101
221: Prichard JC. A treatise on diseases of the nervous system. London: Underwood, 1822.
222: Primavera A, Audenino D, Cocito L. Ifosfamide encephalopathy and nonconvulsive status epilepticus. Can J Neurol Sci 2002;29:180-3. PMID 12035842
223: Primavera A, Bo GP, Venturi S. Aphasic status epilepticus. Eur Neurol 1988;28:255-7. PMID 3224619
224: Primavera A, Cocito L, Audenino D. Nonconvulsive status epilepticus during cephalosporin therapy. Neuropsychobiology 2004;49:218-22. PMID 15118360
225: Privitera MD, Hoffman M, Moore JL, Jester D. EEG detection of non tonic-clonic status epilepticus in patients with altered consciousness. Epilepsy Res 1994;18:155-66. PMID 7957038
226: Privitera MD, Strawsburg RH. Electroencephalographic monitoring in the emergency department. Emerg Med Clin North Am 1994;12:1089-100. PMID 7956889
227: Quintas S, Ródriguez-Carrillo JC, Toledano R, et al. When aphasia is due to aphasic status epilepticus: a diagnostic challenge. Neurol Sci 2018; 39:757-60. PMID 29255963
228: Rabending G, Fischer W. Epileptic psychosis and nonconvulsive status epilepticus with ictal bradycardia and asystole. Psychiatr Neurol Med Psychol (Leipz) 1986;38:184-8. PMID 3090578
229: Rao KM, Gangadhar BN, Janakiramaiah N. Nonconvulsive status epilepticus after the ninth electroconvulsive therapy. Convuls Ther 1993;9:128-9. PMID 11941202
230: Roberg LE, Monsson O, Kristensen SB, et al. Prediction of long-term survival after status epilepticus using the ACD score. JAMA Neurol 2022;79(6):604-13. PMID 35404392
231: Rogawski MA, Gryder D, Castaneda D, Yonekawa W, Banks MK, Lia H. GluR5 kainate receptors, seizures, and the amygdala. Ann N Y Acad Sci 2003;985:150-62. PMID 12724156
232: Roger J, Lob H, Tassinari CA. Status epilepticus. In: Magnus O, Lorentz de Haas AM, editors. The epilepsies. Handbook of clinical neurology. Vol 15. Amsterdam: North Holland Publishing Company, 1974:145-88.
233: Rona S, Rosenow F, Arnold S, et al. A semiological classification of status epilepticus. Epileptic Disord 2005;7:5-12. PMID 15741134
234: Rosenfeld MR, Dalmau JO. Paraneoplastic disorders of the CNS and autoimmune synaptic encephalitis. Continuum (Minneap Minn) 2012;18(2):366-83. PMID 22810133
235: Rosenow F, Knake S. Status epilepticus in adults. Handb Clin Neurol 2012;108:813-9. PMID 22939067
236: Roze E, Oubary P, Chédru F. Status-like recurrent pilomotor seizures: case report and review of the literature. Neurol Neurosurg Psychiatry 2000;68:647-9. PMID 10766899
237: Ruegg SJ, Dichter MA. Diagnosis and treatment of nonconvulsive status epilepticus in an intensive care unit setting. Curr Treat Options Neurol 2003;5:93-110. PMID 12628059
238: Rupprecht S, Franke K, Fitzek S, Witte OW, Hagemann G. Levetiracetam as a treatment option in non-convulsive status epilepticus. Epilepsy Res 2007;73(3):238-44. PMID 17161587
239: Saengpattrachai M, Sharma R, Hunjan A, et al. Nonconvulsive seizures in the pediatric intensive care unit: etiology, EEG, and brain imaging findings. Epilepsia 2006;47:1510-8. PMID 16981868
240: Salas-Puig J, Suarez-Moro R, Mateos V. Status epilepticus. Neurologia 1996;11(Suppl 4):108-21. PMID 9052951
241: Schaeffler L, Karbowski K. Recurring paroxysmal abdominal pains of cerebral origin. Schweiz Med Mochenschr 1981;111:1352-60. PMID 6794144
242: Schapel G, Chadwick D. Tiagabine and non-convulsive status epilepticus. Seizure 1996;5:153-6. PMID 8795133
243: Schulze-Bonhage A, Hefft S, Oehl B. Termination of complex partial status epilepticus by intravenous levetiracetam - a case report. J Neurol Neurosurg Psychiatry 2009;80(8):931-3. PMID 17353254
244: Seegers U, Potschka H, Loscher W. Transient increase of P-glycoprotein expression in endothelium and parenchyma of limbic brain regions in the kainate model of temporal lobe epilepsy. Epilepsy Res 2002;51:257-68. PMID 12399076
245: Seshia SS, McLachlan RS. Aura continua. Epilepsia 2005;46:454-5. PMID 15730546
246: Sheth RD, Drazkowski JF, Sirven JI, Gidal BE, Hermann BP. Protracted ictal confusion in elderly patients. Arch Neurol 2006;63:529-32. PMID 16606764
247: Shinawi M, Shahar E. Neurodevelopmental delay associated with nonconvulsive status epilepticus in a toddler. J Child Neurol 2001;16:215-7. PMID 11305690
248: Shinnar S, Maytal J, Krasnoff L, Moshe SL. Recurrent status epilepticus in children. Ann Neurol 1992;31:598-604. PMID 1514772
249: Shorvon S. Status epilepticus. Cambridge: University Press, 1994:382.
250: Shorvon S. The historical evolution of, and the paradigms shifts in, the therapy of convulsive status epilepticus over the past 150 years. Epilepsia 2013;54 Suppl 6:64-7. PMID 24001077
251: Shorvon S, Trinka E. Nonconvulsive status epilepticus and the postictal state. Epilepsy Behav 2010;19(2):172-5. PMID 20692208
252: Shorvon S, Trinka E. The London-Innsbruck Status Epilepticus Colloquia 2007-2011, and the main advances in the topic of status epilepticus over this period. Epilepsia 2013;54 Suppl 6:11-3. PMID 24001061
253: Siegel AM, Williamson PD, Roberts DW, Thadani VM, Darcey TM. Localized pain associated with seizures originating in the parietal lobe. Epilepsia 1999;40:845-55. PMID 10403207
254: Silbergleit R, Durkalski V, Lowenstein D, et al. Intramuscular versus intravenous therapy for prehospital status epilepticus. N Engl J Med 2012;366(7):591-600. PMID 22335736
255: Simon R. Physiological consequences of status epilepticus. Epilepsia 1985;26(Suppl):558-66. PMID 3922751
256: Skardoutsou A, Voudris KA, Vagiakou EA. Non-convulsive status epilepticus associated with tiagabine therapy in children. Seizure 2003;12:599-601. PMID 14630501
257: Sloviter RS. "Epileptic" brain damage in rats induced by sustained electrical stimulation of the perforant paths. I. Acute electrophysiological and light microscopic studies. Brain Res Bull 1983;10:675-97. PMID 6871737
258: So EL, Ruggles KH, Ahmann PA, Trudeau SK, Weatherford KJ, Trennery MR. Clinical significance and outcome of subclinical status epilepticus in adults. J Epilepsy 1995,8:11-5.
259: Solomons K, Holliday S, Illing M. Non-convulsive status epilepticus complicating electroconvulsive therapy. Int J Geriatr Psychiatry 1998;13:731-4. PMID 9818310
260: Specchio N, Wirrell EC, Scheffer IE, et al. International League Against Epilepsy classification and definition of epilepsy syndromes with onset in childhood: Position paper by the ILAE Task Force on Nosology and Definitions. Epilepsia 2022;63(6):1398-442. PMID 35503717
261: Srzich A, Turbott J. Nonconvulsive generalised status epilepticus following electroconvulsive therapy. Aust N Z J Psychiatry 2000;34(2):334-6. PMID 10789539
262: Staufenberg EF, Brown SW. Some issues in non-convulsive status epilepticus in children and adolescents with learning difficulties. Seizure 1994;3:95-105. PMID 7521725
263: Stecker MM, Kramer TH, Raps EC, O'Meeghan R, Dulaney E, Skaar DJ. Treatment of refractory status epilepticus with propofol: clinical and pharmacokinetic findings. Epilepsia 1998;39(1):18-26. PMID 9578008
264: Stodieck SR, Wieser HG. Autonomic phenomena in temporal lobe epilepsy. J Autonom Nerv Syst 1986;(Suppl):611-21.
265: Suopanki J, Lintunen M, Lahtinen H, et al. Status epilepticus induces changes in the expression and localization of endogenous palmitoyl-protein thioesterase 1. Neurobiol Dis 2002;10:247-57. PMID 12270687
266: Sutter R, Kaplan PW. The neurophysiologic types of nonconvulsive status epilepticus: EEG patterns of different phenotypes. Epilepsia 2013;54 Suppl 6:23-7. PMID 24001065
267: Sutter R, Marsch S, Fuhr P, Kaplan PW, Rüegg S. Anesthetic drugs in status epilepticus: risk or rescue? A 6-year cohort study. Neurology 2014;82(8):656-64. PMID 24319039
268: Sutter R, Semmlack S, Kaplan PW. Nonconvulsive status epilepticus in adults - insights into the Invisible. Nat Rev Neurol 2016;12(5):281-93. PMID 27063108
269: Szabo K, Poepel A, Pohlmann-Eden B, et al. Diffusion-weighted and perfusion MRI demonstrates parenchymal changes in complex partial status epilepticus. Brain 2005;128:1369-76. PMID 15743871
270: Tassinari CA, Rubboli G, Volpi L, et al. Encephalopathy with electrical status epilepticus during slow sleep or ESES syndrome including the acquired aphasia. Clin Neurophysiol 2000;111(Suppl)2:94-102. PMID 10996561
271: Tay SK, Hirsch LJ, Leary L, Jette N, Wittman J, Akman CI. Nonconvulsive status epilepticus in children: clinical and EEG characteristics. Epilepsia 2006;47:1504-9. PMID 16981867
272: Taylor J. Selected writings of John Hughlings Jackson. On epilepsy and epileptiform convulsions. Vol 1. London: Hodder and Stoughton, 1931.
273: Tedrus GM, Fonseca LC. Autonomic seizures and autonomic status epilepticus in early onset benign childhood occipital epilepsy (Panayiotopoulos syndrome). Arq Neuropsiquiatr 2006;64:723-6. PMID 17057874
274: Thomas P. Status epilepticus with confusional symptomatology. Neurophysiol Clin 2000;30:147-54. PMID 10916821
275: Thomas P, Beaumanoir A, Genton P, Dolisi C, Chatel M. "De novo" absence status of late onset: report of 11 cases. Neurology 1992;42:104-10. PMID 1734289
276: Tomson T, Lindbom U, Nilsson B, et al. Serum prolactin during status epilepticus. J Neurol Neurosurg Psychiatry 1989;52:1435-7. PMID 2614444
277: Towne AR, Garnett LK, Waterhouse EJ, Morton LD, DeLorenzo RJ. The use of topiramate in refractory status epilepticus. Neurology 2003;60:332-4. PMID 12552056
278: Treiman DM. Status epilepticus. Baillieres Clin Neurol 1996;5:821-39. PMID 9068883
279: Treiman DM, Delgado-Escueta AV. Complex partial status epilepticus. In: Delgado-Escueta AV, Wasterlain CG, Treimann DM, Porter RJ, editors. Status epilepticus. Advances in neurology. New York: Raven Press, 1983:34:15-35.
280: Treiman DM, Myers PD, Walton NY, et al. A comparison of four treatments for generalized convulsive status epilepticus. N Engl J Med 1998;339:792-8. PMID 9738086
281: Trimble MR, Bolwig TG, editors. The temporal lobes and the limbic system. Petersfield, UK: Wrightson Biomed Publ, 1992.
282: Trinka E, Cock H, Hesdorffer D, et al. A definition and classification of status epilepticus--report of the ILAE Task Force on classification of status epilepticus. Epilepsia 2015a;56(10):1515-23. PMID 26336950
283: Trinka E, Dilitz E, Unterberger I, et al. Non convulsive status epilepticus after replacement of valproate with lamotrigine. J Neurol 2002a;249:1417-22. PMID 12382160
284: Trinka E, Höfler J, Leitinger M, Brigo F. Pharmacotherapy for status epilepticus. Drugs 2015b;75(13):1499-521. PMID 26310189
285: Trinka E, Leitinger M. Which EEG patterns in coma are nonconvulsive status epilepticus? Epilepsy Behav 2015;49:203-22. PMID 26148985
286: Trinka E, Leitinger M. Management of status epilepticus, refractory status epilepticus, and super-refractory status epilepticus. Continuum (Minneap Minn) 2022;28(2):559-602. PMID 35393970
287: Trinka E, Unterberger I, Spiegel M, et al. De novo aphasic status epilepticus as presenting symptom of multiple sclerosis. J Neurol 2002b;249:782-3. PMID 12173579
288: Trousseau A. Clinique médicale de L'Hôtel Dieu de Paris, tome premiere. Paris: Baillière et fils, 1868.
289: Tsai MH, Lee LH, Chen SD, Lu CH, Chen MT, Chuang YC. Complex partial status epilepticus as a manifestation of Hashimoto's encephalopathy. Seizure 2007;16(8):713-6. PMID 17600734
290: Tsuji M, Tanaka H, Yamakawa M, Sagawa R, Azuma H. A case of systemic lupus erythematosus with complex partial status epilepticus. Epileptic Disord 2005;7:249-51. PMID 16162435
291: Ueki Y, Terada K, Otsuka A, Kanda M, Akiguchi I. A case of non-convulsive status epilepticus worsened Wernicke's aphasia reversely [in Japanese]. Rinsho Shinkeigaku 2000;40:339-43. PMID 10967650
292: Van Buren JM. The abdominal aura: a study of abdominal sensations occurring in epilepsy and produced by depth stimulation. Electroenceph Clin Neurophysiol 1963;15:1-19. PMID 13995971
293: Varon D, Pritchard PB 3rd, Wagner MT, Topping K. Transient Kluver-Bucy syndrome following complex partial status epilepticus. Epilepsy Behav 2003;4:348-51. PMID 12791340
294: Velioglu SK, Gazioglu S. Non-convulsive status epilepticus secondary to valproic acid-induced hyperammonemic encephalopathy. Acta Neurol Scand 2007;116(2):128-32. PMID 17661800
295: Vernea JJ. Partial status epilepticus with speech arrest. Proc Aust Assoc Neurol 1974;11:224-8. PMID 4219959
296: Vespa PM, Nenov V, Nuwer MR. Continuous EEG monitoring in the intensive care unit: early findings in clinical efficacy. J Clin Neurophysiol 1999;16:1-13. PMID 10082088
297: Villalobos-Chavez F, Rodriguez-Uranga JJ, Sanz-Fernandez G. Sequential changes in magnetic resonance in a limbic status epilepticus. Revista de Neurol 2005;40:354-7. PMID 15795872
298: Vincent A, Bien CG, Irani SR, Waters P. Autoantibodies associated with diseases of the CNS: new developments and future challenges. Lancet Neurol 2011;10(8):759-72. PMID 21777830
299: Vincent A, Buckley C, Schott JM, Baker I, Dewar BK, Detert N. Potassium channel antibody-associated encephalopathy: a potentially immunotherapy-responsive form of limbic encephalitis. Brain 2004;127:701-12. PMID 14960497
300: Vinton A, Kornberg AJ, Cowley M, Matkovic Z, Kilpatrick C, O’Brien TJ. Tiagabine-induced generalised non convulsive status epilepticus in patients with lesional focal epilepsy. J Clin Neurosci 2005;12:128-33. PMID 15749411
301: Walker MC. Diagnosis and treatment of nonconvulsive status epilepticus. CNS Drugs 2001;15:931-9. PMID 11735613
302: Walker MC. Treatment of nonconvulsive status epilepticus. Int Rev Neurobiol 2007;81:287-97. PMID 17433932
303: Walker M, Cross H, Smith S, et al. Nonconvulsive status epilepticus: Epilepsy Research Foundation workshop reports. Epileptic Disord 2005;7:253-96. PMID 16162436
304: Wang CP, Hsieh PF, Chen CC, et al. Hyperglycemia with occipital seizures: images and visual evoked potentials. Epilepsia 2005;46:1140-4. PMID 16026568
305: Wasterlain CG, Liu H, Mazarati AM, et al. Self-sustaining status epilepticus: a condition maintained by potentiation of glutamate receptors and by plastic changes in substance P and other peptide neuromodulators. Epilepsia 2000;41(Suppl 6):S134-43. PMID 10999535
306: Waterhouse E. Status epilepticus. Continuum (Minneap Minn) 2010;16(3 Epilepsy):199-227. PMID 22810322
307: Waterhouse EJ, Vaughan JK, Barnes PY, et al. Synergistic effect of status epilepticus and ischemic brain injury on mortality. Epilepsy Res 1998;29:175-83. PMID 9551779
308: Waxman SG, Geschwind N. The interictal behavioral syndrome of temporal lobe epilepsy. Arch Gen Psychiatry 1975;32:1580-6. PMID 1200777
309: Wells CR, Labor DR, Solomon GE. Aphasia as the sole manifestation of simple partial status epilepticus. Epilepsia 1992;33:84-7. PMID 1370801
310: Wessels T, Blaes F, Rottger C, Hugens M, Huge S, Jauss M. Kortikale Amaurosis und Status epilepticus bei akuter Porphyrie [Cortical amaurosis and status epilepticus with acute porphyria]. Nervenarzt 2005;76:992-5, 997-8. PMID 15791420
311: Whitty CM. Causalgic pain as an epileptic aura. Epilepsia 1953;2:37-41.
312: Wieser HG. "Psychische Anfälle" und deren stereoelektroenzephalographisches Korrelat. Z EEG-EMG 1979;10:197-206.
313: Wieser HG. Temporal lobe of psychomotor status epilepticus: a case report. Electroencephalogr Clin Neurophysiol 1980;48:558-72. PMID 6153964
314: Wieser HG. Depth recorded limbic seizures and psychopathology. Neurosci Biobehav Rev 1983;7:427-40. PMID 6366646
315: Wieser HG. Spontane und evozierte spitzentätigkeit im tiefen- und oberflächen-EEG. EEG-Labor 1988;10:8-30.
316: Wieser HG. Ictal manifestation of temporal lobe seizures. In: Smith DB, Treiman D, Trimble M, editors. Neurobehavioral problems in epilepsy. Advances in neurology. Vol 55. New York: Raven Press, 1991:301-15.
317: Wieser HG. Stereoelectroencephalography and foramen ovale electrode recording. In: Niedermeyer E, Lopes da Silva F, editors. Electroencephalography. 3rd ed. Baltimore: Williams and Wilkins, 1993:679-93.
318: Wieser HG. Simple partial status epilepticus. In: Engel J Jr, Pedley TA, editors. Epilepsy: a comprehensive textbook. Philadelphia: Lippincott-Raven Publishers, 1997:709-23.
319: Wieser HG. Temporal lobe epilepsies. In: Meinardi H, editor. The Epilepsies, part II. Handbook of clinical neurology. Vol 73. Amsterdam: Elsevier, 2000:53-96.
320: Wieser HG, Hailemariam S, Regard M, Landis T. Unilateral limbic epileptic status activity: stereo EEG, behavioral, and cognitive data. Epilepsia 1985;26:19-29. PMID 3971948
321: Wieser HG, Hajek M. Epilepsia partialis continua des Kindesalters. In: Froscher W, Vasella F, editors. Die Epilepsien. Berlin: W de Gruyter, 1994:273-80.
322: Wieser HG, Landis T. Is the "interictal behaviour syndrome of temporal lobe epilepsy" really an "interictal" phenomenon. Neurol Psychiatr 1983;6:70-8.
323: Wieser HG, Schindler K, Zumsteg D. EEG in Creutzfeldt-Jakob disease. Clin Neurophysiol 2006;117(5):935-51. PMID 16442343
324: Wieser HG, Siegfried J, Bernoulli C. Corrélations stéréo-electroencéphalographiques des manifestations psychiatriques dans l'épilepsie. Med Hyg 1981;39:1920-8.
325: Wieser HG, Williamson PD. Ictal semiology. In: Engel J Jr, editor. Surgical treatment of the epilepsies. 2nd ed. New York: Raven Press 1993:161-71.
326: Wieser S, Kelemen A, Barsi P, et al. Pilomotor seizures and status in non-paraneoplastic limbic encephalitis. Epileptic Disord 2005;7:205-11. PMID 16162429
327: Wilkinson HA. Epileptic pain. An uncommon manifestation with localizing value. Neurology 1973;25:518-20. PMID 4735469
328: Wolf P. Zur klinik und psychopathologie des status psychomotoricus. Nervenarzt 1970;41:603-10. PMID 4992752
329: Worster-Drought C. An unusual form of acquired aphasia in children. Dev Med Child Neurol 1971;13:563-71. PMID 5119912
330: Yoshimura K. A case of nonconvulsive status epilepticus associated with focal cortical dysplasia. Brain Dev 2003;25:207-10. PMID 12689702
331: Yoshino A. Psychotropic agents may induce de novo nonconvulsive status epilepticus. Nihon Shinkei Seishin Yakurigaku Zasshi 2000;20:1-10. PMID 10890017
332: Young GB, Blume WT. Painful epileptic seizures. Brain 1983;106:537-54. PMID 6640268
333: Young GB, Jordan KG. Do nonconvulsive seizures damage the brain. - Yes. Arch Neurol 1998;55:117-9. PMID 9443718
334: Young GB, Kreeft JH, McLachlan RS, Demelo J. EEG and clinical association with mortality in comatose patients in general intensive care unit. J Clin Neurophysiol 1999;16:354-60. PMID 10478708
335: Zarovnaya EL, Jobst BC, Harris BT. Propofol-associated fatal myocardial failure and rhabdomyolysis in an adult with status epilepticus. Epilepsia 2007;48(5):1002-6. PMID 17381434
336: Zhang G, Raol YH, Hsu FC, Coulter DA, Brooks-Kayal AR. Effects of status epilepticus on hippocampal GABAA receptors are age-dependent. Neuroscience 2004;125:299-303. PMID 15062973
337: Zuliani L, Graus F, Giometto B, Bien C, Vincent A. Central nervous system neuronal surface antibody associated syndromes: review and guidelines for recognition. J Neurol Neurosurg Psychiatry 2012;83(6):638-45. PMID 22448032

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Fernando Cendes MD PhD

Dr. Cendes of the University of Campinas - UNICAMP has no relevant financial relationships to disclose.
See Profile

Editor

Jerome Engel Jr MD PhD

Dr. Engel of the David Geffen School of Medicine at the University of California, Los Angeles, has no relevant financial relationships to disclose.
See Profile

Former Authors

Heinz Gregor Wieser MD

This is an article preview.
Start a Free Account
to access the full version.

Nearly 3,000 illustrations, including video clips of neurologic disorders.
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
Full spectrum of neurology in 1,200 comprehensive articles.
Listen to MedLink on the go with Audio versions of each article.

Questions or Comment?

MedLink®, LLC

3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122

Toll Free (U.S. + Canada): 800-452-2400

US Number: +1-619-640-4660

Support: service@medlink.com

Editor: editor@medlink.com

ISSN: 2831-9125

Focal unaware status epilepticus

Differential Diagnosis

focal neurologic deficits
Wernicke aphasia
neuropsychiatric manifestations
confusion
learning difficulties
- absence status
- Landau-Kleffner syndrome
- electrical status epilepticus in sleep

Also Relevant

Aura continua
Benign myoclonic epilepsy in infancy
Electrical status epilepticus during slow sleep
Epilepsy
Landau-Kleffner syndrome
- Lennox-Gastaut syndrome
- Subtle status epilepticus
- West syndrome

Focal unaware status epilepticus …

Focal unaware status epilepticus

Introduction

Overview

Key points

Historical note and terminology

Definition and problems with definition

Clinical manifestations

Presentation and course

Table 1. Criteria for the Diagnosis of Focal Unaware Status Epilepticus

Prognosis and complications

Clinical vignette

Biological basis

Localization

Pathophysiology

Differential diagnosis

Confusing conditions

Table 2. Classification of Status Epilepticus Along the Axes (1) Convulsive - Nonconvulsive, and (2) Generalized - Focal

Table 3. Criteria for absence status epilepticus

Associated and underlying disorders

Diagnostic workup

Management

References

Contributors

Author

Editor

Former Authors

Patient Profile

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Anti-LGI1 encephalitis

Self-limited (familial) neonatal epilepsy

Alcohol withdrawal seizures

Epileptic lesions due to malformation of cortical development

Epileptic spasms

Sleep and epilepsy

Neocortical temporal lobe seizures

Jacksonian seizures

Focal unaware status epilepticus

Introduction

Overview

Key points

Historical note and terminology

Definition and problems with definition

Clinical manifestations

Presentation and course

Table 1. Criteria for the Diagnosis of Focal Unaware Status Epilepticus

Prognosis and complications

Clinical vignette

Biological basis

Localization

Pathophysiology

Differential diagnosis

Confusing conditions

Table 2. Classification of Status Epilepticus Along the Axes (1) Convulsive - Nonconvulsive, and (2) Generalized - Focal

Table 3. Criteria for absence status epilepticus

Associated and underlying disorders

Diagnostic workup

Management

References

Contributors

Author

Editor

Former Authors

Patient Profile

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Anti-LGI1 encephalitis

Self-limited (familial) neonatal epilepsy

Alcohol withdrawal seizures

Epileptic lesions due to malformation of cortical development

Epileptic spasms

Sleep and epilepsy

Neocortical temporal lobe seizures

Jacksonian seizures

This is an article preview.
Start a Free Account
to access the full version.