Aura continua …

Maromi Nei MD

Epilepsy & Seizures

Updated 01.18.2024
Released 05.04.2001
Expires For CME 01.18.2027

Aura continua

Author: Maromi Nei MD

See Contributor Disclosures

Editor: Jerome Engel Jr MD PhD

Aura continua

In This Article

Quick Link

Introduction

Overview

Focal seizures may begin with a somatosensory, special sensory, visceral, or experiential aura, depending on the localization of the epileptic discharge. Typically, an aura lasts seconds to minutes, is stereotyped, and evolves to other ictal clinical features, including loss of awareness. If an aura occurs in isolation without further progression, it is more appropriately called a focal aware seizure, according to the 2017 ILAE Classification of the Epilepsies. Rarely, such symptoms last hours to days (and rarely even years) and are then called “aura continua,” ie, representing a form of focal status epilepticus. As with epilepsia partialis continua, the motor counterpart to aura continua, the understanding of the nature of the aura continua in terms of exact pathophysiology awaits clarification.

Key points

	• Aura continua is a rare phenomenon, difficult to diagnosis, and often occurring with other forms of seizures in the same individual.
	• Therapeutic medication trials or specialized testing may be needed to firmly establish the diagnosis.
	• Aura continua has varied clinical manifestations, depending on the cortical region of origin, and is often associated with an underlying focal cortical lesion.
	• Treatment of aura continua is often difficult and complete seizure freedom is not always possible.

Historical note and terminology

The term "aura" usually refers to that portion of a seizure experienced before impaired awareness occurs and for which memory is retained. In the case of a focal aware seizure, the aura is the entire seizure; however, where awareness is subsequently impaired, the aura is, in fact, the first symptom of a focal seizures with impaired awareness (19).

Scott and Masland first describe somatosensory hallucinations as a "continuous symptom" of an "aura continua” (66). The term "aura continua" can be found in Karbowski as a synonym for continuous psychomotor status (37; 93). Wolf used it as synonym for "status epilepticus of focal sensory seizures" or for hallucinosis (98).

The revised 2015 ILAE status epilepticus classification utilizes four axes: (1) seizure semiology, (2) etiology, (3) EEG correlates, and (4) age to classify status epilepticus (78). In this classification system, aura continua is listed in axis 1 under “Section B.2.b.a,” which includes seizures without prominent motor symptoms and without impairment of consciousness. Under this classification system, there is no specific minimum time duration for seizures to be considered status epilepticus. Instead, seizures are considered to be status epilepticus when there is “failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms which lead to abnormally prolonged seizures (after time point t1). It is a condition that can have long-term consequences (after time point t2), including neuronal death, neuronal injury, and alteration of neuronal networks, depending on the type and duration of seizures.” For focal status epilepticus with impaired consciousness, t1 (time when a seizure is likely to be prolonged leading to continuous seizure activity) is thought to occur at around 10 minutes. However, a t1 time duration has not been proposed specifically for focal seizures without impaired consciousness, including aura continua.

In the unified EEG terminology and criteria for nonconvulsive status epilepticus published in 2013, aura continua is classified as a form of nonconvulsive status epilepticus without coma or stupor with focal onset and without impairment of consciousness (04).

Clinical manifestations

Presentation and course

The term “aura continua” typically refers to seizures consisting of subjective feelings without visible motor phenomena. Thus, focal status epilepticus with motor phenomena or any other objective phenomena, such as aphasia, is not included. In the 2017 ILAE Classification of Seizure Types, aura continua is classified as a focal aware seizure type with nonmotor onset (22).

The EEG may reveal a focal ictal discharge on scalp EEG during aura continua, but in many cases there is no clear ictal change. When seen, the ictal change on scalp EEG may be subtle and remains focal, without significant spread (27). Even with intracranial EEG recordings, the ictal activity may be highly localized (94; 29).

From a clinical point of view, aura continua can be classified into four types: (1) somatosensory (ie, dysesthesia phenomena that involve the trunk, head and extremities); (2) aura continua that involve the special senses (ie, visual, auditory, vertiginous, gustatory and olfactory); (3) aura continua with predominantly autonomic symptoms; and (4) aura continua with psychic symptoms (83).

A special subtype in children, the so-called abdominal aura continua (abdominal epilepsy, recurring abdominal pain), has been described (64; 47; 57).

Pain as an epileptic aura (86), and painful epileptic seizures are likewise uncommon but described (97; 99; 68). Direct evidence that long-lasting pain occurs as aura continua (ie, as a special form of focal status epilepticus) is also sparse, but some data support this possibility. In 2005, Seshia and McLachlan report two patients with aura continua consisting of long-lasting pain (nasal pain for 2 years in one case and epigastric pain for 8 years in the other) (67). In both cases, the pain resolved after focal resection of the presumed seizure focus in the temporal lobe (left sided surgery in the case of nasal pain and right temporal resection for glioma in the case of epigastric pain).

Aura continua with elementary visual phenomena have been described by Gastaut, and prolonged complex visual hallucinations are described by Gastaut, and Sowa and Pituck (24; 71). Status epilepticus amauroticus is described by Barry and colleagues, and ictal visual hallucinations with reversible postictal hemianopia with anosognosia are described by Barry and colleagues, and Spatt and Mamoli (02; 72). Hadjikoutis and Sawhney described a case with occipital seizures presenting with bilateral visual loss (28).

Various medical conditions have been associated with epileptic visual hallucinations. Ghosh and colleagues reported a 34-year-old woman who developed simple partial seizures with ictal visual hallucinations and interictal right homonymous hemianopia due to left posterior quadrant seizures (27). These initially occurred 8 days after liver transplant surgery and occurred up to 22 times per day, with persistent interictal amaurosis. These continued for 1 week before EEG testing confirmed the epileptic etiology for her symptoms. The seizures ceased after levetiracetam treatment. In this case the etiology was not clear, as no lesion was seen on MRI, but it may have been related to immunosuppressive therapy. Donat and associates also described two men who developed visual hallucinations and hemianopia due to occipital seizures in the setting of nonketotic hyperglycemia (18). Kataoka and Ueno described a case of persistent headache and ictal palinopsia and polyopia in a 54-year-old woman with occipital lobe seizures (38). In this case as well, the MRI was normal. Gabapentin reduced the patient’s headaches and visual symptoms. Aura continua with visual allesthesia (visual images from one half of the visual field transposed to the other half) was reported in a 57-year-old man with a prior right parietal traumatic brain injury due to a gunshot wound (45). In this unusual case, the patient suffered from seizures during which images from his right visual field were transposed to his left. These symptoms eventually became continuous over an hour and correlated with seizures arising from the right parietal-temporal region on EEG. After treatment with lorazepam, levetiracetam, divalproex sodium, and gabapentin, his seizure frequency improved and he experienced occasional simple partial seizures on discharge from the hospital. Paredes-Aragon and colleagues reported a case of aura continua with visual symptoms in a patient with presumed autoimmune epilepsy related to both NMDA and GAD65 receptor antibodies (53).

Schiffter and Straschill as well as Wieser described aura continua musicalis (65; 88). Wieser’s patient was published under the heading psychomotor status epilepticus because, eventually, the aura continua with musical hallucinations (the patient experienced a song well-known and familiar to her) in "endless repetition" and with stereo-EEG documented restricted epileptiform discharges near Heschl gyrus spread to the ipsilateral mesiobasal limbic structures, accompanied by alteration of consciousness. The beginning of this electrical epileptiform status activity was accompanied by musical hallucinations only. Blanke and colleagues describe a patient with epilepsy (secondary to left parieto-temporal brain damage) suffering from the paroxysmal unilateral experience of hearing a person in her near-extrapersonal space associated with a deficit in spatial auditory perception and other paroxysmal disorders of somatognosia (06).

Mesial temporal limbic status with olfactory symptoms has been documented (89). A "gustatory aura continua" occurred, with left hippocampal continuous ictal activity in the depth EEG (94). It was also associated with subtle higher cognitive deficits detected with a lexical decision task. Seshia and McLachlan report one patient with long-lasting metallic taste for 2 years (a 46-year-old with left temporal seizure origin; symptom abolished after surgery; oligodendroglioma) and another with foul taste for 5 years (a 34-year-old with right temporal seizure origin; symptom abolished after surgery; mesial temporal sclerosis) (67).

Hamasaki and colleagues reported a case of a 42-year-old man with a 12-year history of persistent olfactory auras that resolved after focal resection of the prepiriform cortex and focal amygdala resection, where an ictal discharge was seen on intracranial electrode monitoring (29). As in many other cases of aura, the scalp EEG showed no ictal change.

The main clinical features of autonomic seizures are abdominal sensations, apnea, arrhythmias and bradyarrhythmias, chest pain, cyanosis, erythema, flushing, genital sensations and orgasm, hyperventilation, lacrimation, miosis, mydriasis, or hippus, palpitations, perspiration, pilomotor excitation ("gooseflesh"), tachycardia, urinary urgency and incontinence, and vomiting. Focal seizures with autonomic symptoms as the leading feature are well known (96). Under the category nonconvulsive status epilepticus, Rabending and Fischer describe ictal bradycardia and asystole (59). For reference, though not a series of aura, another study evaluating focal epileptic seizures in 43 patients with refractory epilepsy found that 39% had rhythm and/or repolarization abnormalities on ictal ECG, including atrial fibrillation, supraventricular tachycardia, asystole, and other abnormalities (50). It is unclear how often aura continua causes purely cardiac abnormalities, though it is likely uncommon. Autonomic seizures and autonomic status epilepticus have been best studied in Panayiotopoulus syndrome (51). In this syndrome with good prognosis, seizures start with autonomic symptoms, mainly emesis, while the child is fully conscious. Half of the seizures last longer than 30 minutes, constituting autonomic status epilepticus (52; 40). Although many patients have a relatively benign course, there are rare cases of more severe autonomic status epilepticus, including respiratory arrest requiring intubation (17).

Umbilical sensations in children (82), long-lasting borborygmi, widened pupils, pilomotor phenomena, goose-flesh or periodically shivering, etc. have been described (07; 90; 91; 92; 73). Autonomic phenomena may be associated with overt or subtle behavioral changes such as irritability, fear, panic, and sometimes, existential emptiness or some other form of pathological self-perception. One of Seshia and McLachlan’s patients suffered from epigastric fear for 8 years, which started after surgery (left temporal seizure origin; mesial temporal sclerosis) (67).

A particularly rare ictal or status symptom is aggression (14).

Limbic encephalitis might be associated with autonomic aura continua, and pilomotor status epilepticus has been reported in a case with voltage-gated potassium channel antibody positive non-paraneoplastic limbic encephalitis (95).

Ictal depression and anxiety in temporal lobe epilepsy is far more frequent (85); Henriksen as well as McLachlan and Blume describe a status with fear as the outstanding clinical expression (32; 44). A large amount of literature exists on this topic (70; 77). Ictal laughter (48) is usually associated with hypothalamic pathology, mainly hamartoma, in which gelastic seizures are the hallmark. Di Giacomo and colleagues reported a case of a patient with recurrent aura continua consisting of feeling “anxiety, motor agitation, fear and sensation of not being able to breathe” without overt clinical signs (16). She underwent intracranial EEG monitoring, which revealed that these symptoms were due to seizures arising from the left temporal region (recorded via left foramen oval electrodes). Her seizures were eliminated by left anterior temporal lobectomy.

Kim and colleagues evaluated headache as aura via video-EEG monitoring (39). They found that six (0.8%) of 775 patients with focal epilepsy reported a headache aura. The interval between headache onset and clinical seizure onset ranged from 1 to 35 seconds, with interval between headache onset and first EEG change ranging between -5 to 14 seconds. Four of these patients had right temporal seizures, and two had left sided onset (one temporal, one central). Although headache aura was rare, 30.7% of this same cohort reported a postictal headache, which is typically more commonly reported in epilepsy. However, prolonged ictal headaches, a form of aura continua, may rarely occur. A rare ictal phenomenon is "hemicrania epileptica" (34; 01), which may last longer than 30 minutes and, therefore, can then be labeled as a form of status epilepticus. “Hemicrania epileptica” by the International Headache Society (HIS) is defined as an ictal epileptic headache with “ipsilateral location of headache and ictal EEG paroxysms" (31). Thus, by this definition, it encompasses both short as well as long duration headaches associated with seizures and does not solely refer to conditions consistent with aura continua. In contrast, hemicrania continua is a primary headache disorder that is characterized by a continuous unilateral headache of moderate severity, exacerbations of severe pain, and complete responsiveness to indomethacin. In hemicrania continua, visual auras may precede or accompany the pain exacerbations (58; 10). However, due to the multiple clinical similarities between migraine with visual aura (including some cases of hemicrania continua) and occipital lobe seizures, it is possible that they share similar underlying electrophysiologic mechanisms (11).

Penfield introduced the term "experiential" to describe such mental phenomena and divided the patients’ past experience into illusions and hallucinations, which could be predominantly visual, auditory, or both, or an "unclassified" experience such as a dream, a flashback, or a memory without further description. Lennox referred to three categories of "psychic seizures,” which are (1) dream states, feeling of unreality or illusions; (2) hallucinations; and (3) mild confusion or disorientation, a feeling of strangeness without loss of memory and consciousness. Experiential means that the mental phenomena have a relevance to the patient’s past; Gloor specified that they typically combine elements of perception, memory, and affect (25). A series of patients undergoing evaluation for epilepsy surgery reported that experiential auras were highly associated with a left hemisphere dominant seizure focus, with 11 out of 12 patients in that series having a left temporal seizure focus localization (33). In contrast, the investigators did not find that déjà vu was highly lateralized to one hemisphere versus the other. Mesial temporal lobe seizures may present as anxiety disorders (100). Di Giacomo and colleagues reported a case of a 60-year-old woman who was originally diagnosed with anxiety disorder and psychogenic nonepileptic seizures, but later diagnosed with aura continua with psychic symptoms consisting of “anxiety, motor agitation, fear and sensation of not being able to breathe” during intracranial EEG monitoring (16). This case highlights the multitude of difficulties that may arise in establishing this diagnosis when scalp EEG is negative.

The principal ictal "psychic phenomena" may be listed as follows (21):

• Perceptual hallucinations
	- Visual - Auditory - Olfactory - Gustatory
• Mnemonic
	- Déjà vu - Jamais vu - Memory recall - Memory gaps/amnesia
• Emotional
	- Fear - Sadness - Pleasure - Sexual emotion - Emotional distress - Anger
• Other
	- Change in reality - Depersonalization - Feeling of other presence, Doppelganger – heautoscopy (08) - Forced thinking (87; 89) - Distortion of body image

Prognosis and complications

Aura continua appears to cause no lasting clinical negative sequelae, likely due to the highly focal nature of ictal activity that occurs in this entity. This contrasts with focal status epilepticus with impaired awareness in which case cognitive and other deficits may occur (76; 23).

Clinical vignette

A 50-year-old man with focal epilepsy presented to our epilepsy center with a history of seizures beginning at the age of 10 years. He had a history of (1) focal motor seizures causing tightening of the left lower extremity, at times spreading to cause whole body stiffening for 5 to 15 seconds; (2) rare focal to bilateral tonic-clonic seizures (only when antiseizure medications were missed or changed); and (3) a continuous feeling of tingling in the left foot for years (consistent with aura continua). His convulsive seizures were completely controlled with antiseizure medication. He underwent video-EEG monitoring, which revealed no ictal change during his focal motor seizures, though the motor manifestations recorded by video were consistent with an epileptic semiology. There was also no ictal pattern seen despite his continuous tingling foot sensation. However, his EEG did reveal rare spikes at Cz in wakefulness. His MRI brain was normal. At that time he had multiple focal motor seizures daily despite treatment trials with carbamazepine, lamotrigine, sodium valproate, and phenobarbital. Further trials of topiramate and levetiracetam were also ineffective in fully controlling his seizures. His seizures became milder after further medication changes, but he continued to experience the focal motor seizures affecting his foot once or twice daily and a continuous feeling of left foot tingling despite treatment with phenytoin and zonisamide. Eventually, his zonisamide was tapered and replaced with lacosamide. This caused complete resolution of his continuous foot tingling and a significant reduction in his focal motor seizures. Initially, after beginning lacosamide 200 mg/day (in addition to phenytoin), he had no seizures of any kind, including the aura continua, for 2 months. Now, at greater than 10 years of additional follow-up, after further increases in lacosamide to 500 mg/day and tapering of the phenytoin, he experiences only rare and very mild focal motor seizures consisting of left foot tightening, or brief auras. Soon after beginning lacosamide, his aura continua resolved completely.

This case illustrates the complexity in confirming an epileptic origin for the aura continua, as there was no ictal change on his EEG during his symptoms of continuous left foot tingling (or even during his focal motor seizures). It also illustrates the longevity of symptoms that can occur in some cases of aura continua. Despite lack of ictal EEG confirmation, his clinical history of discrete focal motor seizures affecting the same foot, as well as rare focal to bilateral tonic-clonic seizures and spikes consistent with a seizure focus affecting his foot region strongly support an epileptic origin for the continuous symptoms as well. In his case, no SPECT or PET imaging was available during or after resolution of his aura continua. In many cases, such ancillary tests may be helpful diagnostically as ictal focal hyperperfusion on SPECT or hypermetabolism on PET could be supportive of the ictal mechanism for the symptoms. In this case, his clinical history was strongly supportive of aura continua, and expensive ancillary confirmatory tests would likely not have altered his medical treatment because he also had focal motor seizures for which he underwent medication changes. Ultimately, the resolution of continuous foot tingling with antiseizure medication changes strongly supported the diagnosis of aura continua.

Biological basis

Aura continua appears to arise due to prolonged, long-lasting epileptic discharges arising from very localized cortical regions and possibly deep nuclei as well. Chronic neocortical stimulation may disrupt epilepsy partials continua, as described by Valentin and colleagues (81). The authors described two patients whose seizure focus in the primary motor cortex precluded resection. They, thus, underwent placement of neurostimulator devices and underwent chronic cortical stimulation via subdural strip electrodes at the seizure focus in this region (previously mapped by intracranial electrode monitoring). Both patients had greater than 90% seizure reduction. In both cases, epilepsy partialis continua returned after battery depletion, but replacement again reduced seizures by greater than 90%.

Subcortical structures are involved in other types of focal seizures and may also be important in aura continua. In another case of epilepsy partials continua, Courtin and colleagues report a case of left faciobrachial myoclonus, which responded to neurostimulation of the sensorimotor part of the globus pallidus internus (13). The authors noted that epileptic activity was recorded within the globus pallidus internus, suggesting potential downward spread of the ictal activity from the motor cortex.

The above data suggest that aura continua may similarly involve both cortical and subcortical processes, and neurostimulation for aura continua has not been reported.

Localization

Theoretically, each part of the cortex, and probably deep nuclei as well (09), can give rise to long-lasting localized epileptiform discharges. According to their functional specialization, the epileptic dysfunction of a localized ganglionic structure of the brain may give rise to "positive" or "negative" symptoms of a particular quality.

The most common localization of sensory seizures that involve the trunk, head, and extremities (somatosensory) as well as the special senses (visual, auditory, vertiginous, gustatory and olfactory) are listed in Table 1 together with some references.

Table 1. Principal Ictal “Psychic Phenomena”

I. Somatosensory symptoms: contralateral
	Localization: (post-) central
	• tingling • numbness • sense of movement • desire to move • somatic pain • heat or cold • electric shock • agnosia for a body part • phantom sensation (60; 55; 56; 42; 99; 80; 79)
II. Somatosensory symptoms: bilateral, contralateral, or ipsilateral
	Localization: Second sensory area localization (termination of the motor strip of the frontal parietal operculum), superior bank of the fronto-parietal Sylvian fissure
	• often affects fingertips, feet, lips, or tongue (perioral region)
III. Macular and peripheral visual symptoms
	Localization: Calcarine and pericalcarine occipital cortex (61; 62)
IV. Auditory symptoms
	Localization: Auditory cortex, Heschl gyrus, tonotopical organization (65; 88)
V. Vertigo
	Localization: Vestibular cortex in superior temporal gyrus rostral to auditory cortex (87; 89)
VI. Taste
	Localization: Parietal operculum near insula, anterior insula, probably the anterior mesial structures (55; 30)
VII. Olfaction
	Localization: Projection areas are:
		- anterior perforate - prepiriform cortex - lateral olfactory gyrus - periamygdalar cortex - entorhinal cortex - amygdala - septal nuclei - hypothalamus (Jackson and Beevor 1890; Jackson and Stewart 1899; 35; 29)

VIII. Experiential phenomena
	Localization: amygdala predominates; hippocampus, parahippocampal gyrus, temporal neocortex; possible left hemisphere dominance (26; 33)

It is not clear whether certain brain regions are more likely to cause the well-circumscribed and long-lasting discharge behavior seen in aura continua. By analogy with epilepsia partialis continua and focal status epilepticus with impaired awareness, it is reasonable to assume that certain brain regions are more likely to cause continuous ictal activity (93). From posttraumatic epilepsy, it is well known that the central and mesiotemporal lobe cortices are more seizure-prone than other cortices, but it is less clear whether region-specific differences exist to limit seizure discharges in time.

Etiology and pathogenesis

Aura continua occurs in many different medical conditions, as noted above. It is often associated with an underlying focal cortical abnormality but may occur in individuals without evidence of focal abnormalities on brain imaging. It has been described in patients with focal lesions, including brain tumors and traumatic brain injury, but has also been described during severe metabolic derangements and in individuals with chronic epilepsy. Any condition causing focal seizures could potentially cause aura continua.

Pathophysiology

The exact pathophysiology of aura continua awaits clarification. The ongoing ictal activity of aura continua reflects the intrinsic epileptogenic properties of a discharging epileptogenic focus that remains well localized. There is no further propagation of the epileptiform discharge and no significant ictal spread over time. A hippocampal epileptic focus causing electrographic focal status epilepticus may be limited to a volume of less than 1 cm in diameter (94; 20). Mechanistically, status epilepticus represents the failure of the natural seizure-suppressing mechanisms responsible for seizure termination (84).

Although a detailed discussion regarding the pathophysiology of status epilepticus is beyond the scope of this article, both cellular and network alterations appear to be involved (09). GABAA, NMDA, and AMPA receptors appear to be involved, along with depletion of inhibitory peptides (12). GABAA receptor-mediated inhibition is reduced in animal models of status epilepticus during status epilepticus (36). This reduced inhibition mediated by GABA receptors may be a basic mechanism underlying the self-sustaining and progressive nature of status epilepticus, including aura continua. Additionally, there are important changes in the intracellular and extracellular ionic environment during seizures, which are likely important in enabling ongoing seizure activity. Although local mechanisms are important, larger scale network activity, such as via recruitment of subcortical regions, may also be important (09).

Specialized imaging and cortical stimulation studies have helped to further refine the localization of specific symptoms of aura. Kovacs and associates reported a case of déjà vu occurring during deep brain stimulation only at specific stimulation parameters (41). SPECT imaging during the stimulated déjà vu showed increased perfusion in the right medial temporal regions. Similarly, Takeda and colleagues found that aura continua consisting of continuous déjà vu correlated with hyperperfusion in the entorhinal cortex in SPECT coregistered with MRI (74). Additionally, Bartolomei and associates found that stimulation of the entorhinal cortex in patients with epilepsy elicited déjà vu more readily than during stimulation of the hippocampus (03). However, their EEG data, which showed increased EEG signal correlation between several medial temporal lobe structures during déjà vu, suggested that déjà vu was likely caused by a transient cooperation between these various structures and not solely due to entorhinal cortex activation.

Differential diagnosis

Confusing conditions

An ongoing continuous or recurrent intermittent epileptic discharge might be suspected, and consequently proven, with EEG and/or response to antiseizure medication treatment in someone with epilepsy with known focal pathology and prolonged aura symptoms that fit well with the localization of the epileptic discharge. However, in the absence of clear-cut EEG findings, aura continua could be difficult to diagnose. Not infrequently, convincing ictal discharges cannot be detected without intracranial recordings. Such techniques, of course, are only justified in the context of surgical epilepsy therapy. Autonomic signs and symptoms occur in focal aware seizures and are frequent in focal with impaired awareness seizures. Prolonged autonomic ictal features can mimic psychiatric, endocrine, cardiac, and gastrointestinal disorders (15). Table 2 lists the most important differential diagnosis of autonomic phenomena.

Autoimmune epilepsy may cause aura continua, as well as other forms of status epilepticus. As noted in a review by Toledano and Pittock, there are several neural-specific autoantibodies targeting both intracellular and plasma membrane antigens that are associated with autoimmune epilepsy (75). Status epilepticus, including nonconvulsive status epilepticus, can occur at presentation. A subacute onset of cryptogenic epilepsy, history of autoimmunity or viral prodrome, psychiatric or cognitive features of limbic encephalitis, or history of tumor are some of the clinical features that may raise suspicion for an autoimmune epilepsy. Furthermore, the opercular syndrome (also known by the eponym Foix-Chavany-Marie), and in particular the anterior (frontal) opercular syndrome, which comprises essentially difficulties in speech and swallowing due to the loss of voluntary control of the oro-facio-linguo-pharyngo-masticatory muscles, can be associated with seizures and even with focal status epilepticus (63; 05). Lingual epilepsia partialis continua with disabling dysarthria due to impairment of the left half of the tongue has been reported by Nayak and colleagues in a patient with suspected Rasmussen encephalitis (49). As noted in a previous section, continuous visual focal status epilepticus was reported in a patient with GAD65-R and NMDA-R autoimmune epilepsy (53). Systemic lupus erythematosus may also cause aura continua (46).

Table 2. Differential Diagnosis of Autonomic Aura Continua

• Endocrine disorders
	- Carcinoid - Pheochromocytoma - Hypoglycemia


• Organic gastrointestinal disease • Panic attacks • Paroxysmal autonomic dysfunction
(43)

Table 3. Differential Diagnosis of Aura Continua with Psychic Phenomena and Psychic Seizures

• Normal experiences • Migraine • Psychoses
	- Postictal - Recurrent intermittent psychoses - Schizophrenia - Schizophrenia-like (69)
• Psychological disorders
	- Panic attacks - Hyperventilation attacks - Other psychiatric conditions
• Hallucinations/illusions due to a loss of primary sense • Drug-induced flashbacks • Cardiovascular disorders • Sleep disorders
	- Nightmares - Night terrors - REM sleep behavior disorder
• Metabolic disorder
	- Recurrent drug abuse - Hypoglycemia - Porphyria
• Acute CNS disorders, including limbic encephalitis
(43)

Associated and underlying disorders

Aura continua might occur de novo, but in most instances occurs in patients with known focal epilepsies, particularly temporal lobe epilepsy. It may be more common in patients with underlying focal pathology, but due to the scarcity of cases, clear evidence from the literature is unavailable. And it is notable that various medical conditions are associated with aura continua, even in the absence of an underlying focal lesion, as noted in prior sections.

Management

	• As discussed above, no convincing evidence exists that aura continua will lead to significant irreversible neurologic deficits.
	• Thus, the use of any treatment options must be tempered by the risk of adverse effects that may arise with overaggressive therapy.

Aura continua may respond to various standard antiseizure medications. However, similarly to epilepsy partials continua, aura continua is frequently difficult to treat and may be refractory to multiple medications, as in the case of visual allesthesia reported by Mendez and Chen (45). There are various antiseizure medications, which have been reported to be effective, but there are not sufficient data to guide treatment or suggest that specific medications may be superior to others. Treatment should follow standard antiseizure medication guidelines and is outside the scope of this review. Various medications have been reported to be useful. Treatment goals must take into account the risks of possible adverse medication side effects, which could outweigh potential benefits of treatment. Treatment of any underlying etiology should also be a focus of therapy, as in autoimmune epilepsy (54).

Outcomes

There are limited data regarding outcome in aura continua because case reports and small case series constitute the bulk of the available data. Aura continua is often refractory to multiple antiseizure medications. As noted above, potential risks of treatment must be weighed against the benefits of treating the aura continua symptoms, which could vary in severity. Benzodiazepines and antiseizure medication polytherapy are necessary to completely control aura continua in some cases. Although epilepsy surgery has been reported to be effective in some cases, those individuals also had other types of seizures as well, which were the prime clinical indication for surgery. Oversedation, cognitive side effects, dizziness, and other common side effects of antiseizure medications could occur in such cases. Thus, treatment of aura continua must balance the severity of the symptoms with quality of life.

References

01: Andermann F, Lugaresi E, editors. Migraine and epilepsy. Boston: Butterworth, 1987.
02: Barry E, Sussmann NM, Bosley TM, et al. Ictal blindness and status epilepticus amauroticus. Epilepsia 1985;26:577-84. PMID 4076063
03: Bartolomei F, Barbeau EJ, Nguyen T, et al. Rhinal-hippocampal interactions during déjà vu. Clin Neurophysiol 2012;123(3):489-95. PMID 21924679
04: Beniczky S, Hirsch LJ, Kaplan PW, et al. Unified EEG terminology and criteria for nonconvulsive status epilepticus. Epilepsia 2013;54 Suppl 6:28-9. PMID 24001066
05: Benninger DH, Mueller SG, Treyer V, Kollias S, Buck A, Wieser HG. Transient epileptic opercular syndrome. Seizure 2007;16:276-82. PMID 17270469
06: Blanke O, Ortigue S, Coeytaux A, Martory MD, Landis T. Hearing of a presence. Neurocase. 2003;9(4):329-39. PMID 12925946
07: Brody JA, Odom GL, Kunkle EC. Pilomotor seizures: report of a case associated with a central glioma. Neurology 1960;10:993-7.
08: Brugger P, Agosti R, Regard M, Wieser HG, Landis T. Heautoscopy, epilepsy, and suicide. J Neurol Neurosurg Psychiatry 1994;57(7):838:9. PMID 8021672
09: Burman RJ, Raimondo JV, Jefferys JGR, Sen A, Akerman CJ. The transition to status epilepticus: how the brain meets the demands of perpetual seizure activity. Seizure 2020;75:137-44. PMID 31870785
10: Castellanos-Pinedo F, Zurdo M, Martinez-Acebes E. Hemicrania continua evolving from episodic paroxysmal hemicrania. Cephalalgia 2006;26:1143-5. PMID 16919066
11: Cianchetti C, Pruna D, Ledda M. Epileptic seizures and headache/migraine: a review of types of association and terminology. Seizure 2013;22(9):679-85. PMID 23831147
12: Chen JWY, Naylor DE, Wasterlain CG. Advances in the pathophysiology of status epilepticus. Acta Neurol Scand 2007(S186):7-15. PMID 17784531
13: Courtin E, Guillaud E, Cuny E, et al. Globus pallidus internen deep brain stimulation: An alternative treatment for Epilepsy partialis continua? Brain Stimul 2022;15(3):635-7. PMID 35443223
14: Delgado-Escueta AV, Mattson RA, King L, et al. The nature of aggression during epileptic seizures. N Engl J Med 1981;305:711-6. PMID 7266614
15: Devinsky O, Price BH, Cohen SI. Cardiac manifestations of complex partial seizures. Am J Med 1986;80(2):195-202. PMID 3946434
16: Di Giacomo R, Gnatkovsky V, Deleo F, et al. How deep do we have to go? Recurrent episodes of aura continua with psychic symptoms may be misdiagnosed without intracranial recordings. Clin Neurophysiology 2020;131(2):580-2. PMID 31831266
17: Dirani M, Yamak W, Beydoun A. Panayiotopoulos syndrome presenting with respiratory arrest: a case report and literature review. Epilepsy Behav Case Rep 2015;3:12-4. PMID 25737964
18: Donat A, Guilloton L, Bonnet C, Depreux G, Lamboley JL, Drouet A. Partial visual seizures induced by non-ketosic hyperglycemia: magnetic resonance imaging and visual evoked potential descriptions: A study of two case reports with radiologic and electrophysiologic abnormalities [Article in French]. Rev Neurol (Paris) 2013;169(2):154-61. PMID 23079857
19: Dreifuss F. Classification of epileptic seizures. In: Engel J Jr, Pedley TA, editors. Epilepsy; A comprehensive textbook. Philadelphia: Lippincott-Raven Publishers, 1997:517-24.
20: Fauser S, Schulze-Bonhage A. How large must an epileptic focus be to cause an electrographic status epilepticus - a case report. Clin Neurophysiol 2004;115:2274-9. PMID 15351369
21: Fish DR. Psychic seizures. In: Engel J Jr, Pedley TA, editors. Epilepsy; A comprehensive textbook. Philadelphia: Lippincott-Raven Publishers, 1997:543-8.
22: 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
23: Fountain NB. Status epilepticus: risk factors and complications. Epilepsia 2000;41 Suppl 2:S23-30. PMID 10885737
24: 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.
25: Gloor P. Experiential phenomena of temporal lobe epilepsy: facts and hypotheses. Brain 1990;113:1673-94. PMID 2276040
26: Gloor P, Olivier A, Quesney LF, Andermann F, Horowitz S. The role of the limbic system in experiential phenomena of temporal lobe epilepsy. Ann Neurol 1982;12:129-44. PMID 7125603
27: Ghosh P, Motamedi G, Osborne B, Mora CA. Reversible blindness: simple partial seizures presenting as ictal and postictal hemianopia. J Neuroophthalmol 2010;30(3):272-5. PMID 20531226
28: Hadjikoutis S, Sawhney IM. Occipital seizures presenting with bilateral visual loss. Neurol India 2003;51(1):115-6. PMID 12865542
29: Hamasaki T, Otsubo H, Uchikawa H, Yamada K, Kuratsu J. Olfactory auras caused by a very focal isolated epileptic network in the amygdala. Epilepsy and Beh Case Reports 2014;2:142-4. PMID 25667893
30: Hausser-Hauw C, Bancaud J. Gustatory hallucinations in epileptic seizures. Brain 1987;110:339-59. PMID 3105808
31: Headache Classification Committee of the International Headache Society. The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia 2013;33(9):629-808. PMID 23771276
32: 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
33: Heydrich L, Marillier G, Evans N, Blanke O, Seeck M. Lateralising value of experiential hallucinations in temporal lobe epilepsy. J Neurol Neurosurg Psychiatry 2015;86(11):1273-6. PMID 25587072
34: Isler HR, Wieser HG, Egli M. Hemicrania epileptica. In: Rose FC, editors. Progress in migraine research 2. London: Pitman Books, 1984:69-82.
35: Jackson JH. On a particular variety of epilepsy ("intellectual aura"), one case with symptoms of organic brain disease 1889. In: Taylor J, editor. Selected writings of J.H. Jackson. Vol 1. New York: Basic Books Inc, 1958:308-17, 385-405.
36: Joshi S, Kapur J. GABAA receptor plasticity during status epilepticus. In: Noebels JL, Avoli M, Rogawski MA, et al., editors. Jasper's Basic Mechanisms of the Epilepsies. [Internet] 4th ed. Bethesda (MD): National Center for Biotechnology Information, 2012.
37: Karbowski K. Epileptische Anfälle. Heidelberg: Springer, 1985.
38: Kataoka H, Ueno S. Cerebral polyopia and palinopsia in a patient with occipital lobe epilepsy. Epilepsy Behav 2009;14(4):684-6. PMID 19435573
39: Kim DW, Sunwoo JS, Lee SK. Headache as an aura of epilepsy: video-EEG monitoring study. Headache 2016;56(4):762-8. PMID 26893212
40: Koutroumanidis M, Rowlinson S, Sanders S. Recurrent autonomic status epilepticus in Panayiotopoulus syndrome: Video/EEG studies. Epilepsy Behav 2005;7:543-7. PMID 16105750
41: Kovacs N, Auer T, Balas I, et al. Neuroimaging and cognitive changes during déjà vu. Epilepsy Behav 2009;14(1):190-6. PMID 18804184
42: Lende RA, Popp AJ. Sensory jacksonian seizures. J Neurosurg 1976;44:706-11. PMID 818344
43: Liporace JD, Sperling MR. Simple autonomic seizures. In: Jengel J Jr, Pedley TA, editors. Epilepsy: a comprehensive textbook. Philadelphia: Lippincott-Raven Publishers, 1997:549-55.
44: McLachlan RS, Blume WT. Isolated fear and complex partial status epilepticus. Ann Neurol 1980;8:639-41. PMID 7212655
45: Mendez MF, Chen JW. Epilepsy partialis continua with visual allesthesia. J Neurol 2009;256(6):1009-11. PMID 19240953
46: Mikdashi J, Krumholz K. Long-term outcome of status epilepticus-related to systemic lupus erythematosus: an observational study and a systematic review. Semin Arthritis Rheum 2023;63:152250. PMID 37595509
47: Mitchell WG, Greenwood RS, Messenheimer JA. Abdominal epilepsy. Cyclic vomiting as the major symptom of simple partial seizures. Arch Neurol 1983;40:251-2. PMID 6403002
48: Mueller D, Mueller J. Lachen als epileptische Manifestation. VEB G. Fischer: Jena, 1980.
49: Nayak D, Abraham M, Kesavadas C, Radhakrishnan K. Lingual epilepsia partialis continua in Rasmussen's encephalitis. Epileptic Disord 2006;8:114-7. PMID 16793572
50: Nei M, Ho RT, Sperling MR. EKG abnormalities during partial seizures in refractory epilepsy. Epilepsia 2000;41(5):542-8. PMID 10802759
51: Panayiotopoulus CP. Panayiotopoulus syndrome: a common and benign childhood epileptic syndrome. London: John Libbey, 2002.
52: Panayiotopoulus CP. Autonomic seizures and autonomic status epilepticus peculiar to childhood: diagnosis and management. Epilepsy Behav 2004;5:286-95. PMID 15145296
53: Paredes-Aragon EM, Valdez-Ruvalcaba HE, Santos-Peyret A, et al. Continuous visual focal status epileptics as the primary presentation of NMDA-R and GAD65-R autoimmune epilepsy. Front Neurol 2020;11:598974. PMID 33324338
54: Patel A, Meng Y, Najjar A, Lado F, Najjar S. Autoimmune encephalitis: a physician’s guide to the clinical spectrum diagnosis and management. Brain Sci 2022;12(9):1130. PMID 36138865
55: Penfield W, Jasper HH. Epilepsy and functional anatomy of the human brain. Boston: Little Brown, 1954.
56: Penfield W, Rasmussen T. The cerebral cortex of man. A clinical study of localization and function. New York: MacMillan, 1957.
57: Peppercorn MA, Herzog AG. The spectrum of abdominal epilepsy in adults. Am J Gastroenterol 1989;84:1294-6. PMID 2801681
58: Peres MF, Siow HC, Rozen TD. Hemicrania continua with aura. Cephalalgia 2002;22(3):246-8. PMID 12047466
59: Rabending G, Fischer W. Epileptic psychosis and nonconvulsive status epilepticus with ictal bradycardia and asystole [in German] Psychiatr Neurol Med Psychol (Leipz) 1986;38(4):184-8. PMID 3090578
60: Russel WR, Whitty CM. Studies in traumatic epilepsy. 2. Focal motor and somatic sensory fits. A study of 85 cases. J Neurol Neurosurg Psychiatry 1953;16:73-97. PMID 13053229
61: Russel WR, Whitty CM. Studies in traumatic epilepsy. 3. Visual fits. J Neurol Neurosurg Psychiatry 1955;18:79-96. PMID 14381917
62: Salanova V, Andermann F, Olivier A, Rasmussen T, Quesney LF. Occipital lobe epilepsy: electroclinical manifestations, electrocorticography, cortical stimulation and outcome in 42 patients treated between 1939 and 1991. Brain 1992;115:1655-80. PMID 1486456
63: Salas-Puig J, Pérez-Jiménez A, Thomas P, et al. Opercular epilepsies with oromotor dysfunction. In: Guerrini R, Aicardi J, Andermann F, Hallet M, editors. Epilepsy and Movement Disorders. Cambridge University Press, 2002:251-68.
64: Schaeffler L, Karbowski K. Recurring paroxysmal abdominal pains of cerebral origin. Schweiz Med Mochenschr 1981;111:1352-60. PMID 1486456
65: Schiffter R, Straschill M. Aura continua musicalis - Bericht über einen Krankheitsfall mit sensorischem Status epilepticus. Nervenarzt 1977;48:321-35.
66: Scott JS, Masland RL. Occurrence of "continuous symptoms" in epilepsy patients. Neurology 1953;3:297-301. PMID 13054857
67: Seshia SS, McLachlan RS. Aura continua. Epilepsia 2005;46:454-5. PMID 15730546
68: 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
69: Slater E, Beard AW. The schizophrenia-like psychoses of epilepsy. Br J Psychiatry 1963, 109:95-150. PMID 13989174
70: Smith DB, Treiman DM, Trimble MR, editors. Neurobehavioral problems in epilepsy. Advances in neurology. Vol 55. New York: Raven Press, 1991.
71: Sowa MV, Pituck S. Prolonged spontaneous complex visual hallucinations and illusions as ictal phenomena. Epilepsia 1989;30:524-6. PMID 2792027
72: Spatt J, Mamoli B. Ictal visual hallucinations and post-ictal hemianopsia with anosognosia. Seizure 2000;9:502-4. PMID 11034876
73: Stodieck SR, Wieser HG. Autonomic phenomena in temporal lobe epilepsy. J Autonom Nerv Syst 1986;(Suppl):611-21.
74: Takeda Y, Kurita T, Sakurai K, Shiga T, Tamaki N, Koyama T. Persistent déjà vu associated with hyperperfusion in the entorhinal cortex. Epilepsy Behav 2011;21(2):196-9. PMID 21555251
75: Toledano M, Pittock SJ. Autoimmune epilepsy. Semin Neurol 2015;35(3):245-58.** PMID 26060904
76: 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.
77: Trimble MR, Bolwig TG, editors. The temporal lobes and the limbic system. Petersfield, UK: Wrightson Biomed Publ, 1992.
78: Trinka E, Cock H, Hesdorffer D, Rossetti AI, et al. A definition and classification of status epilepticus – Report of the ILAE Task Force on Classification of Status Epilepticus. Epilepsia 2015;56(10):1515-23. PMID 26336950
79: Uematsu S, Lesser RP, Fischer RS, et al. Motor and sensory cortex in humans: topography studied with chronic subdurale stimulation. Neurosurgery 1992b;31:59-72. PMID 1641111
80: Uematsu S, Lesser RP, Gordon B. Localization of sensorimotor cortex: the influence of Sherrington and Cushir on the modern concept. Neurosurgery 1992a;30:904-13. PMID 1614594
81: Valentin A, Ughratdar I, Cheserem B, Morris R, Selway R, Alarcon G. Epilepsia partialis continua responsive to neocortical electrical stimulation. Epilepsia 2015;56:e104-9. PMID 26174165
82: VanBuren 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
83: VanNess PC, Lesser RP, Duchowny MS. Simple sensory seizures. In: Engel J Jr, Pedley TA, editors. Epilepsy: a comprehensive textbook. Philadelphia: Lippincott-Raven Publishers, 1997:533-42.
84: Wasterlain CG, Treiman DM, editors. Status epilepticus: Mechanisms and management. Boston: MIT Press, 2006.
85: Weil AA. Ictal depression and anxiety in temporal lobe disorders. Am J Psychiatry 1956;113:149-57. PMID 13340016
86: Whitty CW. Causalgic pain as an epileptic aura. Epilepsia 1953;2:37-41.
87: Wieser HG. "Psychische Anfälle" und deren stereoelektroenzephalographisches Korrelat. Z EEG-EMG 1979;10:197-206.
88: Wieser HG. Temporal lobe of psychomotor status epilepticus: a case report. Electroencephalogr Clin Neurophysiol 1980;48:558-72. PMID 6153964
89: Wieser HG. Zur Frage der lokalisatorischen Bedeutung epileptischer Halluzinationen. In: Karbowski K, editor. Halluzinationen bei Epilepsien und Differentialdiagnose. Bern: Hans Huber Verlag, 1982:67-92.
90: Wieser HG. Electroclinical features of the psychomotor seizure. A stereo-electroencephalographic study of ictal symptoms and chronotopographical seizure patterns including clinical effects of intracerebral stimulation. Stuttgart-London: Fischer-Butteworths, 1983a:242.
91: Wieser HG. Depth recorded limbic seizures and psychopathology. Neurosci Biobehav Rev 1983b;7:427-40. PMID 6366646
92: 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.
93: Wieser HG. Epilepsia partialis continua. In: Gilman S, editor. MedLink Neurology. 3rd ed. San Diego: MedLink Corporation, 2001.
94: 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
95: Wieser S, Kelemen A, Barsi P, et al. Pilomotor seizures and status in non-paraneoplastic limbic encephalitis. Epileptic Disord 2005;7(3):205-11. PMID 16162429
96: 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.
97: Wilkinson HA. Epileptic pain. An uncommon manifestation with localizing value. Neurology 1973;23(5):518-20. PMID 4735469
98: Wolf P. Zur Klinik und Psychopathologie des Status psychomotoricus. Nervenarzt 1970;41:603-10. PMID 4992752
99: Young G, Blume WT. Painful epileptic seizures. Brain 1983;106:537-54. PMID 6640268
100: Young GB, Chandarana PC, Blume WT, McLachlan RS, Munoz DG, Girvin JP. Mesial temporal lobe seizures presenting as anxiety disorders. J Neuropsychiatry Clin Neurosci 1995;7:352-7. PMID 7580198

Contributors

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

Author

Maromi Nei MD

Dr. Nei of Sidney Kimmel Medical College of Thomas Jefferson University received research/clinical trial support from Eisai and UCB Pharma as clinical trial principal investigator.
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

Aura continua

Differential Diagnosis

psychiatric disorders
endocrine disorders
cardiac disorders
gastrointestinal disorders
cardiovascular symptoms
- thoracic symptoms
- papillary dilation
- carcinoid
- limbic encephalitis
- porphyria
- pheochromocytoma
- hypoglycemia
- organic gastrointestinal disease
- panic attacks
- paroxysmal autonomic dysfunction
- nonparaneoplastic limbic encephalitis
- status epilepticus

Aura continua

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Localization

Table 1. Principal Ictal “Psychic Phenomena”

Etiology and pathogenesis

Pathophysiology

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Table 2. Differential Diagnosis of Autonomic Aura Continua

Table 3. Differential Diagnosis of Aura Continua with Psychic Phenomena and Psychic Seizures

Associated and underlying disorders

Diagnostic workup

Management

Outcomes

Special considerations

Pregnancy

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

Photosensitive occipital lobe epilepsy

Intermittent explosive disorder

Pyridoxine/P5P-dependent developmental epileptic encephalopathy

Reflex seizures

Anti-LGI1 encephalitis

Self-limited (familial) neonatal epilepsy

Epilepsy with auditory features

Alcohol withdrawal seizures

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