Focal seizures with experiential symptoms …

Fernando Cendes MD PhD

Epilepsy & Seizures

Updated 03.05.2024
Released 11.19.2011
Expires For CME 03.05.2027

Focal seizures with experiential symptoms

Author: Fernando Cendes MD PhD

See Contributor Disclosures

Editor: Jerome Engel Jr MD PhD

Focal seizures with experiential symptoms

In This Article

Quick Link

Introduction

Overview

The term “experiential phenomena” includes various types of transitory mental states and sensory and memory illusions (28; 17). At the most fundamental level, experiential symptoms are illusions or hallucinations that result in erroneous interpretations of the present experience. Frequent types of experiential symptoms include sensations of déjà-vu or jamais-vu, episodes of disorienting hyperfamiliarity, and a variety of out-of-body experiences termed “autoscopy” (28). If epileptic in origin, experiential symptoms occur almost exclusively in temporal lobe epilepsy.

Experiential phenomena also occur in the context of psychiatric disease or during the aura phase of migraine headaches and have been associated with mass lesions or inflammatory conditions of the temporal lobe.

Déjà vu is a French term that means "already seen." It refers to the subjective feeling of recognizing a current situation, even though there is no clear memory of experiencing it before (43). It is estimated that occasional experiences of déjà vu occur in 60% to 80% of healthy individuals (12).

Key points

	• Experiential symptoms are illusions or hallucinations that result in erroneous interpretations of the present experience.
	• Frequent types of experiential symptoms include déjà-vu, jamais-vu, hyperfamiliarity, sensory and memory illusions, and out-of-body experiences termed “autoscopy.”
	• Seizures with experiential symptoms are most frequently symptoms of focal epilepsy arising from the temporal lobe, most likely the mesial structures.
	• Similar phenomena can occur in patients with no neurologic disease, in the context of psychiatric disease, or during the aura phase of migraine headache and have been associated with mass lesions or inflammatory conditions of the temporal lobe.
	• Occasional episodes of déjà-vu and jamais-vu may also occur in healthy people.

Historical note and terminology

Hughlings Jackson compiled the first study of experiential seizures in 1891 and called them “dreamy states” (32). He described patients with “epileptic convulsions” who experienced episodes of “dreams mixing up with present thoughts.” In the 1950s and 1960s, Wilder Penfield, working at the Montreal Neurological Institute, described patients who experienced vivid memories during electrical stimulation of the lateral temporal lobe (48). Penfield called them “experiential phenomena” because they had a “compelling immediacy similar to or sometimes more vivid than the patient’s recall of his or her own past experiences.” In the 1990s, Jean Bancaud studied experiential symptoms induced by seizures using intracranial electrocorticography and found that experiential phenomena occurred during ictal activation of the mesial temporal structures (04). In 2007, Jean-Pierre Vignal confirmed their findings likewise using intracranial EEG. In 2010, the ILAE Commission on Classification and Terminology classified experiential symptoms as “focal seizures involving subjective sensory or psychic phenomena only” (08). The 2017 operational classification of seizure types by the ILAE replaced the term “psychic” with “cognitive” (24; 23). A cognitive seizure also includes positive cognitive phenomena such as déjà vu, jamais vu, illusions, or hallucinations (24). This newer classification also introduced the term awareness, which is defined as knowledge and understanding that something is happening or exists. If awareness is impaired for any portion of the seizure, then the seizure is classified as a focal seizure with impaired awareness (24; 23). A focal aware seizure replaces the previously termed simple partial seizure, and a focal impaired awareness seizure replaces the term complex partial seizure (24; 45). Therefore, according to this newer operational classification, experiential seizures are defined as focal aware cognitive seizures (24; 23).

Symptoms experienced during epileptic seizure are closely related to the region of the brain where the seizure originated. For example, if a seizure arises from the primary auditory cortex of the temporal lobe, the patient commonly perceives elementary sounds. In this instance, the patient experiences an alteration in a single sensory modality, ie, hearing. If a seizure arises from regions involved in integrating sensation, emotion, and memory, the patient may experience a much more complex alteration of their mental state. For instance, seizures that originate from the temporal lobe may cause the patient to feel a false sense of familiarity and generate the illusion that the patient is reliving a past event. Such complex disruptions in conscious experience have gone by many names, including experiential symptoms, psychical auras, and dreamy states. Symptoms designated as experiential include vivid memories, episodes of hyperfamiliarity or unfamiliarity, states of depersonalization, out-of-body experiences, feeling that someone is nearby, and accompanied by multiple types of emotions such as fear, pleasure, and sadness (21).

Seizures with experiential symptoms have common features. Firstly, at the most basic level, all experiential symptoms are illusions or hallucinations that result in erroneous interpretations of the present experience. The stream of consciousness is mislabeled and contaminated by remote memories and false emotions. Secondly, experiential symptoms result from faulty associations between perception, memory, and effect (28). For example, a patient may report feeling good because the room feels familiar, like something from their past. Thirdly, experiential seizures commonly produce a disruption in multiple sensory modalities. For instance, a patient reports seeing and hearing falsely familiar experiences. Lastly, seizures with experiential symptoms usually do not produce a loss of awareness or an inability to interact. They produce an alteration in the content but not in the level of conscious experience.

Clinical manifestations

Presentation and course

Experiential symptoms most frequently occur during seizures arising from temporal lobe regions (53; 18; 19; 07). This conclusion is robustly supported by multiple lines of evidence (17; 52). The most important evidence comes from intracranial EEG studies and electrical stimulations demonstrating that a dreamy state, including déjà vu and reminiscences, can arise from temporal lobe structures, in particular the perirhinal cortex and hippocampus (27). For instance, Bancaud studied patients with intracranial EEG and observed a temporal correlation between ictal EEG discharge and the appearance of experiential symptoms (04). Furthermore, the relationship between focal epilepsy and experiential phenomena is supported by functional brain mapping using electrical stimulation (06; 05). Penfield was the first to report that the “dreamy state” could be induced by electrical stimulation of the temporal lobe (48).

Temporal lobe areas integrate past and present experiences and encode them with appropriate emotion (38; 02). Seizures that arise from the occipital, parietal, and frontal lobes have not been strongly associated with experiential symptoms (46). One exception relates to seizures that originate in the frontal pole, which present with “forced thinking” (37). Penfield and Jasper observed this phenomenon but thought that it was substantially different from experiential symptoms. In addition, cortical stimulation during stereo-EEG recordings produced psychic phenomena in the posterior cingulum, precuneus, and inferior parietal lobule (03), although much less frequently than other somatosensory symptoms and with characteristics that appeared to be not too much more similar than those occurring when stimulating temporal lobe structures (28; 06; 05). The posterior cingulum and inferior parietal lobule are multimodal association cortical areas that have direct functional and anatomical connections to the temporal lobe; therefore, it is not surprising that seizures originating in these areas may also produce experiential phenomena. One study analyzed clinical, neuropsychological, imaging, and EEG (some with stereo-EEG) data in nine patients with ictal depersonalization (described as the sensation of being detached from one's body) and seven patients with derealization (described as the altered perception of the surroundings) (31). They found that ictal depersonalization originated in the dorsal premotor frontal cortex in seven of nine patients (77%) and in the mesial temporal lobe in the remaining two (23%). By contrast, all patients with ictal derealization had temporal lobe epilepsy seizure onset.

Experiential symptoms most frequently arise during the first portion of a larger seizure, such as a dyscognitive seizure or focal to bilateral tonic-clonic seizure. That is, patients describe experiential symptoms before they lose awareness and experience a focal seizure with impaired awareness or a generalized convulsion. Rarely, a patient may feel repetitive experiential symptoms lasting hours or days not leading to loss of awareness or automatisms (50), characterizing a nonconvulsive status epilepticus with focal aware cognitive seizures, previously called simple partial status epilepticus or aura continua (24; 23).

The most frequent type of experiential symptom described by patients with temporal lobe epilepsy is a sensation of visually experiencing an event multiple times, termed “dejà-vu” (from the French, “already saw”). The converse situation occurs when a patient reports a feeling of unfamiliarity associated with seeing familiar places or people, termed “jamais-vu” (from the French, “never seen”). These phenomena have also been reported in the auditory modality and termed “déjà-entendu” and “jamais-entendu” (from the French, “already heard” and “never heard”). One study showed that ictal fear was significantly associated with jamais-vu, déjà-vu, and derealization (16).

Patients with temporal lobe epilepsy sometimes report a feeling as if they are conscious and aware but not in control of their body, termed “depersonalization.” Others may report a visual illusion that they are looking at themselves from outside of their body, termed “autoscopy,” and a sensation that someone is standing beside them. Autoscopy appears to be more common in the nondominant hemisphere, sometimes associated with a sense of paralyzed limb (misoplegia) (41), but overall, experiential seizures do not have a preferential hemispheric lateralization (30; 17).

Prognosis and complications

If epileptic in origin, experiential phenomena most often occur in the context of temporal lobe epilepsy (07). The proportion of patients who become fully controlled using medical treatment follows the proportions outlined by Kwan and Brodie (34) in that approximately 60% to 70% of patients have their seizures controlled with medications. Most patients who become refractory to multiple antiepileptic medications become good candidates for epilepsy surgery and have a favorable prognosis (56).

Biological basis

Localization

From extensive autopsy studies, Hughlings Jackson concluded that patients who experienced “dreamy states” had lesions in the mesial temporal structures (32). Conversely, Wilder Penfield concluded from electrical stimulation of exposed lateral temporal neocortex during epilepsy surgery that experiential phenomena depended primarily on the lateral temporal neocortex (48). These divergent conclusions on the neuroanatomical origins of experiential symptoms by the founding fathers of epilepsy ushered in an era of strong controversy on this subject. Proponents of Jackson’s theory favored the mesial temporal region as the origin of experiential phenomena, arguing that a strong role in the processing of emotion and memory by this region made neuroanatomical sense. Furthermore, they argued that Penfield did not record the EEG from the mesial structures when stimulating the lateral temporal cortex. In contrast, proponents of Penfield’s theory were compelled by the vivid memories that were induced by stimulation of the lateral temporal neocortex.

Bancaud studied 20 patients with experiential symptoms using intracranial EEG (04). He concluded that “the dreamy state probably depends upon a neuronal network that engages both medial and lateral aspects of the temporal lobe, and that the anterior hippocampus, amygdala, and superior temporal gyrus have relatively privileged access to this circuit.” Further studies by Bancaud revealed that experiential symptoms of seizures did not occur unless mesial temporal structures were affected in some way (04). The lateral temporal neocortex was frequently involved but not essential. This was true for all sorts of experiential phenomena, which included emotions, activation of previous memories, or alteration of familiarity. Furthermore, Gloor found that stimulation of the amygdala resulted in the easiest elicitation of experiential phenomena. This conclusion was supported by Vignal, who concluded, based on intracranial EEG, that mesial temporal stimulation is enough to elucidate the “dreamy state” (55).

In contrast to studies using intracranial EEG, which localizes experiential symptoms to the mesial temporal lobe, postsurgical observations have offered different conclusions. A retrospective comparison of seizure semiology of mesial temporal and lateral temporal epilepsy suggests that experiential symptoms are much more common if the epileptic focus is located on the lateral surface of the temporal lobe (26). Nine out of 19 patients with neocortical-onset epilepsy reported experiential symptoms, compared to none out of 16 patients with mesial onset. Localization of experiential phenomena to the mesial or to the lateral temporal lobe probably should not be made. Moriarity and colleagues reported a patient in whom direct stimulation over the temporal neocortex elicited experiential phenomena, even after anterior temporal lobectomy and amygdalohippocampectomy (40).

Pathophysiology

Mechanisms by which seizures generate experiential symptoms are poorly understood (28). Hypothetical explanations center on whether experiential symptoms are secondary to “ictal activation” or to “ictal inhibition” of the cerebral cortex. Jackson speculated that experiential phenomena arise because regions of the cerebral cortex distant from the seizure focus are released from tonic inhibition. Penfield observed experiential symptoms during stimulation of the cerebral cortex and postulated that activation of stored memory traces produces experiential phenomena. Gloor provided an excellent observation noting that experiential symptoms are related to the normal function of the temporal lobe, which suggests that a seizure can activate normal temporal lobe functions such as memory or sense of familiarity (29). Gloor suggested that ictal activation results in disordered activation and disordered association of normal temporal lobe functions.

Accumulated experience from intracranial EEG recordings and electrical brain stimulation over 80 years demonstrates the role of inappropriate activation of the circuit involving the perirhinal cortex, parahippocampus, and hippocampus in the pathophysiology of ictal experiential phenomena (17; 27). Interestingly, electrical stimulation around the perirhinal cortex produces déjà vu more often and with a lower threshold than stimulation of the hippocampus (06).

A hypothesis of cortico-limbic networks proposes that déjà-vu results from an abnormal synchronization between rhinal cortices and the hippocampus, whereas focal seizures with dreamy state and reminiscences arise from hyperactivation between the hippocampus and a network of temporal neocortical areas associated with episodic memory (27).

Differential diagnosis

Confusing conditions

Patients who present with troubling experiential symptoms should be approached with a sensible differential diagnosis. Other than focal epilepsy arising from the temporal lobe, the differential should include normal mental states, psychiatric illness, manifestation of a generalized epilepsy syndrome, postictal phenomena, focal brain lesions, and migraine. Consideration of the duration of symptoms, associated features, risk factors, laboratory investigation, and response to treatment help to establish the diagnosis.

Experiential symptoms are frequently normal phenomena reported by people without any brain pathology. For instance, the experience of déjà-vu is common (12; 57). In these instances, the experiential symptoms are infrequent, brief, lasting several seconds, and isolated, never leading to unresponsiveness; frequently, the person lacks specific risk factors for epilepsy. In healthy subjects, déjà-vu occurs mostly in psychological states such as precognitive dreams or daydreams, indicating that the memory function is well preserved, whereas in people with epilepsy, déjà-vu is associated with dissociative experiences indicating an impairment of the visual-memory network (35).

A functional MRI (fMRI) study showed different neural responses of brain regions involved in memory and emotional processes in healthy subjects with versus without déjà-vu (42). Those with déjà-vu had a relatively reduced fMRI activation in the right parahippocampal, bilateral hippocampi, temporal middle gyri, superior frontal gyri, thalami, and caudate nuclei (42).

The differential diagnosis of experiential symptoms includes a variety of postictal phenomena. For instance, hyperfamiliarity for faces may be seen as postictal phenomena in temporal lobe epilepsy (13). In addition, postictal psychosis may present with features reminiscent of experiential phenomena, such as the experience of altered reality. The evaluation of refractory experiential phenomena should, therefore, include an attempt at temporal association of symptoms and the discharge on EEG (ie, whether the symptoms are associated with ictal or postictal phenomena). This is important as postictal psychosis frequently responds to antipsychotics (01).

Static lesions such as brain tumors or strokes can produce certain experiential symptoms such as delusions of misidentification (14), reduplicative paramnesia (36), and depersonalization (51). In instances in which experiential symptoms are of acute onset, are persistent, lasting days or weeks, and are not responsive to antiepileptic medications, a focal lesion should be considered, and a high-resolution MRI with an epilepsy protocol should be performed.

Experiential symptoms can occur as part of a migraine aura. The most significant distinction between symptoms of migraine aura and epilepsy is the duration of symptoms. Migraine aura lasts between 5 and 60 minutes and precedes a headache (49). In contrast, typical experiential auras associated with epilepsy last 20 to 40 seconds. Migraine can cause a variety of complex mental states generally before a migraine attack, including sensations of familiarity, sensations of depersonalization, or complex visual illusions such as mosaic vision (58).

Associated and underlying disorders

Temporal lobe epilepsy. Seizures with experiential symptoms have almost exclusively been reported in temporal lobe epilepsy. Most frequently, patients report experiential phenomena as the first part of a focal impaired awareness seizure. The duration of the experiential phenomena is generally in the order of 30 seconds to several minutes and is rarely longer. A comparison of semiology between mesial and lateral temporal lobe epilepsy suggests that experiential symptoms are most frequently encountered in patients who have seizures arising from the lateral temporal lobe (26; 07). These include autoscopic phenomena, sensations of déjà vu, and depersonalization. This has further been reported in cases of neocortical surgery in which experiential auras stopped following neocortical resection (10). Auditory auras and other experiential symptoms also occur in autosomal dominant familial lateral temporal lobe epilepsy with or without LGI1 mutation (54; 39). Experiential seizures have also been reported in other forms of benign familial temporal lobe epilepsy with normal MRI (25; 35).

Limbic encephalitis. Déjà-vu and other ictal experiential phenomena can occur in antibody-associated autoimmune encephalitis, particularly in those with glutamic acid decarboxylase and less frequently in N-methyl-D-aspartate receptor (NMDAR) antibodies (33). New-onset focal status with experiential symptoms and acute memory complaints is more frequent in NMDAR encephalitis (33).

Idiopathic generalized epilepsy. Experiential symptoms may appear in the context of idiopathic generalized epilepsy. Although rarely reported, complex visual illusions, negative and positive affective states, and distortions of time can occur in patients who present with absence status epilepticus (11; 47; 22). The importance of identifying idiopathic generalized epilepsy lies in differential response to antiepileptic medications; for instance, phenytoin or carbamazepine in absence status epilepticus is not effective and may exacerbate the conditions (44).

References

01: Alper KR, Barry JJ, Balabanov AJ. Treatment of psychosis, aggression, and irritability in patients with epilepsy. Epilepsy Behav 2002;3(5S):13-18. PMID 12609315
02: Anderson AK, Phelps EA. Is the human amygdala critical for the subjective experience of emotion? Evidence of intact dispositional affect in patients with amygdala lesions. J Cogn Neurosci 2002;14(5):709-20. PMID 12167256
03: Balestrini S, Francione S, Mai R, et al. Multimodal responses induced by cortical stimulation of the parietal lobe: a stereo-electroencephalography study. Brain 2015;138(Pt 9):2596-607. PMID 26129769
04: Bancaud J, Brunet-Bourgin F, Chauvel P, Halgren E. Anatomical origin of déjà vu and vivid 'memories' in human temporal lobe epilepsy. Brain 1994;117(Pt 1):71-90. PMID 8149215
05: Barbeau E, Wendling F, Régis J, et al. Recollection of vivid memories after perirhinal region stimulations: synchronization in the theta range of spatially distributed brain areas. Neuropsychologia 2005;43(9):1329-37. PMID 15949517
06: Bartolomei F, Barbeau E, Gavaret M, et al. Cortical stimulation study of the role of rhinal cortex in déjà vu and reminiscence of memories. Neurology 2004;63(5):858-64. PMID 15365137
07: Baulac M. MTLE with hippocampal sclerosis in adult as a syndrome. Rev Neurol (Paris) 2015;171(3):259-66. PMID 25727907
08: Berg, AT, Berkovik SF, Brodie MJ, et al. Revised terminology and concepts for organization of seizures and epilepsies: report of the ILAE Commission on Classification and Terminology, 2005-2009. Epilepsia 2010;51(4):676-85. PMID 20196795
09: Bien CG, Urbach H, Schramm J, et al. Limbic encephalitis as a precipitating event in adult-onset temporal lobe epilepsy. Neurology 2007;69(12):1236-44. PMID 17875912
10: Blume WT, Girvin JP, Stenerson P. Temporal neocortical role in ictal experiential phenomena. Neurol 1993;33(1):105-7. PMID 8388185
11: Boyd O, Whittingham F, Clements D, Rhodes J. Petit mal status: an unusual cause of confusion. Br J of Hosp Med 1990;43(3):230-1. PMID 2107953
12: Brown AS. A review of the déjà vu experience. Psychol Bull 2003;129(3):394-413. PMID 12784936
13: Bujarski K, Sperling MR. Post-ictal hyperfamiliarity in focal epilepsy. Epilepsy Behav 2008;13(3):567-9. PMID 18588998
14: Carota A, Staub F, Bogousslavsky J. Emotions, behaviors and mood changes in stroke. Curr Opin Neurol 2002;15(1):57-69. PMID 11796952
15: Casale MJ, Marcuse LV, Young JJ, et al. The sensitivity of scalp EEG at detecting seizures-a simultaneous scalp and stereo EEG study. J Clin Neurophysiol 2022;39(1):78-84. PMID 32925173
16: Chong DJ, Dugan P, EPGP Investigators. Ictal fear: associations with age, gender, and other experiential phenomena. Epilepsy Behav 2016;62:153-8. PMID 27479777
17: Curot J, Busigny T, Valton L, et al. Memory scrutinized through electrical brain stimulation: A review of 80 years of experiential phenomena. Neurosci Biobehav Rev 2017;78:161-77. PMID 28445741
18: Elliott B, Joyce E, Shorvon S. Delusions, illusions and hallucinations in epilepsy: 1. Elementary phenomena. Epilepsy Res 2009a;85(2-3):162-71. PMID 19423297
19: Elliott B, Joyce E, Shorvon S. Delusions, illusions and hallucinations in epilepsy: 2. Complex phenomena and psychosis. Epilepsy Res 2009b;85(2-3):172-86. PMID 19442490
20: Engel J Jr, McDermott MP, Wiebe S, et al. Early surgical therapy for drug-resistant temporal lobe epilepsy: a randomized trial. JAMA 2012;307(9):922-30. PMID 22396514
21: Feichtinger M, Pauli E, Schafer I, et al. Ictal fear in temporal lobe epilepsy: surgical outcome and focal hippocampal changes revealed by proton magnetic resonance spectroscopy imaging. Arch Neurol 2001;58(5):771-7. PMID 11346372
22: Ferner RE, Panayiotopoulos CP. 'Phantom' typical absences, absence status and experiential phenomena. Seizure 1993;2(3):253-6. PMID 8162390
23: Fisher RS, Cross JH, D'Souza C, et al. Instruction manual for the ILAE 2017 operational classification of seizure types. Epilepsia 2017b;58(4):531-42. PMID 28276064
24: 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 2017a;58(4):522-30. PMID 28276060
25: Gambardella A, Messina D, Le Piane E, et al. Familial temporal lobe epilepsy autosomal dominant inheritance in a large pedigree from southern Italy. Epilepsy Res 2000;38(2-3):127-32. PMID 10642040
26: Gil-Nagel A, Risinger MW. Ictal semiology in hippocampal versus extrahippocampal temporal lobe epilepsy. Brain 1997;120(Pt 1):183-92. PMID 9055806
27: Gillinder L, Liegeois-Chauvel C, Chauvel P. What déjà vu and the "dreamy state" tell us about episodic memory networks. Clin Neurophysiol 2022;136:173-81. PMID 35189480
28: Gloor P. Experiential phenomena of temporal lobe epilepsy. Facts and hypotheses. Brain 1990;113(Pt 6):1673-94. PMID 2276040
29: 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(2):129-44. PMID 7125603
30: 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
31: Heydrich L, Marillier G, Evans N, Seeck M, Blanke O. Depersonalization- and derealization-like phenomena of epileptic origin. Ann Clin Transl Neurol 2019;6(9):1739-47. PMID 31437864
32: Jackson JH, Colman WS. Case of epilepsy with tasting movements and 'dreamy state' —very small patch of softening in the left uncinate gyrus. Brain 1898;21:580-90.
33: Kaaden T, Madlener M, Angstwurm K, et al. Seizure semiology in antibody-associated autoimmune encephalitis. Neurol Neuroimmunol Neuroinflamm 2022;9(6):e200034. PMID 36266054
34: Kwan P, Brodie MJ. Early identification of refractory epilepsy. N Engl J Med 2000;342(5):314-9. PMID 10660394
35: Labate A, Baggetta R, Trimboli M, et al. Insight into epileptic and physiological déjà vu: from a multicentric cohort study. Eur J Neurol 2019;26(3):407-14. PMID 30184312
36: Lee K, Shinbo M, Kanai H, Nagumo Y. Reduplicative paramnesia after a right frontal lesion. Cogn Behav Neurol 2011;24(1):35-9. PMID 21467922
37: Mendez MF, Cherrier MM, Perryman KM. Epileptic forced thinking from left frontal lesions. Neurology 1996;47(1):79-83. PMID 8710129
38: Mesulam M. Principles of Behavioral and Cognitive Neurology. Second edition. Oxford University Press, 2000:55.
39: Michelucci R, Pasini E, Malacrida S, et al. Low penetrance of autosomal dominant lateral temporal epilepsy in Italian families without LGI1 mutations. Epilepsia 2013;54(7):1288-97. PMID 23621105
40: Moriarity JL, Boatman D, Krauss GL, Storm PB, Lenz FA. Human "memories" can be evoked by stimulation of the lateral temporal cortex after ipsilateral medial temporal lobe resection. J Neurol Neurosurg Psychiatry 2001;71(4):549-51. PMID 11561047
41: Moss AD, Turnbull OH. Hatred of the hemiparetic limbs (misoplegia) in a 10 year old child. J Neurol Neurosurg Psychiatry 1996;61(2):210-1. PMID 8708701
42: Nigro S, Cavalli SM, Cerasa A, et al. Functional activity changes in memory and emotional systems of healthy subjects with déjà vu. Epilepsy Behav 2019;97:8-14. PMID 31181431
43: O'Connor AR, Moulin CJ. Recognition without identification, erroneous familiarity, and déjà vu. Curr Psychiatry Rep 2010;12(3):165-73. PMID 20425276
44: Osorio I, Reed RC, Peltzer JN. Refractory idiopathic absence status epilepticus: A probable paradoxical effect of phenytoin and carbamazepine. Epilepsia 2000;41(7):887-94. PMID 10897162
45: Pack AM. Epilepsy overview and revised classification of seizures and epilepsies. Continuum (Minneap Minn) 2019;25(2):306-21. PMID 30921011
46: Palmini A, Gloor P. The localizing value of auras in partial seizures; a prospective and retrospective study. Neurology 1992;42(4):801-8. PMID 1565234
47: Panayiotopoulos CP, Chroni E, Daskalopoulos C, Baker A, Rowlinson S, Walsh P. Typical absence seizures in adults: clinical, EEG, video-EEG findings and diagnostic/syndromic considerations. J Neurol Neurosurg Psychiatry 1992;55(11):1002-8. PMID 1469393
48: Penfield W, Perot P. The brain’s record of auditory and visual experience. A final summary and discussion. Brain 1963;86:595-696. PMID 14090522
49: Sacks O. Migraine: understanding a common disorder. University of California Press, 1985.
50: Seshia S, McLachlan RS. Aura continua. Epilepsia 2005;46(3):454-5. PMID 15730546
51: Sierra M, Berrios GE. Depersonalization: neurobiological perspectives. Biol Psychiatry 1998;44(9):898-908. PMID 9807645
52: Sjoberg RL. Brain stimulation and elicited memories. Acta Neurochir (Wien) 2023;165(10):2737-45. PMID 35804269
53: So NK. Epileptic auras. In: Willie E, editor. The Treatment of Epilepsy: Principles and Practice. 4th edition. Philadelphia, PA: Lippincott Williams & Wilkins, 2006:237.
54: Striano P, Busolin G, Santulli L, et al. Familial temporal lobe epilepsy with psychic auras associated with a novel LGI1 mutation. Neurology 2011;76(13):1173-6. PMID 21444903
55: Vignal JP, Maillard L, McGonigal A, Chauvel P. The dreamy state: hallucinations of autobiographic memory evoked by temporal lobe stimulations and seizures. Brain 2007;130(Pt 1):88-99. PMID 17142246
56: Wiebe S, Blume WT, Girvin JP, Eliasziw M; Effectiveness and Efficiency of Surgery for Temporal Lobe Epilepsy Study Group. A randomized, controlled trial of surgery for temporal-lobe epilepsy. N Engl J Med 2001;345(5):311-8. PMID 11484687
57: Wild E. Deja vu in neurology. J Neurol 2005;252(1):1-7. PMID 15654548
58: Wilkinson M, Robinson D. Migraine art. Cephalalgia 2005;5(3):151-7. PMID 4042153

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

Krzysztof A Bujarski MD and Barbara C Jobst 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 seizures with experiential symptoms

Differential Diagnosis

normal mental states
psychiatric illness
manifestation of a generalized epilepsy syndrome
postictal phenomena
focal brain lesions
- migraine

Also Relevant

Absence status epilepticus
Aura continua
Familial mesial temporal lobe epilepsy
Mesial temporal lobe epilepsy with hippocampal sclerosis
Seizures of the posterior neocortex

Clinical Categories

Epilepsy & Seizures

Focal seizures with experiential symptoms …

Focal seizures with experiential symptoms

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Biological basis

Localization

Pathophysiology

Differential diagnosis

Confusing conditions

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

Epilepsy with auditory features

Alcohol withdrawal seizures

Epileptic lesions due to malformation of cortical development

Epileptic spasms

Sleep and epilepsy

Neocortical temporal lobe seizures

Focal seizures with experiential symptoms

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Biological basis

Localization

Pathophysiology

Differential diagnosis

Confusing conditions

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

Epilepsy with auditory features

Alcohol withdrawal seizures

Epileptic lesions due to malformation of cortical development

Epileptic spasms

Sleep and epilepsy

Neocortical temporal lobe seizures

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