# Temporal lobe epilepsy

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Chronic focal seizure disorder

Medical condition

Temporal lobe epilepsy Lobes of the brain. Temporal lobe in green Specialty Neurology, Psychiatry

In the field of neurology, **temporal lobe epilepsy** is an enduring [brain disorder](/source/Neurological_disorder) that causes [unprovoked seizures](/source/Seizure#Causes) from the [temporal lobe](/source/Temporal_lobe). Temporal lobe [epilepsy](/source/Epilepsy) is the most common type of [focal](/source/Focal_seizure) onset epilepsy among adults.[1] Seizure symptoms and behavior distinguish seizures arising from the [mesial (medial) temporal lobe](/source/Anatomical_terms_of_location) from seizures arising from the [lateral (neocortical) temporal lobe](/source/Anatomical_terms_of_location).[2] [Memory](/source/Memory) and psychiatric [comorbidities](/source/Comorbidity) may occur. Diagnosis relies on [electroencephalographic](/source/Electroencephalogram) (EEG) and [neuroimaging](/source/Neuroimaging) studies.[3][4] [Anticonvulsant medications](/source/Anticonvulsant_medication), [epilepsy surgery](/source/Epilepsy_surgery), and [dietary treatments](/source/Dietary_management) may improve seizure control.[5][6][7][8]

## Types

Under the [International League Against Epilepsy](/source/International_League_Against_Epilepsy) (ILAE) 2017 [classification of the epilepsies](/source/Seizure_types), focal onset epilepsy occurs from seizures arising from a [biological neural network](/source/Neural_circuit) within a single [cerebral hemisphere](/source/Cerebral_hemisphere).[9][10] Temporal lobe epilepsy occurs from seizures arising within the lobe.[10] It is the most common focal onset epilepsy, and 80% of temporal lobe epilepsy is *mesial (medial) temporal lobe epilepsy*, temporal lobe epilepsy arising from the inner ([medial](/source/Anatomical_terms_of_location)) part of the temporal lobe that may involve the [hippocampus](/source/Hippocampus), [parahippocampal gyrus](/source/Parahippocampal_gyrus), or [amygdala](/source/Amygdala).[2][11] The less common *lateral temporal lobe* or *neocortical temporal lobe* seizures arise from the outer ([lateral](/source/Anatomical_terms_of_location)) temporal lobe.[2] These types of TLE are very rare due to the genetic cause or lesions such as tumor, birth defect, or blood vessel abnormalities in the temporal lobe.[12]

The ILAE 2017 classification distinguishes *focal aware* from *focal impaired* seizures.[10] A *focal aware* temporal lobe seizure occurs if a person remains aware of what occurs during the entire seizure; awareness may be retained even if impaired responsiveness occurs during the seizure.[10] A *focal impaired awareness* temporal lobe seizure occurs if a person becomes unaware during any part of the seizure.[10]

Approximately 80% of seizures in the temporal lobe begin in the mesial temporal region, frequently starting in or around the hippocampus.[13] The hippocampus, found in both temporal lobes, is essential for memory and learning.[12]

## Symptoms and behavior

### Mesial temporal lobe epilepsy

During a temporal lobe seizure, a person may experience a seizure *aura*; an aura is an autonomic, cognitive, emotional, or sensory experience that commonly occurs during the beginning part of a seizure.[10][2] The common mesial temporal lobe seizure auras include a rising [epigastric](/source/Epigastrium) feeling, abdominal discomfort, taste (gustatory), smell (olfactory), tingling (somatosensory), fear, [*déjà vu*](/source/D%C3%A9j%C3%A0_vu), [*jamais vu*](/source/Jamais_vu), [flushing](/source/Flushing_(physiology)), or rapid heart rate ([tachycardia](/source/Tachycardia)).[2] A person may then stare blankly, appear motionless (*behavioral arrest*) and lose awareness.[2] Repeated stereotyped motor behaviors ([automatisms](/source/Seizure_types)) may occur; these include repeated swallowing, lip smacking, picking, fumbling, patting, or vocalizations.[2] *Dystonic posture* is an unnatural stiffening of one arm occurring during a seizure.[14] A dystonic posture on one side of the body commonly indicates seizure onset from the [opposite side of the brain](/source/Contralateral_brain) e.g. right arm dystonic posture arising from a left temporal lobe seizure.[14] Impaired language function ([dysphasia](/source/Aphasia)) during, or soon following, a seizure is more likely to occur when seizures arise from the [language dominant](/source/Lateralization_of_brain_function) side of the brain.[14]

### Lateral temporal lobe epilepsy

The common auras from seizures arising from the primary auditory cortex include [vertigo](/source/Vertigo), humming sounds, ringing sounds, buzzing sounds, songs or voices, or altered sensations.[2] Lateral temporal lobe seizures arising from the temporal-[parietal lobe](/source/Parietal_lobe) junction may cause [complex visual hallucinations](/source/Complex_visual_hallucination).[2] In comparison to mesial temporal lobe seizures, lateral temporal lobe seizures are briefer in duration, occur with earlier loss of awareness, and are more likely to become focal than [bilateral tonic-clonic](/source/Generalized_tonic%E2%80%93clonic_seizure) seizures.[2] Impaired language function (dysphasia) during or soon following a seizure is more likely to occur when seizures arise from the language dominant side of the brain.[14]

## Comorbidities

### Memory

The major cognitive impairment in mesial temporal lobe epilepsy is a progressive memory impairment.[15]: 71 This involves [declarative memory](/source/Declarative_memory) impairment, including [episodic memory](/source/Episodic_memory) and [semantic memory](/source/Semantic_memory), and is worse when medications fail to control seizures.[16][17][15]: 71 Mesial temporal lobe epilepsy arising from the language dominant hemisphere impairs [verbal memory](/source/Verbal_memory), and mesial temporal lobe epilepsy arising from the language non-dominant hemisphere impairs [nonverbal memory](/source/Verbal_memory).[15]: 71[17]

### Psychiatric comorbidities

Psychiatric disorders are more common among those with epilepsy, and the highest prevalence occurs among those with temporal lobe epilepsy.[18] The most common psychiatric comorbidity is [major depressive disorder](/source/Major_depressive_disorder).[18] Other disorders include [post-traumatic stress disorder](/source/Post-traumatic_stress_disorder), [generalized anxiety disorder](/source/Generalized_anxiety_disorder), [psychosis](/source/Psychosis), [obsessive–compulsive disorder](/source/Obsessive%E2%80%93compulsive_disorder), [schizophrenia](/source/Schizophrenia), [bipolar disorder](/source/Bipolar_disorder), [substance use disorder](/source/Substance_use_disorder), and a ~9% prevalence of [suicidality](/source/Suicidality).[18]

### Personality

Main article: [Geschwind syndrome](/source/Geschwind_syndrome)

[Geschwind syndrome](/source/Geschwind_syndrome) is a syndrome of altered [sexuality](/source/Human_sexuality) (most often [hyposexuality](/source/Hyposexuality)), [religiosity](/source/Religiosity), and compulsive or extensive writing and drawing occurring in persons with temporal lobe epilepsy.[19]: 347–348 However, subsequent studies did not support the association of these behavioral traits with temporal lobe epilepsy.[19]: 347–348 There are reports of religious behaviors occurring in persons with temporal lobe epilepsy.[20][21][22][23][24]

## Causes

[Hippocampal sclerosis](/source/Hippocampal_sclerosis), [brain tumor](/source/Brain_tumor), [traumatic brain injury](/source/Traumatic_brain_injury), cerebral [vascular malformation](/source/Vascular_malformation), [neuronal migration disorders](/source/Neuronal_migration_disorder), infections such as [encephalitis](/source/Encephalitis) and [meningitis](/source/Meningitis), [autoimmune disease](/source/Autoimmune_disease) ([limbic encephalitis](/source/Limbic_encephalitis)), and [genetic disorders](/source/Genetic_disorder) may cause temporal lobe epilepsy.[25]

## Risk factors

Many persons with uncontrolled temporal lobe epilepsy had childhood [febrile seizures](/source/Febrile_seizure).[26] A brief febrile seizure only slightly increases the risk for developing nonfebrile seizures (also known as afebrile seizures).[27] However, the prolonged seizure of febrile [status epilepticus](/source/Status_epilepticus) leads to a 9% risk for developing epilepsy.[27] There is no clear relationship between febrile seizures and development of hippocampal sclerosis.[27] Those who experienced any sort of brain injury in their early life have a higher risk of developing epilepsy.[12]

## Mechanisms

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The neural circuit of the hippocampus shows dentate gyrus (DG). subiculum (SB). entorhinal cortex (EC), CA1 sector and CA3 sector

Scalp electrodes are placed to record an electroencephalogram

Brain MRI with hippocampus identified by cross hairs.

[Brain positron emission tomography](/source/Brain_positron_emission_tomography) (PET) scan

### Neuronal loss

[Hippocampal sclerosis](/source/Hippocampal_sclerosis) occurs with severe [CA1](/source/Hippocampal_subfields) and less severe [CA3](/source/Hippocampal_subfields) and [CA4](/source/Hippocampal_subfields) neuronal loss.[28][29] Experimental research has shown that [N-methyl-d-aspartate (NMDA) receptor](/source/NMDA_receptor) activation causes neuronal cell loss, and electrical stimulation-induced [animal models of temporal lobe epilepsy](/source/Animal_models_of_epilepsy) duplicate the cell loss pattern of temporal lobe epilepsy in humans.[28] Repetitive seizures irreversibly damage [interneurons](/source/Interneuron) leading to persistent loss of [recurrent inhibition](/source/Hippocampus).[28] Damage of [GABAergic](/source/GABAergic) interneurons lead to loss of inhibition, uncontrolled [neuronal firing](/source/Action_potential), leading to seizures.[28] The *secondary epileptogenesis* hypothesis is that repetitive seizures lead to interneuron loss, loss of [glutamatergic](/source/Glutamatergic) [principal neurons](/source/Dentate_nucleus), axonal sprouting, and formation of new recurrent glutamatergic [excitatory](/source/Excitatory_synapse) circuits leading to a more severe epilepsy.[30] Mechanisms related to neuronal loss incompletely account for temporal lobe epilepsy as temporal lobe epilepsy may occur with only minimal neuronal cell loss.[28]

### Neuron-specific type 2 K+/Cl− cotransporter (KCC2) mutation

This [KCC2](/source/Chloride_potassium_symporter_5) mutation prevents [subicular](/source/Subiculum) neurons from potassium and chloride [ion](/source/Ion) extrusion, leading to intracellular chloride accumulation, and positive [γ-Aminobutyric acid](/source/%CE%93-Aminobutyric_acid) (GABA) mediated currents.[28] Accumulated chloride efflux through GABA [receptors](/source/Chemical_synapse) leads to [neuronal depolarization](/source/Depolarization), increased neuronal excitability and ultimately seizures.[28] Persons with this mutation have mesial temporal lobe epilepsy with hippocampal sclerosis.[28]

### Granule cell dispersion

Dentate gyrus [granule cell dispersion](/source/Granule_cell_dispersion) refers to a granule cell layer that is widened, poorly demarcated, or accompanied by granule cells outside the layer (ectopic granule cells).[31]: 1318 In the normal brain, dentate granule cells block seizure spread from [entorhinal cortex](/source/Entorhinal_cortex) to the hippocampus.[28] A hypothesis is that granule cell dispersion may disrupt the normal [mossy fiber pathway](/source/Mossy_fiber_(hippocampus)) connecting granule cells and CA3 [pyramidal cells](/source/Pyramidal_cell) leading to mossy fiber sprouting and new excitatory networks capable of generating seizures.[28] However, a study has shown that a similar pattern of granule cell dispersion may occur in persons without epilepsy.[32]

### Cortical developmental malformations

[Focal cortical dysplasia](/source/Focal_cortical_dysplasia) is a brain malformation that may cause temporal lobe epilepsy.[28] This malformation may cause abnormal [cortical layers](/source/Cerebral_cortex) (*dyslamination*), occur with abnormal neurons (*[dysmorphic neurons, balloon cells](/source/Focal_cortical_dysplasia)*) and may occur with a brain tumor or vascular malformation.[28] An abnormality of the [MTOR](/source/MTOR) pathway leads to hyperexcitable [glutamate](/source/Glutamic_acid) mediated neurons leading to seizures.[28]

## Diagnosis

A surgeon performs epilepsy brain surgery

[Vagus nerve stimulation](/source/Vagus_nerve_stimulation)

[Responsive neurostimulation device](/source/Responsive_neurostimulation_device)

Surgeon implants a brain electrode for [deep brain stimulation](/source/Deep_brain_stimulation)

### Electroencephalogram

The temporal lobe *epileptiform* discharge is a pattern seen on the [electroencephalgram](/source/Electroencephalography) (EEG) test; temporal lobe epileptiform discharges occur between seizures and confirm the diagnosis of temporal lobe epilepsy.[3] [Long-term video-EEG monitoring](/source/Long-term_video-EEG_monitoring) may record the behavior and EEG during a seizure.[3] [Magnetoencephalography](/source/Magnetoencephalography) may diagnose temporal lobe epilepsy by recording epileptiform discharges or seizure patterns arising from the magnetic fields of neural electrical currents.[3]

### Neuroimaging

Neuroimaging tests may identify the cause for seizures and the *seizure focus*, the brain location where seizures begin.[4] In newly diagnosed epilepsy, [magnetic resonance imaging](/source/Magnetic_resonance_imaging) (MRI) can detect brain lesion in up to 12 to 14% of persons with epilepsy.[33] However, for those with chronic epilepsy, MRI can detect brain lesion in 80% of the persons with epilepsy.[33] 3-tesla MRI scan is advised for those with evidence of focal epilepsy such as temporal lobe epilepsy.[4] Abnormalities identified by MRI scan include hippocampal sclerosis, focal cortical dysplasia, other cortical developmental brain malformations, developmental and low-grade tumors, [cavernous hemangioma](/source/Cavernous_hemangioma), [hypoxic-ischemic brain injury](/source/Cerebral_hypoxia), traumatic brain injury and encephalitis.[4]

18F-fluorodeoxyglucose (18F-FDG) [brain positron emission tomography](/source/Brain_positron_emission_tomography) (PET) may show a brain region of decreased [glucose](/source/Glucose) [metabolism](/source/Metabolism) at a time between seizures; this *hypometabolic* region may correspond to the seizure focus, and PET scan is more sensitive for temporal lobe seizure focus localization compared to epilepsy arising from other brain lobes.[4] [Single-photon emission computed tomography](/source/Single-photon_emission_computed_tomography) (SPECT) may show a region of decreased blood flow occurring 40–60 seconds after injection during the seizure; this reduced blood flow region may correspond to the seizure focus.[4]

[Computed tomography](/source/CT_scan) (CT) scan is less sensitive than MRI scan for identifying small tumors, vascular malformations, cortical developmental brain malformations, and abnormalities in the medial temporal lobe.[33] CT scan is advised in emergencies when the suspected cause of epilepsy may be [intracerebral hemorrhage](/source/Intracerebral_hemorrhage), [brain abscess](/source/Brain_abscess), large [cerebral infarction](/source/Cerebral_infarction) or [subdural empyema](/source/Subdural_empyema).[4][33] A person who requires neuroimaging but cannot have an MRI scan due to implanted devices such as a [cardiac pacemaker](/source/Cardiac_pacemaker), [defibrillator](/source/Defibrillator) or [cochlear implant](/source/Cochlear_implant) may receive a CT scan. CT scan may better demonstrate calcium containing brain abnormalities causing epilepsy such as in [tuberous sclerosis](/source/Tuberous_sclerosis) and [Sturge–Weber syndrome](/source/Sturge%E2%80%93Weber_syndrome).[4][33]

## Treatment

### Medical treatment

[Anticonvulsant](/source/Anticonvulsant) oral medications control seizures in about two-thirds of persons with epilepsy, and control commonly occurs with one or two medications.[34]

### Surgical treatment

Those with uncontrolled seizures despite treatment with multiple anticonvulsant medications have *[pharmacoresistant](/source/Management_of_drug-resistant_epilepsy)* epilepsy, and they may require [epilepsy surgery](/source/Epilepsy_surgery) to achieve seizure control.[9][34]

[Penfield](/source/Wilder_Penfield) and Flanigan first described [anterior temporal lobectomy](/source/Anterior_temporal_lobectomy), partial surgical removal of the temporal lobe, for treatment of mesial temporal lobe epilepsy in 1950.[35] In a prospective [randomized controlled trial](/source/Randomized_controlled_trial) comparing anterior temporal lobectomy to medical therapy for pharmacoresistant temporal lobe epilepsy, surgery was more effective than medical therapy with 1-year seizure free outcome occurring in 58% of persons with anterior temporal lobectomy compared to 8% of persons with drug treatment.[5] Among those with intractable mesial temporal lobe epilepsy and hippocampal sclerosis, about 70% become seizure-free after epilepsy surgery.[36]: 751 Studies show that language dominant anterior temporal lobectomy may lead to verbal memory decline.[17] However, study outcomes are more variable on language non-dominant anterior temporal lobectomy leading to nonverbal memory decline.[17]

*Magnetic resonance-guided laser interstitial thermal therapy*, *[stereotactic radiosurgery](/source/Radiosurgery)*, and *[stereotactic radiofrequency ablation](/source/Stereotactic_surgery)* are surgical methods that treat epilepsy by destroying the abnormal brain tissue that causes seizures.[37][38][39]

Neurostimulation may also improve seizure control.[6] The *[vagus nerve stimulator](/source/Vagus_nerve_stimulation)* (VNS) is surgically implanted in the chest, and delivers programmed electrical stimulation to the [vagus nerve](/source/Vagus_nerve) in the neck.[40] The *[responsive neurostimulation device](/source/Responsive_neurostimulation_device)* is implanted in the skull, monitors electrical brain activity for seizures, and responds to seizures with programmed electrical stimulation to one or two brain areas.[41] Programmed *[deep brain stimulation](/source/Deep_brain_stimulation)* of the anterior thalamic nucleus may treat seizures arising from more than 2 brain areas.[6]

### Dietary treatment

The [ketogenic diet](/source/Ketogenic_diet) and [modified Atkins diet](/source/Ketogenic_diet) are additional temporal lobe epilepsy treatment options.[7][8]

## Remission

Among those who develop childhood temporal lobe epilepsy, epilepsy remits in about one-third of children.[42] Remission was more likely among those without [hippocampal sclerosis](/source/Hippocampal_sclerosis), brain tumor, or focal cortical dysplasia on MRI scan.[42]

## See also

- [Geschwind syndrome](/source/Geschwind_syndrome)

- [List of people with epilepsy](/source/List_of_people_with_epilepsy)

## Notes

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1. ^ [***a***](#cite_ref-FOOTNOTEJavidan2012_3-0) [***b***](#cite_ref-FOOTNOTEJavidan2012_3-1) [***c***](#cite_ref-FOOTNOTEJavidan2012_3-2) [***d***](#cite_ref-FOOTNOTEJavidan2012_3-3) [Javidan 2012](#CITEREFJavidan2012).

1. ^ [***a***](#cite_ref-FOOTNOTEDuncan2019_4-0) [***b***](#cite_ref-FOOTNOTEDuncan2019_4-1) [***c***](#cite_ref-FOOTNOTEDuncan2019_4-2) [***d***](#cite_ref-FOOTNOTEDuncan2019_4-3) [***e***](#cite_ref-FOOTNOTEDuncan2019_4-4) [***f***](#cite_ref-FOOTNOTEDuncan2019_4-5) [***g***](#cite_ref-FOOTNOTEDuncan2019_4-6) [***h***](#cite_ref-FOOTNOTEDuncan2019_4-7) [Duncan 2019](#CITEREFDuncan2019).

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1. **[^](#cite_ref-FOOTNOTEQuiroga2012_16-0)** [Quiroga 2012](#CITEREFQuiroga2012).

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1. ^ [***a***](#cite_ref-FOOTNOTELuPyatkaBurantSajatovic2021_18-0) [***b***](#cite_ref-FOOTNOTELuPyatkaBurantSajatovic2021_18-1) [***c***](#cite_ref-FOOTNOTELuPyatkaBurantSajatovic2021_18-2) [Lu et al. 2021](#CITEREFLuPyatkaBurantSajatovic2021).

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1. **[^](#cite_ref-FOOTNOTETedrusFonsecaFagundesda_Silva2015_20-0)** [Tedrus et al. 2015](#CITEREFTedrusFonsecaFagundesda_Silva2015).

1. **[^](#cite_ref-FOOTNOTEd'OrsiTinuper2006_21-0)** [d'Orsi & Tinuper 2006](#CITEREFd'OrsiTinuper2006).

1. **[^](#cite_ref-FOOTNOTESirvenDrazkowskiNoe2007_22-0)** [Sirven, Drazkowski & Noe 2007](#CITEREFSirvenDrazkowskiNoe2007).

1. **[^](#cite_ref-FOOTNOTEArzySchurr2016_23-0)** [Arzy & Schurr 2016](#CITEREFArzySchurr2016).

1. **[^](#cite_ref-FOOTNOTETedrusFonsecaHöehr2013_24-0)** [Tedrus, Fonseca & Höehr 2013](#CITEREFTedrusFonsecaHöehr2013).

1. **[^](#cite_ref-FOOTNOTEVadlamudi2003_25-0)** [Vadlamudi 2003](#CITEREFVadlamudi2003).

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1. ^ [***a***](#cite_ref-FOOTNOTEMewasinghChinScott2020_27-0) [***b***](#cite_ref-FOOTNOTEMewasinghChinScott2020_27-1) [***c***](#cite_ref-FOOTNOTEMewasinghChinScott2020_27-2) [Mewasingh, Chin & Scott 2020](#CITEREFMewasinghChinScott2020).

1. ^ [***a***](#cite_ref-FOOTNOTEOng2019_28-0) [***b***](#cite_ref-FOOTNOTEOng2019_28-1) [***c***](#cite_ref-FOOTNOTEOng2019_28-2) [***d***](#cite_ref-FOOTNOTEOng2019_28-3) [***e***](#cite_ref-FOOTNOTEOng2019_28-4) [***f***](#cite_ref-FOOTNOTEOng2019_28-5) [***g***](#cite_ref-FOOTNOTEOng2019_28-6) [***h***](#cite_ref-FOOTNOTEOng2019_28-7) [***i***](#cite_ref-FOOTNOTEOng2019_28-8) [***j***](#cite_ref-FOOTNOTEOng2019_28-9) [***k***](#cite_ref-FOOTNOTEOng2019_28-10) [***l***](#cite_ref-FOOTNOTEOng2019_28-11) [***m***](#cite_ref-FOOTNOTEOng2019_28-12) [Ong 2019](#CITEREFOng2019).

1. **[^](#cite_ref-29)** Hokkanen, Suvi R. K.; Hunter, Sally; Polvikoski, Tuomo M.; Keage, Hannah A. D.; Minett, Thais; Matthews, Fiona E.; Brayne, Carol (4 July 2018). ["Hippocampal sclerosis, hippocampal neuron loss patterns and TDP-43 in the aged population"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6099461). *Brain Pathology*. **28** (4): 548–559. [doi](/source/Doi_(identifier)):[10.1111/bpa.12556](https://doi.org/10.1111%2Fbpa.12556). [ISSN](/source/ISSN_(identifier)) [1015-6305](https://search.worldcat.org/issn/1015-6305). [PMC](/source/PMC_(identifier)) [6099461](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6099461). [PMID](/source/PMID_(identifier)) [28833898](https://pubmed.ncbi.nlm.nih.gov/28833898).

1. **[^](#cite_ref-FOOTNOTEBen-AriDudek2010_30-0)** [Ben-Ari & Dudek 2010](#CITEREFBen-AriDudek2010).

1. **[^](#cite_ref-FOOTNOTEBlümckeThomAronicaArmstrong2013_31-0)** [Blümcke et al. 2013](#CITEREFBlümckeThomAronicaArmstrong2013).

1. **[^](#cite_ref-FOOTNOTERoyMillenKapur2020_32-0)** [Roy, Millen & Kapur 2020](#CITEREFRoyMillenKapur2020).

1. ^ [***a***](#cite_ref-FOOTNOTESalmenperaDuncan2005_33-0) [***b***](#cite_ref-FOOTNOTESalmenperaDuncan2005_33-1) [***c***](#cite_ref-FOOTNOTESalmenperaDuncan2005_33-2) [***d***](#cite_ref-FOOTNOTESalmenperaDuncan2005_33-3) [***e***](#cite_ref-FOOTNOTESalmenperaDuncan2005_33-4) [Salmenpera & Duncan 2005](#CITEREFSalmenperaDuncan2005).

1. ^ [***a***](#cite_ref-FOOTNOTEKwanBrodie2000_34-0) [***b***](#cite_ref-FOOTNOTEKwanBrodie2000_34-1) [Kwan & Brodie 2000](#CITEREFKwanBrodie2000).

1. **[^](#cite_ref-FOOTNOTEPenfieldFlanigan1950_35-0)** [Penfield & Flanigan 1950](#CITEREFPenfieldFlanigan1950).

1. **[^](#cite_ref-FOOTNOTELamberinkOtteBlümckeBraun2020_36-0)** [Lamberink et al. 2020](#CITEREFLamberinkOtteBlümckeBraun2020).

1. **[^](#cite_ref-FOOTNOTEChenLamoureuxShlobinElkaim2023_37-0)** [Chen et al. 2023](#CITEREFChenLamoureuxShlobinElkaim2023).

1. **[^](#cite_ref-FOOTNOTEKerezoudisTsayemLundstromVan_Gompel2022_38-0)** [Kerezoudis et al. 2022](#CITEREFKerezoudisTsayemLundstromVan_Gompel2022).

1. **[^](#cite_ref-FOOTNOTEMustafaZaben2022_39-0)** [Mustafa & Zaben 2022](#CITEREFMustafaZaben2022).

1. **[^](#cite_ref-FOOTNOTEGogginsMitaniTanaka2022_40-0)** [Goggins, Mitani & Tanaka 2022](#CITEREFGogginsMitaniTanaka2022).

1. **[^](#cite_ref-FOOTNOTEGeller2018_41-0)** [Geller 2018](#CITEREFGeller2018).

1. ^ [***a***](#cite_ref-FOOTNOTESpoonerBerkovicMitchellWrennall2006_42-0) [***b***](#cite_ref-FOOTNOTESpoonerBerkovicMitchellWrennall2006_42-1) [Spooner et al. 2006](#CITEREFSpoonerBerkovicMitchellWrennall2006).

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- Tatum, William O. (2012). "Mesial Temporal Lobe Epilepsy". *Journal of Clinical Neurophysiology*. **29** (5): 356–365. [doi](/source/Doi_(identifier)):[10.1097/WNP.0b013e31826b3ab7](https://doi.org/10.1097%2FWNP.0b013e31826b3ab7). [PMID](/source/PMID_(identifier)) [23027091](https://pubmed.ncbi.nlm.nih.gov/23027091). [S2CID](/source/S2CID_(identifier)) [29616130](https://api.semanticscholar.org/CorpusID:29616130).

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- Zeman, Adam; Kapur, Narinder; Jones-Gotman, Marilyn (2012). [*Epilepsy and memory*](https://books.google.com/books?id=cwJREAAAQBAJ&dq=Epilepsy+and+memory&pg=PP1) (1. ed.). Oxford: Oxford Univ. Press. [ISBN](/source/ISBN_(identifier)) [978-0-19-958028-6](https://en.wikipedia.org/wiki/Special:BookSources/978-0-19-958028-6).

Classification D ICD-10: G40.1-G40.2 ICD-9-CM: 345.4 MeSH: D004833 DiseasesDB: 29433 External resources MedlinePlus: 001399 eMedicine: neuro/365 Patient UK: Temporal lobe epilepsy

v t e Seizures and epilepsy Basics Seizure types Aura (warning sign) Postictal state Epileptogenesis Neonatal seizure Epilepsy in children Management Anticonvulsants Investigations Electroencephalography Epileptologist Personal issues Epilepsy and driving Epilepsy and employment Seizure types Focal Seizures Preserved consciousness Impaired consciousness Gelastic seizure Epilepsy Temporal lobe epilepsy Frontal lobe epilepsy Rolandic epilepsy Sleep-related hypermotor epilepsy Transient epileptic amnesia Panayiotopoulos syndrome Vertiginous epilepsy Generalised Tonic–clonic Absence seizure Atonic seizure Automatism Benign familial neonatal seizures Lennox–Gastaut syndrome Myoclonic astatic epilepsy Epileptic spasms Febrile seizure Status epilepticus Epilepsia partialis continua Complex partial status epilepticus Myoclonic epilepsy Progressive myoclonus epilepsy Dentatorubral–pallidoluysian atrophy Unverricht–Lundborg disease MERRF syndrome Lafora disease Early myoclonic encephalopathy Juvenile myoclonic epilepsy Related disorders CACNA1C-related disorders KCNH1-related disorders Sudden unexpected death in epilepsy Todd's paresis Landau–Kleffner syndrome Psychogenic non-epileptic seizure Epilepsy in animals Organizations International League Against Epilepsy Citizens United for Research in Epilepsy (US) Epilepsy Action (UK) Epilepsy Action Australia Epilepsy Foundation (US) Epilepsy Outlook (UK) Epilepsy Research UK Epilepsy Society (UK)

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Adapted from the Wikipedia article [Temporal lobe epilepsy](https://en.wikipedia.org/wiki/Temporal_lobe_epilepsy) by Wikipedia contributors ([contributor history](https://en.wikipedia.org/wiki/Temporal_lobe_epilepsy?action=history)). Available under [Creative Commons Attribution-ShareAlike 4.0 International](https://creativecommons.org/licenses/by-sa/4.0/). Changes may have been made.