{{Short description|Chronic focal seizure disorder}} {{Use dmy dates|date=April 2022}} {{Infobox medical condition (new) |name=Temporal lobe epilepsy |synonyms= |image=File:Lobes of the brain NL.svg |caption=[[Lobes of the brain]]. [[Temporal lobe]] in green |pronounce= |field= |speciality=[[Neurology]], [[Psychiatry]] |symptoms= |complications= |onset= |duration= |types= |causes= |risks= |diagnosis= |differential= |prevention= |treatment= |medication= |prognosis= |frequency= |deaths= }}
In the field of neurology, '''temporal lobe epilepsy''' is an enduring [[neurological disorder|brain disorder]] that causes [[Seizure#Causes|unprovoked seizures]] from the [[temporal lobe]]. Temporal lobe [[epilepsy]] is the most common type of [[focal seizure|focal]] onset epilepsy among adults.{{sfn|Muhlhofer|Tan|Mueller|Knowlton|2017}} Seizure symptoms and behavior distinguish seizures arising from the [[Anatomical terms of location|mesial (medial) temporal lobe]] from seizures arising from the [[Anatomical terms of location|lateral (neocortical) temporal lobe]].{{sfn|Chowdhury|Silva|Whatley|Walker|2021}} [[Memory]] and psychiatric [[Comorbidity|comorbidities]] may occur. Diagnosis relies on [[electroencephalogram|electroencephalographic]] (EEG) and [[neuroimaging]] studies.{{sfn|Javidan|2012}}{{sfn|Duncan|2019}} [[Anticonvulsant medication]]s, [[epilepsy surgery]], and [[Dietary management|dietary treatments]] may improve seizure control.{{sfn|Wiebe|Blume|Girvin|Eliasziw|2001}}{{sfn|Touma|Dansereau|Chan|Jetté|2022}}{{sfn|Freeman|Kossoff|Hartman|2007}}{{sfn|Rezaei|Abdurahman|Saghazadeh|Badv|2019}} {{TOC limit}}
==Types== Under the [[International League Against Epilepsy]] (ILAE) 2017 [[seizure types|classification of the epilepsies]], focal onset epilepsy occurs from seizures arising from a [[Neural circuit|biological neural network]] within a single [[cerebral hemisphere]].{{sfn|Scheffer|Berkovic|Capovilla|Connolly|2017}}{{sfn|Fisher|Cross|French|Higurashi|2017}} Temporal lobe epilepsy occurs from seizures arising within the lobe.{{sfn|Fisher|Cross|French|Higurashi|2017}} It is the most common focal onset epilepsy, and 80% of temporal lobe epilepsy is <em>mesial (medial) <!--not a misspelling-->temporal lobe epilepsy</em>, temporal lobe epilepsy arising from the inner ([[Anatomical terms of location|medial]]) part of the temporal lobe that may involve the [[hippocampus]], [[parahippocampal gyrus]], or [[amygdala]].{{sfn|Chowdhury|Silva|Whatley|Walker|2021}}{{sfn|Tatum|2012}} The less common ''lateral temporal lobe'' or ''neocortical temporal lobe'' seizures arise from the outer ([[Anatomical terms of location|lateral]]) temporal lobe.{{sfn|Chowdhury|Silva|Whatley|Walker|2021}} 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.<ref name=":0">{{Cite web |title=Temporal Lobe Epilepsy (TLE) |url=https://my.clevelandclinic.org/health/diseases/17778-temporal-lobe-seizures |publisher=Temporal Lobe Epilepsy (TLE)}}</ref>
The ILAE 2017 classification distinguishes ''focal aware'' from ''focal impaired'' seizures.{{sfn|Fisher|Cross|French|Higurashi|2017}} 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.{{sfn|Fisher|Cross|French|Higurashi|2017}} A ''focal impaired awareness'' temporal lobe seizure occurs if a person becomes unaware during any part of the seizure.{{sfn|Fisher|Cross|French|Higurashi|2017}}
Approximately 80% of seizures in the temporal lobe begin in the mesial temporal region, frequently starting in or around the hippocampus.<ref>{{Citation |last1=Nayak |first1=Chetan S. |title=Mesial Temporal Lobe Epilepsy |date=2025 |work=StatPearls |url=https://www.ncbi.nlm.nih.gov/books/NBK554432/ |access-date=2025-03-25 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=32119319 |last2=Bandyopadhyay |first2=Susanta}}</ref> The hippocampus, found in both temporal lobes, is essential for memory and learning.<ref name=":0" />
==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.{{sfn|Fisher|Cross|French|Higurashi|2017}}{{sfn|Chowdhury|Silva|Whatley|Walker|2021}} The common mesial temporal lobe seizure auras include a rising [[Epigastrium|epigastric]] feeling, abdominal discomfort, taste (gustatory), smell (olfactory), tingling (somatosensory), fear, [[Déjà vu|{{em|déjà vu}}]], [[Jamais vu|{{em|jamais vu}}]], [[Flushing (physiology)|flushing]], or rapid heart rate ([[tachycardia]]).{{sfn|Chowdhury|Silva|Whatley|Walker|2021}} A person may then stare blankly, appear motionless (''behavioral arrest'') and lose awareness.{{sfn|Chowdhury|Silva|Whatley|Walker|2021}} Repeated stereotyped motor behaviors ([[seizure types|automatisms]]) may occur; these include repeated swallowing, lip smacking, picking, fumbling, patting, or vocalizations.{{sfn|Chowdhury|Silva|Whatley|Walker|2021}} ''Dystonic posture'' is an unnatural stiffening of one arm occurring during a seizure.{{sfn|Rusu|Chassoux|Landre|Bouilleret|2005}} A dystonic posture on one side of the body commonly indicates seizure onset from the [[Contralateral brain|opposite side of the brain]] e.g. right arm dystonic posture arising from a left temporal lobe seizure.{{sfn|Rusu|Chassoux|Landre|Bouilleret|2005}} Impaired language function ([[aphasia|dysphasia]]) during, or soon following, a seizure is more likely to occur when seizures arise from the [[Lateralization of brain function|language dominant]] side of the brain.{{sfn|Rusu|Chassoux|Landre|Bouilleret|2005}}
===Lateral temporal lobe epilepsy=== The common auras from seizures arising from the primary auditory cortex include [[vertigo]], humming sounds, ringing sounds, buzzing sounds, songs or voices, or altered sensations.{{sfn|Chowdhury|Silva|Whatley|Walker|2021}} Lateral temporal lobe seizures arising from the temporal-[[parietal lobe]] junction may cause [[complex visual hallucination]]s.{{sfn|Chowdhury|Silva|Whatley|Walker|2021}} 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 [[Generalized tonic–clonic seizure|bilateral tonic-clonic]] seizures.{{sfn|Chowdhury|Silva|Whatley|Walker|2021}} 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.{{sfn|Rusu|Chassoux|Landre|Bouilleret|2005}}
==Comorbidities== ===Memory=== The major cognitive impairment in mesial temporal lobe epilepsy is a progressive memory impairment.{{sfn|Zeman|Kapur|Jones-Gotman|2012}}{{rp|71}} This involves [[declarative memory]] impairment, including [[episodic memory]] and [[semantic memory]], and is worse when medications fail to control seizures.{{sfn|Quiroga|2012}}{{sfn|Bauman|Devinsky|Liu|2019}}{{sfn|Zeman|Kapur|Jones-Gotman|2012}}{{rp|71}} Mesial temporal lobe epilepsy arising from the language dominant hemisphere impairs [[verbal memory]], and mesial temporal lobe epilepsy arising from the language non-dominant hemisphere impairs [[verbal memory|nonverbal memory]].{{sfn|Zeman|Kapur|Jones-Gotman|2012}}{{rp|71}}{{sfn|Bauman|Devinsky|Liu|2019}}
===Psychiatric comorbidities=== Psychiatric disorders are more common among those with epilepsy, and the highest prevalence occurs among those with temporal lobe epilepsy.{{sfn|Lu|Pyatka|Burant|Sajatovic|2021}} The most common psychiatric comorbidity is [[major depressive disorder]].{{sfn|Lu|Pyatka|Burant|Sajatovic|2021}} Other disorders include [[post-traumatic stress disorder]], [[generalized anxiety disorder]], [[psychosis]], [[obsessive–compulsive disorder]], [[schizophrenia]], [[bipolar disorder]], [[substance use disorder]], and a ~9% prevalence of [[suicidality]].{{sfn|Lu|Pyatka|Burant|Sajatovic|2021}} ===Personality=== {{Main|Geschwind syndrome}}[[Geschwind syndrome]] is a syndrome of altered [[Human sexuality|sexuality]] (most often [[hyposexuality]]), [[religiosity]], and compulsive or extensive writing and drawing occurring in persons with temporal lobe epilepsy.{{sfn|David|Fleminger|Kopelman|Lovestone|2012}}{{rp|347-348}} However, subsequent studies did not support the association of these behavioral traits with temporal lobe epilepsy.{{sfn|David|Fleminger|Kopelman|Lovestone|2012}}{{rp|347-348}} There are reports of religious behaviors occurring in persons with temporal lobe epilepsy.{{sfn|Tedrus|Fonseca|Fagundes|da Silva|2015}}{{sfn|d'Orsi|Tinuper|2006}}{{sfn|Sirven|Drazkowski|Noe|2007}}{{sfn|Arzy|Schurr|2016}}{{sfn|Tedrus|Fonseca|Höehr|2013}}
==Causes== [[Hippocampal sclerosis]], [[brain tumor]], [[traumatic brain injury]], cerebral [[vascular malformation]], [[neuronal migration disorder]]s, infections such as [[encephalitis]] and [[meningitis]], [[autoimmune disease]] ([[limbic encephalitis]]), and [[genetic disorder]]s may cause temporal lobe epilepsy.{{sfn|Vadlamudi|2003}}
==Risk factors== Many persons with uncontrolled temporal lobe epilepsy had childhood [[febrile seizure]]s.{{sfn|Patterson|Baram|Shinnar|2014}} A brief febrile seizure only slightly increases the risk for developing nonfebrile seizures (also known as afebrile seizures).{{sfn|Mewasingh|Chin|Scott|2020}} However, the prolonged seizure of febrile [[status epilepticus]] leads to a 9% risk for developing epilepsy.{{sfn|Mewasingh|Chin|Scott|2020}} There is no clear relationship between febrile seizures and development of hippocampal sclerosis.{{sfn|Mewasingh|Chin|Scott|2020}} Those who experienced any sort of brain injury in their early life have a higher risk of developing epilepsy.<ref name=":0" />
==Mechanisms== {{Too technical|section|date=January 2024}} [[File:CajalHippocampus (modified).png|thumb|The neural circuit of the hippocampus shows dentate gyrus (DG). subiculum (SB). entorhinal cortex (EC), CA1 sector and CA3 sector]] [[file:EEG Recording Cap.jpg|thumb|Scalp electrodes are placed to record an electroencephalogram]] [[File:Hippocampus-mri.jpg|thumb|Brain MRI with hippocampus identified by cross hairs.]] [[File:PET Normal brain.jpg|thumb|260px|[[Brain positron emission tomography]] (PET) scan]] ===Neuronal loss=== [[Hippocampal sclerosis]] occurs with severe [[Hippocampal subfields|CA1]] and less severe [[Hippocampal subfields|CA3]] and [[Hippocampal subfields|CA4]] neuronal loss.{{sfn|Ong|2019}}<ref>{{Cite journal |last1=Hokkanen |first1=Suvi R. K. |last2=Hunter |first2=Sally |last3=Polvikoski |first3=Tuomo M. |last4=Keage |first4=Hannah A. D. |last5=Minett |first5=Thais |last6=Matthews |first6=Fiona E. |last7=Brayne |first7=Carol |date=2018-07-04 |title=Hippocampal sclerosis, hippocampal neuron loss patterns and TDP-43 in the aged population |journal=Brain Pathology |language=en |volume=28 |issue=4 |pages=548–559 |doi=10.1111/bpa.12556 |pmid=28833898 |issn=1015-6305|pmc=6099461 }}</ref> Experimental research has shown that [[NMDA receptor|N-methyl-d-aspartate (NMDA) receptor]] activation causes neuronal cell loss, and electrical stimulation-induced [[Animal models of epilepsy|animal models of temporal lobe epilepsy]] duplicate the cell loss pattern of temporal lobe epilepsy in humans.{{sfn|Ong|2019}} Repetitive seizures irreversibly damage [[interneuron]]s leading to persistent loss of [[Hippocampus|recurrent inhibition]].{{sfn|Ong|2019}} Damage of [[GABAergic]] interneurons lead to loss of inhibition, uncontrolled [[Action potential|neuronal firing]], leading to seizures.{{sfn|Ong|2019}} The ''secondary epileptogenesis'' hypothesis is that repetitive seizures lead to interneuron loss, loss of [[glutamatergic]] [[Dentate nucleus|principal neurons]], axonal sprouting, and formation of new recurrent glutamatergic [[Excitatory synapse|excitatory]] circuits leading to a more severe epilepsy.{{sfn|Ben-Ari|Dudek|2010}} Mechanisms related to neuronal loss incompletely account for temporal lobe epilepsy as temporal lobe epilepsy may occur with only minimal neuronal cell loss.{{sfn|Ong|2019}}
===Neuron-specific type 2 K+/Cl− cotransporter (KCC2) mutation=== This [[Chloride potassium symporter 5|KCC2]] mutation prevents [[Subiculum|subicular]] neurons from potassium and chloride [[ion]] extrusion, leading to intracellular chloride accumulation, and positive [[γ-Aminobutyric acid]] (GABA) mediated currents.{{sfn|Ong|2019}} Accumulated chloride efflux through GABA [[Chemical synapse|receptors]] leads to [[depolarization|neuronal depolarization]], increased neuronal excitability and ultimately seizures.{{sfn|Ong|2019}} Persons with this mutation have mesial temporal lobe epilepsy with hippocampal sclerosis.{{sfn|Ong|2019}}
===Granule cell dispersion=== Dentate gyrus [[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).{{sfn|Blümcke|Thom|Aronica|Armstrong|2013}}{{rp|1318}} In the normal brain, dentate granule cells block seizure spread from [[entorhinal cortex]] to the hippocampus.{{sfn|Ong|2019}} A hypothesis is that granule cell dispersion may disrupt the normal [[Mossy fiber (hippocampus)|mossy fiber pathway]] connecting granule cells and CA3 [[pyramidal cell]]s leading to mossy fiber sprouting and new excitatory networks capable of generating seizures.{{sfn|Ong|2019}} However, a study has shown that a similar pattern of granule cell dispersion may occur in persons without epilepsy.{{sfn|Roy|Millen|Kapur|2020}}
===Cortical developmental malformations=== [[Focal cortical dysplasia]] is a brain malformation that may cause temporal lobe epilepsy.{{sfn|Ong|2019}} This malformation may cause abnormal [[cerebral cortex|cortical layers]] (''dyslamination''), occur with abnormal neurons (''[[focal cortical dysplasia|dysmorphic neurons, balloon cells]]'') and may occur with a brain tumor or vascular malformation.{{sfn|Ong|2019}} An abnormality of the [[MTOR]] pathway leads to hyperexcitable [[Glutamic acid|glutamate]] mediated neurons leading to seizures.{{sfn|Ong|2019}}
==Diagnosis== [[File:Epilepsy-surgery-in-progress.jpg|thumb|260px|A surgeon performs epilepsy brain surgery ]] [[File:Vagus nerve stimulation.jpg|thumb|260px|[[Vagus nerve stimulation]] ]] [[File:מערכת RNS.jpg|thumb|260px|[[Responsive neurostimulation device]] ]] [[Image:Peds DBS.jpg|thumb|260px|Surgeon implants a brain electrode for [[deep brain stimulation]] ]] ===Electroencephalogram=== The temporal lobe ''epileptiform'' discharge is a pattern seen on the [[Electroencephalography|electroencephalgram]] (EEG) test; temporal lobe epileptiform discharges occur between seizures and confirm the diagnosis of temporal lobe epilepsy.{{sfn|Javidan|2012}} [[Long-term video-EEG monitoring]] may record the behavior and EEG during a seizure.{{sfn|Javidan|2012}} [[Magnetoencephalography]] may diagnose temporal lobe epilepsy by recording epileptiform discharges or seizure patterns arising from the magnetic fields of neural electrical currents.{{sfn|Javidan|2012}} ===Neuroimaging=== Neuroimaging tests may identify the cause for seizures and the ''seizure focus'', the brain location where seizures begin.{{sfn|Duncan|2019}} In newly diagnosed epilepsy, [[magnetic resonance imaging]] (MRI) can detect brain lesion in up to 12 to 14% of persons with epilepsy.{{sfn|Salmenpera|Duncan|2005}} However, for those with chronic epilepsy, MRI can detect brain lesion in 80% of the persons with epilepsy.{{sfn|Salmenpera|Duncan|2005}} 3-tesla MRI scan is advised for those with evidence of focal epilepsy such as temporal lobe epilepsy.{{sfn|Duncan|2019}} Abnormalities identified by MRI scan include hippocampal sclerosis, focal cortical dysplasia, other cortical developmental brain malformations, developmental and low-grade tumors, [[cavernous hemangioma]], [[Cerebral hypoxia|hypoxic-ischemic brain injury]], traumatic brain injury and encephalitis.{{sfn|Duncan|2019}}
<sup>18</sup>F-fluorodeoxyglucose (<sup>18</sup>F-FDG) [[brain positron emission tomography]] (PET) may show a brain region of decreased [[glucose]] [[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.{{sfn|Duncan|2019}} [[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.{{sfn|Duncan|2019}}
[[CT scan|Computed tomography]] (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.{{sfn|Salmenpera|Duncan|2005}} CT scan is advised in emergencies when the suspected cause of epilepsy may be [[intracerebral hemorrhage]], [[brain abscess]], large [[cerebral infarction]] or [[subdural empyema]].{{sfn|Duncan|2019}}{{sfn|Salmenpera|Duncan|2005}} A person who requires neuroimaging but cannot have an MRI scan due to implanted devices such as a [[cardiac pacemaker]], [[defibrillator]] or [[cochlear implant]] may receive a CT scan. CT scan may better demonstrate calcium containing brain abnormalities causing epilepsy such as in [[tuberous sclerosis]] and [[Sturge–Weber syndrome]].{{sfn|Duncan|2019}}{{sfn|Salmenpera|Duncan|2005}}
==Treatment== ===Medical treatment=== [[Anticonvulsant]] oral medications control seizures in about two-thirds of persons with epilepsy, and control commonly occurs with one or two medications.{{sfn|Kwan|Brodie|2000}}
===Surgical treatment===
Those with uncontrolled seizures despite treatment with multiple anticonvulsant medications have ''[[Management of drug-resistant epilepsy|pharmacoresistant]]'' epilepsy, and they may require [[epilepsy surgery]] to achieve seizure control.{{sfn|Scheffer|Berkovic|Capovilla|Connolly|2017}}{{sfn|Kwan|Brodie|2000}}
[[Wilder Penfield|Penfield]] and Flanigan first described [[anterior temporal lobectomy]], partial surgical removal of the temporal lobe, for treatment of mesial temporal lobe epilepsy in 1950.{{sfn|Penfield|Flanigan|1950}} In a prospective [[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.{{sfn|Wiebe|Blume|Girvin|Eliasziw|2001}} Among those with intractable mesial temporal lobe epilepsy and hippocampal sclerosis, about 70% become seizure-free after epilepsy surgery.{{sfn|Lamberink|Otte|Blümcke|Braun|2020}}{{rp|751}} Studies show that language dominant anterior temporal lobectomy may lead to verbal memory decline.{{sfn|Bauman|Devinsky|Liu|2019}} However, study outcomes are more variable on language non-dominant anterior temporal lobectomy leading to nonverbal memory decline.{{sfn|Bauman|Devinsky|Liu|2019}}
''Magnetic resonance-guided laser interstitial thermal therapy'', ''[[radiosurgery|stereotactic radiosurgery]]'', and ''[[Stereotactic surgery|stereotactic radiofrequency ablation]]'' are surgical methods that treat epilepsy by destroying the abnormal brain tissue that causes seizures.{{sfn|Chen|Lamoureux|Shlobin|Elkaim|2023}}{{sfn|Kerezoudis|Tsayem|Lundstrom|Van Gompel|2022}}{{sfn|Mustafa|Zaben|2022}}
Neurostimulation may also improve seizure control.{{sfn|Touma|Dansereau|Chan|Jetté|2022}} The ''[[vagus nerve stimulation|vagus nerve stimulator]]'' (VNS) is surgically implanted in the chest, and delivers programmed electrical stimulation to the [[vagus nerve]] in the neck.{{sfn|Goggins|Mitani|Tanaka|2022}} The ''[[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.{{sfn|Geller|2018}} Programmed ''[[deep brain stimulation]]'' of the anterior thalamic nucleus may treat seizures arising from more than 2 brain areas.{{sfn|Touma|Dansereau|Chan|Jetté|2022}}
===Dietary treatment=== The [[ketogenic diet]] and [[Ketogenic diet|modified Atkins diet]] are additional temporal lobe epilepsy treatment options.{{sfn|Freeman|Kossoff|Hartman|2007}}{{sfn|Rezaei|Abdurahman|Saghazadeh|Badv|2019}}
==Remission== Among those who develop childhood temporal lobe epilepsy, epilepsy remits in about one-third of children.{{sfn|Spooner|Berkovic|Mitchell|Wrennall|2006}} Remission was more likely among those without [[hippocampal sclerosis]], brain tumor, or focal cortical dysplasia on MRI scan.{{sfn|Spooner|Berkovic|Mitchell|Wrennall|2006}}
==See also== * [[Geschwind syndrome]] * [[List of people with epilepsy]]
==Notes== {{Reflist|colwidth=25em}}
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{{Medical resources |ICD10={{ICD10|G|40.1||g|40}}-{{ICD10|G|40.2||g|40}} |ICD9={{ICD9|345.4}} |MedlinePlus=001399 |eMedicineSubj=neuro |eMedicineTopic=365 |DiseasesDB=29433 |MeshID=D004833 }} {{Seizures and epilepsy}} {{Medicine}} {{Authority control}}
{{DEFAULTSORT:Temporal Lobe Epilepsy}} [[Category:Epilepsy types]] [[Category:Neurotheology]] [[Category:Temporal lobe]]