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Temporal lobe epilepsy

January 01, 1970

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

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

Types edit

Under the International League Against Epilepsy (ILAE) 2017 classification of the epilepsies, focal onset epilepsy occurs from seizures arising from a biological neural network within a single cerebral hemisphere.[9][10] Temporal lobe epilepsy occurs from seizures arising within the temporal lobe.[10] Temporal lobe epilepsy 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) part of the temporal lobe that may involve the hippocampus, parahippocampal gyrus or amygdala.[2][11] The less common lateral temporal lobe or neocortical temporal lobe seizures arise from the outer (lateral) temporal lobe.[2] 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]

Symptoms and behavior edit

Medial temporal lobe epilepsy edit

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 medial temporal lobe seizure auras include a rising epigastric feeling, abdominal discomfort, taste (gustatory), smell (olfactory), tingling (somatosensory), fear, déjà vu, jamais vu, flushing, or rapid heart rate (tachycardia).[2] A person may then stare blankly, appear motionless (behavioral arrest) and lose awareness.[2] Repeated stereotyped motor behaviors (automatisms) may occur such as repeated swallowing, lip smacking, picking, fumbling, patting or vocalizations.[2] Dystonic posture is an unnatural stiffening of one arm occurring during a seizure.[12] A dystonic posture on one side of the body commonly indicates seizure onset from the opposite side of the brain e.g. right arm dystonic posture arising from a left temporal lobe seizure.[12] 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.[12]

Lateral temporal lobe epilepsy edit

The common auras from seizures arising from primary auditory cortex include vertigo, humming sound, ringing sound, buzzing sound, hearing a song, hearing voices or altered hearing sensation.[2] Lateral temporal lobe seizures arising from the temporal-parietal lobe junction may cause complex visual hallucinations.[2] In comparison to medial temporal lobe seizures, lateral temporal lobe seizures are briefer duration seizures, occur with earlier loss of awareness, and are more likely become a focal to bilateral tonic-clonic seizure.[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.[12]

Comorbidities edit

Memory edit

The major cognitive impairment in mesial temporal lobe epilepsy is a progressive memory impairment.[13]: 71  This involves declarative memory impairment, including episodic memory and semantic memory, and is worse when medications fail to control seizures.[14][15][13]: 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 nonverbal memory.[13]: 71 [15]

Psychiatric comorbidities edit

Psychiatric disorders are more common among those with epilepsy, and the highest prevalence occurs among those with temporal lobe epilepsy.[16] The most common psychiatric comorbidity is major depressive disorder.[16] Other disorders include post-traumatic stress disorder, general anxiety disorder, psychosis, obsessive-compulsive disorder, schizophrenia, bipolar disorder, substance use disorder and a ~9% prevalence of suicide.[16]

Personality edit

Main article: Geschwind syndrome

Geschwind syndrome is a syndrome of altered sexuality (most often hyposexuality), religiosity, and compulsive or extensive writing and drawing occurring in persons with temporal lobe epilepsy.[17]: 347–348  However, subsequent studies did not support the association of these behavioral traits with temporal lobe epilepsy.[17]: 347–348  There are reports of religious behaviors occurring in persons with temporal lobe epilepsy.[18][19][20][21][22]

Causes edit

Hippocampal sclerosis, brain tumor, traumatic brain injury, cerebral vascular malformation, neuronal migration disorders, infections such as encephalitis and meningitis, autoimmune disease (limbic encephalitis) and genetic disorders may cause temporal lobe epilepsy.[23]

Risk factors edit

Many persons with uncontrolled temporal lobe epilepsy had childhood febrile seizures.[24] A brief febrile seizure only slighty increases the risk for developing afebrile seizures.[25] However, the prolonged seizure of febrile status epilepticus leads to a 9% risk for developing epilepsy.[25] There is no clear relationship between febrile seizures and development of hippocampal sclerosis.[25]

Mechanisms edit

 
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 (PET) scan

Neuronal loss edit

Hippocampal sclerosis occurs with severe CA1 and less severe CA3 and CA4 neuronal loss.[26] Experimental research has shown that N-methyl-d-aspartate (NMDA) receptor activation causes neuronal cell loss, and electrical stimulation-induced animal models of temporal lobe epilepsy duplicate the cell loss pattern of temporal lobe epilepsy in humans.[26] Repetitive seizures irreversibly damage interneurons leading to persistent loss of recurrent inhibition.[26] Damage of GABAergic interneurons lead to loss of inhibition, uncontrolled neuronal firing, leading to seizures.[26] The secondary epileptogenesis hypothesis is that repetitive seizures lead to interneuron loss, loss of glutamatergic principal neurons, axonal sprouting, and formation of new recurrent glutamatergic excitatory circuits leading to a more severe epilepsy.[27] Mechanisms related to neuronal loss incompletely account for temporal lobe epilepsy as temporal lobe epilepsy may occur with only minimal neuronal cell loss.[26]

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

This KCC2 mutation prevents subicular neurons from potassium and chloride ion extrusion, leading to intracellular chloride accumulation, and positive γ-Aminobutyric acid (GABA) mediated currents.[26] Accumulated chloride efflux through GABA receptors leads to neuronal depolarization, increased neuronal excitability and ultimately seizures.[26] Persons with this mutation have mesial temporal lobe epilepsy with hippocampal sclerosis.[26]

Granule cell dispersion edit

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).[28]: 1318  In the normal brain, dentate granule cells block seizure spread from entorhinal cortex to the hippocampus.[26] A hypothesis is that granule cell dispersion may disrupt the normal mossy fiber pathway connecting granule cells and CA3 pyramidal cells leading to mossy fiber sprouting and new excitatory networks capable of generating seizures.[26] However, a study has shown that a similar pattern of granule cell dispersion may occur in persons without epilepsy.[29]

Cortical developmental malformations edit

Focal cortical dysplasia is a brain malformation that may cause temporal lobe epilepsy.[26] This malformation may cause abnormal cortical layers (dyslamination ), occur with abnormal neurons (dysmorphic neurons, balloon cells ) and may occur with a brain tumor or vascular malformation.[26] An abnormality of the MTOR pathway leads to hyperexcitable glutamate mediated neurons leading to seizures.[26]

Diagnosis edit

 
A surgeon performs epilepsy brain surgery
 
Vagus nerve stimulation
 
Responsive neurostimulation device
 
Surgeon implants a brain electrode for deep brain stimulation

Electroencephalogram edit

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

Neuroimaging edit

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 (MRI) can detect brain lesion in up to 12 to 14% of persons with epilepsy.[30] However, for those with chronic epilepsy, MRI can detect brain lesion in 80% of the persons with epilepsy.[30] 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, hypoxic-ischemic brain injury, traumatic brain injury and encephalitis.[4]

18F-fluorodeoxyglucose (18F-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.[4] 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 (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.[30] CT scan is advised in emergencies when the suspected cause of epilepsy may be intracerebral hemorrhage, brain abscess, large cerebral infarction or subdural empyema.[4][30] 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.[4][30]

Treatment edit

Medical treatment edit

Anticonvulsant oral medications control seizures in about two-thirds of persons with epilepsy, and control commonly occurs with one or two medications.[31]

Surgical treatment edit

Those with uncontrolled seizures despite treatment with multiple anticonvulsant medications have pharmacoresistant epilepsy, and they may require epilepsy surgery to achieve seizure control.[9][31]

Penfield and Flanigan first described anterior temporal lobectomy, partial surgical removal of the temporal lobe, for treatment of mesial temporal lobe epilepsy in 1950.[32] 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.[5] Among those with intractable mesial temporal lobe epilepsy and hippocampal sclerosis, about 70% become seizure-free after epilepsy surgery.[33]: 751  Studies show that language dominant anterior temporal lobectomy may lead to verbal memory decline.[15] However, study outcomes are more variable on language non-dominant anterior temporal lobectomy leading to nonverbal memory decline.[15]

Magnetic resonance-guided laser interstitial thermal therapy, stereotactic radiosurgery, and stereotactic radiofrequency ablation are surgical methods that treat epilepsy by destroying the abnormal brain tissue that causes seizures.[34][35] [36]

Neurostimulation may also improve seizure control.[6] The vagus nerve stimulator (VNS) is surgically implanted in the chest, and delivers programmed electrical stimulation to the vagus nerve in the neck.[37] 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.[38] Programmed deep brain stimulation of the anterior thalamic nucleus may treat seizures arising from more than 2 brain areas.[6]

Dietary treatment edit

The ketogenic diet and modified Atkins diet are additional temporal lobe epilepsy treatment options.[7][8]

Remission edit

Among those who develop childhood temporal lobe epilepsy, epilepsy remits in about one-third of children.[39] Remission was more likely among those without hippocampal sclerosis, brain tumor, or focal cortical dysplasia on MRI scan.[39]

See also edit

Notes edit

  1. ^ Muhlhofer et al. 2017.
  2. ^ a b c d e f g h i j Chowdhury et al. 2021.
  3. ^ a b c d Javidan 2012.
  4. ^ a b c d e f g h Duncan 2019.
  5. ^ a b Wiebe et al. 2001.
  6. ^ a b c d Touma et al. 2022.
  7. ^ a b Freeman, Kossoff & Hartman 2007.
  8. ^ a b Rezaei et al. 2019.
  9. ^ a b Scheffer et al. 2017.
  10. ^ a b c d e f Fisher et al. 2017.
  11. ^ Tatum 2012.
  12. ^ a b c d Rusu et al. 2005.
  13. ^ a b c Zeman, Kapur & Jones-Gotman 2012.
  14. ^ Quiroga 2012.
  15. ^ a b c d Bauman, Devinsky & Liu 2019.
  16. ^ a b c Lu et al. 2021.
  17. ^ a b David et al. 2012.
  18. ^ Tedrus et al. 2015.
  19. ^ d'Orsi & Tinuper 2006.
  20. ^ Sirven, Drazkowski & Noe 2007.
  21. ^ Arzy & Schurr 2016.
  22. ^ Tedrus, Fonseca & Höehr 2013.
  23. ^ Vadlamudi 2003.
  24. ^ Patterson, Baram & Shinnar 2014.
  25. ^ a b c Mewasingh, Chin & Scott 2020.
  26. ^ a b c d e f g h i j k l m Ong 2019.
  27. ^ Ben-Ari & Dudek 2010.
  28. ^ Blümcke et al. 2013.
  29. ^ Roy, Millen & Kapur 2020.
  30. ^ a b c d e Salmenpera & Duncan 2005.
  31. ^ a b Kwan & Brodie 2000.
  32. ^ Penfield & Flanigan 1950.
  33. ^ Lamberink et al. 2020.
  34. ^ Chen et al. 2023.
  35. ^ Kerezoudis et al. 2022.
  36. ^ Mustafa & Zaben 2022.
  37. ^ Goggins, Mitani & Tanaka 2022.
  38. ^ Geller 2018.
  39. ^ a b Spooner et al. 2006.

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January 01, 1970
temporal, lobe, epilepsy, field, neurology, temporal, lobe, epilepsy, enduring, brain, disorder, that, causes, unprovoked, seizures, from, temporal, lobe, most, common, type, focal, onset, epilepsy, among, adults, seizure, symptoms, behavior, distinguish, seiz. In the field of neurology temporal lobe epilepsy is an enduring brain disorder that causes unprovoked seizures from the temporal lobe Temporal lobe epilepsy is the most common type of focal onset epilepsy among adults 1 Seizure symptoms and behavior distinguish seizures arising from the medial temporal lobe from seizures arising from the lateral neocortical temporal lobe 2 Memory and psychiatric comorbidities may occur Diagnosis relies on electroencephalographic EEG and neuroimaging studies 3 4 Anticonvulsant medications epilepsy surgery and dietary treatments may improve seizure control 5 6 6 7 8 Temporal lobe epilepsyLobes of the brain Temporal lobe in greenSpecialtyNeurology Psychiatry Contents 1 Types 2 Symptoms and behavior 2 1 Medial temporal lobe epilepsy 2 2 Lateral temporal lobe epilepsy 3 Comorbidities 3 1 Memory 3 2 Psychiatric comorbidities 3 3 Personality 4 Causes 5 Risk factors 6 Mechanisms 6 1 Neuronal loss 6 2 Neuron specific type 2 K Cl cotransporter KCC2 mutation 6 3 Granule cell dispersion 6 4 Cortical developmental malformations 7 Diagnosis 7 1 Electroencephalogram 7 2 Neuroimaging 8 Treatment 8 1 Medical treatment 8 2 Surgical treatment 8 3 Dietary treatment 9 Remission 10 See also 11 Notes 12 ReferencesTypes editUnder the International League Against Epilepsy ILAE 2017 classification of the epilepsies focal onset epilepsy occurs from seizures arising from a biological neural network within a single cerebral hemisphere 9 10 Temporal lobe epilepsy occurs from seizures arising within the temporal lobe 10 Temporal lobe epilepsy 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 part of the temporal lobe that may involve the hippocampus parahippocampal gyrus or amygdala 2 11 The less common lateral temporal lobe or neocortical temporal lobe seizures arise from the outer lateral temporal lobe 2 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 Symptoms and behavior editMedial temporal lobe epilepsy edit 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 medial temporal lobe seizure auras include a rising epigastric feeling abdominal discomfort taste gustatory smell olfactory tingling somatosensory fear deja vu jamais vu flushing or rapid heart rate tachycardia 2 A person may then stare blankly appear motionless behavioral arrest and lose awareness 2 Repeated stereotyped motor behaviors automatisms may occur such as repeated swallowing lip smacking picking fumbling patting or vocalizations 2 Dystonic posture is an unnatural stiffening of one arm occurring during a seizure 12 A dystonic posture on one side of the body commonly indicates seizure onset from the opposite side of the brain e g right arm dystonic posture arising from a left temporal lobe seizure 12 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 12 Lateral temporal lobe epilepsy edit The common auras from seizures arising from primary auditory cortex include vertigo humming sound ringing sound buzzing sound hearing a song hearing voices or altered hearing sensation 2 Lateral temporal lobe seizures arising from the temporal parietal lobe junction may cause complex visual hallucinations 2 In comparison to medial temporal lobe seizures lateral temporal lobe seizures are briefer duration seizures occur with earlier loss of awareness and are more likely become a focal to bilateral tonic clonic seizure 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 12 Comorbidities editMemory edit The major cognitive impairment in mesial temporal lobe epilepsy is a progressive memory impairment 13 71 This involves declarative memory impairment including episodic memory and semantic memory and is worse when medications fail to control seizures 14 15 13 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 nonverbal memory 13 71 15 Psychiatric comorbidities edit Psychiatric disorders are more common among those with epilepsy and the highest prevalence occurs among those with temporal lobe epilepsy 16 The most common psychiatric comorbidity is major depressive disorder 16 Other disorders include post traumatic stress disorder general anxiety disorder psychosis obsessive compulsive disorder schizophrenia bipolar disorder substance use disorder and a 9 prevalence of suicide 16 Personality edit Main article Geschwind syndromeGeschwind syndrome is a syndrome of altered sexuality most often hyposexuality religiosity and compulsive or extensive writing and drawing occurring in persons with temporal lobe epilepsy 17 347 348 However subsequent studies did not support the association of these behavioral traits with temporal lobe epilepsy 17 347 348 There are reports of religious behaviors occurring in persons with temporal lobe epilepsy 18 19 20 21 22 Causes editHippocampal sclerosis brain tumor traumatic brain injury cerebral vascular malformation neuronal migration disorders infections such as encephalitis and meningitis autoimmune disease limbic encephalitis and genetic disorders may cause temporal lobe epilepsy 23 Risk factors editMany persons with uncontrolled temporal lobe epilepsy had childhood febrile seizures 24 A brief febrile seizure only slighty increases the risk for developing afebrile seizures 25 However the prolonged seizure of febrile status epilepticus leads to a 9 risk for developing epilepsy 25 There is no clear relationship between febrile seizures and development of hippocampal sclerosis 25 Mechanisms edit nbsp The neural circuit of the hippocampus shows dentate gyrus DG subiculum SB entorhinal cortex EC CA1 sector and CA3 sector nbsp Scalp electrodes are placed to record an electroencephalogram nbsp Brain MRI with hippocampus identified by cross hairs nbsp Brain positron emission tomography PET scan Neuronal loss edit Hippocampal sclerosis occurs with severe CA1 and less severe CA3 and CA4 neuronal loss 26 Experimental research has shown that N methyl d aspartate NMDA receptor activation causes neuronal cell loss and electrical stimulation induced animal models of temporal lobe epilepsy duplicate the cell loss pattern of temporal lobe epilepsy in humans 26 Repetitive seizures irreversibly damage interneurons leading to persistent loss of recurrent inhibition 26 Damage of GABAergic interneurons lead to loss of inhibition uncontrolled neuronal firing leading to seizures 26 The secondary epileptogenesis hypothesis is that repetitive seizures lead to interneuron loss loss of glutamatergic principal neurons axonal sprouting and formation of new recurrent glutamatergic excitatory circuits leading to a more severe epilepsy 27 Mechanisms related to neuronal loss incompletely account for temporal lobe epilepsy as temporal lobe epilepsy may occur with only minimal neuronal cell loss 26 Neuron specific type 2 K Cl cotransporter KCC2 mutation edit This KCC2 mutation prevents subicular neurons from potassium and chloride ion extrusion leading to intracellular chloride accumulation and positive g Aminobutyric acid GABA mediated currents 26 Accumulated chloride efflux through GABA receptors leads to neuronal depolarization increased neuronal excitability and ultimately seizures 26 Persons with this mutation have mesial temporal lobe epilepsy with hippocampal sclerosis 26 Granule cell dispersion edit 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 28 1318 In the normal brain dentate granule cells block seizure spread from entorhinal cortex to the hippocampus 26 A hypothesis is that granule cell dispersion may disrupt the normal mossy fiber pathway connecting granule cells and CA3 pyramidal cells leading to mossy fiber sprouting and new excitatory networks capable of generating seizures 26 However a study has shown that a similar pattern of granule cell dispersion may occur in persons without epilepsy 29 Cortical developmental malformations edit Focal cortical dysplasia is a brain malformation that may cause temporal lobe epilepsy 26 This malformation may cause abnormal cortical layers dyslamination occur with abnormal neurons dysmorphic neurons balloon cells and may occur with a brain tumor or vascular malformation 26 An abnormality of the MTOR pathway leads to hyperexcitable glutamate mediated neurons leading to seizures 26 Diagnosis edit nbsp A surgeon performs epilepsy brain surgery nbsp Vagus nerve stimulation nbsp Responsive neurostimulation device nbsp Surgeon implants a brain electrode for deep brain stimulation Electroencephalogram edit The temporal lobe epileptiform discharge is a pattern seen on the electroencephalgram EEG test temporal lobe epileptiform discharges occur between seizures and confirm the diagnosis of temporal lobe epilepsy 3 Long term video EEG monitoring may record the behavior and EEG during a seizure 3 Magnetoencephalography may diagnose temporal lobe epilepsy by recording epileptiform discharges or seizure patterns arising from the magnetic fields of neural electrical currents 3 Neuroimaging edit 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 MRI can detect brain lesion in up to 12 to 14 of persons with epilepsy 30 However for those with chronic epilepsy MRI can detect brain lesion in 80 of the persons with epilepsy 30 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 hypoxic ischemic brain injury traumatic brain injury and encephalitis 4 18F fluorodeoxyglucose 18F 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 4 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 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 30 CT scan is advised in emergencies when the suspected cause of epilepsy may be intracerebral hemorrhage brain abscess large cerebral infarction or subdural empyema 4 30 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 4 30 Treatment editMedical treatment edit Anticonvulsant oral medications control seizures in about two thirds of persons with epilepsy and control commonly occurs with one or two medications 31 Surgical treatment edit Those with uncontrolled seizures despite treatment with multiple anticonvulsant medications have pharmacoresistant epilepsy and they may require epilepsy surgery to achieve seizure control 9 31 Penfield and Flanigan first described anterior temporal lobectomy partial surgical removal of the temporal lobe for treatment of mesial temporal lobe epilepsy in 1950 32 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 5 Among those with intractable mesial temporal lobe epilepsy and hippocampal sclerosis about 70 become seizure free after epilepsy surgery 33 751 Studies show that language dominant anterior temporal lobectomy may lead to verbal memory decline 15 However study outcomes are more variable on language non dominant anterior temporal lobectomy leading to nonverbal memory decline 15 Magnetic resonance guided laser interstitial thermal therapy stereotactic radiosurgery and stereotactic radiofrequency ablation are surgical methods that treat epilepsy by destroying the abnormal brain tissue that causes seizures 34 35 36 Neurostimulation may also improve seizure control 6 The vagus nerve stimulator VNS is surgically implanted in the chest and delivers programmed electrical stimulation to the vagus nerve in the neck 37 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 38 Programmed deep brain stimulation of the anterior thalamic nucleus may treat seizures arising from more than 2 brain areas 6 Dietary treatment edit The ketogenic diet and modified Atkins diet are additional temporal lobe epilepsy treatment options 7 8 Remission editAmong those who develop childhood temporal lobe epilepsy epilepsy remits in about one third of children 39 Remission was more likely among those without hippocampal sclerosis brain tumor or focal cortical dysplasia on MRI scan 39 See also editList of people with epilepsy Religious figuresNotes edit Muhlhofer et al 2017 a b c d e f g h i j Chowdhury et al 2021 a b c d Javidan 2012 a b c d e f g h Duncan 2019 a b Wiebe et al 2001 a b c d Touma et al 2022 a b Freeman Kossoff amp Hartman 2007 a b Rezaei et al 2019 a b Scheffer et al 2017 a b c d e f Fisher et al 2017 Tatum 2012 a b c d Rusu et al 2005 a b c Zeman Kapur amp Jones Gotman 2012 Quiroga 2012 a b c d Bauman Devinsky amp Liu 2019 a b c Lu et al 2021 a b David et al 2012 Tedrus et al 2015 d Orsi amp Tinuper 2006 Sirven Drazkowski amp Noe 2007 Arzy amp Schurr 2016 Tedrus Fonseca amp Hoehr 2013 Vadlamudi 2003 Patterson Baram amp Shinnar 2014 a b c Mewasingh Chin amp Scott 2020 a b c d e f g h i j k l m Ong 2019 Ben Ari amp Dudek 2010 Blumcke et al 2013 Roy Millen amp Kapur 2020 a b c d e Salmenpera amp Duncan 2005 a b Kwan amp Brodie 2000 Penfield amp Flanigan 1950 Lamberink et al 2020 Chen et al 2023 Kerezoudis et al 2022 Mustafa amp Zaben 2022 Goggins Mitani amp Tanaka 2022 Geller 2018 a b Spooner et al 2006 References editArzy S Schurr R 2016 God has sent me to you Right temporal epilepsy left prefrontal psychosis Epilepsy amp Behavior 60 7 10 doi 10 1016 j yebeh 2016 04 022 PMID 27176877 S2CID 3886939 Bauman Kristie Devinsky Orrin Liu Anli A 2019 Temporal lobe surgery and memory Lessons risks and opportunities Epilepsy amp Behavior 101 Pt A 106596 doi 10 1016 j yebeh 2019 106596 PMC 6885125 PMID 31711868 Ben Ari Yehezkel Dudek F Edward 2010 Primary and Secondary Mechanisms of Epileptogenesis in the Temporal Lobe There is a before and an After Epilepsy Currents 10 5 118 125 doi 10 1111 j 1535 7511 2010 01376 x ISSN 1535 7597 PMC 2951692 PMID 20944823 Blumcke Ingmar Thom Maria Aronica Eleonora Armstrong Dawna D et al 2013 International consensus classification of hippocampal sclerosis in temporal lobe epilepsy A Task Force report from the ILAE Commission on Diagnostic Methods Epilepsia 54 7 1315 1329 doi 10 1111 epi 12220 PMID 23692496 S2CID 37906434 Chen Jia Shu Lamoureux Audrey Anne Shlobin Nathan A Elkaim Lior M et al 2023 Magnetic Resonance guided Laser Interstitial Thermal Therapy for Drug Resistant Epilepsy A Systematic Review and Individual Participant Data Meta Analysis Epilepsia 64 8 1957 1974 doi 10 1111 epi 17560 ISSN 0013 9580 PMID 36824029 S2CID 257153269 Chowdhury Fahmida A Silva Rui Whatley Benjamin Walker Matthew C 2021 Localisation in focal epilepsy a practical guide Practical Neurology 21 6 481 491 doi 10 1136 practneurol 2019 002341 PMID 34404748 S2CID 237156420 David Daniel Fleminger Simon Kopelman Michael Lovestone Simon Mellers John 2012 Lishman s Organic Psychiatry A Textbook of Neuropsychiatry John Wiley amp Sons ISBN 978 0 470 67507 6 d Orsi Giuseppe Tinuper Paolo 2006 I heard voices from semiology a historical review and a new hypothesis on the presumed epilepsy of Joan of Arc Epilepsy amp Behavior 9 1 152 157 doi 10 1016 j yebeh 2006 04 020 PMID 16750938 S2CID 24961015 Duncan John S 2019 Brain imaging in epilepsy Practical Neurology 19 5 438 443 doi 10 1136 practneurol 2018 002180 ISSN 1474 7758 PMID 31420416 S2CID 201041577 Fisher RS Cross JH French JA Higurashi N et al 2017 Operational classification of seizure types by the International League Against Epilepsy Position Paper of the ILAE Commission for Classification and Terminology Epilepsia 58 4 522 530 doi 10 1111 epi 13670 hdl 11343 292620 PMID 28276060 Freeman JM Kossoff EH Hartman AL 2007 The ketogenic diet one decade later Pediatrics 119 3 535 43 doi 10 1542 peds 2006 2447 PMID 17332207 S2CID 26629499 Geller Eric B 1 November 2018 Responsive neurostimulation Review of clinical trials and insights into focal epilepsy Epilepsy amp Behavior 88 11 20 doi 10 1016 j yebeh 2018 06 042 ISSN 1525 5050 PMID 30243756 S2CID 52341485 Goggins Eibhlin Mitani Shuhei Tanaka Shinji 2022 Clinical perspectives on vagus nerve stimulation present and future Clinical Science 136 9 695 709 doi 10 1042 CS20210507 PMC 9093220 PMID 35536161 Javidan Manouchehr 2012 Electroencephalography in Mesial Temporal Lobe Epilepsy A Review Epilepsy Research and Treatment 2012 1 17 doi 10 1155 2012 637430 PMC 3420622 PMID 22957235 Kerezoudis Panagiotis Tsayem Idriss N Lundstrom Brian N Van Gompel Jamie J 2022 Systematic review and patient level meta analysis of radiofrequency ablation for medically refractory epilepsy Implications for clinical practice and research Seizure 102 113 119 doi 10 1016 j seizure 2022 10 003 ISSN 1059 1311 PMID 36219914 S2CID 252690018 Kwan P Brodie M J 2000 Early identification of refractory epilepsy NEJM 342 5 314 319 doi 10 1056 NEJM200002033420503 PMID 10660394 Lamberink Herm J Otte Willem M Blumcke Ingmar Braun Kees P J et al 2020 Seizure outcome and use of antiepileptic drugs after epilepsy surgery according to histopathological diagnosis a retrospective multicentre cohort study The Lancet Neurology 19 9 748 757 doi 10 1016 S1474 4422 20 30220 9 PMID 32822635 S2CID 221162302 Lu Elaine Pyatka Nataliya Burant Christopher J Sajatovic Martha 2021 Systematic Literature Review of Psychiatric Comorbidities in Adults with Epilepsy Journal of Clinical Neurology 17 2 176 186 doi 10 3988 jcn 2021 17 2 176 PMC 8053555 PMID 33835737 Mewasingh Leena D Chin Richard F M Scott Rod C 2020 Current understanding of febrile seizures and their long term outcomes Developmental Medicine amp Child Neurology 62 11 1245 1249 doi 10 1111 dmcn 14642 PMID 32748466 S2CID 220966202 Muhlhofer Wolfgang Tan Yee Leng Mueller Susanne G Knowlton Robert 2017 MRI negative temporal lobe epilepsy What do we know Epilepsia 58 5 727 742 doi 10 1111 epi 13699 PMID 28266710 S2CID 10691471 Mustafa Mohamed Zaben Malik 2022 Minimal invasive brain surgery for epilepsy can it be the future Journal of Neurology 269 11 6178 6180 doi 10 1007 s00415 022 11360 z ISSN 1432 1459 PMC 9553844 PMID 36098841 Ong Leong Tung 2019 Temporal Lobe Epilepsy Pathophysiology and Mechanisms European Neurological Review 14 2 66 doi 10 17925 ENR 2019 14 2 66 S2CID 213850147 Patterson Katelin P Baram Tallie Z Shinnar Shlomo 2014 Origins of Temporal Lobe Epilepsy Febrile Seizures and Febrile Status Epilepticus PDF Neurotherapeutics 11 2 242 250 doi 10 1007 s13311 014 0263 4 PMC 3996115 PMID 24604424 Penfield Wilder Flanigan Herman 1950 Surgical therapy of temporal lobe seizures Archives of Neurology and Psychiatry 64 4 491 500 doi 10 1001 archneurpsyc 1950 02310280003001 PMID 14770593 Quiroga Rodrigo Quian 2012 Concept cells the building blocks of declarative memory functions Nature Reviews Neuroscience 13 8 587 597 doi 10 1038 nrn3251 PMID 22760181 S2CID 12802960 Rezaei Shahabeddin Abdurahman Ahmed Abdulahi Saghazadeh Amene Badv Reza Shervin Mahmoudi Maryam 2019 Short term and long term efficacy of classical ketogenic diet and modified Atkins diet in children and adolescents with epilepsy A systematic review and meta analysis Nutritional Neuroscience 22 5 317 334 doi 10 1080 1028415X 2017 1387721 PMID 29069983 S2CID 21117747 Roy Achira Millen Kathleen J Kapur Raj P 2020 Hippocampal granule cell dispersion a non specific finding in pediatric patients with no history of seizures Acta Neuropathologica Communications 8 1 54 doi 10 1186 s40478 020 00928 3 PMC 7171777 PMID 32317027 Rusu V Chassoux F Landre E Bouilleret V et al 2005 Dystonic posturing in seizures of mesial temporal origin Electroclinical and metabolic patterns Neurology 65 10 1612 1619 doi 10 1212 01 wnl 0000184510 44808 50 PMID 16301490 S2CID 29551407 Salmenpera T M Duncan J S 2005 Imaging in epilepsy Journal of Neurology Neurosurgery amp Psychiatry 76 suppl 3 iii2 iii10 doi 10 1136 jnnp 2005 075135 ISSN 0022 3050 PMC 1765703 PMID 16107387 Scheffer Ingrid E Berkovic Samuel Capovilla Giuseppe Connolly Mary B et al 2017 ILAE classification of the epilepsies Position paper of the ILAE Commission for Classification and Terminology Epilepsia 58 4 512 521 doi 10 1111 epi 13709 PMC 5386840 PMID 28276062 Sirven Joseph I Drazkowski Joseph F Noe Katherine H 2007 Seizures among public figures lessons learned from the epilepsy of Pope Pius IX Mayo Clinic Proceedings 82 12 1535 1540 doi 10 1016 S0025 6196 11 61100 2 PMID 18053463 Spooner C G Berkovic S F Mitchell L A Wrennall J A et al 2006 New onset temporal lobe epilepsy in children Lesion on MRI predicts poor seizure outcome Neurology 67 12 2147 2153 doi 10 1212 01 wnl 0000248189 93630 4f PMID 17082466 S2CID 1238402 Tatum William O 2012 Mesial Temporal Lobe Epilepsy Journal of Clinical Neurophysiology 29 5 356 365 doi 10 1097 WNP 0b013e31826b3ab7 PMID 23027091 S2CID 29616130 Tedrus Gloria Maria Almeida Souza Fonseca Lineu Correa Hoehr Gabriela Chaves 2013 Spirituality aspects in patients with epilepsy Seizure 23 1 25 8 doi 10 1016 j seizure 2013 09 005 PMID 24094727 Tedrus Gloria Maria Almeida Souza Fonseca Lineu Correa Fagundes Tatiane Mariani da Silva Gabriela Leopoldino 2015 Religiosity aspects in patients with epilepsy Epilepsy amp Behavior 50 67 70 doi 10 1016 j yebeh 2015 06 003 PMID 26133113 S2CID 22703938 Touma Lahoud Dansereau Benedicte Chan Alvin Y Jette Nathalie et al 2022 Neurostimulation in people with drug resistant epilepsy Systematic review and meta analysis from the ILAE Surgical Therapies Commission Epilepsia 63 6 1314 1329 doi 10 1111 epi 17243 ISSN 1528 1167 PMID 35352349 S2CID 247792263 Vadlamudi L 2003 Genetics of temporal lobe epilepsy Journal of Neurology Neurosurgery amp Psychiatry 74 10 1359 1361 doi 10 1136 jnnp 74 10 1359 PMC 1757393 PMID 14570824 Wiebe Samuel Blume Warren T Girvin John P Eliasziw Michael 2001 A Randomized Controlled Trial of Surgery for Temporal Lobe Epilepsy New England Journal of Medicine 345 5 311 318 doi 10 1056 NEJM200108023450501 PMID 11484687 S2CID 31539171 Zeman Adam Kapur Narinder Jones Gotman Marilyn 2012 Epilepsy and memory 1 ed Oxford Oxford Univ Press ISBN 978 0199580286 Retrieved from https en wikipedia org w index php title Temporal lobe epilepsy amp oldid 1221922233, wikipedia, wiki, book, books, library,

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