Padaczka płata czołowego
Patofizjologia i mechanizm

Padaczka płata czołowego (FLE) jest drugą najczęstszą postacią padaczki ogniskowej, charakteryzującą się napadami zogniskowanymi w płacie czołowym, który obejmuje obszary grzbietowo-boczne, przyśrodkowo-oczodołowe i dolno-oczodołowe. Etiologia FLE jest heterogenna i obejmuje wady rozwojowe korowe (zwłaszcza dysplazję korową typu II), guzy mózgu (stanowiące około 33% przypadków lekoopornej FLE), urazy głowy, malformacje naczyniowe, gliozę, infekcje oraz czynniki genetyczne, w tym mutacje w genach CHRNA2, CHRNA4 i CHRNB2 związane z autosomalnie dominującą nocną padaczką płata czołowego (ADNFLE/SHE). Na poziomie komórkowym napady wynikają z nierównowagi między pobudzeniem a hamowaniem w sieciach neuronów korowych, manifestującej się elektroencefalograficznie jako ogniskowe międzynapadowe wyładowania epileptogenne (iglice, fale ostre) oraz napadowe przesunięcie depolaryzacyjne (PDS). Mechanizmy patofizjologiczne obejmują zmniejszenie hamowania, wadliwą aktywację neuronów GABA oraz zwiększoną aktywację pobudzającą, co może prowadzić do farmakologicznej oporności.

Patogeneza padaczki płata czołowego

Padaczka płata czołowego (ang. frontal lobe epilepsy, FLE) jest drugą co do częstości występowania postacią padaczki ogniskowej, charakteryzującą się nawracającymi napadami, których ognisko znajduje się w płacie czołowym mózgu. Płat czołowy stanowi największy płat mózgu i jest podzielony na obszary grzbietowo-boczne, przyśrodkowo-oczodołowe i dolno-oczodołowe. Ze względu na swoją wielkość i złożoność połączeń, napady wywodzące się z różnych obszarów płata czołowego mogą wykazywać odmienne cechy kliniczne.123

Czynniki etiologiczne i patofizjologiczne

Padaczka płata czołowego może mieć różnorodną etiologię. Zmiany w tkance mózgowej, infekcje, urazy, udary mózgu, guzy lub inne choroby mogą wywoływać napady padaczkowe w płacie czołowym. U około połowy osób z padaczką płata czołowego przyczyna pozostaje nieznana.456

Do najczęstszych przyczyn padaczki płata czołowego należą:

  • Wady rozwojowe korowe (dysplazja korowa typu II jest najczęstszym podłożem etiologicznym w lekoopornej padaczce płata czołowego)78
  • Guzy mózgu (stanowią około jednej trzeciej przypadków lekoopornej padaczki płata czołowego)9
  • Urazy głowy (bardzo częsta przyczyna uszkodzeń płatów czołowych)10
  • Malformacje naczyniowe (tętniczo-żylne, naczyniaki jamiste i żylne)11
  • Glioza (identyfikowana w wielu próbkach patologicznych po resekcji chirurgicznej)12
  • Infekcje mózgu (chociaż zapalenie mózgu częściej wywołuje padaczkę płata skroniowego, napady płata czołowego również mogą występować)13
  • Czynniki genetyczne (szczególnie w przypadku autosomalnie dominującej padaczki nocnej płata czołowego)1415

Mechanizmy molekularne i komórkowe

Na poziomie komórkowym, wystąpienie napadu padaczkowego wiąże się z nagłą nierównowagą między siłami pobudzającymi i hamującymi w sieci neuronów korowych na korzyść nagłego, netto pobudzenia. Elektroencefalograficznym (EEG) wyznacznikiem napadów padaczkowych płata czołowego są ogniskowe międzynapadowe wyładowania epileptogenne w postaci iglic lub fal ostrych.16

Komórkowy korelat neuropsychologiczny międzynapadowego ogniskowego wyładowania epileptogennego w pojedynczych neuronach korowych to napadowe przesunięcie depolaryzacyjne (ang. paroxysmal depolarization shift, PDS). W normalnych warunkach po każdym potencjale czynnościowym występuje okres refrakcji, ale w PDS brak okresu refrakcji powoduje przedłużoną depolaryzację błony komórkowej.17

Kilka mechanizmów może współistnieć w różnych kombinacjach, powodując napady ogniskowe płata czołowego:

  • Zmniejszenie hamowania
  • Wadliwa aktywacja neuronów GABA
  • Zwiększona aktywacja

Jeśli mechanizmy prowadzące do zwiększonej pobudliwości staną się trwałymi zmianami, u pacjentów może rozwinąć się farmakologicznie oporna padaczka ogniskowa.18

Genetyczne podłoża padaczki płata czołowego

Szczególnie interesująca z perspektywy patogenezy jest autosomalnie dominująca nocna padaczka płata czołowego (ADNFLE), obecnie nazywana również autosomalnie dominującą padaczką z napadami hipermotorycznymi związanymi ze snem (SHE). Ten zespół padaczkowy jest związany z mutacjami w genach kodujących podjednostki nikotynowego receptora acetylocholiny (nAChR): CHRNA2, CHRNA4 i CHRNB2.192021

Badania wykazały, że mutacje w tych genach wpływają na normalnie uwalnianie i wychwyt niektórych neuroprzekaźników w mózgu. Wynikające z tego zmiany w sygnalizacji między neuronami prawdopodobnie wyzwalają nieprawidłową aktywność mózgu związaną z napadami. Nie jest jednak jasne, dlaczego mutacje w genach CHRNA2, CHRNA4 i CHRNB2 powodują napady w płatach czołowych, a nie w innych częściach mózgu, a także dlaczego napady te występują najczęściej podczas snu.22

Mutacja Ser284Leu w genie CHRNA4 została zidentyfikowana w kilku niepowiązanych ze sobą rodzinach. Badania ekspresji in vitro wskazują, że wszystkie mutacje CHRNA4 zwiększają wrażliwość receptora na acetylocholinę, sugerując zysk funkcji.2324

Mechanizmy napadów w padaczce płata czołowego

Sieci neuronalne i neuroanatomiczne podłoże napadów

Napady padaczkowe płata czołowego można kategoryzować pod względem semiologii, co koreluje z organizacją anatomiczną wzdłuż osi przednio-tylnej, zgodnie z obecnymi hipotezami dotyczącymi hierarchicznej organizacji płata czołowego. Analiza napadowych zachowań ruchowych w napadach przedczołowych, w tym stereotypii, prowadzi do rozszyfrowania sieci korowo-podkorowych, które produkują takie zachowania.25

W zależności od zajętego obszaru płata czołowego, napady wykazują charakterystyczne cechy. Napady pochodzące z kory ruchowej mają wczesne manifestacje ruchowe, mogą występować podczas snu i brakuje im fazy ponapadowej.26

Napady wywodzące się z różnych obszarów płata czołowego charakteryzują się odmiennymi wzorcami:2728

  • Kora ruchowa pierwotna: Jednostronne skurcze kloniczne lub czasem toniczne lub miokloniczne po stronie przeciwnej do ogniska padaczkowego. Mogą rozprzestrzeniać się na sąsiednie obszary (marsz Jacksona)
  • Dodatkowa kora ruchowa (SMA): Asymetryczne obustronne napięcie toniczne, z zaburzeniami świadomości lub bez nich. Może wystąpić wyprost kończyny górnej przeciwstronnej do półkuli, w której rozpoczął się napad, oraz zgięcie ipsilateralnej kończyny górnej (postawa szermiercza)
  • Kora oczodołowo-czołowa: Zazwyczaj zaburzenie świadomości i automatyzmy, które mogą ewoluować do złożonych napadów ruchowych. Czasami występują aury węchowe i mogą występować objawy autonomiczne, takie jak tachykardia napadowa
  • Kora biegunowa czołowa: Często rozpoczyna się od zaburzeń świadomości i postępuje, pokazując inne cechy ruchowe
  • Regiony brzuszno-przyśrodkowe przedczołowe, w tym przednia część zakrętu obręczy: Związane z wymuszonym myśleniem i mają cechy hiperkinetyczne; pacjenci mogą wydawać się przestraszeni

Mechanizmy zaburzenia świadomości w napadach płata czołowego

Zaburzenie świadomości jest poważną manifestacją kliniczną padaczki, mającą negatywne konsekwencje dla jakości życia. Mechanizmy zaburzonej świadomości w napadach płata czołowego różnią się od mechanizmów obserwowanych w napadach płata skroniowego.2930

W napadach płata skroniowego zaburzona świadomość jest związana z rozproszonymi wolnymi falami korowymi (1-4 Hz), podczas gdy w napadach płata czołowego zaburzona świadomość wiąże się z szerokimi wzrostami mocy wysokiej częstotliwości w całej korze.31

Badania z wykorzystaniem wewnątrzczaszkowego EEG wykazały, że napady płata czołowego z zachowaną świadomością wykazują około 40% wzrost mocy EEG zlokalizowany w płacie czołowym, gdzie rozpoczyna się napad, z relatywnie mniejszymi zmianami w innych regionach korowych. Napady płata czołowego z zaburzoną świadomością wykazują około 50% wzrost mocy EEG, znacząco większy niż napady z zachowaną świadomością w innych szerokich regionach korowych.32

W przeciwieństwie do zmniejszonego pobudzenia podkorowego wywołującego wolne fale korowe w napadach płata skroniowego, napady płata czołowego wydają się upośledzać świadomość z powodu szerokiego rozprzestrzeniania się aktywności napadowej w różnych pasmach częstotliwości w całym mózgu.33

Zmiany strukturalne i funkcjonalne w padaczce płata czołowego

U pacjentów z padaczką płata czołowego obserwuje się zmienioną łączność strukturalną i przyczynową. Wykazano zmniejszenie objętości istoty szarej w obu jądrach ogoniastych i prawej gałce bladej, a także zmienioną przyczynowość ze zwiększonym i zmniejszonym przepływem przyczynowym z prawego jądra ogoniastego do dolnego zakrętu czołowego-trójkątnego, z obustronnej gałki bladej do prawego środkowego zakrętu czołowego i przyśrodkowo-oczodołowego zakrętu czołowego, reprezentujących obszary wykonawcze płata czołowego.34

Obserwacje te wskazują na upośledzenie w obrębie układu wykonawczego i kontrolowanego motorycznie, obejmującego móżdżek, regiony czołowe, jądro ogoniaste i gałkę bladą u pacjentów z padaczką płata czołowego.35

U pacjentów z lekooporną padaczką płata czołowego zaobserwowano znaczące zmniejszenie amplitudy fluktuacji niskiej częstotliwości (ALFF) w brzuszno-przyśrodkowej korze przedczołowej (vmPFC), ważnym węźle sieci stanu spoczynkowego (DMN), ściśle połączonym z układem limbicznym. Zmniejszenie ALFF w vmPFC wskazuje na bardziej specyficzną interakcję padaczki z układem afektywnym, co może tłumaczyć współwystępujące zaburzenia behawioralne i emocjonalne u pacjentów z padaczką płata czołowego.36

Dysplazja korowa typu II w patogenezie padaczki płata czołowego

Dysplazja korowa typu II (typu Taylora) jest najczęstszym podłożem etiologicznym padaczki nocnej płata czołowego. Charakteryzuje się obecnością dysplastycznych neuronów, połączonych przez nieprawidłowy obwód GABAergiczny, oraz tzw. komórek balonowatych (BC).37

Dysplazja korowa typu IIb stanowi interesujący model in vivo do badania związku między mechanizmami snu a epileptogenezą, a także szczególny model in vitro do badań farmakologicznych.38

Inhibicja w napadach płata czołowego

W porównaniu do napadów płata skroniowego, napady płata czołowego mają swoją specyfikę w zakresie mechanizmów hamujących. W badaniach porównujących czas trwania napadów płata czołowego i skroniowego stwierdzono, że wtórne uogólnienie napadów nie przedłuża czasu trwania napadu w padaczce płata czołowego, w przeciwieństwie do padaczki płata skroniowego.39

Sugeruje to, że w padaczce płata czołowego mechanizmy hamujące są aktywowane wcześniej niż w padaczce płata skroniowego, dlatego wtórne uogólnienie nie przedłuża czasu trwania napadu w padaczce płata czołowego.40

Inne mechanizmy patofizjologiczne

Napady asymetryczne toniczne pochodzące z płata ciemieniowego

Interesującym mechanizmem jest możliwość wystąpienia napadów toniczno-asymetrycznych przypominających napady płata czołowego u pacjentów z obustronnymi zmianami w płatach ciemieniowych. W tych przypadkach napady toniczne najprawdopodobniej wynikają z rozprzestrzeniania się aktywności napadowej z uszkodzeń ciemieniowych poprzez górny pęczek podłużny do dodatkowej kory ruchowej (SMA).41

Hipoteza zakłada, że obustronne homologiczne zmiany ciemieniowe mogą powodować odhamowanie aktywności napadowej, która może łatwo rozprzestrzeniać się do płata czołowego, generując napady pochodzące z płata czołowego jako strefę symptomatogenną, odległą od strefy epileptogennej.42

Zmiany metaboliczne i funkcjonalne

Badania z zastosowaniem nowoczesnych technik neuroobrazowania, takich jak tomografia emisyjna pojedynczego fotonu (SPECT) i SISCOM (subtraction ictal SPECT coregistered to MRI), pomagają zidentyfikować obszar generujący napady. Techniki te umożliwiają obserwację zmian metabolicznych i funkcjonalnych towarzyszących napadom padaczkowym płata czołowego.43

Typ napadu płata czołowego Obszar anatomiczny Główne manifestacje kliniczne Mechanizmy patofizjologiczne
Napady ruchowe ogniskowe Kora ruchowa pierwotna Jednostronna aktywność kloniczna, toniczno-kloniczna, toniczna lub mioklonia Bezpośrednia aktywacja kory ruchowej, marsz Jacksona
Napady dodatkowej kory ruchowej Dodatkowa kora ruchowa (SMA) Asymetryczne obustronne napięcie toniczne, postawa szermiercza Aktywacja sieci neuronalnych SMA
Napady czołowo-oczodołowe Kora oczodołowo-czołowa Objawy sensomotoryczne ust i języka, trudności w mówieniu (dyzartria) i ślinienie się Zaangażowanie sieci autonomicznych, emocjonalnych i poznawczych
Napady hiperkinetyczne Przednia część płata czołowego Ruchy pedałujące, kopanie, pchnięcia miednicy Odhamowanie funkcji ruchowych
Napady nocne płata czołowego Różne obszary płata czołowego Krótkie napady motoryczne nocne, często występujące w klastrach Mutacje genów nAChR, dysregulacja cyklu sen-czuwanie

Podsumowanie mechanizmów patogenetycznych

Padaczka płata czołowego jest heterogennym zespołem o różnorodnej etiologii, charakteryzującym się występowaniem napadów związanych ze snem o różnych manifestacjach ruchowych i afektywnych, zależnych od zaangażowanych sieci neuronalnych w obrębie płata czołowego.44

Mechanizmy leżące u podstaw tej padaczki obejmują zarówno czynniki genetyczne (zwłaszcza mutacje w genach kodujących podjednostki receptorów nikotynowych), jak i strukturalne (dysplazja korowa, guzy, urazy). W przeciwieństwie do napadów płata skroniowego, gdzie zaburzona świadomość wiąże się z wolnymi falami korowymi, w napadach płata czołowego zaburzona świadomość jest związana z szerokim wzrostem aktywności mózgu w różnych zakresach częstotliwości.45

Zrozumienie mechanizmów padaczki płata czołowego przyczynia się do opracowania skuteczniejszych metod leczenia, zarówno farmakologicznych, jak i chirurgicznych, a także do lepszego zarządzania zaburzeniami snu i świadomości związanymi z tą chorobą.46

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  1. 10.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 The Anatomical Basis of Seizures – Epilepsy – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK580614/
    The frontal lobe is divided into dorsolateral, medial orbital, and inferior orbital. […] Frontal lobe seizures originating in the primary motor area has early motor manifestations, it may occur during sleep, and lack post-ictal phase. […] Frontal lobe epilepsy is one of the commonest types of focal epilepsy. […] Frontal lobe pathology may lead to atrophy of the rostral corpus callosum in juvenile myoclonic epilepsy. […] Frontal lobe epilepsy is presented as contralateral clonic movement, unilateral or bilateral tonic activity or complex automatism. […] Abnormal thalamus and frontal lobe volumes are seen in children with idiopathic generalized epilepsies.
  • #2 FRONTAL LOBE SEIZURE
    https://www.epilepsydiagnosis.org/seizure/frontal-lobe-overview.html
    The frontal lobe is the largest lobe. Seizures involving frontal lobe network have distinctive features depending on the area of the frontal lobe involved. Motor features are prominent and may be hyperkinetic (e.g. pelvic thrusting, bipedal kicking or pedalling) or asymmetric tonic in nature. […] Seizures are typically brief overall, and can have prominent vocalization, bizarre behavior, urinary incontinence, and head and eye deviation. Seizures may be exclusively nocturnal and often cluster. The ictal EEG may not show ictal patterns or may be obscured by movement artifact. […] When awareness is impaired, focal impaired awareness seizures of frontal origin can be difficult to distinguish from absence seizures. […] Frontal lobe seizures may be mis-diagnosed as non-epileptic seizures as there may be bilateral motor phenomena with preserved awareness, and the ictal EEG can be normal.
  • #3 Localisation in focal epilepsy: a practical guide | Practical Neurology
    https://pn.bmj.com/content/21/6/481
    The frontal lobe is the largest lobe of the brain. Its high connectivity with other cortical regions can result in rapid, widespread ictal propagation. Moreover, some of the semiological features from more rostral areas may result more from disinhibition (removal of higher cortical control) than from direct activation. Together, these can make frontal lobe seizure semiology complex and difficult to interpret. Nevertheless, seizures have characteristic patterns depending on the area of the frontal lobe involved. In general, frontal lobe seizures are typically brief, may cluster, can have prominent vocalisation and commonly occur from sleep. Motor features are prominent and include various different motor phenomena, including simple clonic movements, tonic posturing and eye deviation, or more complex movements such as cycling, rocking and grimacing. Seizures can appear bizarre, with bilateral motor phenomena, but with retained awareness. Ictal scalp EEG may show no changes if there is a deep source, or may be obscured by movement artefact, and so frontal lobe seizures may be mistaken for dissociative (non-epileptic) attacks.
  • #4 Frontal lobe seizures – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/frontal-lobe-seizures/symptoms-causes/syc-20353958
    Frontal lobe seizures are a common form of epilepsy. Epilepsy is a brain disorder in which clusters of brain cells send a burst of electrical signals. This causes movements that can’t be controlled, known as seizures. Frontal lobe seizures begin in the front of the brain, the area known as the frontal lobe. […] Changes in brain tissue, infection, injury, stroke, tumors or other conditions can cause frontal lobe seizures. […] Frontal lobe seizures can be caused by tumors, stroke, infection or traumatic injuries in the brain’s frontal lobes. […] For about half of people who have frontal lobe epilepsy, the cause is not known.
  • #5 Frontal lobe seizures | Health Library | Memorial Health System
    https://www.mhsystem.org/health-library/con-20197154/
    Frontal lobe seizures are a common form of epilepsy. […] Changes in brain tissue, infection, injury, stroke, tumors or other conditions can cause frontal lobe seizures. […] Frontal lobe seizures can be caused by tumors, stroke, infection or traumatic injuries in the brains frontal lobes. […] Frontal lobe seizures also are associated with a rare inherited disorder called autosomal dominant nocturnal frontal lobe epilepsy. […] For about half of people who have frontal lobe epilepsy, the cause is not known. […] Frontal lobe seizures tend to occur in clusters. […] Seizures that last longer than five minutes are medical emergencies. […] Frontal lobe epilepsy can be hard to diagnose. […] To make a diagnosis, a health care professional reviews your symptoms and medical history. […] Imaging techniques can help identify the area generating seizures. […] If your seizures cant be controlled with medicines, surgery might be an option. […] If you have surgery for frontal lobe seizures, its likely youll need anti-seizure medicine after the surgery. […] Researchers are continuing to look for new and more-effective medicines.
  • #6 Frontal lobe seizures | Beacon Health System
    https://www.beaconhealthsystem.org/library/diseases-and-conditions/frontal-lobe-seizures?content_id=CON-20197154
    Frontal lobe seizures are a common form of epilepsy. Epilepsy is a brain disorder in which clusters of brain cells send a burst of electrical signals. This causes movements that can’t be controlled, known as seizures. Frontal lobe seizures begin in the front of the brain, the area known as the frontal lobe. […] Changes in brain tissue, infection, injury, stroke, tumors or other conditions can cause frontal lobe seizures. […] Frontal lobe seizures can be caused by tumors, stroke, infection or traumatic injuries in the brain’s frontal lobes. […] Frontal lobe seizures also are associated with a rare inherited disorder called autosomal dominant nocturnal frontal lobe epilepsy. This form of epilepsy causes brief seizures during sleep. […] For about half of people who have frontal lobe epilepsy, the cause is not known.
  • #7 Frontal Lobe Epilepsy: Practice Essentials, Background, Etiology
    https://emedicine.medscape.com/article/1184076-overview
    Frontal lobe epilepsy is characterized by recurrent seizures arising from the frontal lobes. Frequently, seizure types are focal onset with preserved or impaired awareness, often with progression to bilateral tonic-clonic activity. […] Disease conditions commonly associated with frontal lobe epilepsy are frequently symptomatic, including congenital causes (such as cortical dysgenesis, gliosis, vascular malformations), neoplasms, head trauma, infections, and anoxia. […] With improvements in neuroimaging, focal cortical dysplasias are increasingly being identified as epileptogenic lesions. […] Reviews indicate that the epileptogenic lesion in approximately one third of patients with refractory frontal lobe seizures is a tumor. […] Head trauma is a very frequent cause of damage to the frontal lobes.
  • #8
    https://link.springer.com/article/10.1007/s11910-013-0424-6
    Studies, conducted in patients with drug-resistant epilepsy, have shown that type II focal cortical dysplasia (type II FCD; Taylor-type cortical dysplasia) is the most frequent etiological substrate of NFLE. […] Type IIb FCD is characterized by the presence of dysmorphic neurons, connected through an abnormal GABAergic circuit, and the so-called balloon cells (BC). […] Type IIb FCD seems to be an interesting in vivo model to study the relationship between sleep mechanisms and epileptogenesis, as well as a peculiar in vitro model for pharmacological studies. […] The increasing complexity of NFLE ictal motor behaviors, from minor to major events, reflects a different duration and propagation of the discharge within the frontal lobe. […] It has been shown that the seizure onset in patients with asymmetric tonic or dystonic posturing is generally localized in the posterior portion of the frontal cingulated gyrus and in the posterior mesial frontal cortex with a primary involvement of the supplementary motor area.
  • #9 Frontal Lobe Epilepsy: Practice Essentials, Background, Etiology
    https://emedicine.medscape.com/article/1184076-overview
    Frontal lobe epilepsy is characterized by recurrent seizures arising from the frontal lobes. Frequently, seizure types are focal onset with preserved or impaired awareness, often with progression to bilateral tonic-clonic activity. […] Disease conditions commonly associated with frontal lobe epilepsy are frequently symptomatic, including congenital causes (such as cortical dysgenesis, gliosis, vascular malformations), neoplasms, head trauma, infections, and anoxia. […] With improvements in neuroimaging, focal cortical dysplasias are increasingly being identified as epileptogenic lesions. […] Reviews indicate that the epileptogenic lesion in approximately one third of patients with refractory frontal lobe seizures is a tumor. […] Head trauma is a very frequent cause of damage to the frontal lobes.
  • #10 Frontal Lobe Epilepsy: Practice Essentials, Background, Etiology
    https://emedicine.medscape.com/article/1184076-overview
    Frontal lobe epilepsy is characterized by recurrent seizures arising from the frontal lobes. Frequently, seizure types are focal onset with preserved or impaired awareness, often with progression to bilateral tonic-clonic activity. […] Disease conditions commonly associated with frontal lobe epilepsy are frequently symptomatic, including congenital causes (such as cortical dysgenesis, gliosis, vascular malformations), neoplasms, head trauma, infections, and anoxia. […] With improvements in neuroimaging, focal cortical dysplasias are increasingly being identified as epileptogenic lesions. […] Reviews indicate that the epileptogenic lesion in approximately one third of patients with refractory frontal lobe seizures is a tumor. […] Head trauma is a very frequent cause of damage to the frontal lobes.
  • #11 Frontal Lobe Epilepsy: Practice Essentials, Background, Etiology
    https://emedicine.medscape.com/article/1184076-overview
    Three main types are recognized: arteriovenous malformations, cavernous angiomas, and venous angiomas. […] Gliosis is identified in many pathologic specimens following surgical resection for frontal lobe epilepsy. […] Although encephalitis commonly produces temporal lobe epilepsy, frontal lobe seizures may occur. […] The seizures of autosomal dominant sleep-related hypermotor epilepsy (SHE)(formerly known as ADNFLE for autosomal dominant nocturnal frontal lobe epilepsy), which are mostly originating in the frontal lobe, are clinically characterized by brief, nocturnal motor seizures that often occur in clusters, mainly during non-REM sleep. Seizure onset is typically in childhood, but can range from infancy to adulthood. […] Approximately 65-75% of patients with frontal lobe seizures respond to appropriate antiseizure medications and become seizure free. However, approximately 30% of patients will be intractable, many of whom will continue to have frequent nocturnal seizures.
  • #12 Frontal Lobe Epilepsy: Practice Essentials, Background, Etiology
    https://emedicine.medscape.com/article/1184076-overview
    Three main types are recognized: arteriovenous malformations, cavernous angiomas, and venous angiomas. […] Gliosis is identified in many pathologic specimens following surgical resection for frontal lobe epilepsy. […] Although encephalitis commonly produces temporal lobe epilepsy, frontal lobe seizures may occur. […] The seizures of autosomal dominant sleep-related hypermotor epilepsy (SHE)(formerly known as ADNFLE for autosomal dominant nocturnal frontal lobe epilepsy), which are mostly originating in the frontal lobe, are clinically characterized by brief, nocturnal motor seizures that often occur in clusters, mainly during non-REM sleep. Seizure onset is typically in childhood, but can range from infancy to adulthood. […] Approximately 65-75% of patients with frontal lobe seizures respond to appropriate antiseizure medications and become seizure free. However, approximately 30% of patients will be intractable, many of whom will continue to have frequent nocturnal seizures.
  • #13 Frontal Lobe Epilepsy: Practice Essentials, Background, Etiology
    https://emedicine.medscape.com/article/1184076-overview
    Three main types are recognized: arteriovenous malformations, cavernous angiomas, and venous angiomas. […] Gliosis is identified in many pathologic specimens following surgical resection for frontal lobe epilepsy. […] Although encephalitis commonly produces temporal lobe epilepsy, frontal lobe seizures may occur. […] The seizures of autosomal dominant sleep-related hypermotor epilepsy (SHE)(formerly known as ADNFLE for autosomal dominant nocturnal frontal lobe epilepsy), which are mostly originating in the frontal lobe, are clinically characterized by brief, nocturnal motor seizures that often occur in clusters, mainly during non-REM sleep. Seizure onset is typically in childhood, but can range from infancy to adulthood. […] Approximately 65-75% of patients with frontal lobe seizures respond to appropriate antiseizure medications and become seizure free. However, approximately 30% of patients will be intractable, many of whom will continue to have frequent nocturnal seizures.
  • #14 Frontal Lobe Epilepsy: Practice Essentials, Background, Etiology
    https://emedicine.medscape.com/article/1184076-overview
    Three main types are recognized: arteriovenous malformations, cavernous angiomas, and venous angiomas. […] Gliosis is identified in many pathologic specimens following surgical resection for frontal lobe epilepsy. […] Although encephalitis commonly produces temporal lobe epilepsy, frontal lobe seizures may occur. […] The seizures of autosomal dominant sleep-related hypermotor epilepsy (SHE)(formerly known as ADNFLE for autosomal dominant nocturnal frontal lobe epilepsy), which are mostly originating in the frontal lobe, are clinically characterized by brief, nocturnal motor seizures that often occur in clusters, mainly during non-REM sleep. Seizure onset is typically in childhood, but can range from infancy to adulthood. […] Approximately 65-75% of patients with frontal lobe seizures respond to appropriate antiseizure medications and become seizure free. However, approximately 30% of patients will be intractable, many of whom will continue to have frequent nocturnal seizures.
  • #15 Frontal Lobe Seizures: Causes, Symptoms & Treatment
    https://my.clevelandclinic.org/health/diseases/17011-frontal-lobe-epilepsy
    Frontal lobe epilepsy is a pattern of abnormal electrical activity in the front part of your brain, behind your forehead. It causes frontal lobe seizures that usually happen at night. […] Frontal lobe epilepsy is a type of seizure disorder affecting your frontal lobes. It causes frontal lobe seizures, which is a pattern of abnormal electrical activity in your brain. […] Frontal lobe seizures are a type of focal (partial) seizure. This means that the seizures start in one area of your brain. Seizures can start on either the left or right frontal lobe. […] Abnormal electrical activity in your frontal lobe causes frontal lobe epilepsy. Neurons (nerve cells) usually send signals to other cells in your brain. When a frontal lobe seizure happens, neurons fire signals uncontrollably. […] Common reasons why this may happen could include: Abnormal formation of your brain during fetal development, Brain infections, Stroke, Traumatic brain injury, Brain tumor, Genetic variations.
  • #16 Epilepsy and Seizures: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/1184846-overview
    Seizures are paroxysmal manifestations of the electrical properties of the cerebral cortex. A seizure results when a sudden imbalance occurs between the excitatory and inhibitory forces within the network of cortical neurons in favor of a sudden-onset net excitation. […] The pathophysiology of focal-onset seizures differs from the mechanisms underlying generalized-onset seizures. Overall, cellular excitability is increased, but the mechanisms of synchronization appear to substantially differ between these 2 types of seizure and are therefore discussed separately. […] The electroencephalographic (EEG) hallmark of focal-onset seizures is the focal interictal epileptiform spike or sharp wave. The cellular neurophysiologic correlate of an interictal focal epileptiform discharge in single cortical neurons is the paroxysmal depolarization shift (PDS).
  • #17 Epilepsy pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Epilepsy_pathophysiology
    It is understood that epileptic seizure is the result of uncontrolled unusual synchronized, localized or widely distributed neuronal electrical discharges. […] The underlying event in all types of seizures is the paroxysmal depolarization shift (PDS) which also causes the EEG changes. […] In a normal circumstance we have a refractory period after every action potential, but in PDS, the absence of refractory period causes a prolonged membrane depolarization. […] The likelihood of PDS happening depends on so many factors such as intrinsic neuronal characteristic (channelopathies) and extrinsic characteristics (excess excitatory or inadequate inhibitory neurotransmitters). […] In order to cause a seizure, so many PDSs most happen in the same time. […] Any alternation in a synaptic characteristics can prone a person to epilepsy. They include: Amount of neurotransmitters, Function of inhibitory neurons, Function of excitatory neurons, Synaptic structure, Ion channels involved in neurotransmitter release and conduction of action potential.
  • #18 Epilepsy and Seizures: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/1184846-overview
    Several factors may be associated with the transition from an interictal spike to an epileptic seizure. The spike has to recruit more neural tissue to become a seizure. When any of the mechanisms that underlie an acute seizure becomes a permanent alteration, the person presumably develops a propensity for recurrent seizures (ie, epilepsy). […] The following mechanisms (discussed below) may coexist in different combinations to cause focal-onset seizures: Decreased inhibition, Defective activation of gamma-aminobutyric acid (GABA) neurons, Increased activation. […] If the mechanisms leading to a net increased excitability become permanent alterations, patients may develop pharmacologically intractable focal-onset epilepsy. […] Currently available medications were screened using acute models of focal-onset or generalized-onset convulsions. In clinical use, these agents are most effective at blocking the propagation of a seizure (ie, spread from the epileptic focus to secondary generalized tonic-clonic seizures). Further understanding of the mechanisms that permanently increase network excitability may lead to development of true antiepileptic drugs that alter the natural history of epilepsy.
  • #19 Autosomal dominant nocturnal frontal lobe epilepsy: MedlinePlus GeneticsLock
    https://medlineplus.gov/genetics/condition/autosomal-dominant-nocturnal-frontal-lobe-epilepsy/
    Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is an uncommon form of epilepsy that runs in families. […] The seizures associated with ADNFLE begin in areas of the brain called the frontal lobes. These regions of the brain are involved in many critical functions, including reasoning, planning, judgment, and problem-solving. […] Researchers believe that mutations in the CHRNA2, CHRNA4, and CHRNB2 genes affect the normal release and uptake of certain neurotransmitters in the brain. The resulting changes in signaling between neurons likely trigger the abnormal brain activity associated with seizures. […] It is unclear why mutations in the CHRNA2, CHRNA4, and CHRNB2 genes cause seizures in the frontal lobes rather than elsewhere in the brain. Researchers are also working to determine why these seizures occur most often during sleep.
  • #20 Nocturnal frontal lobe epilepsy: Symptoms, causes, and more
    https://www.medicalnewstoday.com/articles/nocturnal-frontal-lobe-epilepsy
    Mutations in specific genes, including CHRNA2, CHRNA4, and CHRNB2, can lead to SHE, as can KCNT1, DEPDC5, NPRL2, and others. […] SHE is autosomal dominant, which means a person only needs to inherit a single copy of the mutated gene to develop the condition. […] The healthcare professional will use the video EEG to confirm SHE and other measures to guide diagnosis. […] Treatment for SHE usually involves medications. […] Medications cannot stop seizures for around 3 in 10 people with SHE. […] No cure is available for SHE, but medications and other treatments may help people control symptoms. […] SHE does not get worse over time. […] However, for many people, seizures become milder and less frequent as they get older. […] SHE can occur due to focal cortical dysplasia, injury, or genetic mutations. […] Diagnosing SHE can be complex, but a video EEG and genetic testing can help confirm an SHE diagnosis. […] Treatment typically includes anti-seizure medications, but these do not always work.
  • #21
    https://omim.org/entry/600513
    A number sign (#) is used with this entry because of evidence that nocturnal frontal lobe epilepsy-1 (ENFL1) is caused by heterozygous mutation in the gene encoding the neuronal nicotinic acetylcholine receptor (nAChR) alpha-4 subunit (CHRNA4; 118504) on chromosome 20q13. […] Autosomal dominant nocturnal frontal lobe epilepsy (ENFL, ADNFLE) is a partial epilepsy with frontal lobe seizure semiology. It is characterized by childhood onset of frequent violent and brief motor seizures occurring at night. […] Nocturnal frontal lobe seizures are also observed in some patients with familial focal epilepsy with variable foci (FFEVF; 604364), caused by mutation in the DEPDC5 gene (614191) on chromosome 22q12. […] The transmission pattern of nocturnal frontal lobe epilepsy in the large Australian family reported by Scheffer et al. (1995) was consistent with autosomal dominant inheritance with incomplete penetrance.
  • #22 Autosomal dominant nocturnal frontal lobe epilepsy: MedlinePlus GeneticsLock
    https://medlineplus.gov/genetics/condition/autosomal-dominant-nocturnal-frontal-lobe-epilepsy/
    Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is an uncommon form of epilepsy that runs in families. […] The seizures associated with ADNFLE begin in areas of the brain called the frontal lobes. These regions of the brain are involved in many critical functions, including reasoning, planning, judgment, and problem-solving. […] Researchers believe that mutations in the CHRNA2, CHRNA4, and CHRNB2 genes affect the normal release and uptake of certain neurotransmitters in the brain. The resulting changes in signaling between neurons likely trigger the abnormal brain activity associated with seizures. […] It is unclear why mutations in the CHRNA2, CHRNA4, and CHRNB2 genes cause seizures in the frontal lobes rather than elsewhere in the brain. Researchers are also working to determine why these seizures occur most often during sleep.
  • #23 Autosomal dominant nocturnal frontal lobe epilepsy: a genotypic comparative study of Japanese and Korean families carrying the CHRNA4 Ser284Leu mutation | Journal of Human Genetics
    https://www.nature.com/articles/jhg201169
    Autosomal dominant nocturnal frontal lobe epilepsy is a familial partial epilepsy syndrome and the first human idiopathic epilepsy known to be related to specific gene defects. […] ADNFLE is the first human idiopathic epilepsy known to be related to specific gene defects. […] Among the four mutations in CHRNA4 (Ser280Phe, Ser284Leu, Leu291dup and Thr293Ile), Ser280Phe and Ser284Leu have been identified in several unrelated families […] The results obtained here do not support the hypothesis that the Ser284Leu mutations originated with a common founder. Association with a CpG site accounts for the independent occurrence of the Ser284Leu mutation. […] To explain it, we need to take into account ADNFLE development. One possible explanation is that ADNFLE is caused by mutations on a few functionally important sites within the M2.
  • #24 Autosomal dominant nocturnal frontal lobe epilepsy: a genotypic comparative study of Japanese and Korean families carrying the CHRNA4 Ser284Leu mutation | Journal of Human Genetics
    https://www.nature.com/articles/jhg201169
    Together with S280F, in vitro expression studies indicate that all CHRNA4 mutations increase receptor sensitivity to acethylcholine, suggesting gain of function. […] This is the first report comparing the haplotype structure of Japanese and Korean ADNFLE families. Further functional studies will be required to ascertain the ADNFLE’s pathophysiology.
  • #25 Frontal lobe seizures: from clinical semiology to localization – PubMed
    https://pubmed.ncbi.nlm.nih.gov/24372328/
    Frontal lobe seizures are difficult to characterize according to semiologic and electrical features. […] Four main groups of patients were identified according to semiologic features, and correlated with specific patterns of anatomic seizure localization. […] Meaningful categorization of frontal seizures in terms of semiology is possible and correlates with anatomic organization along a rostrocaudal axis, in keeping with current hypotheses of frontal lobe hierarchical organization. […] Furthermore, analysis of ictal motor behavior in prefrontal seizures, including stereotypies, leads to deciphering the cortico-subcortical networks that produce such behaviors.
  • #26 The Anatomical Basis of Seizures – Epilepsy – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK580614/
    The frontal lobe is divided into dorsolateral, medial orbital, and inferior orbital. […] Frontal lobe seizures originating in the primary motor area has early motor manifestations, it may occur during sleep, and lack post-ictal phase. […] Frontal lobe epilepsy is one of the commonest types of focal epilepsy. […] Frontal lobe pathology may lead to atrophy of the rostral corpus callosum in juvenile myoclonic epilepsy. […] Frontal lobe epilepsy is presented as contralateral clonic movement, unilateral or bilateral tonic activity or complex automatism. […] Abnormal thalamus and frontal lobe volumes are seen in children with idiopathic generalized epilepsies.
  • #27 Localisation in focal epilepsy: a practical guide | Practical Neurology
    https://pn.bmj.com/content/21/6/481
    The ictal onset patterns during intracranial studies with stereo-EEG show that elementary motor signs (clonic, tonic, versive) arise from precentral and premotor regions, while more complex motor signs arise from more rostral frontal regions. Non-integrated (less natural) gestural behaviour with proximal stereotypies, such as rocking and turning, are from premotor and posterior prefrontal regions, and more integrated (natural) gestural behaviour with distal stereotypies, such as manual automatisms, arise from more anterior prefrontal regions (orbitofrontal cortex, frontal pole, anterior cingulate). In clinical practice, these distinctions may be confounded by rapid propagation. […] Seizures from primary motor cortex comprise contralateral unilateral clonic or sometimes tonic or myoclonic activity that can spread to adjacent areas: the Jacksonian march, reflecting ictal activity spread through the motor cortex along the homunculus. It is therefore possible to distinguish lateral from medial precentral seizures, depending on whether the seizure starts in face, upper or lower limb. The spread is typically slow, representing the slow recruitment of neurones during tangential spread of the ictal wavefront.
  • #28 Localisation in focal epilepsy: a practical guide | Practical Neurology
    https://pn.bmj.com/content/21/6/481
    Seizures arising in the supplementary motor area (SMA) are characterised by asymmetric bilateral tonic posturing, with or without impaired awareness. There may be extension of the upper limb contralateral to the hemisphere of onset, and flexion of the ipsilateral upper limb, known as a fencing posture, along with head and eye deviation contralateral to the hemisphere of onset. […] Seizures arising from orbitofrontal cortex tend to have impaired awareness and automatisms, and may evolve to complex motor seizures. Olfactory auras occasionally occur and there may be autonomic features such as ictal tachycardia. Seizures arising from frontopolar cortex can also start with impaired awareness and progress to show other motor features. Seizures arising from ventromedial prefrontal regions, including anterior cingulate, have been associated with forced thinking and have hyperkinetic features; patients may appear to be frightened.
  • #29
    https://aesnet.org/abstractslisting/mechanism-of-impaired-consciousness-in-frontal-lobe-seizures-investigated-with-intracranial-eeg
    Consciousness is essential to normal human life, and its transient loss can have severe effects on morbidity and mortality. […] the mechanisms of impaired consciousness in frontal lobe seizures are not known. […] These results suggest that broad increases in high frequency power throughout the cortex are associated with impaired consciousness in focal frontal lobe seizures. […] These findings contrast with impaired consciousness in focal temporal lobe seizures, where impaired consciousness is associated with widespread cortical slow wave (1-4Hz) activity. […] We can speculate that different focal seizure types produce impaired consciousness by impacting widespread cortical regions but through different mechanisms.
  • #30 Frontal Lobe Seizures: Intracranial Markers Of Loss Of Consciousness
    https://elischolar.library.yale.edu/ymtdl/2124/
    Loss of consciousness is an important morbidity associated with epileptic seizures, and understanding how altered consciousness occurs could have impact on future therapies. […] Research on the mechanisms of loss of consciousness in frontal lobe epilepsy is not well defined, though loss of consciousness in frontal lobe seizures may be associated with widespread low voltage fast activity. […] Based on this data analysis, there is an increase of low voltage fast activity associated with frontal lobe seizures exhibiting loss of consciousness. […] These findings suggest a novel mechanism for loss of consciousness during frontal lobe seizures which may differ from temporal lobe seizures, and could guide improved treatments for frontal lobe epilepsy.
  • #31
    https://aesnet.org/abstractslisting/mechanism-of-impaired-consciousness-in-frontal-lobe-seizures-investigated-with-intracranial-eeg
    Consciousness is essential to normal human life, and its transient loss can have severe effects on morbidity and mortality. […] the mechanisms of impaired consciousness in frontal lobe seizures are not known. […] These results suggest that broad increases in high frequency power throughout the cortex are associated with impaired consciousness in focal frontal lobe seizures. […] These findings contrast with impaired consciousness in focal temporal lobe seizures, where impaired consciousness is associated with widespread cortical slow wave (1-4Hz) activity. […] We can speculate that different focal seizure types produce impaired consciousness by impacting widespread cortical regions but through different mechanisms.
  • #32 Widespread brain activity increases in frontal lobe seizures with impaired consciousness | bioRxiv
    https://www.biorxiv.org/content/10.1101/2024.09.20.614207v1
    Impaired consciousness is a serious clinical manifestation of epilepsy with negative consequences on quality of life. Little work has investigated impaired consciousness in frontal lobe seizures, a common form of focal epilepsy. […] We found that frontal lobe focal aware seizures showed approximately 40% increases in intracranial EEG power localized to the frontal lobe of seizure onset across frequency ranges, with relatively smaller changes in other cortical regions. Frontal lobe focal impaired awareness seizures showed approximately 50% increases in intracranial EEG power, not significantly different from focal aware seizures in the frontal lobe of seizure onset (P = 1.038), but significantly greater than focal aware seizures in other broad cortical regions (P < 0.001). [...] Our findings contrast with focal temporal lobe epilepsy, where impaired consciousness is associated with cortical slow waves. We can speculate that different focal seizure types produce impaired consciousness by impacting widespread cortical regions but through different physiological mechanisms. Insights gained by studying mechanisms of impaired consciousness may be the first step towards developing novel treatments to prevent this important negative consequence of epilepsy.
  • #33
    https://aesnet.org/abstractslisting/impaired-consciousness-in-frontal-lobe-seizures-is-associated-with-widespread-broad-band-intracranial-eeg-power-increase
    Impaired consciousness in frontal lobe seizures is associated with widespread broad-band intracranial EEG power increase. The mechanism of impaired consciousness in focal frontal lobe seizures has been studied less, and is the goal of the present investigation. We discovered that frontal lobe seizures with spared consciousness had significantly lower power than seizures with impaired consciousness. This study suggests there is a less specific mechanism occurring with the propagation of EEG signals in frontal lobe seizures compared to temporal lobe seizures that impair consciousness. Unlike the decreased subcortical arousal producing cortical slow waves in temporal lobe seizures, frontal lobe seizures appear to impair consciousness due to widespread dissemination of ictal activity in a variety of frequency bands throughout the brain. […] It is our goal to aid in improving treatments and preventing loss of consciousness in frontal lobe seizures through our future investigations.
  • #34 Altered structural and causal connectivity in frontal lobe epilepsy | BMC Neurology | Full Text
    https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-019-1300-z
    Albeit the few resting-state fMRI neuroimaging studies in frontal lobe epilepsy (FLE) patients, these studies focused on functional connectivity. The aim of this current study was to examine the effective connectivity based on voxel-based morphometry in FLE patients. […] Our results showed altered structural and effective connectivity. Compared with healthy controls, FLE patients showed reduced grey matter volume in bilateral putamen and right caudate as well as altered causality with increased, and decreased causal outflow from the right caudate (seed region) to inferior frontal gyrus-triangular, from bilateral putamen (seed regions) to right middle frontal gyrus and frontal gyrus medial-orbital representing the frontal executive areas, respectively. […] The findings point to the impairment within the executive and motor-controlled system including the cerebellum, frontal, caudate and putamen regions in FLE patients. These results would therefore enhance our understanding of structural and effective mechanisms in FLE.
  • #35 Altered structural and causal connectivity in frontal lobe epilepsy | BMC Neurology | Full Text
    https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-019-1300-z
    The current study shows reduced GMV in the bilateral putamen and caudate of FLE patients, which shows an impairment to various motor related processes. […] The evidence of these areas involvement in motor activity in epilepsy is consistent with our findings, which provides complimentary information about motor processes in FLE. […] The altered EC between the putamen/caudate and the cerebellar networks is thus consistent with functional evidences suggested in some studies of other types of epilepsy.
  • #36 Altered intrinsic brain activity associated with outcome in frontal lobe epilepsy | Scientific Reports
    https://www.nature.com/articles/s41598-019-45413-7
    We observed significant decreased ALFF of the vmPFC, an important hub of default mode network (DMN), closely connected to the limbic system. […] The decreased ALFF of vmPFC that we observed in the present study indicated a more specific, epilepsy-affective interaction, which could account for the behavioral and emotional comorbidities in patients with FLE. […] The implication of this finding could be quite impactful because the SMG is responsible for receptive language function and also involved in the sensation and perception of various stimuli and the SFG is notably associated with executive control and attention regulation. Therefore, the intrinsic function abnormalities in these brain regions could not only result in sensorimotor deficits in FLE, but may reveal further dysfunctional intrinsic activity as frontal lobe seizures become more frequent and intractable. […] This study did have several limitations. […] However, the underlying functional mechanism responsible for the variation in treatment outcomes remains unknown.
  • #37
    https://link.springer.com/article/10.1007/s11910-013-0424-6
    Studies, conducted in patients with drug-resistant epilepsy, have shown that type II focal cortical dysplasia (type II FCD; Taylor-type cortical dysplasia) is the most frequent etiological substrate of NFLE. […] Type IIb FCD is characterized by the presence of dysmorphic neurons, connected through an abnormal GABAergic circuit, and the so-called balloon cells (BC). […] Type IIb FCD seems to be an interesting in vivo model to study the relationship between sleep mechanisms and epileptogenesis, as well as a peculiar in vitro model for pharmacological studies. […] The increasing complexity of NFLE ictal motor behaviors, from minor to major events, reflects a different duration and propagation of the discharge within the frontal lobe. […] It has been shown that the seizure onset in patients with asymmetric tonic or dystonic posturing is generally localized in the posterior portion of the frontal cingulated gyrus and in the posterior mesial frontal cortex with a primary involvement of the supplementary motor area.
  • #38
    https://link.springer.com/article/10.1007/s11910-013-0424-6
    Studies, conducted in patients with drug-resistant epilepsy, have shown that type II focal cortical dysplasia (type II FCD; Taylor-type cortical dysplasia) is the most frequent etiological substrate of NFLE. […] Type IIb FCD is characterized by the presence of dysmorphic neurons, connected through an abnormal GABAergic circuit, and the so-called balloon cells (BC). […] Type IIb FCD seems to be an interesting in vivo model to study the relationship between sleep mechanisms and epileptogenesis, as well as a peculiar in vitro model for pharmacological studies. […] The increasing complexity of NFLE ictal motor behaviors, from minor to major events, reflects a different duration and propagation of the discharge within the frontal lobe. […] It has been shown that the seizure onset in patients with asymmetric tonic or dystonic posturing is generally localized in the posterior portion of the frontal cingulated gyrus and in the posterior mesial frontal cortex with a primary involvement of the supplementary motor area.
  • #39 Thieme E-Journals – Klinische Neurophysiologie / Abstract
    https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0029-1216170?innerWidth=981&offsetWidth=980&device=desktop&id=&lang=de
    Purpose: To evaluate the duration of seizures arising from the frontal and temporal lobes in order to better understand spread and inhibitory mechanisms involved. […] Results: Of the 130 seizures arising from the temporal lobes 13.8% generalized secondarily, compared to 24.3% secondary generalization in 103 seizures of FLE. […] In FLE patients, the average duration of non-generalized seizures (66s) did not differ from seizures that generalized secondarily (68s). Secondary generalization of ictal epileptic activity prolonged seizure duration in TLE but not in FLE. […] Conclusion: We conclude that in FLE, inhibitory mechanisms are activated earlier than in TLE and, therefore, secondary generalization does not prolong seizure duration in FLE.
  • #40 Thieme E-Journals – Klinische Neurophysiologie / Abstract
    https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0029-1216170?innerWidth=981&offsetWidth=980&device=desktop&id=&lang=de
    Purpose: To evaluate the duration of seizures arising from the frontal and temporal lobes in order to better understand spread and inhibitory mechanisms involved. […] Results: Of the 130 seizures arising from the temporal lobes 13.8% generalized secondarily, compared to 24.3% secondary generalization in 103 seizures of FLE. […] In FLE patients, the average duration of non-generalized seizures (66s) did not differ from seizures that generalized secondarily (68s). Secondary generalization of ictal epileptic activity prolonged seizure duration in TLE but not in FLE. […] Conclusion: We conclude that in FLE, inhibitory mechanisms are activated earlier than in TLE and, therefore, secondary generalization does not prolong seizure duration in FLE.
  • #41 JLE – Epileptic Disorders – Asymmetric tonic seizures with bilateral parietal lesions resembling frontal lobe epilepsy
    http://www.jle.com/en/revues/epd/e-docs/asymmetric_tonic_seizures_with_bilateral_parietal_lesions_resembling_frontal_lobe_epilepsy_110221/article.phtml
    We performed long-term video/ EEG monitoring and a single photon emission computed tomographic (SPECT) study to clarify generating mechanism of bilateral tonic motor seizures resembling seizures generated by the supplementary motor area (SMA), in patients with bilateral parietal lesions. […] The present 2 patients had clinically asymmetric tonic seizures, most likely resulting from spreading of the ictal activity from the parietal lesions via the superior longitudinal fasciculus to the SMA. […] Tonic seizures belong to generalized seizures in the ILAE seizure classification of 1981, but clinically tonic seizures involving bilateral body parts are also seen in frontal lobe epilepsy, in which either asymmetric body involvement or focal EEG pattern can correctly lead us to a diagnosis of focal (frontal) epilepsy rather than generalized epilepsy. […] We hypothesize that the bilateral homologous parietal lesions may cause disinhibition of ictal activity, which can easily spread into the frontal lobe, generating seizures of frontal lobe origin as the symptomatogenic zone, distant from the epileptogenic zone.
  • #42 JLE – Epileptic Disorders – Asymmetric tonic seizures with bilateral parietal lesions resembling frontal lobe epilepsy
    http://www.jle.com/en/revues/epd/e-docs/asymmetric_tonic_seizures_with_bilateral_parietal_lesions_resembling_frontal_lobe_epilepsy_110221/article.phtml
    We performed long-term video/ EEG monitoring and a single photon emission computed tomographic (SPECT) study to clarify generating mechanism of bilateral tonic motor seizures resembling seizures generated by the supplementary motor area (SMA), in patients with bilateral parietal lesions. […] The present 2 patients had clinically asymmetric tonic seizures, most likely resulting from spreading of the ictal activity from the parietal lesions via the superior longitudinal fasciculus to the SMA. […] Tonic seizures belong to generalized seizures in the ILAE seizure classification of 1981, but clinically tonic seizures involving bilateral body parts are also seen in frontal lobe epilepsy, in which either asymmetric body involvement or focal EEG pattern can correctly lead us to a diagnosis of focal (frontal) epilepsy rather than generalized epilepsy. […] We hypothesize that the bilateral homologous parietal lesions may cause disinhibition of ictal activity, which can easily spread into the frontal lobe, generating seizures of frontal lobe origin as the symptomatogenic zone, distant from the epileptogenic zone.
  • #43 Frontal lobe seizures | Beacon Health System
    https://www.beaconhealthsystem.org/library/diseases-and-conditions/frontal-lobe-seizures?content_id=CON-20197154
    Over the past decade, treatment options have increased for frontal lobe seizures. There are newer types of anti-seizure medicines. There also are a variety of surgical procedures that might help if medicines don’t work. […] If your seizures can’t be controlled with medicines, surgery might be an option. Before surgery, the goal is to find the areas of the brain where seizures occur. […] Imaging techniques can help identify the area generating seizures. These include single-photon emission computerized tomography (SPECT) and subtraction ictal SPECT coregistered to MRI (SISCOM). […] If you have surgery for frontal lobe seizures, it’s likely you’ll need anti-seizure medicine after the surgery. But surgery may allow you to take a lower dose. […] Surgery for epilepsy might involve: Removing the focal point. If your seizures always begin in one spot in your brain, surgery removes that small portion of brain tissue. This might reduce the number of seizures you have. Or it might stop your seizures. […] Deep brain stimulation (DBS). This newer procedure involves implanting an electrode into your brain. The electrode is connected to a stimulating device under the skin of the chest. The device sends signals to the electrode in the brain to stop the activity that triggers a seizure.
  • #44
    https://link.springer.com/article/10.1007/s11910-013-0424-6
    In summary, ADNFLE is a heterogeneous genetic syndrome that can be incidental to mutations in different genes; to date, mutations have been reported in six genes. […] Mutations in these genes, however, account only for a minority of cases and their mean penetrance ranges from 60 % to 80 %. […] Surgical treatment may provide excellent results for selected drug-resistant NFLE patients both for seizures and for epilepsy-related sleep disturbances, such as fragmented sleep and excessive daytime somnolence. […] In conclusion, NFLE is a syndrome of heterogeneous etiology characterized by the occurrence of sleep-related seizures with various motor and affective clinical manifestations, depending on the involved neuronal networks within the frontal lobe.
  • #45 Widespread brain activity increases in frontal lobe seizures with impaired consciousness | bioRxiv
    https://www.biorxiv.org/content/10.1101/2024.09.20.614207v1.full-text
    However, it is not known whether like in TLE, additional mechanisms may also contribute to impaired consciousness in FLE. […] Our analysis demonstrated that frontal lobe FIA seizures had abnormal increased activity in widespread brain regions in contrast to FA seizures where increased activity was confined mainly to the frontal lobe of seizure onset. […] We found that icEEG signals did indeed increase in frontal lobe FBTC seizures across widespread brain areas and frequencies, but these increases were over 10 times larger than in frontal lobe FIA seizures. […] The mechanisms of physiological disruption may vary in different seizure types and can include a combination of factors such as enhanced synchrony per the global neuronal workspace theory, increased cortical slow wave activity per the network inhibition hypothesis in TLE, increased activity across frequencies in FLE, and other activity patterns in different types of seizures. […] These findings suggest a model in which the behavioral severity of seizures, including degree of impaired consciousness, is related to the physiological severity of seizure activity and its impact on widespread regions of cortex.
  • #46
    https://aesnet.org/abstractslisting/impaired-consciousness-in-frontal-lobe-seizures-is-associated-with-widespread-broad-band-intracranial-eeg-power-increase
    Impaired consciousness in frontal lobe seizures is associated with widespread broad-band intracranial EEG power increase. The mechanism of impaired consciousness in focal frontal lobe seizures has been studied less, and is the goal of the present investigation. We discovered that frontal lobe seizures with spared consciousness had significantly lower power than seizures with impaired consciousness. This study suggests there is a less specific mechanism occurring with the propagation of EEG signals in frontal lobe seizures compared to temporal lobe seizures that impair consciousness. Unlike the decreased subcortical arousal producing cortical slow waves in temporal lobe seizures, frontal lobe seizures appear to impair consciousness due to widespread dissemination of ictal activity in a variety of frequency bands throughout the brain. […] It is our goal to aid in improving treatments and preventing loss of consciousness in frontal lobe seizures through our future investigations.