Neuropharmacology & Neurotherapeutics
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Neocortical temporal lobe seizures …
- Updated 09.22.2025
- Released 02.12.2004
- Expires For CME 09.22.2028
Neocortical temporal lobe seizures
Introduction
Overview
Correct diagnosis and classification of seizures and epilepsies is paramount to ensure the delivery of optimal care to patients with epilepsy (55). Clinical expression of temporal lobe seizures depends on the localization of the epileptogenic zone, type of the epileptogenic lesion, and age. Focal seizures in neocortical temporal lobe epilepsies may manifest with preserved or impaired consciousness (22; 21; 02).
Neocortical temporal lobe focal seizures with preserved consciousness (previously classified as simple partial seizures, focal aware seizures, or auras) can be brief, frequently with auditory features, such as buzzing, roaring, radio- or motor-like sounds, and distortions in sounds and words (22; 21; 02). However, the focal seizures often occur with impaired consciousness, which may present with auditory symptoms, visual misperceptions, language impairment (ictal aphasia), or ill-defined cephalic or vertiginous sensations. These seizures may progress to a bilateral tonic-clonic seizure (focal to bilateral tonic–clonic seizure) (21; 02). Preschool children with neocortical temporal lobe epilepsy have nonspecific seizure patterns without the classic auras, subtle ictal symptoms, or with asymmetric tonic posturing, and up to 11% may have spasms as seizure manifestations, making the clinical diagnosis difficult (23).
The EEG abnormalities are more complex in infants and children than in adults. Motor manifestations, including tonic, clonic, or complex behaviors as well as spasms, predominate in infants. Classical focal preserved consciousness seizures with behavioral arrest and automatisms and clear lateralizing signs are rare in young children and mainly occur after 2 years of age (23).
Key points
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• The most common lesions causing neocortical epilepsies are low-grade tumors, malformations of cortical development, posttraumatic, ischemic, and inflammatory-infectious scars, and cavernous angioma. | |
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• Neocortical temporal lobe seizure semiology varies considerably according to the area of the temporal lobe involved. | |
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• Classical lateral temporal focal seizures are characterized by auditory, language, or visual symptoms or ill-defined cephalic or vertiginous sensations. |
Historical note and terminology
Although nonconvulsive seizures with complex behaviors have been recognized since antiquity (67), their relationship to temporal lobe origin was first described in the late 1800s by Jackson (36; 37). The psychic and motor characteristics of these seizures first prompted the designation of psychomotor seizures (29; 28). With the advent of electroencephalography and the increased interest in surgical intervention, the anatomical significance of these seizures led to them being labeled temporal lobe seizures (65).
Most temporal lobe seizures originate in the mesial structures, primarily in the hippocampus, with the rest beginning in various temporal neocortical regions (72; 41; 25). Seizures originating in the temporal neocortex present with distinctive symptoms as compared to those arising from the mesial temporal lobe. However, in many cases, the seizure semiology alone cannot distinguish between mesial and lateral temporal lobe epilepsy (41; 58). For example, if a seizure arises from the primary auditory cortex of the temporal lobe, the patient commonly perceives elementary sounds. In this instance, the patient experiences an alteration in a single sensory modality, ie, hearing. If a seizure arises from regions involved in integrating sensation, emotion, and memory areas, the patient may experience a much more complex alteration of their mental state. These experiential seizures may originate in the lateral or mesial temporal lobe (54; 69) and probably involves cortico-limbic networks (30).
Clinical manifestations
Presentation and course
Temporal lobe epilepsy is typically divided into mesial and neocortical (25). A distinct electroclinical constellation associated with a specific cause is rare for neocortical temporal lobe epilepsy but has been described for patients with autosomal dominant temporal lobe epilepsy presenting with focal seizures with prominent ictal auditory phenomena, normal MRI (45), and usually a good response to antiseizure medications (53). However, most neocortical temporal lobe seizures are characterized by their etiologic, semiologic, and electroclinical heterogeneity (42).
Neocortical temporal lobe seizure semiology varies considerably according to the area of the temporal lobe involved (25). The classical lateral temporal seizures are characterized by auditory, somatosensory, aphasia, or psychic symptoms followed by staring and contralateral facial and arm clonic movements, sometimes evolving to bilateral tonic-clonic seizures. These “pure” temporal lateral seizures have an epileptogenic zone in the mid-posterior aspect of the superior temporal gyrus, usually involving primary or associative sensory areas for auditory, visual, or language functions (01). This region has few direct limbic connections, which may explain the fact that these auras may be prolonged with fewer automatisms as compared to seizures originating in other areas of the temporal lobe (32). By contrast, the lateral anterior and lateral inferior neocortical structures are highly interconnected with limbic structures (32; 01), explaining that seizures from these areas have semiology often very similar to mesial temporal seizures associated with hippocampal sclerosis (11).
The temporal pole is highly connected with the amygdala, the hippocampus, the parahippocampal gyrus, the cingulate gyrus, the orbitofrontal cortex, and the insula (14). The temporal pole cortex extends topographically to the insula (ventrally) and the entorhinal cortex (medial-inferiorly). A network analysis study revealed that the cortex extending from the temporal pole to the entorhinal area is one of the regions with the most association connections with other parts of the brain (08). Therefore, temporopolar seizures may present with different types of auras (focal preserved consciousness seizures), often similar to mesial temporal seizures, including autonomic and rising epigastric sensations. In addition, tonic or clonic seizures, as well as hypermotor seizures, which are uncommon in temporal lobe epilepsy, may occur in patients with temporopolar seizures (14).
Mesial temporal lobe seizures have been studied more extensively than any other type of seizure and constitute a major manifestation of a recognized syndrome (20; 13). Because of these observations, mesial temporal lobe seizures can be used as a benchmark or gold standard against which other seizures can be compared.
Typical mesial temporal lobe seizures begin with an aura of a rising epigastric sensation and progress to impaired consciousness with variable oro-alimentary (lip-smacking, chewing) and manual automatisms (picking, fumbling) (20). Manual automatisms often occur ipsilateral to the side of seizure origin, and dystonia of the hand may occur contralateral of the side of seizure origin (72). The patient may be partially responsive during a seizure and often has postictal confusion or aphasia.
Several reviews of temporal lobe epilepsy did not attempt to differentiate mesial from lateral temporal lobe seizures, implying there is no difference in clinical manifestations (01; 70). This implication is in agreement with another review that specifically examined this issue and concluded the two seizure types could not be distinguished (09). Extensive reciprocal connections between mesial and neocortical temporal structures could explain the similar clinical features from both regions (33; 07). Experiential and hallucinatory phenomena may require seizures to involve both mesial and neocortical structures (33; 07).
Nevertheless, some clinical features might help identify neocortical temporal lobe seizures.
Initial symptoms. Although mesial and neocortical temporal lobe seizures undeniably share common auras, several symptoms are more typical of seizure onset from the temporal neocortex.
Auditory hallucinations or distortions. Auditory hallucinations of any type should suggest seizure origin in the superior region of the posterior superior temporal gyrus, or at least in the lateral temporal neocortex. In a large, well-documented series of mesial temporal lobe seizures, there were no examples of auditory auras of any kind (26). On the other hand, a later report from that same group described auditory auras from both regions of seizure onset (62). A study using PET associated auditory auras with lateral neocortical onset (74). Simple auditory auras are thought to originate in the Heschl gyrus, the primary auditory area (49).
Vertiginous sensations. Vertigo has been associated with epilepsy since ancient times, but it almost certainly was over-interpreted (67; 05). True vertigo (tornado seizures) as a seizure symptom does occur, but only rarely (27). Over the years, this symptom has been equated with seizure origin in the posterior temporal neocortex or the temporoparietal junction (71); others have reported it with frontal seizure onset (44). There are, overall, few well-documented examples.
Complex visual hallucinations. Elementary visual hallucinations are a well-established symptom of seizures beginning in the occipital region, but the origin of complex visual hallucinations or visual flashbacks are generally thought to originate in the visual association cortex at the occipitotemporal or temporoparietal junctions, often including the posterior fusiform gyrus (33; 64; 07; 50). Therefore, auras of complex visual hallucinations should be equated with neocortical seizure activity unless there is strong evidence to the contrary. Overall, these complex visual epileptic auras are rare.
The typical epigastric aura with a rising sensation in the abdominal area is rare in patients with neocortical temporal lobe seizure onset and should suggest mesial temporal seizure origin (35; 51). By contrast, auditory auras can occur rarely in seizures originating in the mesial temporal region (47).
Signs (objective seizure manifestations). There are many similarities between the objective manifestations of mesial and neocortical temporal lobe seizures, but there may be some trends that help separate them. Several studies have noted that the motor manifestations (automatisms) are less common in lateral neocortical seizures (31; 24; 62). A study found that lateralized motor features (contralateral dystonic posturing, ipsilateral automatisms) seen in mesial temporal lobe seizures occurred with opposite laterality in neocortical temporal seizures (ipsilateral dystonic postures and contralateral automatisms) (17). Neocortical temporal lobe seizures generally lacked the motor activity associated with mesial temporal lobe seizures (57). One study compared patients with mesial temporal lobe epilepsy and hippocampal sclerosis with patients with neocortical temporal lobe epilepsy successfully treated by neocortical resections sparing the hippocampus. Epigastric rising sensation (6% vs. 40%), oral automatisms (29% vs. 80%), gestural automatisms (47% vs. 80%), and dystonic posturing (0% vs. 40%) were significantly less frequent in neocortical temporal lobe epilepsy (51).
Prognosis and complications
Prognosis depends on the etiology, eg, slow-growing neoplasms; vascular malformations carry their own prognostic and complication factors. The overall prognosis of neocortical temporal lobe seizures without detectable lesions has not been established.
Biological basis
Localization
By definition, neocortical temporal lobe seizures have their origin in the temporal neocortex, excluding all mesial structures (25). This would include all of the lateral temporal neocortex, the inferior temporal neocortex (excluding the parahippocampal gyrus), the temporal polar region, and the superior plane of the temporal lobe.
Etiology and pathogenesis
Most etiologies of neocortical epilepsies are low-grade tumors, malformations of cortical development, posttraumatic, ischemic, and inflammatory-infectious scars, and cavernous angioma (03; 10; 06).
Pathophysiology
There is no unique pathophysiology to neocortical temporal lobe seizure origin. Any destructive, neoplastic, vascular, or congenital epileptogenic lesion can result in seizures from these regions. As previously noted, preferential spread patterns may be to mesial structures, producing seizures similar to mesial temporal lobe seizures. Other potential spread patterns have not been extensively studied.
Dipole modeling of ictal and interictal patterns have shown differences between neocortical and mesial temporal lobe seizures. Ictal scalp EEG patterns may also help differentiate the two types of temporal lobe seizures (18; 56; 40; 48), but intracranial EEG recording may be required to differentiate between mesial temporal and lateral neocortical seizure onset. Coherence analysis of ictal data from intracranial studies can identify different subtypes of temporal lobe seizures and assist in distinguishing lateral from mesial temporal lobe seizures (01).
In a study with intracranial stereo-electroencephalography (SEEG), the cortico-cortical evoked potentials responsiveness triggered by single pulse electrical stimulation was abruptly reduced in the onset of mesiotemporal seizures but preserved in neocortical temporal seizures (61). These findings may help to explain the clinical differences between mesial and neocortical temporal lobe seizures.
Differential diagnosis
Confusing conditions
The main differential diagnosis of neocortical temporal lobe seizures is mesial temporal lobe seizures. As noted previously, preferential spread patterns to mesial structures would produce seizures similar to those beginning medially. This is true of some, but not all, temporal neocortical seizures.
As mesial temporal lobe seizures mainly occur in association with mesial hippocampal sclerosis, the presence or absence of certain risk factors such as complicated febrile seizures can help differentiate the two conditions (56; 59; 42; 51), but in clinical practice, the presence of MRI findings of hippocampal sclerosis or a neocortical lesion are the most helpful findings to differentiate mesial from neocortical temporal lobe epilepsies (11). One study suggested some of the lateralizing findings associated with mesial temporal lobe seizures (contralateral dystonic posturing, ipsilateral automatisms, etc.) present in a mirror image fashion in neocortical temporal lobe seizures (17). An auditory aura of any type, complex visual auras, or complex memory flashbacks should suggest neocortical temporal seizure onset, but this needs better documentation. A study analyzing intracranial video-EEG recordings showed that a generalized tonic phase occurred in all seven patients with mesial temporal lobe epilepsy who had focal onset bilateral motor (convulsive) seizures, but in only seven of 13 (54%) of those of neocortical temporal lobe epilepsy (60).
When the MRI reveals potentially epileptogenic structural lesions in mesial or neocortical temporal regions, the differential diagnosis is greatly simplified. Patients with normal MRI and suspected mesial or neocortical temporal origin are much more challenging. Ictal SPECT scanning and coregistration with MRI, although logistically difficult, can provide diagnostic data not otherwise obtainable (12). In addition, proton MR spectroscopy and PET studies can be helpful to distinguish mesial from neocortical temporal lobe seizures (43; 34). The differential diagnosis of the seizure onset zone in patients with MRI negative temporal lobe epilepsy may be difficult without invasive EEG monitoring (16).
In addition, seizures originating outside of the temporal lobe can secondarily invade the mesial or neocortical temporal regions or both. This has been documented for orbitofrontal and occipital seizure onset (39; 68). Clinical seizure characteristics and other diagnostic studies will help identify some, but not all, of these patients (72).
Even in some patients with clearly MRI-defined hippocampal sclerosis, seizure semiology may suggest neocortical temporal lobe onset, and intracranial EEG investigation may reveal seizures originating in temporal pole or other neocortical regions, either independently or simultaneously with the mesial temporal structures (14). Based on stereo-EEG recordings, Kahane and Bartolomei proposed the mesial, temporopolar, mesiolateral, lateral, and temporal “plus” subtypes of temporal lobe epilepsy associated with hippocampal sclerosis (41).
Associated and underlying disorders
An inherited epilepsy syndrome with predominant auditory seizures has been identified in several families. These seizures are thought to originate in the lateral neocortical temporal cortex (52; 73; 45). The syndrome was termed autosomal dominant partial epilepsy with auditory features or familial lateral temporal lobe epilepsy (45). A mutation in one copy of the leucine-rich, glioma-inactivated 1 gene (LGI1) in the 10-cM region on chromosome 10 q24 is present in approximately 50% of families associated with the syndrome (04; 45). Seizures are characterized by prominent auditory hallucinations such as auras. Focal to bilateral tonic-clonic seizures are common (59), and MRIs are usually normal (73). However, others describe abnormalities of the temporal neocortex that can be visualized on MRI (46).
Most cases of temporal neocortical epilepsy are associated with cortical lesions such as focal cortical dysplasias, neoplasms, or vascular malformations and do not represent a specific syndrome.
Diagnostic workup
The diagnostic work will vary greatly in complexity, depending on the response to medical treatment and consideration of surgical therapy. A careful history by an experienced examiner should establish the diagnosis of epilepsy and help define the seizure type. A routine EEG may or may not be helpful, as interictal abnormalities may be lacking. Interictal EEG would not be able to differentiate mesial from neocortical temporal origin, or even extratemporal origin. As noted previously, special EEG analysis techniques might help (66).
In the case of new onset seizures, patients should have MRI scans early in the course of evaluation to look for structural lesions as the cause of seizures. Structural lesions, depending on their location and appearance, can have a significant impact on management and evaluation. In the case of documented pharmacoresistance and possible surgical intervention, the diagnostic evaluation proceeds along well-established lines. Finding a structural lesion on MRI helps to delineate the diagnosis workup (55). Further diagnostic evaluation in the case of pharmacoresistance would include video EEG monitoring, neuropsychological evaluation, and when indicated, intracranial EEG monitoring (23). FDG-PET or ictal SPECT can be very helpful in MRI-negative temporal epilepsies (12).
An 18F-FDG-PET study showed that the hypometabolism in mesial temporal lobe epilepsy was limited to the ipsilateral temporal and insular lobes, whereas in neocortical temporal lobe epilepsy the hypometabolism was more widespread, involving more frequently the ipsilateral temporal, frontal, and parietal lobes (75).
Management
Depending on the results of the evaluation, the management can take one of several directions. If the MRI is normal and neocortical temporal lobe seizures are suspected, medical management should be undertaken.
The choice of antiseizure medication needs to be assessed individually and several factors should be considered, including the adverse effect profile of each medication and the potential teratogenic effect on women, age, and comorbidities. If, after a reasonable trial with appropriate antiseizure medications, seizures remain inadequately controlled, surgery should be considered, recognizing that seizure onset localization can be challenging, particularly on the language-dominant side (72). It is important to recognize pharmacoresistant patients without delay and refer them to a tertiary epilepsy center (38). With careful presurgical evaluation through experienced epilepsy surgery programs, surgical therapy can be successful in lateral neocortical temporal epilepsy, even in patients with no obvious MRI abnormalities (63; 19).
Outcomes
Overall, patients with neocortical temporal lobe epilepsy, particularly those with normal MRI, have better response to antiseizure medications than patients with mesial temporal lobe epilepsy associated with hippocampal sclerosis (15).
Despite the differences in EEG and clinical characteristics between mesial temporal lobe epilepsy with hippocampal sclerosis and lesional neocortical temporal lobe epilepsies, surgical outcomes are similar (70).
References
- 01
- Bartolomei F, Cosandier-Rimele D, McGonigal A, et al. From mesial temporal lobe to temporoperisylvian seizures: a quantified study of temporal lobe seizure networks. Epilepsia 2010;51(10):2147-58. PMID 20738279
- 02
- Beniczky S, Trinka E, Wirrell E, et al. Updated classification of epileptic seizures: Position paper of the International League Against Epilepsy. Epilepsia 2025;66(6):1804-23. PMID 40264351
- 03
- Bercovici E, Kumar BS, Mirsattari SM. Neocortical temporal lobe epilepsy. Epilepsy Res Treat. 2012;2012:103160. PMID 22953057
- 04
- Bisulli F, Tinuper P, Marini C, Avoni P, Carraro G, Nobile C. Partial epilepsy with prominent auditory symptoms not linked to chromosome 10q. Epileptic Disord 2002;4(3):183-7. PMID 12446220
- 05
- Bladin PF. History of "epileptic vertigo": its medical, social, and forensic problems. Epilepsia 1998;39(4):442-7. PMID 9578036
- 06
- Blumcke I, Aronica E, Urbach H, Alexopoulos A, Gonzalez-Martinez JA. A neuropathology-based approach to epilepsy surgery in brain tumors and proposal for a new terminology use for long-term epilepsy-associated brain tumors. Acta Neuropathol 2014;128(1):39-54. PMID 24858213
- 07
- Blume WR, Girvin JP, Stenerson P. Temporal neocortical role in ictal experiential phenomena. Ann Neurol 1993;33:105-7. PMID 8388185
- 08
- Bota M, Sporns O, Swanson LW. Architecture of the cerebral cortical association connectome underlying cognition. Proc Natl Acad Sci U S A 2015;112(16):E2093-101. PMID 25848037
- 09
- Burgerman RS, Sperling MR, French JA, Saykin AJ, O'Connor MJ. Comparison of mesial versus neocortical onset temporal lobe seizures: neurodiagnostic findings and surgical outcome. Epilepsia 1995;36(7):662-70. PMID 7555982
- 10
- Cendes F. Neuroimaging in investigation of patients with epilepsy. Continuum (Minneap Minn) 2013;19(3 Epilepsy):623-42. PMID 23739101
- 11
- Cendes F, Sakamoto AC, Spreafico R, Bingaman W, Becker AJ. Epilepsies associated with hippocampal sclerosis. Acta neuropathologica 2014;128(1):21-37. PMID 24823761
- 12
- Cendes F, Theodore WH, Brinkmann BH, Sulc V, Cascino GD. Neuroimaging of epilepsy. Handb Clin Neurol 2016;136:985-1014. PMID 27430454
- 13
- Cendes F, Engel J. Hippocampal atrophy in epilepsy. In: Roos RP, editor-in-chief. MedLink Neurology. San Diego: MedLink Corporation, 2024.
- 14
- Chabardès S, Kahane P, Minotti L, et al. The temporopolar cortex plays a pivotal role in temporal lobe seizures. Brain 2005;128(Pt 8):1818-31. PMID 15857932
- 15
- Chipaux M, Szurhaj W, Vercueil L, et al. Epilepsy diagnostic and treatment needs identified with a collaborative database involving tertiary centers in France. Epilepsia 2016;57(5):757-69. PMID 27037674
- 16
- Doležalová I, Brázdil M, Chrastina J, et al. Differences between mesial and neocortical magnetic-resonance-imaging-negative temporal lobe epilepsy. Epilepsy Behav 2016;61:21-6. PMID 27263079
- 17
- Dupont S, Semah F, Boon P, et al. Association of ipsilateral motor automatisms and contralateral dystonic posturing: a clinical feature differentiating medial from neocortical temporal lobe epilepsy. Arch Neurol 1999;56(8):927-32. PMID 10448797
- 18
- Ebersole JS, Pacia SV. Localization of temporal lobe foci by ictal EEG patterns. Epilepsia 1996;37(4):386-99. PMID 8603646
- 19
- Engel J Jr, Wiebe S, French J, et al. Practice parameter: temporal lobe and localized neocortical resections for epilepsy: report of the Quality Standards Subcommittee of the American Academy of Neurology, in association with the American Epilepsy Society and the American Association of Neurological Surgeons. Neurology 2003;60(4):538-47. PMID 12601090
- 20
- Engel JJ, Williamson PD, Wieser HG. Mesial temporal lobe epilepsy with hippocampal sclerosis. In: Engel JJ, Pedley TA, editors. Epilepsy: A Comprehensive Textbook. Second Edition. Philadelphia: Lippincott-Raven Publishers, 2008:2479-86.
- 21
- Falco-Walter JJ, Scheffer IE, Fisher RS. The new definition and classification of seizures and epilepsy. Epilepsy Res 2018;139:73-9. PMID 29197668
- 22
- Fisher RS, Cross JH, French JA, et al. Operational classification of seizure types by the International League Against Epilepsy: Position Paper of the ILAE Commission for Classification and Terminology. Epilepsia 2017;58(4):522-30. PMID 28276060
- 23
- Fohlen M, Taussig D, Ferrand-Sorbets S, Chipaux M, Dorfmuller G. Clinical semiology of temporal lobe seizures in preschool children: contribution of invasive recording to anatomical classification. Epileptic Disord 2021;23(4):590-610. PMID 34289959
- 24
- Foldvary N, Lee N, Thwaites G, et al. Clinical and electrographic manifestations of lesional neocortical temporal lobe epilepsy. Neurology 1997;49(3):757-63. PMID 9305337
- 25
- Frazzini V, Cousyn L, Navarro V. Semiology, EEG, and neuroimaging findings in temporal lobe epilepsies. Handb Clin Neurol 2022;187:489-518. PMID 35964989
- 26
- French JA, Williamson PD, Thadani VM, et al. Characteristics of medial temporal lobe epilepsy: I. Results of history and physical examination. Ann Neurol 1993;34:774-80. PMID 8250525
- 27
- Fried I, Spencer DD, Spencer SS. The anatomy of epileptic auras: focal pathology and surgical outcome. J Neurosurg 1995;83(1):60-6. PMID 7782851
- 28
- Gibbs EL, Gibbs FA, Fuster B. Psychomotor epilepsy. Arch Neurol Psychiatr 1948;60:331-69. PMID 18111213
- 29
- Gibbs FA, Gibbs EL, Lennox WG. Cerebral dysrhythmias of epilepsy. Arch Neurol Psychiatr 1938;39:298-314.
- 30
- Gillinder L, Liegeois-Chauvel C, Chauvel P. What déjà vu and the "dreamy state" tell us about episodic memory networks. Clin Neurophysiol 2022;136:173-81. PMID 35189480
- 31
- Gil-Nagel A, Risinger MW. Ictal semiology in hippocampal vs. extrahippocampal temporal lobe epilepsy. [abstract] Neurology 1993;43:273.
- 32
- Gloor P. The temporal lobe and limbic system. New York-Oxford: Oxford University Press, 1997.
- 33
- Gloor P, Olivier A, Quesney LF, Andermann F, Horowitz S. The role of the limbic system in experiential phenomena of temporal lobe epilepsy. Ann Neurol 1982;12:129-44. PMID 7125603
- 34
- Hammen T, Stefan H, Pauli E, Schafer I, Huk W, Tomandl B. 1H-MR spectroscopy: a promising method in distinguishing subgroups in temporal lobe epilepsy. J Neurol Sci 2003;215(1-2):21-5. PMID 14568123
- 35
- Henkel A, Noachtar S, Pfander M, Luders HO. The localizing value of the abdominal aura and its evolution: a study in focal epilepsies. Neurology 2002;58(2):271-6. PMID 11805256
- 36
- Jackson JH. Case of epilepsy with tasting movements and "dreaming state" -- very small patch of softening in the left uncinate gyrus. Brain 1898;21:580-90.
- 37
- Jackson JH. Selected writings of John Hughlings Jackson Volumes 1 and 2. Taylor J, editor. London, England: Staples Press, 1958.
- 38
- Jehi L, Jette N, Kwon CS, et al. Timing of referral to evaluate for epilepsy surgery: Expert Consensus Recommendations from the Surgical Therapies Commission of the International League Against Epilepsy. Epilepsia 2022;63(10):2491-506. PMID 35842919
- 39
- Jobst BC, Siegel AM, Thadani VM, Roberts DW, Rhodes HC, Williamson PD. Intractable seizures of frontal lobe origin. Epilepsia 2000;41(9):1139-52. PMID 10999553
- 40
- Jung WY, Pacia SV, Devinsky R. Neocortical temporal lobe epilepsy: intracranial EEG features and surgical outcome. J Clin Neurophysiol 1999;16(5):419-25. PMID 10576224
- 41
- Kahane P, Bartolomei F. Temporal lobe epilepsy and hippocampal sclerosis: lessons from depth EEG recordings. Epilepsia 2010;51 Suppl 1:59-62. PMID 20331718
- 42
- Kennedy JD, Schuele SU. Neocortical temporal lobe epilepsy. J Clin Neurophysiol 2012;29(5):366-70. PMID 23027092
- 43
- Kim JH, Guimaraes PO, Shen MY, Masukawa LM, Spencer DD. Hippocampal neuronal density in temporal lobe epilepsy with and without gliomas. Acta Neuropathol 1990;80:41-5. PMID 2360416
- 44
- Kluge M, Beyenburg S, Fernandez G, Elger CE. Epileptic vertigo: evidence for vestibular representation in human frontal cortex. Neurology 2000;55(12):1906-8. PMID 11134394
- 45
- Kobayashi E, Engel J. Epilepsy with auditory features. In: Roos RP, editor-in-chief. MedLink Neurology. San Diego, CA: Medlink Corporation, 2022.
- 46
- Kobayashi E, Santos NF, Torres FR, et al. Magnetic resonance imaging abnormalities in familial temporal lobe epilepsy with auditory auras. Arch Neurol 2003;60(11):1546-51. PMID 14623726
- 47
- Kumar S, Nayak DS, Basrur RMR, et al. Auditory aura from the hippocampus - Not all that 'rings' is neocortical temporal lobe epilepsy. Epilepsy Behav Rep 2022;19:100548. PMID 35573059
- 48
- Lee SA, Spencer DD, Spencer SS. Intracranial EEG seizure-onset patterns in neocortical epilepsy. Epilepsia 2000;41(3):297-307. PMID 10714401
- 49
- Liegeois-Chauvel C, Musolino A, Chauvel P. Localization of the primary auditory area in man. Brain 1991;114(Pt 1A):139-51. PMID 1900211
- 50
- Marchi A, Bonini F, Lagarde S, et al. Occipital and occipital "plus" epilepsies: A study of involved epileptogenic networks through SEEG quantification. Epilepsy Behav 2016;62:104-14. PMID 27454330
- 51
- Maizuliana H, Usui N, Terada K, Kondo A, Inoue Y. Clinical, semiological, electroencephalographic, and neuropsychological features of "pure" neocortical temporal lobe epilepsy. Epileptic Disord 2020;22(1):55-65. PMID 32031536
- 52
- Michelucci R, Passarelli D, Pitzalis S, Dal Corso G, Tassinari CA, Nobile C. Autosomal dominant partial epilepsy with auditory features: description of a new family. Epilepsia 2000;41(8):967-70. PMID 10961622
- 53
- Michelucci R, Pasini E, Nobile C. Lateral temporal lobe epilepsies: clinical and genetic features. Epilepsia 2009;50(suppl 5):52-54. PMID 19469848
- 54
- Moriarity JL, Boatman D, Krauss GL, Storm PB, Lenz FA. Human "memories" can be evoked by stimulation of the lateral temporal cortex after ipsilateral medial temporal lobe resection. J Neurol Neurosurg Psychiatry 2001;71(4):549-51. PMID 11561047
- 55
- Nascimento FA, Friedman D, Peters JM, et al. Focal epilepsies: update on diagnosis and classification. Epileptic Disord 2023;25(1):1-17. PMID 36938903
- 56
- O'Brien TJ, Kilpatrick C, Murrie V, Vogrin S, Morris K, Cook MJ. Temporal lobe epilepsy caused by mesial temporal sclerosis and temporal neocortical lesions. A clinical and electroencephalographic study of 46 pathologically proven cases. Brain 1996;119(Pt 6):2133-41. PMID 9010016
- 57
- Pacia SV, Devinsky O, Perrine K, et al. Clinical features of neocortical temporal lobe epilepsy. Ann Neurol 1996;40(5):724-30. PMID 8957013
- 58
- Patel KH, Mitropanopoulos S, Kalamangalam G. Pearls & oy-sters: Mesial temporal seizures in the absence of the mesial temporal lobe. Seizure onset vs seizure network. Neurology 2024;102(2):e208012. PMID 38165343
- 59
- Pfander M, Arnold S, Henkel A, et al. Clinical features and EEG findings differentiating mesial from neocortical temporal lobe epilepsy. Epileptic Disord 2002;4(3):189-95. PMID 12446221
- 60
- Punyawai P, Usui N, Kondo A, et al. Semiological differences of focal onset bilateral motor (convulsive) seizure between mesial temporal lobe epilepsy and neocortical epilepsy. Epilepsy Res 2021;170:106553. PMID 33453690
- 61
- Russo S, Mikulan E, Zauli FM, et al. Neocortical and medial temporal seizures have distinct impacts on brain responsiveness. Epilepsia 2023;64(6):e118-26. PMID 36994648
- 62
- Saygi S, Spencer SS, Scheyer R, Katz A, Mattson R, Spencer DD. Differentiation of temporal lobe ictal behavior associated with hippocampal sclerosis and tumors of temporal lobe. Epilepsia 1994;35:737-42. PMID 8082615
- 63
- Schramm J, Kral T, Grunwald T, Blumcke I. Surgical treatment for neocortical temporal lobe epilepsy: clinical and surgical aspects and seizure outcome. J Neurosurg 2001;94(1):33-42. PMID 11147895
- 64
- Sowa MV, Pituck S. Prolonged spontaneous complex visual hallucinations and illusions as ictal phenomena. Epilepsia 1989;30(5):524-6. PMID 2792027
- 65
- Sutton LN, Packer RJ, Zimmerman RA, Bruce DA, Schut L. Cerebral gangliogliomas of childhood. Prog Exp Tumor Res 1987;30:239-46. PMID 3628809
- 66
- Tatum WO 4th. Mesial temporal lobe epilepsy. J Clin Neurophysiol 2012;29(5):356-65. PMID 23027091
- 67
- Temkin O. The falling sickness. Baltimore: Johns Hopkins Press, 1945.
- 68
- Usui N, Mihara T, Baba K, et al. Early seizure propagation from the occipital lobe to medial temporal structures and its surgical implication. Epileptic Disord 2008;10(4):260-5. PMID 19017566
- 69
- Vignal JP, Maillard L, McGonigal A, Chauvel P. The dreamy state: hallucinations of autobiographic memory evoked by temporal lobe stimulations and seizures. Brain 2007;130(Pt 1):88-99. PMID 17142246
- 70
- Wassenaar M, Leijten FSS, de Haan GJ, Uijl SG, Sander JW. Electro-clinical criteria and surgical outcome: Is there a difference between mesial and lesional temporal lobe epilepsy? Acta Neurol Scand 2017;136(6):708-14. PMID 28626979
- 71
- Wilder BJ, Schmidt RP. Propagation of epileptic discharge from chronic neocortical foci in monkey. Epilepsia 1965;6(4):297-309. PMID 4956069
- 72
- Williamson PD, Engel JJ. Anatomic classification of focal epilepsies. In: Engel JJ, Pedley TA, editors. Epilepsy: A Comprehensive Textbook. Second Edition. Philadelphia: Lippincott-Raven Publishers, 2008:2465-78.
- 73
- Winawer MR, Martinelli Boneschi F, Barker-Cummings C, et al. Four new families with autosomal dominant partial epilepsy with auditory features: clinical description and linkage to chromosome 10q24. Epilepsia 2002;43(1):60-7. PMID 11879388
- 74
- Wunderlich G, Schuller MF, Ebner A, et al. Temporal lobe epilepsy with sensory aura: interictal glucose hypometabolism. Epilepsy Res 2000;38(2-3):139-49. PMID 10642042
- 75
- Zhu HY, Tang YX, Xiao L, et al. Metabolic profiles and correlation with surgical outcomes in mesial versus neocortical temporal lobe epilepsy. CNS Neurosci Ther 2023;29(9):2656-65. PMID 37017415
Contributors
All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.
Author
-
Fernando Cendes MD PhD
Dr. Cendes of the University of Campinas - UNICAMP has no relevant financial relationships to disclose.
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Editor
-
Jerome Engel Jr MD PhD
Dr. Engel of the David Geffen School of Medicine at the University of California, Los Angeles, has no relevant financial relationships to disclose.
See Profile
Former Authors
- Peter D Williamson MD
- Barbara C Jobst MD
Patient Profile
- Age range of presentation
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- 2 to 65+ years
- Heredity
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- The familial forms of neocortical temporal lobe epilepsies are presented the article on familial lateral temporal lobe epilepsy.
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