ACKNOWLEDGEMENTS AND DISCLOSURES

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HISTORICAL NOTE AND NOMENCLATURE

Although nonconvulsive seizures with complex behaviors have been recognized since antiquity (Temkin 1945), their relationship to temporal lobe origin was more recently recognized, being first described in the late 1800s by Jackson (Jackson 1898; 1958). The psychic and motor characteristics of these seizures first prompted the designation of psychomotor seizures (Gibbs et al 1938; 1948). 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 (Sutton et al 1987).

The prominent role of mesial temporal structures in the genesis of temporal lobe seizures was first suspected only 35 years ago (Falconer et al 1964) and was confirmed and widely recognized even more recently (Engel et al 1982; 1997; Williamson 1992; French et al 1993; Engel 1996; Williamson et al 1998). The majority of temporal lobe seizures originate in the mesial structures, primarily in the hippocampus, with the rest beginning in a variety of temporal neocortical regions. If patients with circumscribed, epileptogenic lesions are excluded (not including mesial temporal sclerosis), temporal seizures originating in the hippocampus and related structures are far more common than lateral neocortical seizures (Williamson et al 1997b).

A widely used classification scheme distinguishes 2 types of temporal lobe seizures: the common mesial temporal lobe seizures and the relatively uncommon neocortical temporal lobe seizures. Whether or not these can reliably be separated based on noninvasive evaluation is disputed (Spencer et al 1993b; Saygi et al 1994; Walczak 1995).

The 1981 International Classification of Epilepsy and Epilepsy Syndromes by the International League Against Epilepsy included lateral and mesial temporal lobe seizures in the category of complex partial seizures, which includes any seizure of focal onset with altered or impaired consciousness. The term is not specific for temporal lobe seizure onset (Anonymous 1981).

CLINICAL MANIFESTATIONS

Neocortical temporal lobe seizures are relatively rare, and comprehensive studies of a large series of well-documented cases are not available. Conversely, mesial temporal lobe seizures have been studied more extensively than any other type of seizure and constitute a major manifestation of a recognized syndrome (Engel et al 1997). 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 altered consciousness with variable oro-alimentary (lip smacking, chewing) and manual automatisms (picking, fumbling) (Engel et al 1997). 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 (Williamson et al 1998). The patient may be partially responsive during a seizure and often has postictal confusion or aphasia.

Several recent reviews of temporal lobe epilepsy did not attempt to differentiate mesial from lateral temporal lobe seizures, implying there is no difference in clinical manifestations (Kotagal 1991; Mikati and Holmes 1993; Wieser et al 1993). This implication is in agreement with another recent review that specifically examined this issue and concluded the 2 seizure types could not be distinguished (Burgerman et al 1995). Extensive reciprocal connections between mesial and neocortical temporal structures could explain the similar clinical features from both regions (Gloor et al 1982; Wieser 1986; Blume et al 1993). Experiential and hallucinatory auras may require seizures to involve both mesial and neocortical structures (Gloor et al 1982; Blume et al 1993).

Nevertheless, there are some clinical features that 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 (French et al 1993). On the other hand, a later report from that same group described auditory auras from both regions of seizure onset (Saygi et al 1994). A study using PET associated auditory auras with lateral neocortical onset (Wunderlich et al 2000). Simple auditory auras are thought to originate in the Heschl gyrus, the primary auditory area (Liegeois-Chauvel et al 1991).

Vertiginous sensations. Vertigo has been associated with epilepsy since ancient times, but it almost certainly was over-interpreted (Temkin 1945; Bladin 1998). True vertigo (tornado seizures) as a seizure symptom does occur, but only rarely (Fried et al 1995). Over the years this symptom has been equated with seizure origin in the posterior temporal neocortex or the temporoparietal junction (Wilder and Schmidt 1965), others have reported it with frontal seizure onset (Kluge et al 2000). 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 is not entirely clear. Although some reports suggest mesial temporal origin, they are generally thought to originate in the visual association cortex at the temporoparietal junction (Gloor et al 1982; Sowa and Pituck 1989; Blume et al 1993). 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 only rarely seen in patients with lateral neocortical seizure onset and should suggest mesial temporal seizure origin (Henkel et al 2002).

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 (Gil-Nagel and Risinger 1993; Foldvary et al 1994; 1997; Saygi et al 1994). A recent study found that lateralized motor features (contralateral dystonic posturing, ipsilateral automatisms) seen in neocortical temporal lobe seizures occurred with opposite laterality in neocortical temporal seizures (ipsilateral dystonic postures and contralateral automatisms) (Dupont et al 1999). Another study noted that neocortical temporal lobe seizures generally lacked the motor activity associated with mesial temporal lobe seizures (Pacia et al 1996).

LOCALIZATION

By definition, neocortical temporal lobe seizures have their origin in the temporal neocortex excluding all mesial structures. 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.

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 (Ebersole and Wade 1990; 1991; Assaf and Ebersole 1997). Ictal scalp EEG patterns may also help differentiate the 2 types of temporal lobe seizures (Ebersole and Pacia 1996; O’Brien et al 1996; Jung et al 1999; Lee e al 2000), 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 (Bartolomei et al 1999) and assist to distinguish lateral from mesial temporal lobe seizures.

DIFFERENTIAL DIAGNOSIS

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 temporal sclerosis, the presence or absence of certain risk factors such as complicated febrile seizures can help differentiate the 2 conditions (O’Brien et al 1996; Pfander et al 2002), as can the results of intracranial amytal testing (Hamberger et al 1996). A recent 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 (Dupont et al 1999). An auditory aura of any type, complex visual auras, or complex memory flashbacks should suggest neocortical temporal seizure onset, but this needs better documentation.

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 (Aso et al 1987) and coregistration with MRI, although logistically difficult, can provide diagnostic data not otherwise obtainable (Thadani et al 1998). In addition, proton MR spectroscopy and PET studies can be helpful to distinguish mesial form neocortical temporal lobe seizures (Kim et al 1990; Hammen et al 2003).

Finally, 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 (Jobst et al 2000; Fava and Blume 2002). Clinical seizure characteristics and other diagnostic studies will help identify some, but not all, of these patients (Williamson et al 1992a; 1992b; 1993a; 1993b; Wieser and Williamson 1993; Williamson and Engel 1997a).

DIAGNOSTIC WORKUP

The diagnostic work will vary greatly in complexity, depending on 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 (Ebersole and Wade 1990; 1991).
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. If the MRI is normal or nonspecific, no further evaluation is required and medical management should be initiated or continued. In the case of documented medical intractability and possible surgical intervention, the diagnostic evaluation proceeds along well-established lines (Williamson 1991; Williamson et al 1997c). In addition, magnetic resonance spectroscopy might help differentiate mesial temporal lobe seizures from neocortical temporal lobe seizures (Vermathen et al 1997). Further diagnostic evaluation in the case of medical intractability would include video EEG monitoring, intracarotid amytal testing, ictal SPECT, neuropsychological evaluation and possible intracranial EEG monitoring with depth, strip, and grid electrodes, separately or in combination.

SYNDROMES AND DISEASES IN WHICH THE SEIZURE TYPE OCCURS

Only recently 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 (Michelucci et al 2000; Winawer et al 2002). The syndrome was termed autosomal dominant partial epilepsy with auditory features. A mutation in one copy of the leucine-rich, glioma-inactivated 1 gene (LGI1) in the 10-cM region on chromosome 10 q24 was identified in some but not all families (Bisulli et al 2002) associated with the syndrome. Seizures are characterized by prominent auditory hallucinations such as auras. Secondarily generalized seizures are common (Pfander et al 2002), and MRI findings are usually normal (Winawer et al 2002). However, others describe abnormalities of the temporal neocortex that can be visualized on MRI (Kobayashi et al 2003).
Most cases of temporal neocortical epilepsy are associated with cortical lesions such as cortical dysplasias, neoplasms, or vascular malformations and do not represent a specific syndrome.

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.

MANAGEMENT

Depending on the results of 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. If, after a reasonable trial with appropriate antiepileptic drugs, seizures remain inadequately controlled, surgery can be considered, recognizing that seizure onset localization can be a formidable challenge, particularly on the language-dominant side (Williamson et al 1997c). However, 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 (Schramm et al 2001; Engel et al 2003).

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ABBREVIATIONS
MRI:magnetic resonance imaging
SPECT:single positron emitted computed tomography
EEG:electroencephalography


SUBTOPICS
Occipital lobe seizures
Parietal lobe seizures

MAJOR KEYWORD DESCRIPTORS
auras
automatisms
extrahippocampal temporal lobe seizures
lateral temporal lobe seizures
medial temporal seizures
mesial temporal seizures
neocortex
neocortical temporal seizures
temporal lobe

MINOR KEYWORD DESCRIPTORS
auditory seizures
epileptic vertigo

AGE OF PRESENTATION
02-05 years
06-12 years
13-18 years
19-44 years
45-64 years
65+ years

AGE OF TYPICAL PRESENTATION
2-18 years
45-64 years

GLOSSARY
Neocortical temporal lobe seizures are seizures with focal onset in the neocortex of the temporal lobe. Seizures beginning elsewhere in the temporal lobe or outside of the temporal lobe and spreading to temporal lobe structures would be excluded.

PERMUTED TOPIC, SYNONYMS, VARIANTS
Neocortical temporal lobe seizures
temporal lobe seizures, Neocortical
lobe seizures, Neocortical temporal

RELATED SUMMARIES
Aura continua
Frontal lobe seizures
Gelastic seizures
Mesial temporal lobe epilepsy

DIFFERENTIAL DIAGNOSIS
mesial temporal lobe seizures

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