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Frontal Lobe Seizures
by Peter D. Williamson and Barbara C. Jobst Date of submission: June 4, 2003 Medline SEARCH DATE: June 4, 2003
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Acknowledgements
and disclosures Please disclose any financial or other conflicts of interest that might bias your contributions, or give rise to the perception of such bias. Relevant financial ties can include consultantships, memberships in speaker's bureaus, grants, research support, salaries, royalties, ownership, equity positions, stock options, or other financial arrangements wherein you stand to gain substantially from an increase of stock value or corporate revenues. Disclosures and acknowledgements will be linked to the author name(s) and will display along with appointments and affiliations. Disclosures, acknowledgements, and affiliations can be entered and updated via the "Update My Profile" link in the Online Submission System. Alternatively, you may send such information along with your updated manuscript. Thumbnail So that MedLink Corporation can highlight your clinical summary and your authorship on the MedLink Neurology home page and in our weekly email to subscribers, we ask that you provide here a brief overview of your subject (about 50 to 100 words) aimed at enticing readers to view this clinical summary. For updates, please include a sentence that refers to something new you have added. Refer to yourself in the 3rd person (eg, Dr. Doe of Superior Institution explains the basics…). For more information and examples of thumbnails, please see the Instructions to Authors, which can be downloaded from your "My Writing Assignments" page in the Online Submission System (http://www.medlinkoss.com). HISTORICAL NOTE AND NOMENCLATURE Penfield and Welch performed stimulation experiments of the human and
monkey cortex. They defined the supplementary motor area (Brodmann area 6)
as a region of the brain, that mediates speech and behavioral arrest,
vocalization and asymmetric contralateral posturing when stimulated
(Penfield 1951a). They described supplementary motor area seizures as
seizures with speech arrest, unilateral arm posturing, and head or eye
deviation, later referred to as "fencing posture" (Penfield 1949; Penfield
1954). In a detailed study of pharmacologically induced seizures,
Ajmone-Marsan created the term "M2e" to describe tonic abduction and
external rotation of the shoulder with flexion of the elbow with or
without head turning. He described supplementary motor involvement if M2e
posturing occurred without loss of consciousness and without progression
into a secondarily generalized tonic clonic seizure (Ajmone-Marsan 1957).
With the introduction of intracranial long-term EEG recordings,
supplementary motor area seizures again became the focus of scientific
interest in the late 1980s and early 1990s and were described in greater
detail (Dinner 1987; Morris 1987; Morris 1988; Fried 1991; Tuxhorn 1992;
Lim 1994; Connolly 1995; Roberts 1995; Baumgartner 1996; Janszky 2000;
Fogaresi 2001). As cortical stimulation of the mesial frontal area can
also result in sensory responses, the Cleveland Clinic has proposed the
term "supplementary sensorimotor area;" seizures were termed accordingly.
However, this term may lead to confusion with the supplementary sensory
area. The term “adversive seizure” was also used to describe sensory motor
area seizures. Currently these seizures are listed as supplementary motor
area seizures by the Commission on Classifications and Terminology of the
International League Against Epilepsy (Anonymous 1989), which may be
revised in the near future. Clinically, they are best described as
asymmetric tonic seizures, recognizing that asymmetrical tonic seizures
can also occur with seizure origin outside of the sensory motor area. Complex partial seizures of frontal lobe origin with bizarre
automatisms were initially recognized by Tharp, who described 3 patients
that were misdiagnosed as having psychogenic attacks (Tharp 1972). Using
stereoencephalography, Geier, Bancaud, and Talairach defined frontal lobe
automatisms further (Geier 1976; Geier 1977b) and detailed descriptions of
complex partial seizures of frontal lobe origin followed (Williamson
1985b; Waterman 1987). The term "hypermotor seizure" was proposed for this
type of seizure (Luders 1998). These seizures are also termed "frontal
lobe seizures with hypermotor automatisms," "frontal lobe seizures with
frenetic automatisms," "complex partial seizures frontal lobe type,"
"frontal lobe seizures with agitated behavior," or "seizures with
hyperactive automatisms" (Williamson 2000). Autosomal dominant frontal lobe epilepsy has been recognized recently
and, since then, has been localized to certain genetic defects associated
with the nicotinic acetylcholine receptor (Tinuper 1990; Scheffer 1994;
Steinlein 2002). The frontal lobes contain 40% of the entire cerebral cortex. Epileptiform activity may arise in various areas of the large cortical surface, and several different seizure types are associated with onset in the anterior neocortex dependent, to some extent, on region of seizure origin. These include focal clonic seizures, asymmetric tonic seizures, bizarre hyperactive seizures, frontal lobe absence seizures, and masticatory seizures. These seizure types are discussed below. Seizures of the anterior neocortex are the second most common type of seizures seen at epilepsy centers during presurgical evaluation (Behrens 1998). The average age of onset of patients with intractable seizures of the anterior neocortex usually is in late childhood or early adolescence (Jobst 2000). Men and women are equally affected. General characteristics of frontal lobe seizures. Seizures of the anterior neocortex have been described as brief and frequent with a nocturnal preponderance (Williamson 1985b; Laskowitz 1995; Jobst 2000). Even though this may apply to several seizure types of the frontal lobes, especially asymmetric tonic seizures and hypermotor seizures, it is not a constant parameter of all seizure types of the anterior neocortex, as discussed below. Seizures of the anterior neocortex were shown to be significantly shorter in duration than seizures originating in the temporal lobes (Jobst 1999). Nighttime preponderance and association with sleep wake cycle has been reported by several authors (Williamson 1985b; Niedermeyer 1998; Jobst 2000). Seizures may occur in nightly clusters of as many as 70. Convulsive and nonconvulsive status epilepticus is frequently observed with seizures of the anterior neocortex (Williamson 1985a; Williamson 2000). No specific type of aura has been linked to seizures of the anterior neocortex. Patients often report an unspecific unexplainable feeling, often localized to the head (“cephalic aura”) (Palmini and Gloor 1992; Jobst et al 2000). However, a prospective series could not confirm that this aura distinguishes between seizures of frontal and temporal origin (Palmini 1992). Some asymmetric tonic seizures originating in the sensorimotor area are often preceded by a somatosensory aura (Morris 1988; Chauvel 1995). In seizures of the anterior neocortex, autonomic auras like nausea or palpitations as well as emotional auras such as fear are also reported (Bancaud 1992; Jobst 2000). It was long assumed that generalization occurs rapidly and frequently in seizures of the anterior neocortex (Quesney 1992). However, systematic analysis did not confirm that secondarily generalized seizures occur more frequently than in other localization related epilepsies (Chauvel 1995; Jobst 2000). The notion that seizures of the anterior neocortex frequently generalize may stem from the observation that asymmetric tonic seizures share some clinical similarities with secondarily generalized tonic clonic seizures. In seizures of the anterior neocortex consciousness is often preserved, even when there is bilateral motor involvement. When consciousness is impaired, these seizures typically are followed by minimal, if any, postictal confusion. An exception would occur when the seizure spread to the temporal lobes. When this happens, the postictal confusion associated with temporal lobe seizures would be expected. Specific seizure types. Focal clonic motor seizures (focal motor seizures, primary motor seizure, Jacksonian seizure, somatomotor seizure) Focal clonic seizures consist of unilateral clonic movements of the extremities, trunk, or face. Consciousness is preserved. The clonic activity occurs contralateral to the epileptic discharge. Clonic movements may be restricted to specific muscle groups such as the face or hand (focal clonic seizure without march), or they may spread following the somatotopic organization of the motor cortex (Jacksonian seizure, focal motor seizure with march) or clonic movements can be multifocal involving several unrelated muscle groups. Focal clonic seizures do not have a daytime preponderance. These seizures may continue for hours, days or even months. This type of status epilepticus is termed epilepsia partialis continua. Focal clonic seizures are often seen with diffuse unilateral hemispheric damage, but they are also associated with small circumscribed lesions in the primary motor cortex (Brodmann area 4) (Chauvel 1992b). Epilepsia partialis continua is characteristic of Rasmussen syndrome (McLachlan 1993). In Rasmussen syndrome focal clonic seizures are often multifocal with different muscle groups exhibiting differing frequencies and timing. Although a focal clonic motor seizure clearly implies seizure activity in the primary motor area, it does not equate with seizure origin there. Seizures beginning practically anywhere else in the brain can have a focal motor component. Even when focal clonic motor activity is the sole clinical manifestation of the seizure, origin can be in clinical silent areas of the brain both anterior and posterior to the primary motor cortex. Asymmetric tonic seizures (sensorimotor seizures, supplementary sensorimotor seizures, postural seizures, adversive seizures). During seizures originating in the sensorimotor area patients typically assume a sudden tonic posture of the extremities. Although tonic posturing is usually asymmetric (Morris 1988), it can be very symmetric with few if any lateralizing features. Classically, there is tonic arm extension and elevation with forced head deviation to the side of the extended arm with the patient appearing to be looking at his upraised hand, referred to as fencing posture (Bleasel 1996). The tonic arm may also be flexed at the elbow, externally rotated and abducted, a posture previously termed M2e over 40 years ago by Ajmone-Marsan (Ajmone-Marsan 1957). If one arm is tonically extended the other is often flexed. Fingers of the abducted arm are often spread apart. The opposite hand is often clenched to a fist. Asymmetric tonic posture is more pronounced in the upper extremities but can also be observed in the lower extremities. The patient may also exhibit cycling or stepping movements of the legs. Although typical postures have been described as above, in practice, there are probably no clearly consistent patterns but a wide variety of different tonic manifestations. Individual patients, however, exhibit very stereotyped patterns. Consciousness is often preserved. Speech arrest can occur, but vocalization with the patient crying out for help is also possible (Williamson 2000). Tonic posturing may be followed by some brief clonic jerking, often bilateral (Chauvel 1995). If seizures do not secondarily generalize, patients usually have no postictal confusion and rapidly return to normal. There is often nocturnal preponderance of brief, frequent seizures. These seizures can be distinguished from secondarily generalized seizures by the tonic postures, preservation of consciousness, paucity of clonic movements and rapid postictal clearing. Sensorimotor area seizures, however, can also secondarily generalize. When this happens, careful attention to initial clinical seizure manifestations will often suggest the correct diagnosis but, in some cases, it can prove very difficult. Asymmetrical tonic seizures are associated with seizure origin in the supplementary motor area but may also be observed with seizures origin in other areas of the anterior neocortex (Bleasel 1996; Jobst 2000; Williamson 2000; Ikeda et al 2002). Since many cortical areas of the anterior neocortex are clinically silent in terms of clinical seizure activity, analogous to focal clonic motor seizures, asymmetric tonic posturing can result from spread to the supplementary motor area from other cortical regions. Finally, these types of seizures can occur with seizure origin outside the anterior neocortex and may involve spread to the sensorimotor area (Williamson 1992). When sensorimotor area seizures present with typical characteristics, they can be identified on the basis of these characteristics alone. However, since EEG findings in patients with sensorimotor area seizures are often normal or nonspecific, familiarity with the clinical characteristics is essential to avoid diagnostic error. These patients have been misdiagnosed as psychogenic nonepileptic seizures. Patients with probable sensorimotor area seizures were diagnosed with a specific parasomnia termed "paroxysmal nocturnal dystonia," an entity that is now recognized as a type of frontal lobe epilepsy (Scheffer 1994; Provini et al 2000). Bizarre hyperactive seizures (complex partial seizures of frontal lobe origin, complex partial seizures frontal lobe type, hypermotor seizures). These seizures begin suddenly, sometimes explosively, with the onset of complex behavioral automatisms (Williamson 1985b). Patients may jump around, thrash, rock to-and-fro, pound on objects or rock back and forth. They may jump out of bed and run around in circles. Bicycling movements or stepping movements are frequently described. More subtle seizures consist of awakening and scrambling about the bed. Automatisms with sexual content are also reported (genital manipulation, pelvic thrusting), but sexual sensations are not (Spencer 1983). Motor manifestations are often accompanied by vocalization, such as screaming, yelling, shouting, humming, grunting, laughing, or barking. The patient may swear and produce understandable speech. Because of the prominent motor features these automatisms that are distinctly different than the automatisms seen in temporal lobe seizures, they have been called "hypermotor automatisms" (Luders 1998). Consciousness is often preserved during seizures, and the patient clears rapidly after the seizure. The patient may be unable to speak during the seizure but will recall test phrases afterwards. They often have a nocturnal preponderance with flurries of many brief seizures per night. If consciousness had not been impaired initially, it does become clouded with increasing number of seizures during a flurry; the patient may go several days without seizures until the next flurry. These seizures are often very bizarre in appearance and, when coupled with a paucity of EEG findings are frequently misdiagnosed as psychogenic attacks. These hyperactive seizures are associated with seizure origin in various parts of the anterior neocortex (Jobst 2000; Williamson 2000). Although some authors proposed that bizarre hyperactive seizures are associated with origin in the orbitofrontal (Tharp 1972) or anterior cingulate areas, they are also observed with frontopolar, mesial frontal, and dorsal frontal origin (Quesney 1985; Jobst 2000). Absence type seizures (frontal lobe absence, frontal absence). Absence type seizures with altered consciousness and minimal motor involvement have been described in association with origin in the anterior neocortex (Bancaud 1992; So 1998). The patient loses contact with his environment. He may still respond to his surroundings to some degree, but in a slow and inappropriate way. These seizures can be brief and distinct, but they may also last hours or even days. These episodes, when prolonged, are a type of nonconvulsive status epilepticus. Although this condition has also been called "spike-wave stupor," this term is somewhat misleading because of the great variability in the level of altered consciousness, from a barely perceptible change to bland unresponsiveness. For example, during prolonged episodes of this type of nonconvulsive status patients may seem normal but complain of being mildly confused. They may also be partially or completely amnestic for events occurring during the episode despite appearing alert. The ictal EEG pattern consists of generalized disorganized spike-wave activity, a pattern similar to that described for absence status in adults (Niedermeyer 1979). It is, therefore, important to differentiate this type of frontal lobes seizure from idiopathic generalized absence seizures, as they may be clinically and electrographically very similar. Masticatory seizures (opercular seizures). Masticatory seizures are characterized by prominent mastication, swallowing and excessive salivation (Bancaud 1992; Biraben 1999). Consciousness is preserved. If the seizures originate in the dominant hemisphere, they are accompanied by expressive aphasia. They have been localized to the opercular region of the frontal lobes. Seizures originating in the anterior neocortex but presenting as temporal lobe seizures. Due to the close anatomic relationship of the medial, posterior orbitofrontal cortex to the mesial temporal structures, seizures originating in the orbitofrontal cortex may present clinically as temporal lobe seizures (Jobst 2000). They may begin with olfactory hallucinations followed by an altered state of consciousness with the typical oroalimentary and manual automatisms (Bancaud 1992). These seizures can be clinically indistinguishable from mesial temporal lobe seizures, and only further diagnostic studies such as neuroimaging, intracranial EEG recording, or both can correctly identify extratemporal seizure origin. Combined seizure types. Although the various types of frontal lobe seizures may appear as relatively typical examples, it is not uncommon for them to present as mixed forms. For example, an sensorimotor area type seizure may also have some hypermotor automatisms or a seizure can begin with hypermotor automatisms and then evolves into a temporal lobe seizure as the seizure spreads. LOCALIZATION By definition, these seizure types are associated with seizure origin in various areas of the anterior neocortex. Since large areas of the anterior neocortex, such as the prefrontal cortex, may be clinically silent in terms of clinical seizure manifestations, the first clinical evidence of a seizure may be the result of propagation to areas remote from the region of seizure origin. As a result, clinical presentation may not correlate with seizure onset. Focal clonic seizures indicate involvement of the primary motor cortex, but isolated lesions of the primary motor cortex are relatively uncommon. Focal clonic seizures are most commonly seen with diffuse contralateral hemispheric lesions (Chauvel 1992b). Asymmetric tonic seizures are associated with seizure origin in the supplementary motor area; however, as explained above, they may also be the result of secondary spread to the sensorimotor area. Seizures may spread to the sensorimotor area from the prefrontal cortex or from the parietal cortex (Bleasel 1996; Williamson 2000). Asymmetric tonic seizures occasionally can also occur without direct involvement of the sensorimotor area, but are rarely reported (Bancaud 1992; Bleasel 1996). In asymmetric tonic seizures the predominant and sometimes exclusive tonic posturing is contralateral to the side of seizure origin (Morris 1987; Jobst 2000). The lateralizing value of forced head turning with asymmetric tonic posturing has been discussed extensively in the literature. It occurs more commonly contralateral to the side of seizure origin, but not invariably (Robillard 1983; Ochs 1984; Wyllie et al 1986a). If forced head turning occurs shortly before generalization, it is more consistently contralateral to the side of seizure origin (Wyllie et al 1986b). Bizarre hyperactive seizures seem to localize nonspecifically to the anterior neocortex (Williamson 1985b; Waterman 1987). They have been suspected to originate in the orbitofrontal (Ludwig 1972; Tharp 1972; Chang 1991), mesial frontal (Waterman 1987), anterior cingulate (Anonymous 1989; Bancaud 1992), frontopolar area, and frontal dorsal convexity (Quesney 1992). There is no conclusive evidence that any of these locations is more commonly associated with this type of seizure (Jobst 2000; Williamson 2000) and could also represent a frontal release phenomenon. Absence type seizures were reported to originate at the medial surface of the frontal lobes (Bancaud 1992), but have also been observed with frontopolar and frontal convexity seizure onset (Jobst 2000). Masticatory seizures are associated with onset in the frontal operculum (Bancaud 1992; Biraben 1999; Jobst 2000). As discussed above, seizures originating in the orbitofrontal region can present with typical hyperactive automatisms, or they can clinically mimic seizures originating in the temporal lobes (Munari 1992; Munari 1995; Jobst 2000). It has been proposed that the orbitofrontal area may remain clinically silent, and clinical manifestations are just a manifestation of seizure spread. It has also been proposed that the major clinical manifestations are autonomic in nature and not easily recognized (Munari 1992; Munari 1995). PATHOPHYSIOLOGY The basic pathophysiology of seizures of the anterior neocortex is the same as for other focal seizures, which specifically is a localized breakdown of the balance of inhibition and excitation. The striking tendency of certain types of anterior neocortical seizures to occur in nocturnal clusters of frequent brief seizures with little or no postictal confusion, the preservation of consciousness during some very complicated seizures with documented bilateral brain involvement and the propensity of anterior neocortical seizures of all types to evolve into episodes of status epilepticus would strongly suggest that some special, as yet unknown, pathophysiological mechanisms exist. DIFFERENTIAL DIAGNOSIS Much has been written about frontal lobe seizures during the past decades (Penfield 1954; Ajmone-Marsan 1957; Geier 1976; Williamson 1985b; Bancaud 1992; Cascino 1992; Manford 1996). Despite increased recognition and understanding of these seizures, the potential for diagnostic error remains high for certain types of frontal lobe seizures. For example, hyperactive seizures coupled with loud vocalization can have a very bizarre appearance. When this occurs without epileptiform interictal or ictal EEG findings, diagnostic errors are common. Similar problems are associated with sensorimotor area seizures. Familiarity with the condition is of primary importance. For example, if a patient gives a history of frequent nocturnal episodes consisting of stiffening of one side of the body more than the other, or of multiple nocturnal episodes of awakening, scrambling about the bed, and shouting with at least partial preservation of consciousness, the diagnosis should be strongly suggested based on history alone. On the other hand, there are certain seizures originating in the frontal neocortex that do not have clinical characteristics that help locate their region of origin. Examples include frontal lobe absence type seizures as well as seizures beginning in the medial posterior orbital cortex, which preferentially spread to the medial temporal structures and strongly resemble typical temporal lobe seizures. In both examples, imaging is extremely important as EEG findings alone can be confusing or misleading. If the MRI in these examples is normal, then a carefully planned ictal-interictal SPECT study might provide the correct localizing information. DIAGNOSTIC WORKUP An accurate and complete clinical history and neurologic exam is essential to diagnose seizures originating in the anterior neocortex. Neuroimaging should be performed to search for intracerebral lesions. MRI imaging is preferred to CT. Interictal EEG is often of limited use for the diagnosis of seizures of the anterior neocortex. Even long-term interictal EEG recordings may be completely normal. Even though the interictal EEG can be helpful to establish the diagnosis of epilepsy if interictal spikes are observed, the location of interictal spikes can be falsely localizing. For example, patients with orbitofrontal seizure origin may have anterior temporal spikes on EEG. Video and EEG monitoring is often required to establish diagnosis as well as to record clinical seizures and ictal EEG. As previously noted, in a certain percentage of patients even ictal scalp EEG findings may not show definite epileptiform activity and diagnosis has to rely on seizure characteristics. Neuropsychological testing may show cognitive deficits that correlate with anterior neocortical dysfunction. Reformatted MRI and ictal SPECT studies can be helpful to localize seizure origin but are usually only performed in specialized epilepsy centers. If epilepsy surgery is considered, and the MRI is normal, intracranial video and EEG monitoring with subdural or depth electrodes or both is usually mandatory. Functional mapping may be necessary to identify functionally important regions of the brain such as language areas and the primary motor cortex. SYNDROMES AND DISEASES IN WHICH THE SEIZURE TYPE OCCURS Autosomal dominant nocturnal frontal lobe epilepsy. This is a disorder that usually manifests itself in childhood with clusters of brief, nocturnal seizures (Scheffer 1995; Oldani 1996; Hayman 1997; Provini 1999). These may have the appearance of bizarre hyperactive seizures or asymmetric tonic seizures without loss of consciousness. Seizures occur in clusters, exclusively at night. Patients with this syndrome are cognitively and neurologically intact (Tassinari and Michelucci 1997). Imaging studies do not reveal any structural abnormalities and the seizures usually respond well to standard antiepileptic medications (Scheffer 2000). The syndrome was only been recognized over the last decade (Tinuper 1990). Missense mutations of the gene for the neuronal nicotinic acetylcholine receptor alpha 4 subunit (CHRNA4) have been shown to be responsible for the syndrome (Steinlein 2002). The gene has been mapped to chromosome 20q13.2 and 15q24 (Steinlein 1995; Steinlein 1997) and has been shown in Australian, British, Canadian, Spanish, and Japanese and Norwegian families (Tassinari 1997; Nakken 2000). A gene locus on chromosome 1 encoding the beta2 subunit of the nicotinic receptor (CHRNA2) has been reported in Italian and Scottish families (Gambardella 2000; Phillips 2001). The neuronal nicotinic acetylcholine receptors are widespread throughout the frontal lobes, which may explain the association with the frontal lobes. Rasmussen syndrome. Focal clonic seizures and especially epilepsia partialis continua are associated with Rasmussen syndrome, which is characterized by the development of epilepsia partialis continua, slowly progressive hemiparesis, progressive cognitive deficits, and progressive atrophy of the affected hemisphere (So 1997). Seizures are often unresponsive to standard antiepileptic medications and hemispherectomy should be considered if there is no improvement. Diagnosis is made by the typical clinical picture and histopathologic findings (Granata et al 2003). There typically is microglial proliferation, micronodules, and perivascular infiltrations with cuffing and neuronophagia (So 1997). Because of the underlying inflammatory process, immunosuppressive therapy has been suggested (Hart 1994). Antibodies to the GluR3 subunit of the glutamate receptors have been found in patients with Rasmussen syndrome, but the significance of these autoantibodies needs further investigation (Rogers 1994; So 1997; Granata et al 2003). Benign childhood epilepsy with centrotemporal spikes. This disorder is characterized by partial seizures with or without generalization occurring during childhood with typical centrotemporal spikes. There is a genetic predisposition, no cognitive impairment, and usually good response to standard antiepileptic medications. Remission during the second decade of life is the rule (Lerman 1997). Seizures may present as typical focal clonic seizures with unilateral involvement of face, lips, and tongue or as masticatory seizures with drooling and speech arrest (Lerman 1997). Consciousness is often preserved. Benign childhood epilepsy with centrotemporal spikes is a benign syndrome, and intracranial EEG studies are not indicated to exactly localize regions of seizure origin. Multifocal seizure onset including regions of the anterior neocortex has been suggested but was not studied systematically (Loiseau 1992). Fejerman and colleagues (Fejerman et al 2000) describe a variant with difficult to treat seizures but with good prognosis. PROGNOSIS AND COMPLICATIONS The true percentage of patients with seizures originating in the anterior neocortex is not known, as many patients may respond well to medications. Some patients remain intractable despite optimal management with antiepileptic medications. If epilepsy surgery is performed, reported success rates for a good or seizure free outcome vary between 26% and 80% (Williamson 1985b; Waterman 1987; Cascino 1992; Laskowitz 1995; Salanova 1995a; Baumgartner 1996; Smith 1997; So 1998; Swartz 1998; Jobst 2000; Schramm et al 2002). MANAGEMENT Seizures of the anterior neocortex respond to standard antiepileptic medications. As the seizures are focal in origin, carbamazepine or phenytoin are recommended as first line treatment. Because of less sedating side-effects, lamotrigine is increasingly used as monotherapy. If patients are not responsive to monotherapy, other agents may be added. Valproate may prevent secondarily generalization. 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ILAE Abbreviations EEG:electroencephalography FLAIR:fluid attenuated inversion recovery imaging MRI:magnet resonance imaging SPECT:single photon emission computed tomography Synonyms Frontal lobe epilepsy Seizures of the anterior neocortex Subtopics Absence type seizures Asymmetric tonic seizures Bizarre hyperactive seizures Combined seizure types Masticating seizures Major keyword descriptors adversive seizures anterior neocortex complex partial seizures focal clonic frontal absences frontal convexity seizure frontal lobe absences hypermotor automatisms mesial temporal lobe seizures olfactory hallucinations opercular seizures postural seizures seizures sensorimotor area spike-wave stupor supplementary sensorimotor seizures Minor keyword descriptors altered consciousness automatisms frontal lobar frontopolar Jacksonian sensorimotor Age of presentation: 01-23 months 02-05 years 06-12 years 13-18 years 19-44 years Age of typical presentation: 06-12 years 13-18 years Permuted topic, synonyms, subtopics Frontal lobe seizures (seizures of the cerebral cortex) seizures, Frontal lobe lobe seizures, Frontal cortex, seizures of the cerebral cerebral cortex, seizures epilepsy, Frontal lobe anterior neocortex, seizures of the neocortex, seizures of the anterior Related topics Carbamazepine Epilepsy Gelastic seizures Proprioceptive-induced seizures Typical absence seizures Differential diagnosis hyperactive seizure sensorimotor seizures frontal lobe absence type seizures seizures in the medial posterior orbital complex
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