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Frontal Lobe Epilepsy

  • Author: Sheryl Haut, MD; Chief Editor: Selim R Benbadis, MD  more...
 
Updated: Dec 30, 2015
 

Practice Essentials

Frontal lobe epilepsy is characterized by recurrent seizures arising from the frontal lobes. Frequently, seizure types are simple partial or complex partial, often with secondary generalization. Status epilepticus may be associated more commonly with frontal lobe seizures than with seizures arising from other areas.

Signs and symptoms

Time of day is an important characteristic for seizures originating in the frontal lobe, as the majority of these seizures occur between the hours of 2 am and noon.[5] The following features help to distinguish frontal lobe seizures from nonepileptic events:

  • Stereotyped semiology
  • Occurrence during sleep
  • Brief duration (often < 30 seconds)
  • Rapid secondary generalization
  • Prominent motor manifestations
  • Complex automatisms

Other history findings may vary according to the site of involvement, include the following:

  • Dominant hemisphere involvement - May be indicated by prominent speech disturbances
  • Supplementary motor area (SMA) - Typically involves unilateral or asymmetrical, bilateral tonic posturing; may be associated with facial grimacing, vocalization, or speech arrest; seizures frequently preceded by a somatosensory aura; complex automatisms, such as kicking, laughing, or pelvic thrusting, may be present; responsiveness often preserved
  • Primary motor cortex - Usually simple partial motor seizures with clonic or myoclonic movements and preserved consciousness; jacksonian spread to adjacent cortical areas may occur, and secondary generalization is frequent; speech arrest and contralateral adversive or dystonic posturing may be present
  • Medial frontal, cingulate gyrus, orbitofrontal, or frontopolar regions - Complex behavioral events characterized by motor agitation and gestural automatisms; viscerosensory symptoms and strong emotional feelings often described; motor activity repetitive and may involve pelvic thrusting, pedaling, or thrashing, often accompanied by vocalizations or laughter/crying; seizures often bizarre and may be diagnosed incorrectly as psychogenic
  • Dorsolateral cortex - Tonic posturing or clonic movements often associated with either contralateral head and eye deviation, or less commonly, ipsilateral head turn
  • Operculum - Swallowing, salivation, mastication, epigastric aura, fear, and speech arrest often associated with clonic facial movements; gustatory hallucinations also may occur
  • Nonlocalizable frontal seizures - Rare, manifesting as brief staring spells accompanied by generalized spike/wave on EEG, which may be difficult to distinguish from primarily generalized absence seizures; may present as generalized tonic-clonic seizures without obvious focal onset
  • Nocturnal frontal lobe epilepsy - Autosomal dominant inheritance; seizures occur mainly during sleep; characterized by marked motor manifestations, including dystonic posturing, jerking, bending, and rocking; difficult to distinguish from parasomnias

Physical examination may reveal signs suggestive of syndromes that may be associated with epilepsy, such as the following:

  • Facial dysmorphisms
  • Cafe-au-lait spots, hypomelanotic macules, or neurofibromas

See Clinical Presentation for more detail.

Diagnosis

For new-onset seizures, blood tests should be performed to rule out a metabolic cause (eg, hypoglycemia, hypomagnesemia). For patients with an established diagnosis of epilepsy, blood testing for complications may include the following:

  • CBC - Monitor for neutropenia and thrombocytopenia
  • Liver function tests
  • Anticonvulsant levels

Brain imaging

  • MRI is the imaging modality of choice in patients with frontal lobe seizures
  • Underlying lesions are reported to be present in up to 50% of patients with frontal lobe epilepsy
  • Optimally, MRI with gadolinium should be obtained with high resolution, 1 mm thick slices, and multiple sequences; if EEG or other testing indicates a potential epileptogenic zone, thin slices through the area of interest should be requested
  • A field strength of 3 Tesla (3T) can further increase the identification of lesions [10]
  • PET scanning is being increasingly used in the presurgical evaluation of patients with extratemporal epilepsy.
  • On PET scans, interictal hypometabolism, reflective of focal dysfunction, may be seen in areas that were normal on MRI
  • SPECT scans may be obtained during prolonged video-EEG monitoring; hyperperfusion on ictal SPECT scanning suggests an area of seizure onset

Electroencephalography

  • Indicated for all patients with frontal lobe epilepsy
  • Patients with intractable epilepsy, or in whom the diagnosis is doubtful, should undergo prolonged video-EEG monitoring
  • If the events are primarily or exclusively nocturnal, polysomnography should be considered, with extended EEG montages if available
  • Interictal EEGs may be normal
  • On interictal EEG, spikes or sharp waves may be absent; may appear maximal unilaterally, bilaterally, or in the midline; or may appear generalized due to secondary bilateral synchrony; background rhythm abnormalities, with or without focal slowing, may be present
  • Ictal onset often is seen poorly from the scalp and is highly variable in appearance
  • Postictal slowing can be confirmatory, and at times, localizing or lateralizing
  • Patients with suspected frontal lobe epilepsy frequently require invasive EEG monitoring
  • On intracranial EEG, Ictal onset most often appears as a low-voltage, high-frequency discharge (ie, buzz), although rhythmic activity at alpha, theta, or delta frequencies may be seen

See Workup for more detail.

Management

Anticonvulsant therapy should be initiated once the diagnosis of epilepsy is established. Many nocturnal episodes with prominent motor manifestations respond extremely well to carbamazepine. Monotherapy is desirable, some patients require polytherapy.

Patients with medically intractable epilepsy should be considered for resective epilepsy surgery. Other treatment options include the following:

  • Ketogenic diet
  • Modified Atkins diet
  • Vagal nerve stimulator
  • Corpus callosotomy
  • Multiple subpial transections

See Treatment and Medication for more detail.

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Background

Frontal lobe epilepsy is characterized by recurrent seizures arising from the frontal lobes. Frequently, seizure types are simple partial or complex partial, often with secondary generalization. Clinical manifestations tend to reflect the specific area of seizure onset and range from behavioral to motor or tonic/postural changes. Status epilepticus may be associated more commonly with frontal lobe seizures than with seizures arising from other areas.

Seizures may arise from any of the frontal lobe areas, including orbitofrontal, frontopolar, dorsolateral, opercular, supplementary motor area, motor cortex, or cingulate gyrus.

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.

Owing to advances in genetic analysis, an expanded number of genetically inherited frontal lobe epilepsy syndromes have been described. Many of these syndromes are characterized by autosomal dominant inheritance, belonging to a group known as the autosomal dominant nocturnal frontal lobe epilepsies (ADNFLE).

Quality-of-life issues for patients with epilepsy can include the following:

  • Coping with the social stigma of epilepsy
  • Living with restrictions
  • Living with long-term medical therapy

For more information, see Simple Partial Seizures, Complex Partial Seizures, and Status Epilepticus.

Go to Epilepsy and Seizures for an overview of this topic.

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Etiology

Tumors

Reviews indicate that the epileptogenic lesion in approximately one third of patients with refractory frontal lobe seizures is a tumor.

Common tumors causing frontal lobe epilepsy include gangliogliomas, low-grade gliomas, and epidermoid tumors. High-grade tumors more often present with headache or focal deficits, but many are associated with seizures at some time in their course.

Head trauma

Head trauma is a very frequent cause of damage to the frontal lobes. Risk of later epilepsy depends largely on the severity of trauma. The first seizure usually occurs within months, but may not occur for many years.

Pathologic examination of the frontal lobe frequently reveals meningocerebral cicatrix.

Vascular malformations

Three main types are recognized: arteriovenous malformations, cavernous angiomas, and venous angiomas. Arteriovenous malformations and cavernous angiomas are more likely to cause seizures than are venous angiomas.

Developmental lesions

With improvements in neuroimaging, cortical dysplasias increasingly are being recognized as epileptogenic lesions. Other common developmental causes of frontal lobe seizures include hamartomas and nodular heterotopias.

Gliosis

Gliosis is identified in many pathologic specimens following surgical resection for frontal lobe epilepsy. It may follow head trauma, neonatal anoxia, or previous resection; often, no cause is identified.

Encephalitis

Although encephalitis commonly produces temporal lobe epilepsy, frontal lobe seizures may occur.

Inherited frontal lobe epilepsy

Three types of ADNFLE have been described. They are clinically characterized by brief, nocturnal motor seizures that often occur in clusters, mainly during non-REM sleep. Seizures may also occur during daytime naps. A brief aura is typically followed by hyperkinetic or tonic activity and typically shows a good response to carbamazepine. Differentiation from parasomnias remains a challenge.

ADNFLE was the first partial epilepsy identified as a single gene disorder. Mutations in 2 nicotinic acetylcholine receptor genes (nAChR alpha4 and beta2 subunits) have been associated with ADNFLE, with a third potential locus identified.[1] Nicotine use is reported to be associated with decreased seizure frequency in patients with these mutations.[2]

Positron emission tomography (PET) scan studies in ADNFLE demonstrate decreased nAChR density in the right dorsolateral prefrontal region, but increased density in mesencephalon. Dopaminergic pathways in the striatum have been shown to be altered in ADNFLE.[3]

Other familial frontal lobe epilepsies have been identified, including a familial partial epilepsy with variable foci linked to chromosome 22.

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Epidemiology

The exact incidence of frontal lobe epilepsy is not known. In most centers, however, frontal lobe epilepsy accounts for 20-30% of operative procedures involving intractable epilepsy.

Sex predilection

No significant sex-based frequency difference has been reported for frontal lobe epilepsy in epidemiologic studies. However, a comparison of frontal lobe versus temporal lobe seizures captured during epilepsy monitoring has suggested a male predominance in frontal lobe seizures.[4]

Age predilection

Symptomatic frontal lobe epilepsy may affect patients of all ages.

In a large series of cases, the mean subject age was 28.5 years, with age of epilepsy onset 9.3 years for left frontal epilepsy and 11.1 years for right frontal epilepsy.

Morbidity

Complications of frontal lobe epilepsy may include status epilepticus or a comorbid psychiatric or behavioral disturbance.

Status epilepticus is reported in up to 25% of patients with frontal lobe epilepsy. The episodes may be convulsive, nonconvulsive, or simple partial.

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Prognosis

Approximately 65-75% of patients with frontal lobe seizures respond to appropriate anticonvulsants and become seizure free.

The proportion of patients with medically refractory frontal lobe epilepsy who become seizure free from additional medications or surgical options is lower than in patients with temporal lobe epilepsy.

An important feature in prognosis is the early recognition of frontal lobe seizures as an epileptic syndrome rather than as a parasomnia or a psychiatric condition.

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Patient Education

Patient education is important for all patients with epilepsy. Many patients benefit from joining one of the national or regional epilepsy support groups.

Activity restrictions

Patients with epilepsy who are not seizure free have the following restrictions:

  • Driving - Duration of restriction varies by state
  • Operating heavy machinery
  • Activities that involve unprotected heights
  • Swimming alone
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Contributor Information and Disclosures
Author

Sheryl Haut, MD Professor of Clinical Neurology, Albert Einstein College of Medicine; Director, Adult Epilepsy, Montefiore Medical Center

Sheryl Haut, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, American Neurological Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Consultant/DSMB: Acorda;Upsher Smith;Neurelis;Xeris.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, Assistant Dean for the MD/PhD Program, Program Director of the Clinical Neurophysiology Fellowship, University of Texas School of Medicine at San Antonio; Co-Director, South Texas Comprehensive Epilepsy Center, University Hospital System; Director, San Antonio Veterans Affairs Epilepsy Center of Excellence and Neurodiagnostic Centers, Audie L Murphy Veterans Affairs Medical Center

Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Neurological Association, Society for Neuroscience, American Epilepsy Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Brain Sentinel, consultant.<br/>Stakeholder (<5%), Co-founder for: Brain Sentinel.

Chief Editor

Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cyberonics; Eisai; Lundbeck; Sunovion; UCB; Upsher-Smith<br/>Serve(d) as a speaker or a member of a speakers bureau for: Cyberonics; Eisai; Glaxo Smith Kline; Lundbeck; Sunovion; UCB<br/>Received research grant from: Cyberonics; Lundbeck; Sepracor; Sunovion; UCB; Upsher-Smith.

References
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  2. Brodtkorb E, Picard F. Tobacco habits modulate autosomal dominant nocturnal frontal lobe epilepsy. Epilepsy Behav. 2006 Nov. 9(3):515-520. [Medline].

  3. Fedi M, Berkovic SF, Scheffer IE, O'Keefe G, Marini C, Mulligan R, et al. Reduced striatal D1 receptor binding in autosomal dominant nocturnal frontal lobe epilepsy. Neurology. 2008 Sep 9. 71(11):795-8. [Medline].

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  10. Knake S, Triantafyllou C, Wald LL, Wiggins G, Kirk GP, Larsson PG, et al. 3T phased array MRI improves the presurgical evaluation in focal epilepsies: a prospective study. Neurology. 2005 Oct 11. 65(7):1026-31. [Medline].

  11. Bonelli SB, Lurger S, Zimprich F, Stogmann E, Assem-Hilger E, Baumgartner C. Clinical seizure lateralization in frontal lobe epilepsy. Epilepsia. 2007 Mar. 48(3):517-23. [Medline].

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  13. Elsharkawy AE, Alabbasi AH, Pannek H, Schulz R, Hoppe M, Pahs G, et al. Outcome of frontal lobe epilepsy surgery in adults. Epilepsy Res. 2008 Oct. 81(2-3):97-106. [Medline].

  14. Jeha LE, Najm I, Bingaman W, Dinner D, Widdess-Walsh P, Lüders H. Surgical outcome and prognostic factors of frontal lobe epilepsy surgery. Brain. 2007 Feb. 130:574-84. [Medline].

  15. Kossoff EH, Rowley H, Sinha SR, Vining EP. A prospective study of the modified Atkins diet for intractable epilepsy in adults. Epilepsia. 2008 Feb. 49(2):316-9. [Medline].

  16. FDA approves Aptiom to treat seizures in adults. US Food and Drug Administration. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm374358.htm. Accessed: November 12, 2013.

 
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