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.
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.
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.
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.
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
Picard F, Bruel D, Servent D, et al. Alteration of the in vivo nicotinic receptor density in ADNFLE patients: a PET study. Brain. Aug 2006;129(Pt 8):2047-60. [Medline].
Brodtkorb E, Picard F. Tobacco habits modulate autosomal dominant nocturnal frontal lobe epilepsy. Epilepsy Behav. Nov 2006;9(3):515-520. [Medline].
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. Sep 9 2008;71(11):795-8. [Medline].
O'Brien TJ, Mosewich RK, Britton JW, Cascino GD, So EL. History and seizure semiology in distinguishing frontal lobe seizures and temporal lobe seizures. Epilepsy Res. Dec 2008;82(2-3):177-82. [Medline].
So NK. Mesial frontal epilepsy. Epilepsia. 1998;39 Suppl 4:S49-61. [Medline].
Kotagal P, Arunkumar GS. Lateral frontal lobe seizures. Epilepsia. 1998;39 Suppl 4:S62-8. [Medline].
Williamson PD, Spencer DD, Spencer SS, Novelly RA, Mattson RH. Complex partial seizures of frontal lobe origin. Ann Neurol. Oct 1985;18(4):497-504. [Medline].
Laskowitz DT, Sperling MR, French JA, O'Connor MJ. The syndrome of frontal lobe epilepsy: characteristics and surgical management. Neurology. Apr 1995;45(4):780-7. [Medline].
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. Oct 11 2005;65(7):1026-31. [Medline].
Bonelli SB, Lurger S, Zimprich F, Stogmann E, Assem-Hilger E, Baumgartner C. Clinical seizure lateralization in frontal lobe epilepsy. Epilepsia. Mar 2007;48(3):517-23. [Medline].
Mosewich RK, So EL, O'Brien TJ, Cascino GD, Sharbrough FW, Marsh WR, et al. Factors predictive of the outcome of frontal lobe epilepsy surgery. Epilepsia. Jul 2000;41(7):843-9. [Medline].
Elsharkawy AE, Alabbasi AH, Pannek H, Schulz R, Hoppe M, Pahs G, et al. Outcome of frontal lobe epilepsy surgery in adults. Epilepsy Res. Oct 2008;81(2-3):97-106. [Medline].
Jeha LE, Najm I, Bingaman W, Dinner D, Widdess-Walsh P, Lüders H. Surgical outcome and prognostic factors of frontal lobe epilepsy surgery. Brain. Feb 2007;130:574-84. [Medline].
Kossoff EH, Rowley H, Sinha SR, Vining EP. A prospective study of the modified Atkins diet for intractable epilepsy in adults. Epilepsia. Feb 2008;49(2):316-9. [Medline].
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