Partial Epilepsies 

  • Author: Alberto Figueroa Garcia, MD; Chief Editor: Helmi L Lutsep, MD   more...
 
Updated: Jun 7, 2011
 

Background

Partial epilepsies are epileptic disorders in which seizure semiology or findings on investigation disclose localized origin of seizures. In children, cortical dysplasias and low-grade neoplasms are the most commonly identified causes.

Partial epilepsies represent the most common type of adult-onset epilepsy. Most adult-onset localization-related epilepsies do not have an identifiable etiology (ie, neuroimaging studies are most often normal). When a cause is found, it can include various structural lesions (eg, traumatic scars, neoplasms, vascular malformations, strokes, neuronal heterotopias).

Obtaining a description of the seizures from the patient and any witnesses is critical. The description needs to include a description of the patient’s state of consciousness during the seizure, to determine whether the seizure is a simple or complex partial seizure (see Clinical Presentation). Further evaluation, which may include neuroimaging, is important for determining the specific disorder, in order to determine prognosis and guide therapy (see Workup).

Partial epilepsies are generally treated with antiepileptic drugs (AEDs). Nonpharmacologic treatments in certain refractory cases include surgery and dietary modification (see Treatment and Management).

Go to Epilepsy and Seizures for a general overview of this topic.

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Pathophysiology

Most partial epilepsies are the result of a localized brain abnormality, even though in most patients the abnormality cannot be seen with imaging techniques.

Only a few partial epilepsies are genetic; most are lesional. Unfortunately, in the current classification, they are referred to as idiopathic. The term idiopathic is often misunderstood in this setting. While generally idiopathic means "of unknown cause," idiopathic epilepsies are not truly of unknown cause. This terminology most likely will be corrected in the upcoming classification system of the International League Against Epilepsy (ILAE). Idiopathic epilepsies are determined genetically and have no apparent structural cause, with seizures as the only manifestation of the condition.

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Etiology

Most partial epilepsies are caused by a localized brain abnormality, which may or may not be visible on imaging studies. If the cause is found, the epilepsy is said to be symptomatic. If imaging studies are normal, the cause remains elusive and the disorder is said to be cryptogenic. Although imaging studies often have negative results, advances in neuroimaging techniques have resulted in the identification of lesions in increasing numbers of cases. Such lesions include low-grade tumors, hippocampal sclerosis, and subtle cortical dysplasias.

Because of dramatic differences in electroclinical semiology and management, localization-related epilepsies usually are divided into mesiotemporal and neocortical. The most common localization-related epilepsy in adults is mesiotemporal lobe epilepsy, but, in neonates and young children, this is less common than neocortical epilepsy.

The most common cause of temporal lobe epilepsy in candidates for epilepsy surgery in adults is hippocampal sclerosis, while in children, etiologies are dominated by cortical dysplasias and low-grade neoplasms.

Most adult-onset localization-related epilepsies do not have an identifiable etiology (ie, MRI is most often normal); this is well known. When a cause is found, it can include various structural lesions (eg, traumatic scars, neoplasms, vascular malformations, strokes, neuronal heterotopias).

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Epidemiology

The prevalence of epilepsy is approximately 1% of the population, both in the United States and internationally. Most adult-onset epilepsies are partial epilepsies. Males and females are equally affected. The age-related incidence follows a U-shaped curve, with a peak in the first year of life and an increase during the sixth and seventh decades. (See the image below.)

This graph illustrates the 2 peaks of incidence ofThis graph illustrates the 2 peaks of incidence of epilepsy: early and late in life.
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Prognosis

In the United States, the mortality rate from epilepsy decreased from 0.8 deaths per 100,000 population in 1979 to 0.7 deaths per 100,000 population in 1986; it was 0.6 deaths per 100,000 persons for white males and females but 1.7 deaths per 100,000 persons for black males and 1 death per 100,000 persons for black females. No specific data are available for partial epilepsy.

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Patient Education

For patient education information, see the Brain and Nervous System Center, as well as Epilepsy.

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Contributor Information and Disclosures
Author

Alberto Figueroa Garcia, MD  Resident Physician, Department of Neurology, University of South Florida College of Medicine

Alberto Figueroa Garcia, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Coauthor(s)

Vikas K Agrawal, MD  Attending Neurologist, Medical Director of Stroke Unit, Bronx Lebanon Hospital Center; Clinical Instructor, Albert Einstein College of Medicine

Vikas K Agrawal, MD is a member of the following medical societies: American Academy of Neurology and American Medical Association

Disclosure: Nothing to disclose.

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 Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Specialty Editor Board

Claude G Wasterlain, MD  Chair, Department of Neurology, VA Greater Los Angeles Health Care System; Distinguished Professor and Vice-Chair, Department of Neurology, University of California, Los Angeles, David Geffen School of Medicine

Claude G Wasterlain, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Federation for Medical Research, American Neurological Association, Royal Society of Medicine, and Society for Neuroscience

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

Jose E Cavazos, MD, PhD, FAAN  Associate Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, 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 of the San Antonio Veterans Affairs Epilepsy Center of Excellence and Neurodiagnostic Centers, Audie L Murphy Veterans Affairs Medical Center

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

Disclosure: GXC Global, Inc. Intellectual property rights Medical Director - company is to develop a seizure detecting device. No conflict with any of the eMedicine articles that I wrote or edited.

Chief Editor

Helmi L Lutsep, MD  Professor, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, Oregon Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

References
  1. Cohn A. Stool withholding presenting as a cause of non-epileptic seizures. Dev Med Child Neurol. Oct 2005;47(10):703-5. [Medline].

  2. Rudzinski LA, Shih JJ. The Classification of Seizures and Epilepsy Syndromes. CONTINUUM: Lifelong Learning in Neurology. Jun 2010;16(3):15-35. [Full Text].

  3. Sveinbjornsdottir S, Duncan JS. Parietal and occipital lobe epilepsy: a review. Epilepsia. May-Jun 1993;34(3):493-521. [Medline].

  4. Naritoku DK, Warnock CR, Messenheimer JA, Borgohain R, Evers S, Guekht AB, et al. Lamotrigine extended-release as adjunctive therapy for partial seizures. Neurology. Oct 16 2007;69(16):1610-8. [Medline].

  5. Richy FF, Banerjee S, Brabant Y, Helmers S. Levetiracetam extended release and levetiracetam immediate release as adjunctive treatment for partial-onset seizures: an indirect comparison of treatment-emergent adverse events using meta-analytic techniques. Epilepsy Behav. Oct 2009;16(2):240-5. [Medline].

  6. Powell G, Saunders M, Marson AG. Immediate-release versus controlled-release carbamazepine in the treatment of epilepsy. Cochrane Database Syst Rev. Jan 20 2010;CD007124. [Medline].

  7. Benbadis SR. Evaluation for surgical treatment of partial epilepsy: an overview. Wis Med J. 1995;94(9):500-4. [Medline].

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This graph illustrates the 2 peaks of incidence of epilepsy: early and late in life.
 
 
 
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