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Temporal Lobe Epilepsy

  • Author: David Y Ko, MD; Chief Editor: Selim R Benbadis, MD  more...
 
Updated: Apr 29, 2014
 

Practice Essentials

Temporal lobe epilepsy was defined in 1985 by the International League Against Epilepsy (ILAE) as a condition characterized by recurrent, unprovoked seizures originating from the medial or lateral temporal lobe. The seizures associated with this condition consist of simple partial seizures without loss of awareness and complex partial seizures (ie, with loss of awareness).

Signs and symptoms

Common features of temporal lobe epilepsy include the following:

  • Memory impairment
  • Aura

Auras may be classified by symptom type, as follows:

  • Somatosensory and special sensory – Olfactory, gustatory, and visual illusions and hallucinations; vertigo
  • Autonomic – Changes in heart rate, piloerection, and sweating
  • Psychic – Déjà vu or jamais vu; depersonalization or derealization; fear or anxiety; dissociation

Features of temporal lobe complex partial seizure may include the following:

  • Aura
  • Motionless stare, dilated pupils, and behavioral arrest
  • Oral alimentary automatisms, manual automatisms, or unilateral dystonic limb posturing; reactive automatisms may also be seen
  • Possible evolution to a secondarily generalized tonic-clonic seizure
  • Postictal period that can include confusion, aphasia, or (by definition) amnesia

See Presentation for more detail.

Diagnosis

Diagnostic modalities that may be considered include the following:

  • Magnetic resonance imaging (MRI; the neuroimaging modality of choice for temporal lobe epilepsy)
  • Computed tomography (CT; poor resolution compared to that of MRI)
  • Positron emission tomography (PET; useful for interictal seizure localization in surgical candidates when MRI is normal)
  • Single-photon emission CT (SPECT; also an adjunctive imaging modality useful only for surgical candidates)
  • Magnetic resonance spectroscopy (investigational)
  • Electroencephalography (EEG; indicated in all patients with suspected temporal lobe epilepsy)
  • Magnetoencephalography (MEG; mainly used for coregistration with MRI to give magnetic source imaging in 3-dimensional space)

See Workup for more detail.

Management

Antiepileptic drugs (AEDs) traditionally used for seizure control in temporal lobe epilepsy are as follows:

  • Phenytoin
  • Carbamazepine
  • Valproate
  • Phenobarbital

Newer AEDs, which appear to be comparably effective but with fewer side effects, include the following:

  • Gabapentin
  • Topiramate
  • Lamotrigine
  • Levetiracetam
  • Oxcarbazepine
  • Zonisamide
  • Lacosamide
  • Vigabatrin
  • Ezogabine
  • Rufinamide

Nonpharmacologic treatments for temporal lobe epilepsy are as follows:

  • Vagus nerve stimulation (VNS; approved for treatment of intractable partial epilepsy in patients aged 12 years and older)
  • Temporal lobectomy (the definitive treatment for medically intractable temporal lobe epilepsy)

See Treatment and Medication for more detail.

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Background

The temporal lobe is the most epileptogenic region of the brain. In fact, 90% of patients with temporal interictal epileptiform abnormalities on their electroencephalograms (EEGs) have a history of seizures.

Temporal lobe epilepsy was defined in 1985 by the International League Against Epilepsy (ILAE) as a condition characterized by recurrent, unprovoked seizures originating from the medial or lateral temporal lobe.

The seizures associated with temporal lobe epilepsy consist of simple partial seizures without loss of awareness and complex partial seizures (ie, with loss of awareness). The individual loses awareness during a complex partial seizure because the seizure spreads to involve both temporal lobes, which causes impairment of memory. The partial seizures may secondarily generalize. As humans have 2 temporal lobes, one side is domininant for language function, and, if there is marked aphasia, seizure focus may be lateralized to the left temporal lobe for most right-handed people.

Temporal lobe epilepsy was first recognized in 1881 by John Hughlings Jackson, who described "uncinate fits" seizures arising from the uncal part of temporal lobe and the "dreamy state."

In the 1940s, Gibbs et al introduced the term psychomotor epilepsy.[1] The international classification of epileptic seizures (1981) replaced the term psychomotor seizures with complex partial seizures. Complex means that there is some alteration of conciouness, versus a simple partial seizure, which means there is no alteration of conciouness. The ILAE classification of the epilepsies uses the term temporal lobe epilepsy and divides the etiologies into cryptogenic (presumed unidentified etiology), idiopathic (genetic), and symptomatic (cause known, eg, tumor).

For more information, see Epilepsy and Seizures.

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Etiology

Hippocampal sclerosis

Approximately two thirds of patients with temporal lobe epilepsy treated surgically have hippocampal sclerosis as the pathologic substrate. Hippocampal sclerosis involves hippocampal cell loss in the CA1 and CA3 regions and the dentate hilus. The CA2 region is relatively spared.

Hippocampal sclerosis produces a clinical syndrome called mesial temporal lobe epilepsy (MTLE).

The clinical correlate of hippocampal sclerosis on neuroimaging on magnetic resonance imaging (MRI) is called mesial temporal lobe sclerosis (MTS), which is high-signal intensity on either T2-weighted or fluid-attenuated inversion recovery (FLAIR)–sequence MRIs and/or atrophy of the hippocampi.

The etiologies of temporal lobe epilepsy include the following:

  • Infections, eg, herpes encephalitis, bacterial meningitis, neurocysticercosis
  • Trauma producing contusion or hemorrhage that results in encephalomalacia or cortical scarring; difficult, traumatic delivery such as forceps deliveries
  • Hamartomas
  • Malignancies (eg, meningiomas, gliomas, gangliomas)
  • Paraneoplastic (anti-Hu , NMDA-receptor antibodies)
  • Vascular malformations (ie, arteriovenous malformation, cavernous angioma)
  • Cryptogenic (a cause is presumed but has not been identified)
  • Idiopathic (genetic)

The last of the above etiologies, idiopathic, is rare. Familial temporal lobe epilepsy was described by Berkovic and colleagues,[2] and partial epilepsy with auditory features was described by Scheffer and colleagues.

Febrile seizures

A subset of children with complex febrile convulsions appears to be at risk of developing temporal lobe epilepsy in later life. Complex febrile seizures are febrile seizures that last longer than 15 minutes, have focal features, or recur within 24 hours.

The association of simple febrile seizure with temporal lobe epilepsy has been controversial.

Go to Febrile Seizures for complete information on this topic.

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Epidemiology

Approximately 50% of patients with epilepsy have partial epilepsy. Partial epilepsy is often of temporal lobe origin. However, the true prevalence of temporal lobe epilepsy is not known, since not all cases of presumed temporal lobe epilepsy are confirmed by video-electroencephalography and most cases are classified by clinical history and interictal electroencephalogram (EEG) findings alone.

Sex and age predilection

Temporal lobe epilepsy is not more common in one sex, but female patients may experience catamenial epilepsy, which is an increase in seizures during the menstrual period.

Epilepsy occurs in all age groups. Recently, a significant increase in new-onset seizures in elderly persons has been recognized.

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Prognosis

In comparison with the general population, morbidity and mortality are increased in persons with temporal lobe epilepsy, due to increased accidents from the episodes of consciousness loss.

Mortality also results from sudden unexpected death in epilepsy (SUDEP). Patients with refractory temporal lobe epilepsy, especially those with secondarily generalized tonic clonic seizures, have a risk of sudden death that is 50 times greater than that in the general population.

Epilepsy surgery seems to modify the risk of SUDEP if the patient remains seizure free. In patients who have undergone surgery, the mortality rate becomes equivalent to that of the general age- and sex-matched population.

The presence of a seizure-free state 2 years after anterior temporal lobectomy is predictive of long-term seizure-free outcome for the patient.

About 47-60% of patients become seizure free with medical treatment. After 3 first-line antiepileptic drugs (AEDs) have failed, the chance for seizure freedom is 5-10%. The ILAE now has a formal definition of medically intractable/drug-resistant epilepsy, which defined as after a patient has had an adequate trial with 2 antiepileptic drugs and is still having seizures. Surgery in well-selected patients with refractory temporal lobe epilepsy yields a seizure-free outcome rate of 70-80%.

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Patient Education

Fetal anomalies due to antiepileptic medications

Physicians should carefully document on the chart that they have explained to their female patients with epilepsy about the increased risk of fetal anomalies associated with antiepileptic medications, a 2-fold increase (4-6%), and the increased risk of neural tube defects with valproate (1.5-2.0%) and carbamazepine (0.5%).

Patients should be told that most women with epilepsy have healthy children (90-95%). They also should be told that the chance of a normal pregnancy outcome is increased with planned pregnancies, improved seizure control, folate supplementation (0.4-4 mg each day prior to pregnancy), minimizing the number of AEDs used, and never abruptly discontinuing AEDs without consulting the physician.

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

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Contributor Information and Disclosures
Author

David Y Ko, MD Associate Professor of Clinical Neurology, Associate Director, USC Adult Epilepsy Program, Keck School of Medicine of the University of Southern California

David Y Ko, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Headache Society, American Clinical Neurophysiology Society

Disclosure: Received honoraria from UCB for speaking and teaching; Received consulting fee from Lundbeck for consulting; Received consulting fee from Westward for consulting; Received consulting fee from Esai for consulting; Received consulting fee from Supernus for consulting; Received consulting fee from Sunovion for speaking and teaching.

Coauthor(s)

Soma Sahai-Srivastava, MD Director of Neurology Ambulatory Care Services, LAC and USC Medical Center; Assistant Professor, Department of Neurology, Keck School of Medicine of the University of Southern California

Soma Sahai-Srivastava, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Headache Society

Disclosure: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida Morsani 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, American Medical Association

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 (Livanova); Eisai; Lundbeck; Sunovion; UCB<br/>Received research grant from: Cyberonics (Livanova); GW, Lundbeck; Sunovion; UCB; Upsher-Smith.

Acknowledgements

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 Medscape Reference articles that I wrote or edited.

Erasmo A Passaro, MD, FAAN Director, Comprehensive Epilepsy Program/Clinical Neurophysiology Lab, Bayfront Medical Center, Florida Center for Neurology

Erasmo A Passaro, MD, FAAN is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Association, and American Society of Neuroimaging

Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Forest Honoraria Speaking and teaching

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

References
  1. Gibbs EL, Gibbs FA, Fuster B. Psychomotor epilepsy. Arch Neurol Psychiatry. 1948. 60:331-339.

  2. Berkovic SF, McIntosh A, Howell RA, Mitchell A, Sheffield LJ, Hopper JL. Familial temporal lobe epilepsy: a common disorder identified in twins. Ann Neurol. 1996 Aug. 40(2):227-35. [Medline].

  3. Acharya V, Acharya J, Lüders H. Olfactory epileptic auras. Neurology. 1998 Jul. 51(1):56-61. [Medline].

  4. Engel J Jr, McDermott MP, Wiebe S, Langfitt JT, Stern JM, Dewar S, et al. Early surgical therapy for drug-resistant temporal lobe epilepsy: a randomized trial. JAMA. 2012 Mar 7. 307(9):922-30. [Medline].

  5. Semah F, Picot MC, Adam C, Broglin D, Arzimanoglou A, Bazin B, et al. Is the underlying cause of epilepsy a major prognostic factor for recurrence?. Neurology. 1998 Nov. 51(5):1256-62. [Medline].

  6. Foldvary N, Nashold B, Mascha E, Thompson EA, Lee N, McNamara JO, et al. Seizure outcome after temporal lobectomy for temporal lobe epilepsy: a Kaplan-Meier survival analysis. Neurology. 2000 Feb 8. 54(3):630-4. [Medline].

  7. Bandt SK, Werner N, Dines J, Rashid S, Eisenman LN, Hogan RE, et al. Trans-middle temporal gyrus selective amygdalohippocampectomy for medically intractable mesial temporal lobe epilepsy in adults: Seizure response rates, complications, and neuropsychological outcomes. Epilepsy Behav. 2013 Jul. 28(1):17-21. [Medline].

  8. Anderson P. AED withdrawal postsurgery: no point in waiting. Medscape Medical News. December 12, 2013. [Full Text].

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