eMedicine Specialties > Neurology > Seizures and Epilepsy

Temporal Lobe Epilepsy

Author: David Y Ko, MD, Associate Professor, Department of Neurology, University of Southern California Keck School of Medicine
Coauthor(s): Soma Sahai-Srivastava, MD, Director of Neurology Ambulatory Care Services, LAC and USC Medical Center; Assistant Professor, Department of Neurology, University of Southern California
Contributor Information and Disclosures

Updated: Apr 8, 2009

Introduction

Background

Temporal lobe epilepsy (TLE) 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.

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.6 The international classification of epileptic seizures (1981) replaced the term psychomotor seizures with complex partial seizures. 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).

Pathophysiology

Although the causes of temporal lobe epilepsy are widely varied, hippocampal sclerosis is the most common pathologic finding. Hippocampal sclerosis involves hippocampal cell loss in the CA1 and CA3 regions and the dentate hilus. The CA2 region is relatively spared. The clinical correlate on neuroimaging on MRI is called mesial temporal lobe sclerosis.

For more information, see Pathophysiology in the article Seizures and Epilepsy: Overview and Classification.

Frequency

United States

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-EEG and most cases are classified by clinical history and interictal EEG findings alone. The temporal lobe is the most epileptogenic region of the brain. In fact, 90% of patients with temporal interictal epileptiform abnormalities on their EEG have a history of seizures.

Sex

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

Age

Epilepsy occurs in all age groups, but a group where it was underrecognized is in elderly persons. Epilepsy in elderly persons may not be as dramatic and often may present as confusion or memory lapses. The index for suspicion should be low as patients are often misdiagnosed and not treated appropriately.

Clinical

History

  • Aura
    • Auras occur in approximately 80% of temporal lobe seizures. They are a common feature of simple partial seizures and usually precede complex partial seizures of temporal lobe origin.
    • Auras may be classified by symptom type; the types comprise somatosensory, special sensory, autonomic, or psychic symptoms.
  • Somatosensory and special sensory phenomena
    • Olfactory and gustatory illusions and hallucinations may occur. Acharya et al found that olfactory auras are more commonly associated with temporal lobe tumors than with other causes of temporal lobe epilepsy.1
    • Auditory hallucinations consist of a buzzing sound, a voice or voices, or muffling of ambient sounds. This type of aura is more common with neocortical temporal lobe epilepsy than with other types of temporal lobe epilepsy.
    • Patients may report distortions of shape, size, and distance of objects.
    • These visual illusions are unlike the visual hallucinations associated with occipital lobe seizure in that no formed elementary visual image is noted, such as the visual image of a face that may be seen with seizures arising from the fusiform or the inferior temporal gyrus.
    • Things may appear shrunken (micropsia) or larger (macropsia) than usual.
    • Tilting of structures has been reported. Vertigo has been described with seizures in the posterior superior temporal gyrus.
  • Psychic phenomena
    • Patients may have a feeling of déjà vu or jamais vu, a sense of familiarity or unfamiliarity, respectively.
    • Patients may experience depersonalization (ie, feeling of detachment from oneself) or derealization (ie, surroundings appear unreal).
    • Fear or anxiety usually is associated with seizures arising from the amygdala. Sometimes, the fear is strong, described as an "impending sense of doom."
    • Patients may describe a sense of dissociation or autoscopy, in which they report seeing their own body from outside.
  • Autonomic phenomena are characterized by changes in heart rate, piloerection, and sweating. Patients may experience an epigastric "rising" sensation or nausea.

Physical

  • Following the aura, a temporal lobe complex partial seizure begins with a wide-eyed, motionless stare, dilated pupils, and behavioral arrest. Oral alimentary automatisms such as lip smacking, chewing, and swallowing may be noted. Manual automatisms or unilateral dystonic posturing of a limb also may be observed.
  • Patients may continue their ongoing motor activity or react to their surroundings in a semipurposeful manner (ie, reactive automatisms). They can have repetitive stereotyped manual automatisms.
  • A complex partial seizure may evolve to a secondarily generalized tonic-clonic seizure. Often, the documentation of a seizure only notes the generalized tonic-clonic component of the seizure. A careful history from the patient or an observer is needed to elicit the partial features of either a simple seizure or a complex partial seizure before the secondarily generalized seizure is important.
  • Patients usually experience a postictal period of confusion, which distinguishes temporal lobe epilepsy from absence seizures, which are not associated with postictal confusion. In addition, absence seizures are not associated with auras nor with complex automatisms. Postictal aphasia suggests onset in the language-dominant temporal lobe.
  • Most auras and automatisms last a very short period—seconds or 1-2 minutes. The postictal phase may last for a longer period (several minutes). By definition, amnesia occurs during a complex partial seizure because of bilateral hemispheric involvement.

Causes

  • Approximately two thirds of patients with temporal lobe epilepsy treated surgically have hippocampal sclerosis as the pathologic substrate.
  • 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)
    • Vascular malformations (ie, arteriovenous malformation, cavernous angioma)
    • Cryptogenic: A cause is presumed but has not been identified.
    • Idiopathic (genetic): This is rare. Familial temporal lobe epilepsy was described by Berkovic and colleagues3 , and partial epilepsy with auditory features was described by Scheffer and colleagues.
  • Hippocampal sclerosis produces a clinical syndrome called mesial temporal lobe epilepsy (MTLE).
  • Febrile seizures: The association of simple febrile seizure with temporal lobe epilepsy has been controversial. However, a subset of children with complex febrile convulsions appear 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.

More on Temporal Lobe Epilepsy

Overview: Temporal Lobe Epilepsy
Differential Diagnoses & Workup: Temporal Lobe Epilepsy
Treatment & Medication: Temporal Lobe Epilepsy
Follow-up: Temporal Lobe Epilepsy
References

References

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

  2. Adams RD, Victor M, Ropper AH. Epilepsy and other seizure disorders. Principles of Neurology. 1997;313-343.

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

  4. Engel J, Williamson PD, Heinz-Gregor W. Mesial Temporal Lobe Epilepsy. Epilepsy: A Comprehensive Textbook. 1997;2417-2426.

  5. Foldvary N, Nashold B, Mascha E. Seizure outcome after temporal lobectomy for temporal lobe epilepsy: a Kaplan-Meier survival analysis. Neurology. Feb 8 2000;54(3):630-4. [Medline].

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

  7. Gillham R, Kane K, Bryant-Comstock L. A double-blind comparison of lamotrigine and carbamazepine in newly diagnosed epilepsy with health-related quality of life as an outcome measure. Seizure. Sep 2000;9(6):375-9. [Medline].

  8. Harvey AS, Berkovic SF, Wrennall JA. Temporal lobe epilepsy in childhood: clinical, EEG, and neuroimaging findings and syndrome classification in a cohort with new-onset seizures. Neurology. Oct 1997;49(4):960-8. [Medline].

  9. Harvey AS, Grattan-Smith JD, Desmond PM. Febrile seizures and hippocampal sclerosis: frequent and related findings in intractable temporal lobe epilepsy of childhood. Pediatr Neurol. Apr 1995;12(3):201-6. [Medline].

  10. Hennessy MJ, Langan Y, Elwes RD. A study of mortality after temporal lobe epilepsy surgery. Neurology. Oct 12 1999;53(6):1276-83. [Medline].

  11. Jeong SW, Lee SK, Kim KK. Prognostic factors in anterior temporal lobe resections for mesial temporal lobe epilepsy: multivariate analysis. Epilepsia. Dec 1999;40(12):1735-9. [Medline].

  12. Kim WJ, Park SC, Lee SJ. The prognosis for control of seizures with medications in patients with MRI evidence for mesial temporal sclerosis. Epilepsia. Mar 1999;40(3):290-3. [Medline].

  13. Luciano D. Partial seizures of frontal and temporal origin. Neurol Clin. Nov 1993;11(4):805-22. [Medline].

  14. Passaro EA, Beydoun A. Identification of potential candidates for epilepsy surgery. eMedicine Journal [serial online]. 2001. [Full Text].

  15. Passaro EA, Beydoun A. Presurgical Evaluation of Medically Refractory Epilepsy. eMedicine Journal [serial online]. 2001. [Full Text].

  16. Passaro EA, Beydoun A, Minecan D. Outcome of epilepsy surgery. eMedicine Journal [serial online]. 2001. [Full Text].

  17. Semah F, Picot MC, Adam C. Is the underlying cause of epilepsy a major prognostic factor for recurrence?. Neurology. Nov 1998;51(5):1256-62. [Medline].

  18. Spencer DC, Morrell MJ, Risinger MW. The role of the intracarotid amobarbital procedure in evaluation of patients for epilepsy surgery. Epilepsia. Mar 2000;41(3):320-5. [Medline].

  19. Sperling MR, Feldman H, Kinman J. Seizure control and mortality in epilepsy. Ann Neurol. Jul 1999;46(1):45-50. [Medline].

  20. Wiebe S, Blume WT, Girvin JP. A randomized, controlled trial of surgery for temporal-lobe epilepsy. N Engl J Med. Aug 2 2001;345(5):311-8. [Medline].

  21. Williamson PD, Thadani VM, French JA. Medial temporal lobe epilepsy: videotape analysis of objective clinical seizure characteristics. Epilepsia. Nov 1998;39(11):1182-8. [Medline].

  22. Winawer MR, Ottman R, Hauser WA. Autosomal dominant partial epilepsy with auditory features: defining the phenotype. Neurology. Jun 13 2000;54(11):2173-6. [Medline].

Further Reading

Keywords

temporal lobe epilepsy, psychomotor seizures, limbic seizures, TLE, aura, recurrent unprovoked seizures, simple partial seizures, complex partial seizures, uncinate fits, dreamy state, psychomotor epilepsy, hippocampal sclerosis, partial epilepsy, olfactory illusions, gustatory illusions, temporal lobe tumors, auditory hallucinations, neocortical TLE, visual illusions, micropsia, macropsia, vertigo, depersonalization, derealization, manual automatisms, unilateral dystonic posturing

oral alimentary automatisms, reactive automatisms, repetitive stereotyped manual automatisms, secondarily generalized tonic-clonic seizure, postictal period of confusion, postictal aphasia, amnesia, herpes encephalitis, bacterial meningitis, encephalomalacia, cortical scarring, hamartomas, gliomas, arteriovenous malformation, cavernous angioma, mesial temporal lobe epilepsy, MTLE, febrile seizures, complex febrile convulsions

Contributor Information and Disclosures

Author

David Y Ko, MD, Associate Professor, Department of Neurology, University of Southern California Keck School of Medicine
David Y Ko, MD is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Medical Association, and California Medical Association
Disclosure: Pfizer Honoraria Speaking and teaching; UCB Grant/research funds clinical trials; Johnson and Johnson Grant/research funds clinical trials

Coauthor(s)

Soma Sahai-Srivastava, MD, Director of Neurology Ambulatory Care Services, LAC and USC Medical Center; Assistant Professor, Department of Neurology, University of Southern California
Soma Sahai-Srivastava, MD is a member of the following medical societies: American Academy of Neurology, American Headache Society, and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Erasmo A Passaro, MD, Director, Comprehensive Epilepsy Program/Clinical Neurophysiology Lab, Bayfront Medical Center Florida Center for Neurology
Erasmo A Passaro, 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, and American Society of Neuroimaging
Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Takeda Honoraria Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Jose E Cavazos, MD, PhD, FAAN, Associate Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, University of Texas Health Science Center at San Antonio; Co-Director, South Texas Comprehensive Epilepsy Center; Director of the Epilepsy Center, 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 Society for Neuroscience
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
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: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
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: Nothing to disclose.

 
 
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