Temporal Lobe Epilepsy

Updated: Dec 22, 2017
  • Author: David Y Ko, MD; Chief Editor: Selim R Benbadis, MD  more...
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Overview

Practice Essentials

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 this condition consist of simple partial seizures without loss of awareness, now categorized as focal aware seizures, and complex partial seizures (ie, with loss of awareness), now called focal impaired awareness seizures. Secondarily generalized seizures are now called focal to bilateral tonic-clonic seizures under the updated 2017 ILAE classication. [1]  Temporal lobe epilepsy is a common type of epilepsy that is sometimes difficult to diagnose, but once diagnosed it can be effectively treated with medications. Medically intractable temporal lobe epilepsy is amenable to epilepsy surgery with a very high seizure-free rate.

Signs and symptoms

Common features of temporal lobe epilepsy include the following:

  • Memory impairment

  • Aura (now called focal aware)

Auras/focal aware may be classified by symptom type, as follows:

  • Sensory – auditory, gustatory, hot-cold sensations, olfactory, somatosensory, vestibular, visual

  • Autonomic – Heart rate Change (asytole, bradycardia, palpitations, tachycardia), flushing, gastrorintestinal, pallor, piloerection, respiratory

  • Cognitive/psychic – Déjà vu or jamais vu, dissociation, depersonalization or derealization, forced thinking, aphasia/dysphasia, memory

  • Emotional/affective - agitation, aggression, anger, anxiety, fear, paranoia, pleasure, crying (dacrystic) or laughing 

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

  • Aura/focal ware

  • Motionless stare, dilated pupils, and behavioral arrest

  • Automatism - Oral-facial, eye blinking, alimentary, manual  or unilateral dystonic limb posturing, perserveration, vocalization/speech

  • Possible evolution to a secondarily generalized tonic-clonic seizure, now called bilateral tonic clonic

  • Postictal period that can include confusion, aphasia, or (by definition) amnesia

See Presentation for more detail.

Diagnosis

A good history and physical is tantamount for diagnosis of TLE.  Diagnostic modalities that may be considered include the following:

  • Magnetic resonance imaging (MRI); the neuroimaging modality of choice for temporal lobe epilepsy, especially coronal cuts

  • Computed tomography (CT); poor resolution compared to that of MRI, but is strong for calcified lesion(s)

  • Positron emission tomography (PET); useful for interictal seizure localization in surgical candidates when MRI is normal

  • Single-photon emission CT (SPECT); adjunctive imaging modality useful for surgical candidates, when done as ictal study 

  • Magnetic resonance spectroscopy( MRS); of some use in trying to evaluate lesion for neoplastic signal

  • 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

Older antiepileptic drugs (AEDs) used for seizure control in temporal lobe epilepsy have some long-term side effects and require lab monitoring:

  • Phenytoin

  • Carbamazepine

  • Valproate

  • Phenobarbital

Newer AEDs appear to be comparably effective but with fewer side effects and don't requre lab monitoring for the most part:

  • Gabapentin

  • Pregabalin

  • Topiramate

  • Lamotrigine

  • Levetiracetam

  • Oxcarbazepine

  • Zonisamide

  • Lacosamide

  • Briviacetam

  • Clobazam 

  • Rufinamide

  • Perampanel

  • Vigabatrin (for intractable)
  • Felbamate (for intractable)

Nonpharmacologic treatments for temporal lobe epilepsy are as follows:

  • Vagus nerve stimulation (VNS; approved for treatment of intractable partial epilepsy in patients aged 4 years and older)

  • Responsive neurostimulation (RNS; stimulation of seizure focus when seizure occurs is the goal)

  • Deep brain stimulation (DBS; awating FDA approval but is available in other countries) 

  • Temporal lobectomy (the definitive treatment for medically intractable temporal lobe epilepsy with high seizure-free rate)

  • Dietary therapies are adjunctive such as ketogenic diet and Modified Atkins diet

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 ILAE released an updated classifcation in 2017. [1]

The seizures associated with temporal lobe epilepsy consist of simple partial seizures without loss of awareness (now termed focal aware) and complex partial seizures (ie, with loss of awareness; now termed focal impaired awareness). The individual loses awareness during a complex partial (focal aware) 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.

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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