Temporal lobe epilepsy (TLE) may be simple partial seizures without loss of awareness (with or without aura) or complex partial seizures (with loss of awareness). Loss of awareness occurs during a complex partial seizure when the seizure spreads to involve both temporal lobes.

Epidemiology

Partial epilepsy is often of temporal lobe origin but the true prevalence of temporal lobe epilepsy is not known.¹

Presentation

• Aura occurs in the majority of temporal lobe seizures. Most auras and automatisms last a very short period - seconds or 1 to 2 minutes. Auras may cause sensory, autonomic, or psychic symptoms:¹
  • Somatosensory and special sensory phenomena:
    • Olfactory, auditory and gustatory illusions and hallucinations may occur.
    • Patients may report distortions of shape, size, and distance of objects.
    • These visual illusions differ from the visual hallucinations associated with occipital lobe seizure in that there is no formed visual image.
    • Objects may appear smaller or larger than usual.
    • Vertigo may occur with seizures in the posterior superior temporal gyrus.
  • Psychic phenomena:
    • Feeling of déjà vu (familiarity)or jamais vu (unfamiliarity).
    • Depersonalisation (i.e. feeling of detachment from oneself) or derealisation (surroundings appear unreal).
    • Fear or anxiety.
    • May describe seeing their own body from outside.
  • Autonomic phenomena: changes in heart rate and sweating. Patients may experience an epigastric fullness sensation or nausea.
• Following the aura, a temporal lobe complex partial seizure begins with a wide-eyed, motionless stare, dilated pupils, and behavioural arrest.
• Lip-smacking, chewing and swallowing may be noted.
• Manual automatisms or unilateral dystonic posturing of a limb may also occur.
• A complex partial seizure may evolve to a generalised tonic-clonic seizure.
• Patients usually experience a post-ictal period of confusion. The post-ictal phase may last for several minutes.
• Amnesia occurs during a complex partial seizure because of bilateral hemispheric involvement.

Possible underlying causes

• Past infections, e.g. herpes encephalitis or bacterial meningitis
• Head injury producing contusion or haemorrhage that results in encephalomalacia or cortical scarring
• Hamartomas
• Gliomas
• Vascular malformations (i.e. arteriovenous malformation, cavernous angioma)
• Cryptogenic: a cause is presumed but has not been identified
• Idiopathic (rare)
• Hippocampal sclerosis produces a clinical syndrome called mesial temporal lobe epilepsy, which begins in late childhood, then remits, but reappears in adolescence or early adulthood in a refractory form
• Febrile seizures: some children with complex febrile convulsions appear to be at risk of developing temporal lobe epilepsy in later life

Differential diagnosis

• Absence seizures: have an abrupt onset with no aura, usually last less than 30 seconds, have no post-ictal confusion and are not associated with complex automatisms. Complex partial seizures are usually preceded by a distinct aura, last longer than a minute, and have a period of post-ictal confusion.
• Frontal lobe complex partial seizures appear in clusters of brief seizures with abrupt onset and ending. There is minimal post-ictal state. May cause behavioural changes with vocalisations and complex motor and sexual automatisms. In differentiating from TLE, may need electroencephalograph (EEG) localisation.
• Excessive daytime somnolence, e.g. due to a sleep apnoea or narcolepsy
• Periodic limb movement disorder
• Tardive dyskinesia
• Panic attacks
• Occipital lobe epilepsy: may spread to the temporal lobe and be clinically indistinguishable from a temporal lobe seizure
• Psychogenic seizures: patients with psychogenic seizures may also have epileptic seizures

Investigations

• Inter-ictal EEG: one third of patients with TLE have bilateral, independent, temporal inter-ictal epileptiform abnormalities
• MRI is the neuro-imaging investigation of choice
• Positron emission tomography with 18-fluorodeoxyglucose (PET-FDG) is useful when the MRI result is normal
• Single-photon emission computed tomography (SPECT) is useful for candidates for surgical intervention
• Video-EEG telemetry is used as part of the pre-surgical evaluation. It also is used if the diagnosis of TLE is still uncertain

Management

• About half of all new-onset partial seizures are controlled effectively by the first drug.¹
• Carbamazepine, lamotrigine, oxcarbazepine, and sodium valproate are the drugs of choice for partial (focal) seizures.²
• Second-line drugs include clobazam, gabapentin, levetiracetam, pregabalin, tiagabine, topiramate, and zonisamide.

Surgical

• Vagus nerve stimulation with a high-frequency stimulation rate results in a mean reduction in seizure frequency of 25-28%. A battery-operated stimulator device is implanted in the left vagus nerve in the neck.
• Anterior temporal lobectomy is the definitive treatment for medically intractable temporal lobe epilepsy.^3,4

Prognosis¹

• Patients with refractory temporal lobe epilepsy have an increased risk of sudden death that is 50 times greater than that in the general population.
• Seizure-free state 2 years after anterior temporal lobectomy is predictive of long-term seizure-free outcome.
• About 50% of patients become seizure-free with medical treatment.
• After 3 first-line anti-epileptic drugs (AEDs) have failed, the chance for seizure freedom is 5-10%.
• Surgery in well-selected patients with refractory TLE leads to a seizure-free outcome rate of 70-80%.
• Patients with refractory temporal lobe epilepsy typically have deficits in memory function.
• Those patients with dominant temporal lobe epilepsy often have impaired language function.