Bilateral temporal lobe epilepsy

• Changes in topological properties of brain structural covariance networks and alertness in temporal lobe epilepsy with and without focal to bilateral tonic-clonic seizures
• Symptomatic Emotional Responses and Changes in Networks Elicited by Direct Electrical Stimulation
• Prevalence of Temporal Lobe Epilepsy (TLE) Subtypes and Response to Resective Surgery in Patients with Presumed TLE Undergoing Limbic and Paralimbic Network Exploration with Stereo-Electrodes
• Seizure-related cardiovascular symptoms: Comorbidities or SUDEP risk factors?
• Decreased locus coeruleus multiunit activity in a mouse model of temporal lobe seizures with impaired consciousness
• Predictive value in memory evaluation of the temporal mesial afterdischarges induced by electrical stimulations in stereoelectroencephalography
• Marked differences in the effects of levetiracetam and its analogue brivaracetam on microglial, astrocytic, and neuronal density in the rat model of kainic acid-induced temporal lobe epilepsy
• Parallel transmit 7T MRI for adult epilepsy pre-surgical evaluation

Bilateral Temporal Lobe Epilepsy (BTLE) is a form of drug-resistant epilepsy involving seizure activity in both temporal lobes. It is less common than unilateral temporal lobe epilepsy (TLE) and presents unique diagnostic and therapeutic challenges.

1. Clinical Features Seizure Types: Focal impaired awareness seizures (complex partial seizures) – most common, often with automatisms (lip smacking, fidgeting). Focal aware seizures (auras) – may include déjà vu, fear, auditory or visual distortions. Bilateral tonic-clonic seizures – may occur due to secondary generalization. Cognitive and Behavioral Symptoms: Memory impairment (particularly episodic memory) Emotional dysregulation (anxiety, depression) Language disturbances if involvement is asymmetric (dominant hemisphere more affected) Autonomic Symptoms: Sweating, palpitations, nausea, epigastric sensations. 2. Etiology and Pathophysiology Structural Lesions: Mesial Temporal Sclerosis (MTS) (hippocampal atrophy, gliosis, neuron loss) Bilateral cortical malformations Tumors, vascular malformations, infections Genetic Factors: Some familial cases linked to LGI1, DEPDC5, SCN1A mutations. Autoimmune Causes: Anti-LGI1, Anti-GAD, or Anti-NMDA receptor encephalitis. Post-Traumatic or Infectious (Meningitis, Encephalitis) 3. Diagnosis Video EEG Monitoring: Bilateral independent seizure onset in temporal lobes. MRI Brain: Bilateral hippocampal atrophy or other structural abnormalities. PET/SPECT: Hypometabolism or altered perfusion in both temporal lobes. Neuropsychological Testing: Confirms cognitive and memory impairments.

Antiseizure Medications (ASMs): Levetiracetam, Lacosamide, Zonisamide, Clobazam Caution: Phenytoin and Carbamazepine may exacerbate bilateral onset seizures. Immunotherapy (if autoimmune suspected): IVIG, steroids, plasmapheresis.

Resective Surgery: Poor candidate due to bilateral seizure foci.

see Temporal lobectomy for bilateral temporal lobe epilepsy

Neurostimulation Therapies:

Responsive Neurostimulation (RNS)

Vagus Nerve Stimulation (VNS)

Deep Brain Stimulation (DBS) – Anterior Nucleus of the Thalamus

Laser Interstitial Thermal Therapy (LITT): Experimental in bilateral cases.

Poorer seizure control compared to unilateral TLE. High risk of cognitive decline if seizures remain uncontrolled. Best outcomes with early diagnosis and multimodal treatment.