Temporal Lobe Epilepsy (TLE) is the most common form of focal epilepsy, where seizures begin in a specific, localized area of the brain. TLE arises from abnormal electrical activity originating within one of the two temporal lobes, which are situated behind the temples. It is a chronic neurological condition that can affect people of any age, though it often begins in childhood or adolescence.
Defining Temporal Lobe Epilepsy
Temporal Lobe Epilepsy (TLE) is classified as a type of focal onset epilepsy because the seizures reliably start in one of the two temporal lobes. These lobes are deeply involved in several higher-order functions, including memory, emotion, and the processing of sensory input like sounds and language.
The temporal lobe contains structures like the hippocampus and the amygdala, which are crucial for forming new memories and regulating emotional responses. When a seizure originates in these areas, particularly the hippocampus, it is referred to as mesial temporal lobe epilepsy (MTLE), which accounts for approximately 80% of all TLE cases. Dysfunction in this region is why TLE seizures frequently involve alterations in memory and feelings, rather than dramatic convulsive movements.
Identifying Seizure Types
Seizures related to TLE are characterized by a wide range of manifestations, classified based on whether a person’s awareness is maintained. Many temporal lobe seizures begin with a focal aware seizure, formerly known as a simple partial seizure, which acts as a warning sign called an aura. These auras are highly personalized and often involve sensory or psychic experiences, such as a sudden feeling of déjà vu or unfamiliarity (jamais vu).
Auras can also include autonomic or emotional features, like a rising sensation in the stomach, an unusual smell or taste, or an abrupt feeling of fear or panic. During a focal aware seizure, the individual remains fully conscious and can typically recall the event. This initial phase can last from a few seconds up to a couple of minutes before the seizure either ends or progresses.
The seizure may then evolve into a focal impaired awareness seizure, where consciousness is affected. During this type of seizure, the person may appear awake but is unresponsive and unaware of their surroundings. Characteristic behaviors, known as automatisms, are common, including repetitive, involuntary actions such as lip-smacking, chewing, fumbling with clothes, or purposeless wandering.
These impaired awareness seizures usually last between 30 seconds and two minutes, followed by a period of postictal confusion. They may be disoriented, tired, or have difficulty speaking for several minutes to hours, and they typically have no memory of the seizure itself.
Underlying Causes
The most common underlying cause of TLE, particularly the mesial form, is hippocampal sclerosis (HS). This involves scarring and loss of neurons within the hippocampus. Hippocampal sclerosis is frequently associated with a history of prolonged febrile seizures, which are seizures triggered by a high fever, often occurring in early childhood.
The prolonged electrical activity during a severe febrile seizure is thought to potentially damage the delicate hippocampal tissue, leading to epileptogenesis years later. Other factors that can cause TLE include significant head trauma, infections of the brain such as meningitis or encephalitis, and stroke or vascular malformations.
In many cases, however, the exact cause of TLE remains unknown, classified as idiopathic. Genetic factors are also thought to play a role, predisposing individuals to both febrile seizures and the subsequent development of TLE.
Diagnosis and Management Approaches
Diagnosing Temporal Lobe Epilepsy typically begins with a detailed medical history, where the patient’s and witnesses’ descriptions of the seizure symptoms, especially the auras and automatisms, are crucial. This is followed by an electroencephalogram (EEG), which measures the electrical activity in the brain and can detect abnormal discharges originating in the temporal region. Video-EEG monitoring, which records both brain activity and physical behavior during a seizure, is often used to confirm the diagnosis and pinpoint the seizure focus.
Structural imaging, primarily magnetic resonance imaging (MRI), looks for physical changes in the brain tissue. An MRI can reveal hippocampal sclerosis, which appears as shrinkage or scarring of the hippocampus. Identifying this structural abnormality is important because it often predicts how a patient will respond to treatment.
The primary management approach for TLE is the use of anti-epileptic medications (AEDs) to stabilize electrical activity and reduce seizure frequency. Common first-line drugs include carbamazepine, lamotrigine, and levetiracetam. Approximately 47% to 60% of patients achieve seizure freedom with medication.
If seizures continue despite adequate trials of two or more AEDs, the condition is deemed drug-resistant TLE. For these individuals, surgical options offer the best chance for seizure freedom, with success rates between 70% and 80%. The most common procedure is a temporal lobectomy, which removes the scarred area where the seizures originate. Neuromodulation devices, such as Vagus Nerve Stimulation (VNS) or Responsive Neurostimulation (RNS), are alternatives for patients who are not candidates for resective surgery.