Overview

The most common type of focal epilepsy, known as temporal lobe epilepsy (TLE), is characterised by recurrent seizures that originate in the temporal lobe of the brain. The temporal lobe is important for language, memory, and emotion, all of which impact the symptoms that occur during seizures. TLE is usually divided into two subtypes according to where the seizures originate: mesial temporal lobe epilepsy (MTLE) and lateral temporal lobe epilepsy (LTLE).¹ 

Accurate diagnosis and treatment depend on differentiating between LTLE and MLTE. Despite these conditions sharing the temporal lobe as their origin, both epilepsies differ in their clinical characteristics, EEG patterns, and response to treatment. LTLE is known to have various underlying causes, such as neocortical lesions and genetic abnormalities, which often lead to auditory (hearing) and language-related (speech) symptoms. 

However, MTLE is more likely to be drug-resistant (does not respond to drugs) than LTLE and is usually linked with hippocampal sclerosis. Highlighting the pathology, features, diagnosis and treatment of LTLE, whilst understanding the differences of MLTE, is very important for patient care.² 

The pathophysiology of lateral temporal lobe epilepsy

The temporal lobe is underneath the lateral sulcus on the sides of the brain. LTLE originates in the neocortex of the lateral temporal lobe. Due to its location, seizures frequently manifest with auditory auras, language abnormalities, and less prominent autonomic features than MTLE.³

 LTLE is caused by numerous anatomical and genetic causes including:

• Genetic mutations (e.g. mutations in the LGI1 gene)
• Structural lesions (strokes, brain tumours, and vascular abnormalities)
• Traumatic brain injuries (TBI)⁴

LTLE first appears in the neocortex, which is the brain's outer layer in charge of higher functions. This leads to symptoms such as complex partial seizures, a type of focal seizure that originates in a specific region and can impair awareness during an episode.⁴ 

MTLE, however, arises from the mesial (medial) structures of the temporal lobe, including the hippocampus, amygdala, and parahippocampal gyrus. It is frequently linked to déjà vu, epigastric sensations, and automatisms.⁸ 

Clinical features of LTLE vs MTLE

The specific functions of the lateral temporal cortex are reflected in the seizures of LTLE.⁶ These include the presence of: 

• Auditory auras – distorted sounds or musical hallucinations. This factor is an important local sign of LTLE and differentiates LTLE from MTLE
• Language disturbance – transient speech arrest, difficulties retrieving words and/or subtle impairments in comprehension (understanding). This could lead to brief episodes of aphasia or dysphasia
• Automatisms such as lip-smacking, repetitive hand movements, or other motor behaviours are frequently present with MTLE. For this reason, it may be more difficult to diagnose and differentiate LTLE since these patients may also exhibit stereotypical automatisms
• Cognitive and neuropsychological impacts – LTLE affects language and auditory processing. However, it spares memory, whereas MTLE's association with hippocampal sclerosis is strongly connected to memory impairment and learning difficulties

Better diagnosis and treatment are made easier by the differences in clinical features in both LTLE and MTLE.⁶ 

Diagnostic approaches 

A multimodal approach, such as electroencephalography (EEG), neuroimaging, and neuropsychological assessment, helps with the accurate diagnosis of LTLE and MTLE.^6,7 

EEG 

EEG findings determine the location (brain region) where the seizure started. In LTLE, the recordings can show specific rhythmic activity, focal spikes, or sharp waves in the lateral temporal cortex. On the other hand, MTLE usually shows distinct mesial temporal spikes and sharp waves, which are frequently linked to hippocampal sclerosis and produce a more distinct and repeatable pattern. 

Neuroimaging techniques

Magnetic resonance imaging (MRI) is essential to identify structural abnormalities in LTLE and MTLE. MRIs can help identify tumours, localised cortical dysphasia and other neocortical abnormalities. Hippocampal atrophy and signal alterations on T2-weighted imaging are hallmarks of mesial temporal sclerosis, which is frequently seen in MTLE. 

By identifying regions of hypometabolism, positron emission tomography (PET) helps differentiate these subtypes even more. While LTLE has abnormal metabolic patterns localised to the lateral cortex, MTLE usually shows decreased metabolic activity in the mesial temporal area.

Neuropsychological testing

This evaluates cognitive abilities related to temporal lobe integrity. Patients with LTLE may show difficulties in language processing and auditory (hearing) perception, whereas MTLE more frequently impacts memory. These tests help to locate which area in the brain the seizure started, which also aids with surgical planning and customised treatment plans.

Treatment and prognosis 

Medical and surgical approaches that are specific to the seizure subtype and patient features are necessary for the effective therapy of TLE.^4,5 The first line of treatment for TLE is antiepileptic medications (AEDs). AEDs include carbamazepine, lamotrigine and levetiracetam, and these can help patients control their seizures. LTLE has a variety of underlying causes, including tumours, cortical dysplasia and traumatic brain injuries, which can affect how well the treatment works, therefore, the patients may react differently to the medications. Drug resistance remains an issue, especially with MTLE, which is linked to hippocampal sclerosis. 

Surgical treatments are highly recommended when the drugs are unable to control seizures effectively. However, results are more variable in LTLE compared to MTLE.^4,5 Resection (surgical removal) of the TLE targets in the neocortex in LTLE can be less defined compared to MTLE. Through the use of neuroimaging techniques, the success of these resections has been improved, thereby enhancing the outcomes. However, the seizure-free outcomes may still not be as high as in the MTLE surgeries. 

The underlying pathology, length of epilepsy, and effectiveness of the treatment are some of the variables that affect long-term prognosis.² Whether using AEDs or surgery, patients who successfully manage their seizures typically see notable improvements in their quality of life. 

LTLE patients may experience language problems if the dominant hemisphere is affected. These results could be further improved with ongoing developments in surgical and diagnostic methods, whereas MTLE patients frequently experience long-lasting memory loss as a result of hippocampal damage.

FAQs 

What is the difference between LTLE and MTLE?

LTLE originates in the lateral regions, such as the neocortical temporal lobe, where MTLE arises from mesial (medial) structures such as the hippocampus, amygdala and parahippocampal gyrus. The difference in origin leads to the difference in clinical features.

Can LTLE or MTLE be prevented? 

Prevention is difficult since both LTLE and MTLE frequently develop from underlying genetic or structural causes. Some risk factors include traumatic brain injury, strokes or infections, however, this can be controlled or mitigated by lifestyle changes. Early diagnosis can help manage the severity of the disorder. 

When should I see a doctor? 

It is advisable to see a doctor if you have recurring episodes of odd sensations or other seizure-like symptoms, such as auditory auras or language disturbances. If these symptoms affect your day-to-day life or you have a family history of epilepsy, then it is advised to see a neurologist as soon as possible. Early diagnosis can help manage the severity of the disorder. 

Can LTLE or MTLE affect day-to-day life? 

Yes, both LTLE and MTLE can have a major impact on your day-to-day activities. Seizures can disrupt employment, education and social activities. Cognitive impairments, such as memory and language difficulties, can also affect quality of life. However, with proper medical management, many individuals can maintain sustainable lives. 

What is the long-term prognosis for patients with LTLE and MTLE?

Long-term outcomes are dependent on proper diagnosis, successful treatment, and the underlying cause of epilepsy. Successful seizure management can considerably enhance the quality of life, although cognitive outcomes can vary, with MTLE patients frequently enduring more severe memory problems.

Summary 

• LTLE originates in the lateral neocortical region, while MTLE originates from the mesial structures such as the hippocampus, amygdala, and parahippocampal gyrus
• LTLE presents with auditory auras and language disturbances, whereas MTLE typically presents with automatisms, deja vu and epigastric sensations 
• EEGs, neuroimaging techniques (PET and MRI), and neuropsychological testing are used for accurate diagnosis and localisation of the epileptogenic zone (the brain region where the seizure started)
• AEDs are the first line of management for LTLE and MTLE. Surgery can also be offered, however, the outcomes vary between MTLE and LTLE, as MTLE surgeries are more likely to lead to seizure-free outcomes 
• Ongoing research is focused on improving diagnostic tools and developing targeted therapies for personalised treatments with long-lasting results