Temporal lobe epilepsy (TLE) refers to a chronic disorder of the nervous system characterized by recurrent, unprovoked focal seizures that originate in the temporal lobe of the brain and last about one or two minutes.
It is the most common form of epilepsy with focal seizures.
Temporal lobe epilepsy (TLE) in which the epileptic focus is in the temporal lobe, is one of the most common types of epilepsy in adolescents and adults.
A focal seizure in the temporal lobe may spread to other areas in the brain.
Temporal lobe epilepsy is diagnosed by taking a medical history, blood tests, and brain imaging.
Temporal lobe seizure causes:
head injury, stroke, brain infections, structural lesions in the brain, brain tumors, or it can be of unknown onset.
Distortions in visual perception during a temporal lobe seizure may include size distortion, distorted perception of movement, a sense that surfaces such as ceilings and even entire horizons are moving farther away in a fashion similar to the dolly zoom effect, and other illusions.
Treatment
First line of treatment is through anticonvulsants.
Surgery is considered when there is an observable abnormality in the brain.
Temporal lobe epilepsy (TLE) in which the epileptic focus is in the temporal lobe, is one of the most common types of epilepsy in adolescents and adults.
Temporal lobe resection, during which the whole temporal lobe or just a part of the temporal lobe for example the hippocampus or the amygdala is removed, is the most common epilepsy surgery procedure.
Between 40 and 60% of patients that undergo temporal lobe resection are continuously seizure free.
The surgery itself is very safe with a mortality of 0%.
The risk for neurologic complications from a temporal lobe resection is around 3 to 7%.
Impaired performance in measures of specific cognitive domains like verbal memory, naming, visuo-spatial orientation; it may point to areas
Electrical stimulation of the brain utilizing a vagus nerve stimulator (VNS).
Focal seizures account for approximately sixty percent of all adult cases.
Temporal lobe epilepsy (TLE) is the single most common form of focal seizure.
There are two main types of temporal lobe epilepsy: mesial temporal lobe epilepsy (MTLE), arising in the hippocampus, the parahippocampal gyrus and the amygdala which are located in the medial aspect of the temporal lobe and lateral temporal lobe epilepsy (LTLE), the rarer type, arising in the neocortex at the lateral surface of the temporal lobe.
Lateral TLE seizures are characterized by auditory or visual features.
Autosomal dominant lateral temporal lobe epilepsy is a rare hereditary condition, often associated with mutations in the LGI1 gene.
Classification of TLE uses three key features: where the seizures begin, the level of awareness during a seizure, and other features.
Focal seizures involving then temporal lobe of the brain involve small areas of the lobe such as the amygdala and hippocampus.
There are two types of focal onset seizures: focal aware and focal impaired awareness.
Focal aware means consciousness is not altered during the seizure.
In TLE, a focal seizure usually causes abnormal sensations only:
Sensations such as déjà vu.
Amnesia of a single memory or set of memories.
A sudden sense of unprovoked fear and anxiety.
Nausea
Hallucinations: Auditory, visual, olfactory, gustatory, or tactile
Visual distortions such as macropsia and micropsia
Dissociation
Synesthesia
Dysphoric or euphoric feelings, fear, anger, and other emotions may occur.
Olfactory hallucinations.
Focal aware seizures may serve as a warning sign of a subsequent seizure (aura).
This aura is actually a seizure, and such a focal seizure may or may not progress to a focal impaired awareness seizure.
Focal seizures may not recognized what they are, nor may patients seek medical attention.
If impaired awareness seizures occur they alter the person’s ability to interact normally with their environment.
Impaired awareness seizures usually start as a focal aware seizure, then spread to a larger portion of the temporal lobe, resulting in impaired consciousness.
Signs of temporal lobe seizures may include:
Motionless staring
Automatic movements of the hands or mouth
Confusion and disorientation
Altered ability to respond to others
Unusual speech
Transient aphasia
Temporal lobe seizures tend to have a warning or aura before they occur.
Temporal lobe seizures generally tend to last only 1–2 minutes.
With temporal lobe seizures it is not uncommon for patients to experience being tired or confused for up to 15 minutes following the seizure.
It is not uncommon for an individual to be tired or confused for up to 15 minutes after a seizure has occurred.
Postictal confusion, however, can last for hours or even days.
TLE can be extremely harmful if the individual is left alone in hazardous conditions.
A seizure can begin in the temporal lobe, and then spread to involve both sides of the brain and is termed focal to bilateral seizures.
If both sides of the brain or the whole brain is involved from the onset, it is referred to as generalized seizures and may be tonic clonic.
There is a period of recovery in which neurological function is altered after each of these seizure types-the postictal state.
The degree and length of postictal impairment directly correlates with the severity of the seizure type.
Focal aware seizures often last less than sixty seconds.
Focal with impaired awareness seizures may last up to two minutes.
Generalized tonic clonic seizures may last up to three minutes.
The postictal state in seizures other than focal aware may last much longer than the seizure itself.
Temporal lobe epilepsy patients have a higher prevalence of depression than the general population.
The temporal lobe and the hippocampus play an important role in memory processing.
Declarative memory is formed in the area of the hippocampus called the dentate gyrus.
TLE is associated with memory disorders and loss of memory.
Brain pyramidal cell loss correlates with TLE verbal memory loss.
Brain pyramidal cell loss correlates with left brain verbal memory loss, while neuronal loss on the right is more prominent in visual/spatial memory loss.
After childhood onset,
One third of children with TLE will have a lasting remission up to an average of 20 years.
Patients with TLE that have a lesion such as a hippocampal scar, tumor mass, or dysplasia on MRI have intractable seizures.
The personality and behavioral disorders with TLE can become chronic (Geschwind syndrome).
Gershwind syndrome can be seen in some patients with TLE:
hypergraphia, which is the compulsion to write or draw excessively, hyperreligiosity, hyposexuality, irrelevancy.
The causes of TLE include: mesial temporal sclerosis, traumatic brain injury, brain infections (encephalitis and meningitis) , hypoxic brain injury, stroke, cerebral tumors, and genetic syndromes.
Temporal lobe epilepsy is not the result of psychiatric illness.
There is a link between febrile seizures and subsequent temporal lobe epilepsy, epidemiologically.
In TLE, there is loss of neurons in the hippocampus, with damage to mossy cells and inhibitory interneurons.
GABA-mediated inhibitory interneuron loss may increase the excitability of neurons of the hippocampus leading to recurrent seizures.
Loss of mossy cells lowers the threshold of action potentials of the granule cells of neurons: Mossy fibers are the axons of granule cells.
In TLE, granule cells are lost.
In TLE there are changes in the orientation of dendrites.
Not all patients have granule cell dispersion.
Mossy fibers project into the hilus of the dentate gyrus and stratum lucidum giving inputs to both excitatory and inhibitory neurons.
In the TLE brain, synaptic reorganization occurs where granule cells are damaged or lost, and they mossy fibers sprout
to reconnect to other granule cell dendrites.
In TLE, the sprouting mossy fibers are larger than in the normal brain.
Mossy fiber sprouting continues from one week to two months after injury.
It is theorized that aberrant mossy fiber sprouting may cause excitatory feedback circuits that lead to temporal lobe seizures.
However, aberrant mossy fiber sprouting may inhibit excitatory transmission by synapsing with basket cells which are inhibitory neurons and which are inhibitory neurotransmitters.
The evaluation of TLE can include: Magnetic resonance imaging (MRI), CT scans, positron emission tomography (PET), EEG, and magnetoencephalography.
Differential diagnosis includes: panic attacks, psychosis spectrum disorders, tardive dyskinesia, and occipital lobe epilepsy.
Many anticonvulsant oral medications are available for the management of temporal lobe seizures.
In TLE, the most commonly used older medications are phenytoin, carbamazepine, primidone, valproate, and phenobarbital, with newer agents, such as gabapentin, topiramate, levetiracetam, lamotrigine, pregabalin, tiagabine, lacosamide, and zonisamide having similar effectiveness.
Up to one third of patients with medial temporal lobe epilepsy do not have adequate seizure control with medication alone.
For patients with medial TLE whose seizures remain uncontrolled surgical excision of the affected temporal lobe may be considered.
Other management options include: new anticonvulsants, vagus nerve stimulation.and a ketogenic diet is also for children, and some adults, brain cortex responsive neural stimulators, deep brain stimulation, stereotactic radiosurgery with gamma knife, and laser ablation.
Abnormal symptoms and signs of TLE with the constellation of symptoms that included hypergraphia, hyperreligiosity, collapse, and pedantism, is called Geschwind syndrome.
TLE is associated with emotional responses to religious words, diminished responses to the sexually charged words, and normal responses to the neutral words.
A study reported that religiosity is higher in patients with epilepsy than in controls.
Religiosity in TLE is associated with lower education levels, abnormal background EEG activity, and hippocampus sclerosis.
TLE has been suggested as an explanation for the revelatory experiences of prominent religious figures such as Abraham, Moses, Jesus, Mohammed, Saint Paul, Joan of Arc, Saint Teresa of Ávila and Joseph Smith.
Many have questioned the evidence for a link between temporal lobe epilepsy and religiosity.