Temporal lobe epilepsy ( TLE ) is a chronic disorder of the nervous system characterized by unreasonable recurrent focal seizures originating from the temporal lobe of the brain and lasts about a minute or two. TLE is the most common form of epilepsy with focal seizures. Focal seizures in the temporal lobe can spread to other areas of the brain when it can become focal for bilateral seizures .
TLE is usually diagnosed in childhood or adolescence. TLE is diagnosed by taking a medical history, blood test, and brain imaging. It can have a number of causes such as head injury, stroke, brain infection, structural lesions in the brain, or brain tumors, or may become unknown onset . The first treatment is through anticonvulsants. Surgery can be an option, especially when there are abnormalities that can be observed in the brain. Another treatment option is brain electrical stimulation through an implanted device called a vagus nerve stimulator (VNS).
Video Temporal lobe epilepsy
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More than forty types of epilepsy are recognized and these are divided into two main groups: focal seizures and generalized seizures. Focal seizures account for about sixty percent of all adult cases. Temporal lobe epilepsy (TLE) is the most common form of focal seizures.
The International League Against Epilepsy (ILAE) recognizes two major types of temporal lobe epilepsy: mesial temporal lobe epilepsy (MTLE), arising in the hippocampus, parahippocampal gyrus and the inner medial amygdala of the temporal lobe and lateral temporal lobe epilepsy LTLE), a more rare type, that appears in the neocortex on the outer surface (lateral) of the temporal lobe. LTLE seizures are characterized by auditory or visual features. Autosomal lateral temporal lobe epilepsy (ADLTLE) is a rare hereditary condition, often associated with mutations in the LGI1 gene.
Maps Temporal lobe epilepsy
Signs and symptoms
When the seizure begins in the temporal lobe, the effect depends on the exact location of the point of origin, locus . In 1981, ILAE recognized three types of seizures that occur in temporal lobe epilepsy. Classification based on EEG findings. But by 2017 the general classification of seizures has been revised. The new classification uses three main features: where seizures begin, awareness levels during seizures, and other features.
Focal spasms
Focal seizures in the temporal lobe involve small areas of the lobe such as the amygdala and the hippocampus.
The newer classification provides two types of focal onset attacks, such as focal awareness and focal distraction awareness.
Focal conscious seizures
Focal aware means that the level of consciousness does not change during a seizure. In temporal lobe epilepsy, focal seizures usually cause only abnormal sensations.
This is possible:
- Sensations like dÃÆ' Â © jÃÆ' vu (feelings of intimacy), jamais vu (feelings of unfamiliarity)
- Amnesia; or one memory or series of memory
- Unexpected fear and anxiety suddenly
- Nausea
- Hearing, visual, olfactory, gustatory, or touching hallucinations.
- Visual distortions such as macropsia and micropsia
- Dissociation or derealization
- Synesthesia (sensory stimulation experienced in the second sense) may occur.
- Feelings, fears, anger, and other dis- posical or euphoric emotions may also occur. Often, the patient can not describe the sensation.
The olfactory hallucinations often seem indescribable to patients outside "fun" or "unpleasant".
Focally conscious seizures are often called "auras" when they function as a warning sign of subsequent seizures. Regardless of the aura is actually the seizure itself, and such a focal seizure may or may not develop into a focal spasm of focal consciousness. People who have only a focal conscious seizure may not recognize them for what they are, or seek medical care.
Focal vigilance
Spasm of focal disorder awareness is a seizure that disrupts consciousness to some extent: they change a person's ability to interact normally with his environment. They usually begin with focal conscious seizures, then spread to larger parts of the temporal lobes, resulting in impaired consciousness. They may include autonomic and psychic features present in conscious seizure focus.
Alerts may include:
- No staring gestures
- Automatic hand or mouth movement
- Confusion and disorientation
- Ability to change to respond to others, unusual remarks
- Temporary Aphasia (loss of ability to speak, read, or understand spoken word)
These seizures tend to have a warning or aura before they occur, and when they occur they tend to last only 1-2 minutes. Not infrequently a person becomes tired or confused until 15 minutes after the seizure has occurred, although postical confusion can last for hours or even days. Although they may not seem dangerous, due to the fact that individuals usually do not catch on, they can be very dangerous if the individual is left alone around a dangerous object. For example, if someone with a complex partial seizure drives on their own, this may cause them to run into a ditch, or worse, causing an accident involving multiple people. With this type, some people do not even realize they have seizures and most of the time their memories from just before or after seizures are wiped away. First aid is only necessary if there is an injury or if this is the first time a person has a seizure.
Focal for bilateral seizures
Seizures that begin in the temporal lobes, and then spread to involve both sides of the brain are called focal to bilateral . (Where both sides of the brain or the entire brain are involved from onset, convulsions are known as generalized seizures and may be tonic clonics.The arms, trunk, and legs tighten (tonic phase), either in flexion or extension positions, and then jerk (clonic phase) This was formerly known as the grand mal seal The word 'grand mal is derived from the French term, which means great suffering.
Postiktal period
There are several recovery periods in which neurological functioning changes after each type of seizure. This is postiktal status . The degree and length of direct postic disturbance correlate with the severity of the seizure type. Focal conscious seizures often last less than sixty seconds; focal with seizure awareness disorder may last up to two minutes; and general tonic clonic seizures can last up to three minutes. Postical states in seizures other than focal aware may last longer than the seizure itself.
Because the main function of the temporal lobe is short-term memory, the focus with seizure awareness disorder, and the focus on bilateral seizures can cause amnesia during the period of seizures, which means that the seizures may not be remembered.
Complications and prognosis
Depression
Individuals with temporal lobe epilepsy have a higher prevalence of depression than the general population. Although the psychosocial effects of epilepsy may be the cause, there is also a relationship in the phenomenology and neurobiology of TLE and depression.
Memory
The temporal lobe and especially the hippocampus play an important role in the memory process. Declarative memories (memories that can be consciously remembered) form in the hippocampus area called dentate gyrus .
Temporal lobe epilepsy is associated with memory impairment and memory loss. Animal models and clinical studies show that memory loss correlates with neuronal loss of temporal lobe in temporal lobe epilepsy. The verbal memory deficit correlates with the loss of pyramidal cells in TLE. This is more on the left side of verbal memory loss. Neuronal damage on the right is more prominent in non-verbal (loss of visuospatial memory).
Children's onset
After the onset of childhood, a third will "grow" from TLE, finding lasting remissions to an average of 20 years. The discovery of lesions such as hippocampal sclerosis (scarring in the hippocampus), tumors, or dysplasia, in magnetic resonance imaging (MRI) predict seizure spasms.
Personality
The effect of temporal lobe epilepsy on personality is a historical observation dating from the 1800s. The personality and behavioral changes in temporal lobe epilepsy are seen as chronic conditions when they last for more than three months.
Geschwind syndrome is a set of behavior phenomena seen in some people with TLE. Documented by Norman Geschwind, the signs include: hypergraphia (the necessity for excessive writing (or drawing), hyper-religiosity (deep religious or philosophical experience or interest), hyposexuality (decreased interest or sex drive), instability non-linear thinking patterns, talk at length about irrelevant and trivial details). Personality changes generally vary according to the hemisphere.
The existence of "temporal lobe epilepsy personality" and Geschwind syndrome has been debated and the study can not be concluded.
Diagnosis
Diagnosis of temporal lobe epilepsy may include the following methods: Magnetic Resonance Imaging (MRI), CT scan, positron emission tomography (PET), EEG, and magnetoencephalography.
Differential diagnosis
Other medical conditions with similar symptoms include panic attacks, psychotic spectrum disorders, tardive tardive, and occipital lobe epilepsy.
Cause
Causes of TLE include mesial temporal sclerosis, traumatic brain injury, cerebral infections, such as encephalitis and meningitis, hypoxic brain injury, stroke, cerebral tumor, and genetic syndrome. Temporal lobe epilepsy is not the result of psychiatric illness or the fragility of the personality.
Febrile seizures
Although this theory is controversial, there is a relationship between febrile seizures (seizures coinciding with fever episodes in young children) and subsequent temporal lobe epilepsy, at least epidemiology.
Human herpes virus 6
In the mid-1980s, human herpes 6 virus (HHV-6) was suggested as a possible causal relationship between febrile seizures and temporal temporal lobe epilepsy. However, although the virus is found in temporal lobe tissue during surgery for TLE, it has not been recognized as a major factor in febrile seizures or TLE.
Reelin
The dispersion of granular cell layers in the hippocampal dentate gyrus is sometimes seen in temporal lobe epilepsy and has been associated with a decrease in reelin regulation, a protein that usually maintains a compact layer containing neuronal migration. It is unknown whether changes in the expression of reelin play a role in epilepsy.
Pathophysiology
Neuronal damage
In TLE, there is loss of neurons in CA1 and CA3 regions of the hippocampus. There is also damage to mossy cells and interneuron inhibition in the hippocampal hilar region (region IV) and dentate gyrus granular cells. In animal models, neuronal loss occurs during seizures but in humans, neuronal loss precedes the first seizure and does not always continue with seizure activity. The loss of internalization of GABA-mediated inhibition may improve the hyperexcitability of neurons from the hippocampus leading to recurrent seizures. According to the "cell basket dormitory" hypothesis, mossy cells usually attract basket cells which, in turn, inhibit granular cells. The loss of the cells of the formula decreases the threshold of the granular cell action potential.
GABA Reversal
In certain patients with temporal lobe epilepsy it has been found that the subiculum may produce epilepsy activity. It has been found that GABA's reversal potential is depolarization in pyramidal cell subpopulations due to lack of KCC2 co-transporters. It has been proven that it is theoretically possible to produce seizures within the neural network due to KCC2 down-regulation, consistent with chloride measurements during transition to seizures and KCC2 blockade experiments.
Granular cell dispersion in dentate gyrus
Granular cell dispersion is a type of developmental migration and pathological changes found in the TLE brain first described in 1990. The granular cells of dense dentate gyrus are packed to form a uniform, laminated layer without monosynaptic connections. This structure provides a filter for neuron stimulation.
In TLE, the granular cells are lost, the structure is no longer solid and there is a change in the orientation of dendrites. These changes may or may not be epileptogenic. For example, if granular cell dendrites reconnect, perhaps in a way (via the laminar plane) that allows hyperexcitability. However, not all patients have granular cell dispersion.
Distorted mossy fibers grow
Moss fibers are granular cell axons. They project onto the dentate gyrus and stratum lucidum hilus in the CA3 region providing input for both excitatory and inhibitory neurons.
In the TLE brain, where granular cells are damaged or lost, axons, mossy fibers, 'sprouts' to reconnect to other granular cell dendrites. This is an example of a synaptic reorganization . It was recorded in human tissue in 1974 and in animal models in 1985. In TLE, moss fibers grow larger than in normal brains and their connections may deviate. Fiber moss grew steadily from one week to two months after the injury.
Excess moss fiber fat can create excitatory feedback circuits that lead to temporal lobe seizures. This is evident in the intracellular recording. Stimulating the area of ​​mossy fibers that deviate increases the potential postsynaptic excitatory response.
However, sprouting mossy mossy fibers may inhibit the transmission of excitatory by synapses with basket cells which are the inhibitory neurons and by releasing GABA and neuropeptide Y which are the neurotransmitter inhibitors. Also, in animal models, the stimulation of granular inflammatory cells is noted before mossy mossy mossy shoots have occurred.
Treatment
Antikonvulsan
Many anticonvulsant oral drugs are available for management of temporal lobe seizures. Most anticonvulsants function by reducing the excitation of neurons, for example, by blocking the sodium channel quickly or slowly or by modulating the calcium channel; or by increasing the inhibition of neurons, for example by potentiating the inhibitory neurotransmitter effects such as GABA.
In TLE, the most commonly used drugs are phenytoin, carbamazepine, primidone, valproate, and phenobarbital. New drugs, such as gabapentin, topiramate, levetiracetam, lamotrigine, pregabalin, tiagabine, lacosamide, and zonisamide promise similar effectiveness, with fewer side effects. Felbamate and vigabatrin are newer, but can have serious side effects that are not considered first-line treatments.
Up to one third of patients with temporal medial lobe epilepsy will not have adequate seizure control with medication alone. For patients with medial TLE whose seizures remain uncontrolled after trials of some anticonvulsant species (ie, epilepsy is stubborn ), surgical excision of the affected temporal lobe may be considered.
Surgical intervention
Epilepsy surgery has been done since the 1860s and doctors have observed that it is very effective in generating freedom from seizures. However, it was not until 2001 that scientific scientific research was conducted to test the effectiveness of temporal lobectomy.
Temporal lobe surgery can be complicated by decreased cognitive function. However, after a temporal lobectomy, memory function is supported by opposing temporal lobe; and frontal lobe recruitment. Cognitive rehabilitation can also help.
Other treatments
Where surgery is not recommended, further management options include new anticonvulsants (including experimental), and vagal nerve stimulation. The ketogenic diet is also recommended for children, and some adults. Other options include cortex brain responsive nerve stimulator, deep brain stimulation, stereotactic radiosurgery, such as gamma blades, and laser ablation.
Link with religiosity
The first to record and catalog the abnormal symptoms and signs of TLE is Norman Geschwind. He found a constellation of symptoms that included hypergraphia, hyperreligiosity, collapse, and pedantism, now called Geschwind syndrome .
Vilayanur S. Ramachandran explores the neural base of hyperreligiosity seen in TLE using a galvanic skin response (GSR), which correlates with emotional arousal, to determine whether the hyperreligiosity seen in TLE is due to an emotional state that increases overall or is specific to religion. stimulation. Ramachandran presents two subjects with neutral, sexual and religious words while measuring the GSR. Ramachandran was able to show that patients with TLE showed increased emotional responses to religious words, reduced responses to sexually charged words, and normal responses to neutral words. The study is presented as an abstract at a neuroscience conference and referenced in Ramachandran's book, Phantom in the Brain, but has never been published in peer-reviewed scientific press.
A study by 2015, reported that intrinsic religiosity and religiosity outside organized religion is higher in patients with epilepsy than in controls. Lower levels of education, abnormal background EEG activity, and hippocampal sclerosis have been found to be a contributing factor to religiosity in Temporal Lobe Epilepsy.
Temporal lobe epilepsy has been suggested as a physical explanation for the revelatory experiences of prominent religious leaders such as Abraham, Moses, Jesus, Muhammad, Saint Paul, and Joseph Smith. These experiences are described as complex interactions with their vision, but lack the stereotypes, amnestic periods, and automatisms or general motor events, which are characteristic of TLE. Psychiatric conditions with psychotic spectrum symptoms may be a more sensible physical explanation of this experience. Pope Pius IX's doctrine of clean conception is deemed to have been affected by partially diagnosed forensic epilepsy. It is also suspected that the vision of Joan of Arc may be a partial expression of epilepsy. In 2016, a case history found that temporal lobe epilepsy experienced God's vision after a temporal lobe seizure, while undergoing EEG monitoring. The patient reported that God had sent him into the world to "bring redemption to the people of Israel". The concrete relationship between TLE and religiosity has inspired the work of Michael Persinger and many other researchers in the field of neurotheology, but some have questioned the evidence for the relationship between temporal lobe epilepsy and religiosity. Novel, Lying Awake , by Mark Salzman, deals with the topic of temporal and religious lobe epilepsy.
References
Source of the article : Wikipedia
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