Temporal lobe epilepsy (TLE) is an enduring brain disorder that causes unprovoked seizures from the temporal lobe. Temporal lobe epilepsy is the most common type of focal onset epilepsy among adults. Seizure symptoms and behavior distinguish seizures arising from the mesial (medial) temporal lobe from seizures arising from the lateral (neocortical) temporal lobe. Memory and psychiatric comorbidities may occur. Diagnosis relies on electroencephalographic (EEG) and neuroimaging studies. Anticonvulsant medications, epilepsy surgery, and dietary treatments may improve seizure control.
Types Under the International League Against Epilepsy (ILAE) 2017 classification of the epilepsies, focal onset epilepsy occurs from seizures arising from a biological neural network within a single cerebral hemisphere. Temporal lobe epilepsy occurs from seizures arising within the lobe. It is the most common focal onset epilepsy, and 80% of temporal lobe epilepsy is mesial (medial) temporal lobe epilepsy, temporal lobe epilepsy arising from the inner (medial) part of the temporal lobe that may involve the hippocampus, parahippocampal gyrus, or amygdala. The less common lateral temporal lobe or neocortical temporal lobe seizures arise from the outer (lateral) temporal lobe. These types of TLE are very rare due to the genetic cause or lesions such as tumor, birth defect, or blood vessel abnormalities in the temporal lobe. The ILAE 2017 classification distinguishes focal aware from focal impaired seizures. A focal aware temporal lobe seizure occurs if a person remains aware of what occurs during the entire seizure; awareness may be retained even if impaired responsiveness occurs during the seizure. A focal impaired awareness temporal lobe seizure occurs if a person becomes unaware during any part of the seizure. Approximately 80% of seizures in the temporal lobe begin in the mesial temporal region, frequently starting in or around the hippocampus. The hippocampus, found in both temporal lobes, is essential for memory and learning.
Signs and symptoms
Mesial temporal lobe epilepsy During a temporal lobe seizure, a person may experience a seizure aura; an aura is an autonomic, cognitive, emotional, or sensory experience that commonly occurs during the beginning part of a seizure. The common mesial temporal lobe seizure auras include a rising epigastric feeling, abdominal discomfort, taste (gustatory), smell (olfactory), tingling (somatosensory), fear, déjà vu, jamais vu, flushing, or rapid heart rate (tachycardia). A person may then stare blankly, appear motionless (behavioral arrest) and lose awareness. Repeated stereotyped motor behaviors (automatisms) may occur; these include repeated swallowing, lip smacking, picking, fumbling, patting, or vocalizations. Dystonic posture is an unnatural stiffening of one arm occurring during a seizure. A dystonic posture on one side of the body commonly indicates seizure onset from the opposite side of the brain e.g. right arm dystonic posture arising from a left temporal lobe seizure. Impaired language function (dysphasia) during, or soon following, a seizure is more likely to occur when seizures arise from the language dominant side of the brain.
Lateral temporal lobe epilepsy The common auras from seizures arising from the primary auditory cortex include vertigo, humming sounds, ringing sounds, buzzing sounds, songs or voices, or altered sensations. Lateral temporal lobe seizures arising from the temporal-parietal lobe junction may cause complex visual hallucinations. In comparison to mesial temporal lobe seizures, lateral temporal lobe seizures are briefer in duration, occur with earlier loss of awareness, and are more likely to become focal than bilateral tonic-clonic seizures. Impaired language function (dysphasia) during or soon following a seizure is more likely to occur when seizures arise from the language dominant side of the brain.
Causes Hippocampal sclerosis, brain tumor, traumatic brain injury, cerebral vascular malformation, neuronal migration disorders, infections such as encephalitis and meningitis, autoimmune disease (limbic encephalitis), and genetic disorders may cause temporal lobe epilepsy.
Risk factors Many persons with uncontrolled temporal lobe epilepsy had childhood febrile seizures. A brief febrile seizure only slightly increases the risk for developing nonfebrile seizures (also known as afebrile seizures). However, the prolonged seizure of febrile status epilepticus leads to a 9% risk for developing epilepsy. There is no clear relationship between febrile seizures and development of hippocampal sclerosis. Those who experienced any sort of brain injury in their early life have a higher risk of developing epilepsy.
Mechanism
Neuronal loss Hippocampal sclerosis occurs with severe CA1 and less severe CA3 and CA4 neuronal loss. Experimental research has shown that N-methyl-d-aspartate (NMDA) receptor activation causes neuronal cell loss, and electrical stimulation-induced animal models of temporal lobe epilepsy duplicate the cell loss pattern of temporal lobe epilepsy in humans. Repetitive seizures irreversibly damage interneurons leading to persistent loss of recurrent inhibition. Damage of GABAergic interneurons lead to loss of inhibition, uncontrolled neuronal firing, leading to seizures. The secondary epileptogenesis hypothesis is that repetitive seizures lead to interneuron loss, loss of glutamatergic principal neurons, axonal sprouting, and formation of new recurrent glutamatergic excitatory circuits leading to a more severe epilepsy. Mechanisms related to neuronal loss incompletely account for temporal lobe epilepsy as temporal lobe epilepsy may occur with only minimal neuronal cell loss.
Neuron-specific type 2 K+/Cl− cotransporter (KCC2) mutation This KCC2 mutation prevents subicular neurons from potassium and chloride ion extrusion, leading to intracellular chloride accumulation, and positive γ-Aminobutyric acid (GABA) mediated currents. Accumulated chloride efflux through GABA receptors leads to neuronal depolarization, increased neuronal excitability and ultimately seizures. Persons with this mutation have mesial temporal lobe epilepsy with hippocampal sclerosis.
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