VE is a localized, often symptomatic form of epilepsy, in which the epileptogenic focus is localized in the temporal lobe.
Hughlings Jackson, apparently, was the first who in 1889 associated the occurrence of certain attacks with the defeat of the temporal lobe. He described olfactory hallucinations as an epileptic phenomenon and showed their occurrence when the hook of a hippocampus (uncus) is irritated by a tumor.
Frequency. CE is one of the most common forms of epilepsy, which accounts for up to 4 of all cases, and up to 60% among symptomatic partial epilepsies.
Etiology. The reasons determining the development of CE are diverse and can be represented by two main groups: perinatal and postnatal. A perinatal CNS lesion in history is found in 36% of patients suffering from VE (intrauterine infections, hypoxia, focal cortical dysplasia, birth trauma, etc.).
The most characteristic pathological finding in CE is mesial sclerosis of the temporal lobe of the brain, and more precisely – the hippocampal gyrus. This is due to the fact that when the head of the fetus passes through the birth canal of the mother, this part of the brain is squeezed into the tentrium opening of the cerebellum due to deformation of the skull and under unfavorable childbirth, along with the vessels supplying it, between the edge of the dura mater and the middle brain, with the appearance of foci of destruction here, ischemia, hemorrhage, edema.
All this leads to the formation of foci of hyper-excited neurons. Kunz, Kudin et al. (2000) found a deficiency of complex 1 in the mitochondrial respiratory chain in the hippocampal region of the SAZ in patients suffering from VE with an epileptic focus in the hippocampus. Among postnatal factors, neuroinfection (encephalitis, post-vaccination encephalomyelitis), traumatic brain injury, tumors of the temporal lobes of the brain, cerebral infarction, vascular malformations, tuberous sclerosis and others should be noted.
Before the introduction of neuroimaging techniques into the clinic, it was possible to establish the etiology of EC only in 28% of cases. With the help of MRI, structural abnormalities in the temporal lobe are verified on average in 62% of patients, and during PET and intravital brain biopsy, this figure approaches 100%. MRI is the preferred method of objectification than CT: focal cortical dysplasia of the temporal lobe is visualized with CT only in 5% of cases.
A highly topical and not fully resolved issue of modern epileptology is the interrelation of the appearance of CE with a long episode of febrile seizures and the development of mediobasal temporal sclerosis (MVS). Histologically, with MVS, a decrease in the density of neurons per surface unit is detected due to their necrosis, followed by the growth of astroglia (sclerosis). The reasons determining the development of AIM and its relationship with febrile seizures remain the subject of debate. Of fundamental importance is the question of what comes first: AIM, which later causes CE, or atypical febrile seizures, leading to the development of AIM.
The role of genetic factors in the occurrence of CE is debatable. Separate patterns of inheritance, apparently, does not exist. In general, hereditary burden with symptomatic CE is not more than 5%.
Clinic. CE debut varies over a wide age range depending on the causes of the disease. Clinical manifestations of VE are extremely polymorphic and diverse. VE is manifested by simple, complex partial, secondary-generalized convulsive seizures or their combination (50%). In 75% of cases with CE, seizures begin with an aura. The nature of the aura (somatosensory, visual, olfactory, gustatory, auditory, etc.) has an extremely important topical value, as it indicates the area of the cortex where the epileptogenic focus is localized and where the epileptic discharge begins.
Depending on the localization of the epileptogenic focus and, respectively, clinical manifestations, 4 types of temporal epilepsy are distinguished by modern classification: hippocampal, amygdular, lateral posterior temporal, opercular. Traditionally, for the convenience of clinicians, VE is divided into two large groups: amygdalogip-decal and lateral.
The amygalogue and hippocampal EI (mediobasal, paleocortical) is considered a separate nosological form.