Temporal lobe epilepsy is one of the forms of epilepsy in which the focus of epileptic activity is localized in the temporal lobe of the brain. Disease is characterized by simple and complex partial epi-seizures, and with the further development of the disease, secondary generalized seizures and mental disorders. The diagnosis is made possible by comparing complaints, neurological status data, EEG, polysomnography, MRI and PET of the brain. Temporal lobe epilepsy is treated by mono- or polytherapy with antiepileptic drugs. If they are ineffective, surgical techniques are used, which consist in removing cells from the area of the temporal lobe where the epileptogenic focus is located.
Temporal lobe epilepsy is the most common form of epilepsy. It accounts for almost 25% of cases of epilepsy in general and up to 60% of cases of symptomatic epilepsy. It should be noted that the clinical picture of temporal epilepsy does not always indicate the location of an epileptogenic focus in the temporal lobe of the brain. There are cases when a pathological discharge radiates into the temporal lobe from a focus localized in other areas of the brain.
The study was started in the time of Hippocrates. However, before the introduction of methods of lifetime brain imaging into neurological practice, the causes could be established in less than 1/3 of cases. With the use of MRI in neurology, this indicator has grown to 62%, and with additional PET and stereotactic brain biopsy, it reaches 100%.
Temporal lobe epilepsy can be triggered by a number of factors, which are divided into perinatal, affecting during intrauterine development and during childbirth, and postnatal. According to some data, in about 36% of cases, disease is somehow associated with a perinatal CNS lesion: fetal hypoxia, intrauterine infection (measles, rubella, cytomegaly, syphilis, etc.), birth trauma, asphyxia of the newborn, focal cortical dysplasia.
Pathology under the influence of postnatal etiological factors can develop as a result of traumatic brain injury, neuroinfection (brucellosis, herpes infection, neurosyphilis, tick-borne encephalitis, purulent meningitis, Japanese mosquito encephalitis, postvaccinal encephalomyelitis), hemorrhagic or ischemic stroke. Its cause may be tuberous sclerosis, tumor (angioma, astrocytoma, glioma, glomus tumor, etc.), intracerebral hematoma, abscess, cerebral vascular aneurysm.
In half of the cases, pathology is observed against the background of medial (mesial) temporal sclerosis. However, there is still no clear answer to the question whether medial temporal sclerosis is the cause of temporal epilepsy or it develops as a consequence of it, especially with a long duration of epi-attacks.
According to the localization of the focus of epileptic activity within the temporal lobe, temporal lobe epilepsy is classified into 4 forms: amygdalar, hippocampal, lateral and opercular (insular). For greater convenience, temporal lobe epilepsy is divided into 2 groups in clinical practice: lateral and mediobasal (amygdalogippocampal).
Some authors distinguish bitemporal (bilateral) form. On the one hand, it may be associated with simultaneous damage to both temporal lobes, which is more often observed in perinatal etiology of temporal epilepsy. On the other hand, a “mirror” epileptogenic focus may form as the disease develops.
Depending on the etiology, disease debuts in a different age range. Patients combined with medial temporal sclerosis are characterized by the onset of the disease with atypical febrile seizures that appear in childhood (most often in the period from 6 months to 6 years). Then, within 2-5 years, spontaneous remission is noted, after which psychomotor afebrile seizures occur.
Types of epileptic seizures characterized include: simple seizures, complex partial (CPA) and secondary generalized (SGA) seizures. In half of the cases, disease occurs with a mixed nature of seizures.
Simple seizures are characterized by the preservation of consciousness and are often preceded by CPA or SGA in the form of an aura. By their nature, one can judge the location of the focus of temporal lobe epilepsy. Motor simple seizures manifest themselves in the form of turning the head and eyes towards the localization of the epileptic focus, fixed installation of the hand, less often — the foot. Sensory simple seizures can occur in the form of gustatory or olfactory paroxysms, auditory and visual hallucinations, attacks of systemic dizziness.
There may be attacks of vestibular ataxia, which are often combined with the illusion of changing the surrounding space. In some cases, temporal lobe epilepsy is accompanied by cardiac, epigastric and respiratory somatosensory paroxysms. In such cases, patients complain of a feeling of compression or bursting in the heart, abdominal pain, nausea, heartburn, a feeling of a lump in the throat, an attack of suffocation. Possible occurrence of arrhythmia, vegetative reactions (chills, hyperhidrosis, pallor, feeling of heat), feelings of fear.
Mediobasal temporal lobe epilepsy is more often accompanied by simple epi-attacks with impaired mental function with the phenomena of derealization and depersonalization. The phenomena of derealization consist in a state of “waking sleep”, a sense of acceleration or deceleration of time, the perception of a familiar situation as “never seen” or new events as “previously experienced”. Depersonalization is manifested by the patient identifying himself with some fictional character; the feeling that the patient’s thoughts or his body do not really belong to him.
Complex partial seizures are a shutdown of consciousness with no reaction to external stimuli. With temporal lobe epilepsy, such seizures can occur with a stop of motor activity (the patient seems to freeze in place), without stopping and with a slow fall, which is not accompanied by convulsions. As a rule, CPA forms the basis of the clinical picture of the mediabasal form of temporal lobe epilepsy. Often they are combined with various automatisms — repetitive movements, which can be a continuation of actions started before the attack or occur de novo. Oroalimentary automatism is manifested by smacking, sucking, licking, chewing, swallowing, etc. Mimic automatism is a variety of grimaces, frowning, forced laughter, blinking. Disease can also be accompanied by gesture automatism (stroking, scratching, patting, stomping on the spot, looking around, etc.) and speech automatism (hissing, sobbing, repetition of individual sounds).
Secondary generalized seizures usually occur with the progression. They occur with loss of consciousness and clonic-tonic seizures in all muscle groups. Secondary generalized seizures are not specific in nature. However, the simple or complex partial seizures preceding them indicate that the patient has temporal lobe epilepsy.
Over time, temporal lobe epilepsy leads to mental emotional-personal and intellectual-mnestic disorders. Patients who have temporal lobe epilepsy are characterized by slowness, excessive thoroughness and viscosity of thinking; forgetfulness, decreased ability to generalize; emotional instability and conflict.
In many cases, temporal lobe epilepsy is accompanied by a variety of neuroendocrine disorders. In women, there is a violation of the menstrual cycle, polycystic ovaries, a decrease in fertility; in men, a decrease in libido and a violation of ejaculation. Individual observations indicate cases when temporal lobe epilepsy was accompanied by the development of osteoporosis, hypothyroidism, hyperprolactinemic hypogonadism.
It should be noted that temporal lobe epilepsy presents certain diagnostic difficulties for both ordinary neurologists and epileptologists. Early diagnosis of temporal lobe epilepsy in adults is often not possible, since patients seek medical help only when secondary generalized seizures occur. Simple and complex partial seizures remain unnoticed by patients or are not regarded by them as a reason to consult a doctor. A more timely diagnosis of epilepsy in children is due to the fact that they are brought to a medical consultation by parents who are concerned about attacks of “disconnection” of consciousness, behavioral features and automaticities observed in a child.
Temporal lobe epilepsy is often not accompanied by any changes in neurological status. The corresponding neurological symptoms are noted only in cases when the cause of epilepsy is a focal lesion of the temporal lobe (tumor, stroke, hematoma, etc.). In children, micro-focal symptoms are possible: mild coordination disorders, insufficiency of VII and XII pairs of PMN, increased tendon reflexes. With a prolonged course of the disease, characteristic mnestic and personality disorders are revealed.
Additional diagnostic difficulties are associated with the fact that temporal lobe epilepsy often proceeds without changes on a conventional electroencephalogram (EEG). The detection of epileptic activity can be facilitated by EEG during sleep, which is carried out during polysomnography.
In many cases, MRI of the brain helps to determine the cause of temporal lobe epilepsy. The most common finding during its implementation is medial temporal sclerosis. With the help of MRI, it is also possible to diagnose cortical dysplasia, tumors, vascular malformations, cysts, atrophic changes in the temporal lobe. PET of the brain in temporal epilepsy reveals a decrease in metabolism in the temporal lobe, often affecting the thalamus and basal ganglia.
The main objective of therapy is to reduce the frequency of seizures and achieve remission of the disease, i.e. complete absence of seizures. Treatment of patients diagnosed with temporal lobe epilepsy begins with monotherapy. The drug of the first choice in this case is carbamazepine, if it is ineffective, valproates, hydantoines, barbiturates or reserve drugs (benzodiazepines, lamotrigine) are prescribed. If pathology cannot be treated with monotherapy, then they switch to polytherapy with various combinations of drugs.
In cases where temporal lobe epilepsy is resistant to ongoing antiepileptic therapy, the possibility of its surgical treatment is considered. Most often neurosurgeons perform temporal resection, less often focal resection, selective hippocampotomy or amygdalotomy.
The course of temporal lobe epilepsy and prognosis largely depend on its etiology. Drug remission can be achieved only in 35% of cases. Often conservative treatment leads only to some reduction of seizures. After surgical treatment, the complete absence of seizures is observed in 30-50% of cases, and in 60-70% of patients, their significant reduction is noted. However, the operation can lead to the development of complications such as speech disorders, hemiparesis, alexia and mnestic disorders.