Neurological status. The results of the clinical examination depend on the etiology of CE. With extensive organic lesion of the temporal lobes (porecephalic cysts, tumors), contralateral symptoms of prolapse (hemiparesis) may appear. Often, microfocal symptoms are detected: insufficiency of the VII and XII pairs of cranial nerves according to the central type, revitalization of tendon reflexes, abnormal reflexes, coordinating disorders. However, it is possible and the absence of any changes.
With age, the persistence of seizures in the majority (up to 80%) of patients reveals persistent mental disorders caused by the involvement of both temporal lobes, especially the limbic system. Mental or emotional-personality disorders are noted. Constant forgetfulness, difficulties in memorizing new material are typical. Thinking is slow, it is characterized by excessive viscosity, fixation on the same thought, thoroughness. The level of generalization, abstract thinking decreases, and the intellect can remain intact. Tenacity, slowness, rigidity of mental processes, stagnation of emotional experiences, with angry irritability or depressive tearfulness and exhaustion prevail. The preservation of intelligence in VE depends on the nature of the structural changes in the brain. In other cases, there may be the following changes: peaks, sharp waves, peak-wave activity, more often in front temporal leads; regional temporal retardation; slowing the main activity of the background recording.
In the majority of patients, over time, epileptic activity manifests itself as bitemporal in 25–30% of patients in the form of an acute-slow wave complex (a “mirror focus” is formed).
During an attack on an EEG, pathological changes are detected in 95% of cases: 5-7 seconds before the onset of the attack, low-amplitude rapid P-activity is diffusely recorded, then it is replaced by a regional slowdown in the temporal leads.
In a neuroradiological study, macrostructural changes in the brain are recorded in 40-60% of cases: a decrease in the size of the hippocampus and the temporal lobe as a whole, the expansion of the temporal horn of the lateral ventricle (Engel, 1994). The most common finding with MRI is medial temporal sclerosis. Often, there is also a decrease in the differentiation of the gray and white matter of the cerebral cortex, the expansion of the furrows, ventriculomegaly, and focal cortical dysplasia. With positron emission tomography, hypometabolism in the temporal lobe is found, usually involving the thalamus and the basal ganglia ipsilateral.
Treatment. The drug of first choice in the treatment of VE is carbamazepine. The first step is monotherapy. The starting daily dose of carbamazepine is 10 mg / kg / day, it is gradually increased to 20 mg / kg / day, and in case of insufficient effectiveness, to 30 mg / kg / day. With satisfactory tolerability, a further dose increase is possible until a positive effect or first signs of intoxication appear. If there is no effect, then the use of carbamazepine should be abandoned by prescribing valproate. Daily doses should be quite high – 50-100 mg / kg / day.
It should be remembered that VE is often resistant to treatment, the therapeutic effect is achieved only with the use of anti-epileptic drugs in high doses.
Phenytoin and barbiturates are not the first choice because of toxicity, but in rare cases their use is acceptable. The reserve drugs are lamotrigine and benzodiazepins.
With the ineffectiveness of two consecutive monotherapy attempts, one should switch to polytherapy using combinations of basic and reserve drugs. The most effective combinations are:
- Finlepsin + Valproate (Convulex);
- finlepsin + lamictal.
- With absolute resistance to attacks of anti-epileptic drugs to the maximum
tolerated doses and the presence of frequent severe attacks, as well as a clearly localized epileptogenic focus, neurosurgical intervention is performed. Surgical treatment is not recommended in case of severe somatic status of the patient and pronounced mental,
intellectual and mental disorders. The purpose of the operation is to remove the epileptogenic focus and prevent further epilepticization of the brain. Temporal lobectomy, selective amygdalo- and hippocampotomy, stereotactic bilateral amygdalotomy are performed. A significant decrease in attacks after surgical treatment is achieved in 60-70% of patients, including their complete disappearance in 30-50% of cases.
Forecasting EI is always serious in view of the resistance of temporal attacks to treatment, a high proportion of patients in need of neurosurgical treatment.