Go Leucoencephalitis treatment


Leucoencephalitis is a special form of viral etiology encephalitis . Leukoencephalitis is characterized by predominant damage to the white matter of the brain. Leucoencephalitis in the form of subacute sclerosing encephalitis (see) occurs mainly in children aged 4-16 years.

Clinical course. The disease develops gradually. Generally infectious and cerebral symptoms are rarely observed. The picture of the disease consists of gradually developing dementia (dementia), hyperkinesis (involuntary movements) and autonomic disorders. The earliest symptom is mental disorders, which are rapidly progressing. Already in the early period there are epileptiform seizures, but more often they appear against the background of the unfolded picture of the disease. After 1.5 —2 months. involuntary movements appear, with hyperkinesis being diverse, tonic spasms of the muscles of the trunk and extremities are often observed, leading to a kind of rotational movements. Often there are speech disorders such as sensory or motor aphasia (see). Patients observed violent laughter and crying. Vegetative disorders manifest greasiness of the skin, sweating, drooling, changes in vascular reactions. Losing weight gradually develops, often to the degree of cachexia. The disease is progressive. Death occurs after a few months, and in some cases a few years from the onset of the disease.


Treatment . Rational treatment of the disease does not currently exist. Some effect may be in the treatment of prednisone (under the supervision of a physician). Fortifying treatment, vitamin therapy, anticonvulsants ( phenobarbital at 0.01 g per 1 year of life per day), etc. are shown. Care should be taken for patients (they should be fed, wiped the skin, and care should be taken to prevent bedsores ).

Leucoencephalitis (from the Greek. Leukos - white + encephalitis) is an inflammatory disease of the brain with white matter damage. For a long time, leukoencephalitis was contrasted with encephalitis with an isolated lesion of gray matter (polyencephalitis). Recently, the boundary between these two types of encephalitis is gradually erased, and now we can only speak about the predominance of the inflammatory process in the white or gray matter of the brain.

At first, various lesions of the nervous system, both inflammatory and degenerative, were attributed to leukoencephalitis. As we study the nature of encephalitis, secondary post-infectious encephalitis was isolated from this polymorphic group, observed mainly in acute childhood infections (measles, rubella, etc.), vaccinal and allergic encephalitis, as well as systemic demyelinating diseases of a degenerative nature, such as diffuse sclerosis (Schilder’s disease) , family progressive leukodystrophy, etc.). The remaining primary leukoencephalitis is still difficult to recognize due to the lack of a precise etiological classification. Their diagnosis is possible only by the features of the clinic and histopathology.

The group of primary leukoencephalitis, which is called subacute sclerosing leukoencephalitis with a progressive course, has been studied most accurately. As an independent nosological unit, they were first isolated by Van-Bogart (L. van Bogaert) in 1945. It turned out that a number of encephalitis, previously described under various names, can be completely attributed to subacute sclerosing leucoencephalitis. They are only variants of this form and differ by the presence or absence of intracellular inclusions, the duration of the flow and the intensity of the demyelinating process.


The etiology of subacute sclerosing leukoencephalitis has not yet been established. Intracellular inclusions are evidence of a viral nature, but the virus cannot be isolated. The disease does not have seasonality and epidemic foci. There is an increase in the incidence of the subacute course of the disease in many countries. Initially, it was believed that the disease occurs only in childhood. Last time it is described in adults, but much less frequently and it proceeds less typically.

Pathological subacute sclerosing leukoencephalitis is characterized by demyelinating lesions in the white matter of the cerebral hemispheres and the trunk. The process of demyelination in some cases spreads diffusely, but more often affects the conductor systems of the brain in a certain sequence. The first to suffer are the association systems of the big hemispheres, cortico-strio-pallidar pathways and pontocerebellar conductor bonds. The pyramid system is involved in the process in the later stages of the disease. The proliferation of fibrous glia accompanying demyelination and inflammatory changes vary depending on the duration of the disease. They are more pronounced with a longer course. In cases of rapid course, along with a weak development of demyelination, proliferation of the fibrillary glia comes to the fore, which gave grounds to call encephalitis sclerosing. In fast-flowing forms, intranuclear eosinophilic inclusions of type A are more often detected.

The clinical picture is extremely stereotypical. The disease proceeds in three main stages. The earliest symptoms (first stage) include changes in higher nervous activity that occur in children, who are so healthy and somatic and psychologically healthy and not burdened by pathological heredity. Severe degradation of the intellect with agnosia, apraxia and speech disorders quickly increases. Mutism and complete lack of contact with others are developing.

The second stage is accompanied by a kind of hyperkinesis. At first they may have the character of choreiform or myoclonic, but very quickly acquire the type of large-scale ballism, an extremely stereotypical type, with simultaneous contraction of a number of muscles of the proximal extremities, trunk and neck. They are distinguished by strict rhythm (from 4 to 12 in 1 min.). In the future, a kind of hyperkinesis of the eyeball joins: forcing them to the sides and upwards synchronously with the hyperkinesis of the extremities; at the same time, forced opening of the mouth and pushing out of the tongue, coinciding with the rhythm of the remaining motor discharges. These strictly rhythmic and complex hyperkinesis give subacute leukoencephalitis an originality that allows it to be isolated from a number of other subacute encephalitis. Between bouts of motor discharges, first, neither paralysis of the limbs, nor disorders of the cranial nerves are detected; only hypotonia is noted.

The third stage of the disease is characterized by the cessation of hyperkinesis and the gradual development of decerebration rigidity. There are vegetative disorders and hyperthermal crises with a temperature rise up to 40 ° and above. By this time, pyramidal symptoms in the form of clonus of the feet and pathological reflexes develop. In the cerebrospinal fluid, globulin fractions of protein increase, while the level of gamma globulin in the blood may not increase. The fundus of the eye is normal in all cases. Changes in the electrical activity of the brain with periodic high-voltage discharges, observed in all leads synchronously for both hemispheres, are especially characteristic. These peculiar changes in the EEG can be used to distinguish this form from other encephalitis.

The disease is progressing steadily; the process lasts from several months to 2 years, in all cases ending in a fatal outcome. Treatment unsuccessfully. See also Encephalitis.