Leukoencephalitis Subacute Sclerosing

Subacute sclerosing leukoencephalitis: Understanding and Treatment

Subacute sclerosing leukoencephalitis, also known as van Bogaert's disease or van Bogaert leukoencephalitis, is a rare neurological disease that is characterized by inflammatory changes in the white matter of the brain. This is a serious condition that can lead to progressive damage to the brain and spinal cord. In this article we will look at the main aspects of this disease, its symptoms, causes and treatment options.

Characteristic symptoms of subacute sclerosing leukoencephalitis include progressive weakness and spasticity in the limbs, coordination problems, changes in visual function, and speech problems. Patients may also experience psychiatric disorders, including depression, apathy, and cognitive deficits. Symptoms usually develop gradually and get worse over time.

The causes of subacute sclerosing leukoencephalitis are not completely clear. However, it is believed that autoimmune processes may play an important role in the development of the disease. The body's immune system begins to mistakenly attack its own cells and tissues, including the white matter of the brain, leading to inflammation and subsequent degeneration of nerve fibers.

The diagnosis of subacute sclerosing leukoencephalitis is a complex process, as symptoms may be similar to other neurological diseases. Doctors usually rely on clinical manifestations, neuroimaging findings (such as MRI of the brain and spinal cord), and laboratory tests to rule out other possible causes of symptoms.

Treatment of subacute sclerosing leukoencephalitis is aimed at alleviating symptoms, slowing the progression of the disease and improving the quality of life of patients. Doctors may use immunomodulatory therapy, including corticosteroids and immunosuppressants, to reduce inflammation and suppress autoimmune reactions. Physical therapy, occupational therapy, and speech therapy may also be helpful to relieve physical and cognitive symptoms.

Although subacute sclerosing leukoencephalitis is a chronic and progressive disease, a number of patients can show a positive response to treatment and achieve a stable condition over a long period of time. However, the prognosis may vary for each patient and treatment results may vary.

It is important to note that subacute sclerosing leukoencephalitis requires a comprehensive approach to management and treatment. Regular consultations with a neurologist, physiotherapist and other specialists will help the patient receive support and necessary medical measures.

In addition, patients and their loved ones can turn to organizations and communities that provide information and support to people affected by subacute sclerosing leukoencephalitis. Educational resources, support groups, and online forums can be helpful for obtaining information, sharing experiences, and interacting with others who are facing similar problems.

In conclusion, subacute sclerosing leukoencephalitis is a rare neurological disease that causes inflammation and degeneration of the white matter of the brain. Although the causes of this disease are not fully understood, diagnostic and treatment options are available to relieve symptoms and slow the progression of the disease. It is important to seek professional advice and receive appropriate support to manage this condition and improve patients' quality of life.

**Acute sclerosing leukoencephalitis** is an infectious-allergic disease of the central nervous system with predominant damage to the white matter of the hemispheres and brain stem.

The disease has many synonyms - leukoencephalitis disseminated myelin lesion (disease, Van Giborg syndrome), subacute chaga of the corpus callosum, Marseilles spot. The disease is most often registered at the age of 20-40 years, both men and women are affected, although the female gender predominates. The peak incidence occurs in early spring.

Etiology, pathogenesis. The main etiological factor of the disease is the CMV virus. Having penetrated the body, viruses enter the cerebrospinal fluid and peripheral blood simultaneously. From the cerebrospinal fluid, the pathogen “migrates” to the endothelium, through the vessels it enters the sinuses of the dura mater of the brain. Tissues in contact with venous capillaries come out of the action of the decongestant and numerous hemorrhages form on their surface. The walls of the blood vessels are loosened, through which cells exit during the inflammatory reaction of the brain substance into the cerebrospinal fluid. The result of these processes is the formation of abscesses in the brain. Antibodies to the virus are detected in the blood, microglial cells undergo metabolic disorders, accompanied by the release of cytokines into the cerebrospinal fluid. Plasma rheology worsens and blood viscosity increases. Erythrocyte sedimentation rate and plasma creatinine increase compensatoryly. The presence of antibodies to the virus is confirmed not only by a set of signs of the disease, but also by serological reactions. Often in combination with persistent CMV