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Levamizole is an imidazole derivative used in the treatment of various types of cancer, dermatological diseases and parasitoses. The drug has immunomodulatory properties due to stimulating the activity of macrophages, neutrophils, monocytes and T-lymphocytes. Common side effects are gastrointestinal disorders, skin manifestations and hematological disorders. There is also a wide range of neurological side effects, such as headache, dizziness, vomiting, aphasia, blurred vision, diplopia, weakness, which can be observed in 1.3-5.0% of patients. Multifocal levamizole-induced leukoencephalopathy is one of the most striking neurological side effects of levamizole. MRI of the brain in this pathology reveals numerous foci of demyelination, located mainly periventrically, in the white matter of the cerebral hemispheres, cerebellum, brain stem, corpus callosum, basal ganglia. The treatment with corticosteroids showed the significant improvement in the condition, with almost complete regression of neurological symptoms [8]. Although the symptoms are most often manifested as subacute, over 2-8 weeks of drug use, there were reported cases with clinical manifestations developed both 1 day and months after levamizole administration. It should be noted that the neurotoxic effects of levamizole can manifest independently on the dose, even after a single application of 50 mg, which indicates that its toxic effect is a manifestation of idiosyncrasy. The literature provides a sufficient number of descriptions of clinical manifestations, MRI features and therapy of drug complications of levamizole use in adults. However, observations in pediatric practice are few. We would like to present clinical, laboratory data, imaging results, information on the treatment and follow-up of a 17-year girl who developed levamizole-induced inflammatory leukoencephalopathy and autoimmune hepatitis after self-administration of levamizole for the prevention of helminthic invasion. Leukoencephalopathy caused by levamizole should be taken into account in the differential diagnosis of demyelinating diseases, including acute multiple encephalomyelitis and multiple sclerosis, and the neurotoxic effects of the drug should also be taken into account for the timely initiation of therapy.

Leukodystrophies are a group of hereditary progressive diseases of the central nervous system characterized by selective lesions in white matter with specific involvement of glial cells. There are hypomyelinating (absence of myelin deposition), demyelinating (loss of previously deposited myelin), dysmyelinating (deposition of structurally or biochemically abnormal myelin), and myelinolytic leukodystrophies (myelin vacuolization). Hypomyelinating leukodystrophies (HL), like most leukodystrophies, debut in childhood or adolescence and are characterized by a progressive course of the disease. HL occurs as a result of impaired synthesis of proteins responsible for the development, structure, and integrity of the myelin sheath, involved in the processes of transcription and translation. In the latter group, the main role is assigned to HL associated with biallelic mutations in the genes of the RNA polymerase III transcription complex, POLR3: POLR3A, POLR3B, POLR1C, and POLR3K. The diagnosis can be confirmed by magnetic resonance imaging of the brain. POLR3A-associated HL is manifested by hypomyelination, hypodontia, and hypogonadotropic hypogonadism. The magnetic resonance features of POLR3-associated HL include diffuse hypomyelination with relative preservation of the dentate nuclei, anterolateral nuclei of the thalamus, globus pallidus, pyramidal tracts at the level of the posterior part of the internal capsules, and the corona radiata. In some cases, thinning of the corpus callosum and atrophy of the cerebellum were also noted. The article presents a clinical case of a patient with POL3A-associated HL with spinal cord injury with the debut in early childhood.