The aim of this review is the presentation of molecular mechanisms of action of cytostatic drugs used in the therapy of neurological disorders, mostly of multiple sclerosis (MS). From many years cytostatics like mitoxantrone, cyclophosphamide, cladribine and methotrexate were used in the MS clinical trials. So far only mitoxantrone has been approved by FDA for the treatment of progressive MS. The other cytostatics are still studied in clinical trials, the main problem with their approval for human therapy are their numerous side effects. So far those drugs are mostly used in oncology and haematology where the usage of this type of drugs is better justified. Now there are many studies leading to better understanding of mechanisms of action of cytostatics at the cellular and subcellular level. Mitoxantrone induces apoptosis and reduce the population of inflammatory cells capable to initiate demyelination in the central nervous system (CNS). At the molecular level mitoxantrone damages genome of inflammatory cells by inhibition of activity of topoisomerase II (TOP II) or direct interaction with DNA structure. Cyclophosphamide is a cytostatic acting mainly on dividing cells, in which it alkylates DNA and interferes with replication and cell apoptosis. Methotrexate inhibits activity of dehydrofolate reductase what leads to disturbance of replication and blocks phase S of the cell cycle in leukocytes. Cladribine is an antagonist of transcription. The detailed analysis of these mechanisms may lead to diminishing of the level of their side effects and to increase of their therapeutic potential, also in neurological therapy.