Hysterectomy currently occupies one of the leading places among obstetric and gynecological surgeries and is one of the highly effective and sometimes the only method of treating various diseases of the female genital organs.  Quite often, however, hysterectomy results not only in the elimination of the cause of disease, but also in the development of complications that reduce the quality of life of patients. More and more attention is being paid to neurological complications, which is obviously due to improved diagnostic capabilities, as well as the results of recent research on the pathogenesis and treatment of neurological disorders. Only recently the scientists have begun to think about the true causes  of one of the most important neurologic complications of hysterectomy, namely chronic postoperative pain.The review describes in detail the main neurological disorders that develop after hysterectomy: chronic postoperative pain, traumatic neuroma, residual ovarian syndrome  as possible causes of chronic pain, mononeuropathies, sexual and sleep disorders, decreased cognitive and motor functions, lower  urinary tract and bowel dysfunction.  Considerable  attention is given to the mechanisms of neurological complications and the relationship between the surgery and emotional disturbances in women.

The influence of epigenetic processes on the development of malignant diseases, including gynaecological cancers, is now beyond doubt. DNA methylation, histone modification and post-transcriptional regulation by microRNAs lead to changes in the activity of various genes, contributing to female genital cancers (cervix, endometrium, ovarian). It should be noted that disruptions in gene expression do not only occur in malignant cells, but also in the tumour microenvironment, resulting in disease progression and relapse. However, “epigenetic markers” of carcinogenesis can be useful in the treatment and rehabilitation of patients, making a personalized approach possible.

Huntington’s disease is a serious inherited neurodegenerative disorder characterized by of motor, cognitive and psychiatric features. The disease is caused by an abnormally expanded CAG repeat expansion in the HTT gene and the production of mutant huntingtin protein.The disease usually manifests in adulthood, but the manifestation in childhood and youth is also described, which is noted in 5–10 % of cases. The disease predominantly affects the neostriatum, resulting in a characteristic clinical picture.The most promising approaches to etiotropic therapy of Huntington’s disease are a number of DNA- (CRISPR/Cas9 system) and RNA-directed methods (antisense oligonucleotides, RNA interference), methods that directly reduce the level of mutant gentingtin (chimera molecules), as well as approaches based on inactivating the DNA mismatch repair system using the FAN1 enzyme.