Most of the people diagnosed with sexual sadism disorder come to the attention of authorities by committing sexually motivated crimes. Surveys have also been conducted to include people who are interested in only mild and consensual forms of sexual pain/humiliation (BDSM).Most people with full-blown sexual sadism disorder are male, whereas the sex ratio of people interested in BDSM is closer to 2:1 male-to-female.People with sexual sadism disorder are at an elevated likelihood of having other paraphilic sexual interests. Typology
Criminologist Lee Mellor created a six typology of sexually sadistic homicide offenders, based upon a combination of three binary factors:                             Destructive versus Preservative: Destructive sex sadists mutilate the bodies of their living victims, while Preservative sex sadists do not. Prolonged versus Brief:  The Prolonged sex sadist tortures their victim for an hour or more, while the Brief sex sadist does so over less time. Elaborate versus Simple: Where Simple sex sadists tend to use one or two methods of torture, Elaborate sadists have three of the following four characteristics, (i) variation in torture methods, (ii) complex torture apparatus, (iii) psychological torture, (iv) record making (e.g., using notes/media to document the process).
Mutations generally prevent the production of any functional VHL protein or result in a change of structure of VHL protein. This genetic disorder shows an autosomal dominant inheritance pattern, with about 20% of patients possessing a new mutation. There are usually several other tumors which are part of the syndrome, including tumors of the central nervous system, kidneys, pancreas, adrenal glands, epididymis, broad ligament, along with the endolymphatic sac. The vast majority of patients with an endolymphatic sac tumor have von Hippel-Lindau syndrome. Pathology findings
Tumors range from several millimeters up to 10 cm, with larger tumors more frequently seen in older patients. If the tumor is bilateral, it is almost always seen in a VHL patient. The tumor destroys the mastoid air spaces and extends into the middle ear and/or posterior cranial fossa. The microscopic appearance shows an unencapsulated, destructive growth, remodeling and invading bone. The tumor is arranged as simple, broad, non-complex papillary projections without large cystic spaces. The spaces are often fluid filled, have extravasated erythrocytes and/or inspissated material. The cells are cuboidal, usually single layered along the papillary structures, showing indistinct cell borders. The nuclei are round and hyperchromatic. Immunohistochemistry
The neoplastic cells are reactive with keratin, CK7, and Epithelial membrane antigen, but negative with TTF-1 and CK20. Cytogenetics
The germline mutations of VHL tumor suppressor gene will be found on 3p25-26 (short arm  of chromosome 3), usually between base pair 10,158,318 to 10,168,761. Differential diagnosis
The clinical and pathology differential are different.