These categories are used for forms of pathological dissociation that do not fully meet the criteria of the other specified dissociative disorders; or if the correct category has not been determined; or the disorder is transient.The ICD11 lists dissociative disorders as: 

Dissociative neurological symptom disorder
Dissociative amnesia
Dissociative amnesia with dissociative fugue
Trance disorder
Possession trance disorder
Dissociative identity disorder
Partial dissociative identity disorder
Depersonalization-derealization disorder

Cause and treatment
Dissociative identity disorder
Cause: Dissociative identity disorder is caused by ongoing childhood trauma that occurs before the ages of six to nine. People with dissociative identity disorder usually have close relatives who have also had similar experiences.Treatment: Long-term psychotherapy to improve the patients quality of life. Dissociative amnesia
Cause: A way to cope with trauma. Treatment: Psychotherapy (e.g. talk therapy) counseling or psychosocial therapy which involves talking about your disorder and related issues with a mental health provider. Psychotherapy often involves hypnosis (help you remember and work through the trauma); creative art therapy (using creative process to help a person who cannot express his or her thoughts); cognitive therapy (talk therapy to identify unhealthy and negative beliefs/behaviors); and medications (antidepressants, anti-anxiety medications, or sedatives). These medications help control the symptoms associated with the dissociative disorders, but there are no medications yet that specifically treat dissociative disorders. However, the medication pentothal can sometimes help to restore the memories. The length of an event of dissociative amnesia may be a few minutes or several years. If an episode is associated with a traumatic event, the amnesia may clear up when the person is removed from the traumatic situation.
Sublingual and rectal bioavailabilities are intermediate at approximately 25–50%.After absorption ketamine is rapidly distributed into the brain and other tissues. The plasma protein binding of ketamine is variable at 23 to 47%. In the body ketamine undergoes extensive metabolism. It is biotransformed by CYP3A4 and CYP2B6 isoenzymes into norketamine, which, in turn, is converted by CYP2A6 and CYP2B6 into hydroxynorketamine and dehydronorketamine. Low oral bioavailability of ketamine is due to the first-pass effect and, possibly, ketamine intestinal metabolism by CYP3A4. As a result, norketamine plasma levels are several-fold higher than ketamine following oral administration, and norketamine may play a role in anesthetic and analgesic action of oral ketamine. This also explains why oral ketamine levels are independent of CYP2B6 activity, unlike subcutaneous ketamine levels.After an intravenous injection of tritium-labelled ketamine, 91% of the radioactivity is recovered from urine and 3% from the feces. The medication is excreted mostly in the form of metabolites, with only 2% remaining unchanged. Conjugated hydroxylated derivatives of ketamine (80%) followed by dehydronorketamine (16%) are the most prevalent metabolites detected in urine. Chemistry
Synthesis
2-chlorobenzonitrile is reacted with the Grignard reagent cyclopentylmagnesium bromide to give (2-chlorophenyl)(cyclopentyl)methanone. This is then brominated using bromine to form the corresponding bromoketone, which is then reacted with methylamine in an aqueous solution to form the methylimino derivative, 1-(2-Chloro-N-methylbenzimidoyl)cyclopentanol, with hydrolysis of the tertiary bromine atom. This final intermediate is then heated in decalin or another suitable high-boiling solvent, upon which a ring-expansion rearrangement occurs, forming ketamine. Structure
In chemical structure, ketamine is an arylcyclohexylamine derivative. Ketamine is a chiral compound.