Description
Individuals who experience depersonalization feel divorced from their own personal self by sensing their body sensations, feelings, emotions, behaviors etc. as not belonging to the same person or identity. Often a person who has experienced depersonalization claims that things seem unreal or hazy. Also, a recognition of a self breaks down (hence the name). Depersonalization can result in very high anxiety levels, which further increase these perceptions.Depersonalization is a subjective experience of unreality in ones self, while derealization is unreality of the outside world. Although most authors currently regard depersonalization (personal/self) and derealization (reality/surroundings) as independent constructs, many do not want to separate derealization from depersonalization. Prevalence
Depersonalization is a symptom of anxiety disorders, such as panic disorder. It can also accompany sleep deprivation (often occurring when experiencing jet lag), migraine, 
epilepsy (especially temporal lobe epilepsy,complex-partial seizure, both as part of the aura and during the seizure), 
obsessive-compulsive disorder, severe stress or trauma, anxiety, the use of recreational drugs 
—especially cannabis, hallucinogens, ketamine, and MDMA, certain types of meditation, deep hypnosis, extended mirror or crystal gazing, sensory deprivation, and mild-to-moderate head injury with little or full loss of consciousness (less likely if unconscious for more than 30 minutes). Interoceptive exposure is a non-pharmacological method that can be used to induce depersonalization.In the general population, transient depersonalization/derealization are common, having a lifetime prevalence between 26 and 74%. A random community-based survey of 1,000 adults in the US rural south found a 1-year depersonalization prevalence rate at 19%.
Benzodiazepines are recommended to control seizures. Dialysis is of no use due to the high degree of protein binding with amitriptyline. Interactions
Since amitriptyline and its active metabolite nortriptyline are primarily metabolized by cytochromes CYP2D6 and CYP2C19 (see Amitriptyline#Pharmacology), the inhibitors of these enzymes are expected to exhibit pharmacokinetic interactions with amitriptyline. According to the prescribing information, the interaction with CYP2D6 inhibitors may increase the plasma level of amitriptyline. However, the results in the other literature are inconsistent: the co-administration of amitriptyline with a potent CYP2D6 inhibitor paroxetine does increase the plasma levels of amitriptyline two-fold and of the main active metabolite nortriptyline 1.5-fold, but combination with less potent CYP2D6 inhibitors thioridazine or levomepromazine does not affect the levels of amitriptyline and increases nortriptyline by about 1.5-fold; a moderate CYP2D6 inhibitor fluoxetine does not seem to have a significant effect on the levels of amitriptyline or nortriptyline. A case of clinically significant interaction with potent CYP2D6 inhibitor terbinafine has been reported.A potent inhibitor of CYP2C19 and other cytochromes fluvoxamine increases the level of amitriptyline two-fold while slightly decreasing the level of nortriptyline. Similar changes occur with a moderate inhibitor of CYP2C19 and other cytochromes cimetidine: amitriptyline level increases by about 70%, while nortriptyline decreases by 50%. CYP3A4 inhibitor ketoconazole elevates amitriptyline level by about a quarter. On the other hand, cytochrome P450 inducers such as carbamazepine and St. Johns Wort decrease the levels of both amitriptyline and nortriptylineOral contraceptives may increase the blood level of amitriptyline by as high as 90%.