Relation to other psychiatric disorders
Depersonalization exists as both a primary and secondary phenomenon, although making a clinical distinction appears easy, it is not absolute. The most common comorbid disorders are depression and anxiety, although cases of depersonalization disorder without symptoms of either do exist. Comorbid obsessive and compulsive behaviours may exist as attempts to deal with depersonalization, such as checking whether symptoms have changed and avoiding behavioural and cognitive factors that exacerbate symptoms. Many people with personality disorders such as schizoid personality disorder, schizotypal personality disorder, and borderline personality disorder will have high chances of having depersonalization disorder. History
The word depersonalization itself was first used by Henri Frédéric Amiel in The Journal Intime. The 8 July 1880 entry reads:

 I find myself regarding existence as though from beyond the tomb, from another world; all is strange to me; I am, as it were, outside my own body and individuality; I am depersonalized, detached, cut adrift. Is this madness? Depersonalization was first used as a clinical term by Ludovic Douglas in 1898 to refer to "a state in which there is the feeling or sensation that thoughts and acts elude the self and become strange; there is an alienation of personality – in other words a depersonalization". This description refers to personalization as a psychical synthesis of attribution of states to the self.Early theories of the cause of depersonalization focused on sensory impairment.
If the internal carotid artery ruptures within the cavernous sinus, an arteriovenous fistula is created (more specifically, a carotid-cavernous fistula). Lesions affecting the cavernous sinus may affect isolated nerves or all the nerves traversing through it. The pituitary gland lies between the two paired cavernous sinuses. An abnormally growing pituitary adenoma, sitting on the bony sella turcica, will expand in the direction of least resistance and eventually invade the cavernous sinus. Cavernous sinus syndrome may result from mass effect of these tumors and cause ophthalmoplegia (from compression of the oculomotor nerve, trochlear nerve, and abducens nerve), ophthalmic sensory loss (from compression of the ophthalmic nerve), and maxillary sensory loss (from compression of the maxillary nerve). A complete lesion of the cavernous sinus disrupts CN III, IV, and VI, causing total ophthalmoplegia, usually accompanied by a fixed, dilated pupil. Involvement of CN V (V1 and variable involvement of V2) causes sensory loss in these divisions of the trigeminal nerve. Horners syndrome can also occur due to involvement of the carotid ocular sympathetics, but may be difficult to appreciate in the setting of a complete third nerve injury.Because of its connections with the facial vein via the superior ophthalmic vein, it is possible to get infections in the cavernous sinus from an external facial injury within the danger area of the face. In patients with thrombophlebitis of the facial vein, pieces of the clot may break off and enter the cavernous sinus, forming a cavernous sinus thrombosis. From there the infection may spread to the dural venous sinuses.