If other memory processes are affected, they are usually much less severely affected than retrograde autobiographical memory, which is taken as the hallmark of psychogenic amnesia. However the wide variability of memory impairment among cases of psychogenic amnesia raises questions as to its true neuropsychological criteria, as despite intense study of a wide range of cases there is little consensus of which memory deficits are specific to psychogenic amnesia.Past literature has suggested psychogenic amnesia can be situation-specific or global-transient, the former referring to memory loss for a particular incident, and the latter relating to large retrograde amnesic gaps of up to many years in personal identity. The most commonly cited examples of global-transient psychogenic amnesia are fugue states, of which there is a sudden retrograde loss of autobiographical memory resulting in impairment of personal identity and usually accompanied by a period of wandering. Suspected cases of psychogenic amnesia have been heavily reported throughout the literature since 1935 where it was reported by Abeles and Schilder. There are many clinical anecdotes of psychogenic or dissociative amnesia attributed to stressors ranging from cases of child sexual abuse to soldiers returning from combat. Cause
Neurological cause of psychogenic amnesia is controversial. Even in cases of organic amnesia, where there is lesion or structural damage to the brain, caution must still be taken in defining causation, as only damage to areas of the brain crucial to memory processing is possible to result in memory impairment.
A cholangiocarcinoma occurring at the junction where the left and right hepatic ducts meet to form the common hepatic duct may be referred to eponymously as a Klatskin tumor.Although cholangiocarcinoma is known to have the histological and molecular features of an adenocarcinoma of epithelial cells lining the biliary tract, the actual cell of origin is unknown. Recent evidence has suggested that the initial transformed cell that generates the primary tumor may arise from a pluripotent hepatic stem cell. Cholangiocarcinoma is thought to develop through a series of stages – from early hyperplasia and metaplasia, through dysplasia, to the development of frank carcinoma – in a process similar to that seen in the development of colon cancer. Chronic inflammation and obstruction of the bile ducts, and the resulting impaired bile flow, are thought to play a role in this progression.Histologically, cholangiocarcinomas may vary from undifferentiated to well-differentiated. They are often surrounded by a brisk fibrotic or desmoplastic tissue response; in the presence of extensive fibrosis, it can be difficult to distinguish well-differentiated cholangiocarcinoma from normal reactive epithelium. There is no entirely specific immunohistochemical stain that can distinguish malignant from benign biliary ductal tissue, although staining for cytokeratins, carcinoembryonic antigen, and mucins may aid in diagnosis. Most tumors (>90%) are adenocarcinomas. Diagnosis
Blood tests
There are no specific blood tests that can diagnose cholangiocarcinoma by themselves. Serum levels of carcinoembryonic antigen (CEA) and CA19-9 are often elevated, but are not sensitive or specific enough to be used as a general screening tool.