Due to its non-specific nature, diagnosing CSE requires a multidisciplinary<unk>  Team" typically consisting of a neurologist, occupational physician, occupational hygienist, neuropsychologist, and sometimes a psychiatrist or toxicologist. Together, the team of specialists assess the patient's history of exposure, symptoms, and course of symptom development relative to the amount and duration of exposure, presence of neurological signs, and any existing neuropsychological impairment. Furthermore, CSE must be diagnosed "by exclusion". This means that all other possible causes of the patient's symptoms must first be ruled out beforehand. Because screening and assessing for CSE is a complex and time-consuming procedure requiring several specialists of multiple fields, few cases of CSE are formally diagnosed in the medical field. This may, in part, be a reason for the syndrome's lack of widespread recognition. The<unk> s responsible for neurological effects dissipate quickly after an exposure, leaving only indirect evidence of their presence, in the form of temporary or permanent impairments. Brain imaging techniques which have been explored in research have shown little promise as alternative methods to diagnose CSE. Neuroradiology and functional imaging have shown mild cortical atrophy, and effects in dopamine-mediated frontostriatal circuits in some cases. Examinations of regional cerebral blood flow in some imaging techniques have also shown some cerebrovascular abnormalities in patients with CSE, but the data were not different enough from healthy patients to be considered significant. The most promising brain imaging technique being studied currently is functional magnetic resonance imaging (fMRI) but as of now, no specific brain imaging techniques are available to reliably diagnose CSE. Classification Introduced by a working group from the World Health Organization (WHO) in 1985, WHO diagnostic criteria states that CSE can occur in three stages, organic affective syndrome (type I), mild chronic toxic encephalopathy (type II), and severe chronic toxic encephalopathy (type III). Shortly after, a workshop in Raleigh-Durham, NC (United States) released a second diagnostic criterion which recognizes four stages as symptoms only (type 1), sustained personality or mood swings (type 2A), impairment of intellectual function (type 2B), and dementia (type 3). Though not identical, the WHO and Raleigh criteria are relatively comparable. WHO type I and Raleigh types 1 and 2A are believed to encompass the same stages of CSE, and WHO type II and Raleigh type 2B both involve deficiencies in memory and attention. No other international classifications for CSE have been proposed, and neither the WHO nor Raleigh criteria have been uniformly accepted for epidemiological studies.
Chronic solvent-induced encephalopathy
Toxic encephalopathy
Chronic traumatic encephalopathy
Chronic traumatic encephalopathy in sports
Alcohol-related brain damage
Hashimoto's encephalopathy
Transmissible spongiform encephalopathy
Viral encephalitis