<unk> 's<unk>  is diagnosed by establishing a clinical history of carbon monoxide poisoning, narcotic overdose, myocardial infarction, or other global cerebral hypoxic events. This diagnosis can then be supported by neuroimaging confirmation of broadcast cerebral hemisphere demyelination sparing cerebellar and brainstem tracts. The neuroimaging evidence can also be used to diagnose<unk> 's<unk>  through an elevation in the concentrations of a myelin basic protein in the cerebrospinal fluid . Because this disease shares many of the symptoms with various forms of dementia or hysteria, these possibilities must be eliminated before a diagnosis for<unk> 's<unk>  can be made. Neuroimaging While there are no standard criteria for the diagnosis of<unk> 's<unk> , neuroimaging can be an important diagnostic tool in ruling out other diagnoses. Magnetic resonance imaging (MRI) or computed tomography (CT) scans can be used to demonstrate a decrease in white matter density in the patient's cerebral hemispheres, with the typical exception of overlying cortices. Unexplained, uniform demyelination of white matter can indicate acute onset<unk> 's<unk> .
Grinker myelinopathy
Diffuse myelinoclastic sclerosis
Neuromyelitis optica spectrum disorder
Cerebrotendineous xanthomatosis
Akureyri disease
Fasciolopsiasis
White dot syndromes
Camel spongiform encephalopathy