One or more of:
limb rigidity or akinesia
limb dystonia
limb myoclonus, plus one of:
orobuccal or limb apraxia
cortical sensory deficit
alien limb phenomena (more than simple levitation)More likely (probable sporadic CBS) if:
Asymmetric presentation
Onset after age 50
No family history (2 or more relatives)
No genetic mutation affecting T (e.g. MAPT)
plus two of:limb rigidity or akinesia
limb dystonia
limb myoclonusplus two of:orobuccal or limb apraxia,
cortical sensory deficit
alien limb phenomena (more than simple levitation)

Frontal behavioural-spatial syndrome subtype
Two of:
executive dysfunction
behavioural or personality changes
visuospatial deficits

NAV of primary progressive aphasia subtype
Effortful, agrammatic speech plus at least one of:
impaired grammar/sentence comprehension with relatively preserved single word comprehension or
groping, distorted speech production (apraxia of speech)

Progressive supranuclear palsy syndrome subtype
Three of:
axial or symmetric limb rigidity or akinesia
postural instability or falls
urinary incontinence
behavioural changes
supranuclear vertical gaze palsy or decreased vertical saccade velocity

Exclusion criteria
These apply to all types of CBD. Evidence of Lewy body disease
multiple system atrophy
Alzheimers disease
ALS
semantic or logopenic variant primary progressive aphasia
structural lesion suggestive of focal cause
granulin mutation or reduced plasma progranulin levels
TDP-43 or fused in sarcoma (FUS) mutationsThe diagnostic criteria for clinical use may result in a misdiagnosis of other tau-based diseases.The probable criteria are proposed for clinical research. Clinical vs. postmortem
One of the most significant problems associated with CBD is the inability to perform a definitive diagnosis while an individual exhibiting the symptoms associated with CBD is still alive. A clinical diagnosis of CBD is performed based upon the specified diagnostic criteria, which focus mainly on the symptoms correlated with the disease. However, this often results in complications as these symptoms often overlap with numerous other neurodegenerative diseases.
The current theory on the cause of these reactions is that they may be related to polyphenols found in alcoholic beverages. A 2017 study found that alcohol sensitive patients reacted to catechins in red wine, but not to resveratrol. It has been suggested that steel fermented white wines and clear liquors may cause less of a reaction than other alcoholic beverages. Desensitization to aspirin has been found to reduce reactions to alcohol.Some people have reported relief of symptoms by following a low-salicylate diet such as the Feingold diet. Aspirin is quickly converted in the body to salicylic acid, also known as 2-Hydroxybenzoic acid. A prospective randomized trial with 30 patients following a low-salicylate diet for six weeks demonstrated a clinically significant decrease in both subjective and objective scoring of severity of disease, but made note of the challenge for patients in following what is a fairly stringent diet. Despite these findings, experts on the disease do not believe that dietary salicylates contribute to AERD symptoms. Dietary salicylates do not significantly inhibit the COX-1 enzyme, which is the cause of AERD reactions. One confounding factor in the study that showed a benefit from avoidance of dietary salicylates is that a low salicylate diet involves eliminating wine and beer. The majority of AERD patients react to wine and beer for reasons that do not involve their salicylate content. There is also a strong placebo effect involved with any dietary intervention.