Guideline | Procedures |
---|---|
Step 1: criteria for ‘all cause dementia’ | |
Interferes with the ability to function at work or with usual abilities and | History and observation |
Represents a decline from previous ability and | ■ Evidence of changes in functioning reported by either patient and/or informant or observed by clinician |
Cannot be explained by delirium or major psychiatric disorder | |
Presence of cognitive impairment | History, observation, neuropsychological testing |
■ History-taking from a knowledgeable informant ■ Objective mental status testing and/or neuropsychological testing ■ Neuropsychological testing is recommended when history and mental status testing cannot provide a confident diagnosis | |
The cognitive or behavioural impairment involves a minimum of two domains | History, observation, neuropsychological testing |
■ Impaired ability to acquire/remember new information (eg, repeating questions, forgetting events or appointments, becoming lost in familiar places) ■ Impaired reasoning and handling of complex tasks, poor judgement (eg, inability to handle finances, poor decision making) ■ Impaired visuospatial abilities (eg, difficulty recognising faces or common objects) ■ Impaired language function (speaking, reading, writing; eg, difficulty thinking of common words while speaking, hesitations in speech) ■ Changes in personality, behaviour, comportment (eg, agitation, apathy, social withdrawal) | |
Difference between MCI and dementia | History and observation |
■ The fundamental difference between diagnoses of dementia versus MCI depends upon whether or not there is a significant change in the ability to function at work or in daily activities. This will necessarily require clinical judgment based upon the information provided by the patient and a knowledgeable informant. | |
Step 2: criteria for ‘probable AD dementia’ | |
Meets criteria for dementia | See criteria above for dementia, step 1 |
Insidious onset: symptoms have a gradual onset over months or years, not sudden over hours or days. | History |
■ From patient and knowledgeable informant | |
Clear cut history of worsening of cognition | History, serial neuropsychological testing |
■ From patient and knowledgeable informant | |
Initial cognitive deficits are evident and most prominent in one of the following categories | History, neuropsychological testing |
■ Amnestic presentation – the most common presentation ■ Non-amnestic presentations | Amnestic presentation ■ Impairment of learning and recall of recently learned information |
(1) Language presentation | ■ Deficit in at least one other cognitive area Non-amnestic presentations |
(2) Visuospatial presentation | ■ Language: most prominent deficits are word finding, but should also be deficits in other cognitive areas |
(3) Executive dysfunction | ■ Visuospatial: most prominent deficits are spatial cognition, but should also be deficits in other cognitive areas ■ Executive: most prominent deficits are reasoning, judgment and problem solving, but should also be deficits in other cognitive areas |
Diagnosis of AD should not be made when there is evidence of another dementing illness | History, neuropsychological testing, imaging studies, laboratory studies |
Disorders to rule out include: ■ Vascular cognitive impairment/vascular dementia ■ Dementia with Lewy bodies ■ Frontal-temporal dementia – behavioural variant ■ Primary progressive aphasia ■ Evidence of neurological disease or non-neurological condition or medication that could have a substantial effect on cognition | |
Step 3: criteria for ‘probable AD dementia with increased level of certainty’ | |
Meets criteria for AD dementia | See criteria above for AD dementia, step 2 |
Probable AD dementia with documented decline | History, serial neuropsychological testing |
Evidence of progressive cognitive decline on subsequent evaluations from | |
■ knowledgeable informant or ■ cognitive testing (either formal neuropsychological evaluation or standardised mental status examinations) | |
Probable AD dementia in a carrier of a causative AD genetic mutation | Laboratory studies |
Presence of an early-onset familial genetic mutation | |
■ APP, PSEN1, or PSEN2 | |
(Note that the apolipoprotein E ɛ4 allele was not considered specific enough to meet criteria) | |
Step 4: evaluate the ‘biomarker probability of AD aetiology’ | |
Evaluate for atrophy of temporal (medial, basal, and lateral) and medial parietal cortex and other biomarkers when available and clinically useful | Biomarkers |
■ Although the use of biomarkers is not recommended routinely, they are available to the clinician when desired ■ There are two categories of biomarkers, those associated with Aβ protein deposition and those associated with downstream neurodegeneration (see table 1) ■ We recommend routine review of CT and MRI patterns of atrophy, a marker of downstream neurodegeneration ■ Presence of one biomarker category makes the ‘biomarker probability of AD aetiology’ ‘intermediate;’ both categories must be positive for a ‘high’ probability. The ‘lowest’ probability is present if both categories are negative |
Note: patients who would have met criteria under the 1984 guidelines would also meet criteria under the current guidelines.
Aβ, amyloid β; AD, Alzheimer's disease; APP, amyloid precursor protein; MCI, mild cognitive impairment; PSEN, presenilin.