Erfan Bashar
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Dementia — Diagnosis

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Educational scope notice: This is a study note for medical students, not medical advice, diagnosis, or treatment guidance. Clinical management should follow local protocols and current guidelines.

Dementia requires cognitive or behavioural symptoms that interfere with work or usual activities, mark a decline from a previous level, and are not explained by delirium or major psychiatric illness, with at least two of five domains involved: memory, reasoning and judgment, visuospatial skill, language, or personality and behaviour. Two bedside principles anchor every assessment: examine the patient neurologically, and image the brain.

Informant history

Patients with dementia often lack insight and minimise their deficits, so a family member provides the timeline and functional impact. The characteristic report is gradual withdrawal over months to years: abandoned hobbies and housekeeping, repeated questions, misplaced objects, confused times of day, forgotten medications, swapped names, and getting lost in familiar places. Ask when the change began, how it interferes with daily life, and whether the patient has gotten lost, mishandled finances, or stopped activities they once managed.

Cognitive testing

The Mini-Mental State Examination scores orientation, registration, attention and calculation, recall, language, and construction out of 30. Roughly 24–30 is normal, 20–23 suggests mild dementia, 13–20 moderate dementia, and below 12 severe dementia. The Montreal Cognitive Assessment is more sensitive for mild impairment and early disease, especially executive and visuospatial deficits. Use the same test version for serial comparison, since versions differ in their attention items.

Neurological examination

The examination can point directly to the cause: pyramidal signs and focal findings toward vascular disease, Parkinsonism toward Lewy body disease, frontal release signs toward advancing degeneration. Cortical release reflexes (sucking, grasp, glabella, palmomental) emerge as frontal inhibition is lost and support a neurodegenerative cause over depression or mild impairment alone. MRI may then show white matter disease suggesting vascular dementia, lobar microbleeds suggesting amyloid angiopathy, medial temporal atrophy suggesting Alzheimer disease, or disproportionate ventricular enlargement suggesting normal pressure hydrocephalus.

Reversible-cause workup

Before accepting a neurodegenerative diagnosis, check thyroid function, serum B12, review medications (especially anticholinergics, benzodiazepines, and barbiturates), and obtain brain MRI to exclude hydrocephalus, tumours, and vascular disease. Drug-induced impairment is dose-dependent and can take months to develop and months to resolve.

Nuclear imaging in the workup

FDG-PET measures regional glucose metabolism as a proxy for neuronal activity, because firing neurons consume glucose continuously. Metabolism falls before neurons die, so hypometabolism appears before structural atrophy, and each disease leaves a characteristic pattern: posterior cingulate and temporoparietal hypometabolism with spared primary cortices in Alzheimer disease, occipital hypometabolism in Lewy body dementia, frontal and anterior temporal hypometabolism in frontotemporal dementia, and patchy asymmetric defects following vascular territories in vascular dementia.

Two exclusion principles make these scans clinically powerful: a normal FDG-PET makes neurodegenerative dementia unlikely, pointing instead toward depression, medication effects, or metabolic causes. A negative amyloid PET excludes Alzheimer disease with high confidence.

Amyloid deposition begins 10–20 years before symptoms, so amyloid PET also clarifies prognosis in mild cognitive impairment and suspected mixed dementia. Dopamine transporter SPECT separates Lewy body dementia, where striatal uptake is reduced, from Alzheimer disease, where it is normal. PET resolves cortical detail far better than perfusion SPECT, which is why PET is the functional modality of choice.

Evidence anchors

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