Dementia — Classification

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 is defined clinically: cognitive or behavioural decline from a previous level that interferes with work or usual activities. The decline must span at least two domains among memory, reasoning and judgment, visuospatial skill, language, and personality or behaviour, and it must not be explained by delirium or a major psychiatric disorder. Classification matters because the cause determines the treatment.

Major causes compared

The World Health Organization estimates Alzheimer disease may contribute to 60–70% of cases. Mixed forms often coexist, so single-cause shares never sum cleanly.

Alzheimer disease versus vascular dementia

This distinction carries a direct treatment consequence. Alzheimer disease is managed with cholinesterase inhibitors and memantine alongside non-pharmacological care, while vascular dementia is managed by controlling vascular risk factors such as hypertension, diabetes, and hyperlipidaemia. Mixed dementia is common, so comorbid Alzheimer pathology should be considered even when vascular features dominate; amyloid PET can clarify this when the answer changes management.

The Lewy body spectrum

Dementia with Lewy bodies and Parkinson disease dementia share the same α-synuclein pathology and differ in timing. When dementia appears within about a year of Parkinsonism, the convention is to call it dementia with Lewy bodies; when established Parkinson disease precedes dementia by more than a year, it is Parkinson disease dementia. This timing convention is a clinical rule of thumb rather than a sharp biological boundary.

Frontotemporal variants

Three clinical presentations cover most frontotemporal dementia: the behavioural variant with disinhibition, apathy, and loss of social norms; the nonfluent variant with effortful, halting speech and grammar errors; and the semantic variant with fluent speech that has lost word meaning. A right temporal presentation with progressive loss of face recognition is also recognised. Onset is typically between 50 and 65. Memory stays relatively preserved early, which is the bedside contrast with Alzheimer disease. About 15–20% of patients have an associated motor neuron disease, most often through shared TDP-43 pathology and C9orf72 genetics.

Creutzfeldt-Jakob disease

Creutzfeldt-Jakob disease is a prion disease caused by accumulation of abnormal prion protein. It is the fastest dementia, progressing over weeks to months, with myoclonus, pyramidal or extrapyramidal signs, visual disturbance, and cerebellar signs. The EEG shows characteristic periodic sharp waves. Typical onset is between 57 and 62 years; most cases are sporadic, with smaller familial and iatrogenic shares, and average survival is only a few months. The variant form linked to bovine spongiform encephalopathy presents earlier with prominent psychiatric features.

Mild cognitive impairment

Mild cognitive impairment is measurable decline with daily activities largely preserved. Its staging, yearly progression risk, and how amyloid testing sharpens prognosis are set out under mild cognitive impairment (/notes/neurology/dementia-mci/).

Reversible causes not to miss

Treatable mimics — depression, drug effects, hypothyroidism, and B12 and thiamine deficiency — are compared in full under reversible dementias (/notes/neurology/vascular-dementia/). Every new assessment screens for these before accepting a neurodegenerative diagnosis.

Dementia, delirium, and pseudodementia at a glance

Evidence anchors

• NICE. Dementia: assessment, management and support (NG97): https://www.nice.org.uk/guidance/ng97