Cognitive Connie

Neurocognitive Disorders

Neurocognitive disorders encompass conditions in which cognitive functioning is significantly impaired relative to a prior level of performance — not merely below a population norm. The DSM-5-TR (2022) distinguishes Mild Neurocognitive Disorder (modest decline, independence preserved) from Major Neurocognitive Disorder (significant decline that interferes with daily independence). What DSM-5 calls "major NCD" maps onto what ICD-11 — and most clinicians worldwide — continue to call "dementia"; both terminologies remain in active use.

Defining features

Often progressive

Most neurocognitive disorders — Alzheimer's, Lewy body, frontotemporal — are progressive and not reversible. But not all: cognitive impairment from TBI may stabilise or improve; substance-related NCD can partially resolve with abstinence; delirium is typically reversible.

Prior level

Current

Compared to prior level

Diagnosis requires a measurable decline from the individual's own previous baseline — not a comparison to population norms.

01. Overview

Mild, Major & Delirium.

The DSM-5 organises neurocognitive conditions across a spectrum of severity. Delirium stands apart — it is acute, fluctuating, and often reversible.

MiNDMild

Mild Neurocognitive Disorder

Modest cognitive decline from a prior level that does not interfere significantly with daily independence. Replaces the older term "mild cognitive impairment." Around 10–15% of cases progress to MaND per year.

Daily independence preserved

MaNDMajor

Major Neurocognitive Disorder

Significant cognitive decline in one or more domains (memory, executive function, language, etc.) that interferes with independence in everyday activities. The DSM-5 replacement for "dementia."

Independence significantly affected

DELAcute

Delirium

An acute, fluctuating disturbance of attention and awareness caused by an underlying medical condition, substance intoxication or withdrawal, or medication. Distinguished from dementia by its sudden onset and fluctuating course.

Acute onset · Often reversible

MiNDMild

Mild Neurocognitive Disorder

Daily independence preserved

MaNDMajor

Major Neurocognitive Disorder

Significant cognitive decline in one or more domains (memory, executive function, language, etc.) that interferes with independence in everyday activities. The DSM-5 replacement for "dementia."

Independence significantly affected

DELAcute

Delirium

Acute onset · Often reversible

02, Major types

The major neurocognitive disorders.

Each disorder has a distinct profile of onset, pathology, and affected brain regions. Click a card to expand details.

Early clinical features

Gradual episodic memory loss

VaD

Stepwise decline

LBD

REM sleep behaviour disorder

FTD

Personality change

PDD

Motor symptoms

Key figures

Arnold Pick

1851–1924

Czech neurologist who described cases of progressive dementia associated with focal atrophy of the frontal and temporal lobes. His name was later applied to a specific histological form ("Pick's disease") — but the broader category he helped establish, now called frontotemporal dementia (FTD), is a clinical umbrella encompassing multiple distinct syndromes and neuropathological entities. His work established that different anatomical patterns of neurodegeneration could produce distinct clinical presentations, a foundational insight for syndromic dementia classification.

Emil Kraepelin

1856–1926

German psychiatrist who coined the term "Alzheimer's disease" in the 1910 edition of his psychiatry textbook, bringing Alzheimer's case descriptions to wide clinical attention. Kraepelin's systematic approach to classifying psychiatric disorders laid the groundwork for modern diagnostic systems.

Alois Alzheimer

1864–1915

German psychiatrist and neuropathologist who in 1906 presented one of the earliest described cases of the disease that bears his name — a 51-year-old woman (Auguste Deter) with progressive memory loss, language problems, and behavioural changes. Post-mortem examination revealed the plaques and tangles now recognised as hallmarks of Alzheimer's disease. The eponym was applied by his colleague Emil Kraepelin, and earlier cases had likely been observed but not systematically characterised.

Friedrich Heinrich Lewy

1885–1950

German-American neurologist who discovered the intracellular protein inclusions (Lewy bodies) found in Parkinson's disease while working in Alois Alzheimer's laboratory in 1912. Lewy bodies were later found to be the defining pathology of Dementia with Lewy Bodies, a major dementia subtype.

Key concepts

Major Neurocognitive Disorder (MaND)

The DSM-5-TR term for what most of the world continues to call "dementia." Involves significant cognitive decline from a prior level in one or more of the six cognitive domains — complex attention, executive function, learning/memory, language, perceptual-motor ability, and social cognition — that interferes with independence in everyday activities. ICD-11 retains the explicit "Dementia" category rather than renaming it. Both terminologies are current.

Mild Neurocognitive Disorder (MiND)

Modest cognitive decline that does not interfere significantly with daily independence. Overlaps substantially with the older term "mild cognitive impairment." Progression to MaND varies considerably: in memory-clinic samples the rate is often cited as ~10–15% per year, but population-based studies find lower rates and many individuals remain stable or revert to normal — particularly when the underlying cause is treatable (e.g., depression, medication effects, sleep disorder).

Six DSM cognitive domains

DSM-5-TR specifies six cognitive domains across which decline must be demonstrated: (1) Complex attention — sustained, divided, or selective attention; processing speed. (2) Executive function — planning, decision-making, working memory, inhibition. (3) Learning and memory — immediate and delayed recall, recognition. (4) Language — expressive and receptive; naming, fluency. (5) Perceptual-motor — visual construction, praxis, gnosis. (6) Social cognition — recognising emotions, theory of mind. Both MiND and MaND require documented decline in at least one domain; MaND requires it to interfere with independence.

Normal ageing vs Mild vs Major NCD

Normal ageing involves modest slowing of processing speed and some difficulty with effortful recall, but declarative memory, language, and daily function remain largely intact. Mild NCD involves a measurable decline from the person's own baseline — detected on neuropsychological testing — that does not impair daily independence. Major NCD involves functional impairment. Distinguishing normal ageing from Mild NCD requires longitudinal observation and neuropsychological assessment, not a single cross-sectional comparison with peers.

Delirium

An acute, fluctuating disturbance of attention and awareness arising from an underlying medical condition, substance intoxication/withdrawal, or medication. Onset is sudden (hours to days) and course fluctuates — cardinal features that distinguish it from dementia. Delirium is common in hospitalised older adults (20–30% of general medical inpatients; up to 50% post-surgery in the elderly) and carries significant mortality risk. It can be superimposed on existing dementia, making diagnosis more difficult. Unlike most neurocognitive disorders, delirium is often reversible if the underlying cause is identified and treated promptly.

Mixed aetiology

Post-mortem studies show that mixed pathology — typically Alzheimer's neuropathology co-occurring with cerebrovascular disease — is found in the majority of older adults with dementia. Pure single-aetiology dementia is less common than clinical diagnostic categories imply. The recognition of mixed dementia has therapeutic implications: vascular risk factor management may slow progression even in those with primary Alzheimer's pathology.

Amyloid-beta (Aβ) plaques

Extracellular deposits of misfolded amyloid-beta protein — a hallmark of Alzheimer's disease. The amyloid cascade hypothesis proposes that Aβ accumulation initiates a chain of events leading to neurodegeneration, though the relationship between plaques and symptoms is complex.

Neurofibrillary tangles (tau)

Intracellular aggregates of hyperphosphorylated tau protein, another neuropathological hallmark of Alzheimer's disease. Tau tangles correlate more closely with cognitive decline than amyloid plaques. Tauopathies (e.g., frontotemporal dementia) can occur independently of amyloid pathology.

Lewy bodies

Abnormal intracellular aggregates of alpha-synuclein protein found in neurons. The defining pathology of Dementia with Lewy Bodies (DLB) and Parkinson's disease dementia. Associated with four core diagnostic features per McKeith et al. (2017): fluctuating cognition, recurrent visual hallucinations, Parkinsonism, and REM sleep behaviour disorder.

Cholinergic hypothesis

The proposal that the cognitive symptoms of Alzheimer's disease result substantially from loss of cholinergic neurons in the basal forebrain (nucleus basalis of Meynert). This hypothesis underpins the use of acetylcholinesterase inhibitors (e.g., donepezil) as symptomatic treatments.

Vascular dementia

The second most common dementia, caused by cerebrovascular disease (strokes, small vessel disease, white matter lesions). Often shows a stepwise rather than gradual decline. Risk factors overlap with cardiovascular disease (hypertension, diabetes, smoking).

Frontotemporal dementia (FTD)

A group of dementias characterised by progressive degeneration of the frontal and temporal lobes. Typically presents with personality change, disinhibition, apathy, or language impairment rather than memory loss. Often affects younger adults (40s–60s).

Acetylcholinesterase inhibitors

Drugs (e.g., donepezil, rivastigmine, galantamine) that prevent breakdown of acetylcholine, increasing its availability. Used symptomatically in mild-to-moderate Alzheimer's disease and DLB. Produce modest improvements in cognition and function but do not halt disease progression.

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