Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Alzheimer, vascular, Lewy-body and frontotemporal dementia
Psychiatry · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Subtype does not explain every acute change
Sudden focal deficit, abrupt loss of speech or mobility, hours-to-days fluctuation, reduced consciousness, seizure, severe autonomic change, head injury or new systemic illness requires urgent stroke, delirium or medical assessment rather than attribution to dementia progression.
Action: Assess ABCDE, glucose, onset, attention and focal neurology; activate emergency stroke or acute medical pathways when indicated; establish baseline from collateral sources; and review medicines. In suspected Lewy-body dementia or parkinsonism, avoid reflex haloperidol because severe antipsychotic sensitivity and motor deterioration can be life-threatening.
Overview
Recognise characteristic but overlapping dementia profiles, separate chronic subtype features from delirium and acute stroke, select specialist tests only when they change management, and avoid subtype-specific medication harms and ineffective treatment.
Dementia subtypes are clinicopathological formulations, not personality descriptions. Begin with the sequence of cognitive and functional change, neurological examination and collateral examples. Ask which domain changed first, how progression occurred and which features remain preserved. Alzheimer's, vascular, Lewy-body and frontotemporal diseases frequently overlap with each other and with delirium, depression and medical illness. A confident subtype can guide medicines, counselling, genetic discussion and safety, but false certainty can expose a person to ineffective or harmful treatment.
Typical Alzheimer's disease develops gradually, with impaired learning and retention of recent information followed by orientation, language, executive and visuospatial difficulties. Repetition and getting lost may precede loss of basic self-care. Not every case is amnestic: posterior cortical or language-led presentations need specialist formulation. Structural imaging may show medial temporal and parietal patterns but cannot rule the disease in or out alone. When uncertainty matters, NICE permits specialist FDG-PET or perfusion SPECT, or specified cerebrospinal-fluid tau and amyloid measures.
Practice
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PsychiatryOriginal SBA
Uncertain Lewy-body diagnosis
A person has progressive visuospatial difficulty, recurrent formed visual hallucinations and spontaneous parkinsonism. Delirium and medicine causes have been excluded, but the specialist remains uncertain whether this is dementia with Lewy bodies. Which test does NICE recommend?
Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
NICE NG97 dementia recommendationsSubtype criteria, structural and functional imaging, CSF tests, cognitive medicines and antipsychotic cautions.
NHS dementia subtype symptomsCurrent UK descriptions of Alzheimer's, vascular, Lewy-body and frontotemporal presentations.
Vascular cognitive impairment is heterogeneous. A strategic infarct can cause abrupt domain-specific loss; recurrent strokes may produce steps; small-vessel disease may cause a slowly progressive executive, attentional and processing-speed syndrome with gait or mood change. Focal neurological findings and cardiovascular disease support but do not prove causation. NICE recommends MRI when the subtype is uncertain and vascular dementia is suspected, using CT if MRI is unavailable or contraindicated, and explicitly warns against diagnosis from vascular lesion burden alone.
Dementia with Lewy bodies often affects attention, executive and visuoperceptual function before marked amnesia. Core clues include pronounced spontaneous cognitive fluctuation, recurrent detailed visual hallucinations, REM-sleep behaviour disorder and parkinsonism. Repeated falls, syncope, orthostatic hypotension, constipation and other autonomic symptoms can support the pattern. First exclude delirium, eye disease, medicine effects and sleep phenomena. If diagnosis remains uncertain and would change care, NICE recommends iodine-123 FP-CIT SPECT, with cardiac MIBG scintigraphy as an alternative when FP-CIT is unavailable; normal testing does not exclude DLB alone.
Frontotemporal dementia affects frontal and temporal networks, commonly between midlife and early older age. Behavioural-variant disease may bring disinhibition, apathy, reduced social insight, loss of empathy, stereotyped routines, impulsivity or altered food preference. Primary progressive aphasia variants affect speech production, word meaning or language processing. Describe observed change without calling the person selfish or difficult. Psychiatric illness, autism, bipolar disorder and relationship conflict are differentials, while motor neurone disease or parkinsonian syndromes may coexist.
NICE uses validated clinical criteria and reserves additional investigations for uncertainty where the answer would alter management. Structural imaging is broadly useful. For uncertain Alzheimer's disease, specialist FDG-PET or perfusion SPECT and cerebrospinal-fluid amyloid and tau biomarkers are options; APOE genotyping and EEG are not diagnostic tests for Alzheimer's. For uncertain FTD, NICE recommends FDG-PET or perfusion SPECT, while warning that normal structural or functional imaging cannot independently exclude it. Genetic causes deserve specialist counselling, particularly in young-onset or strongly familial presentations.
Treatment differs by subtype. For mild-to-moderate Alzheimer's disease, NICE recommends donepezil, galantamine or rivastigmine as options; memantine is used in defined moderate or severe pathways and may be added to an AChE inhibitor by stage. For DLB, offer donepezil or rivastigmine in mild-to-moderate disease, with other choices depending on tolerance and severity; NICE identifies these DLB medicine uses as off-label. In vascular dementia, only consider these medicines if comorbid Alzheimer's, Parkinson's disease dementia or DLB is suspected. Do not offer AChE inhibitors or memantine for FTD.
Non-drug support is never subtype-free. Occupational adaptation, cognitive rehabilitation, meaningful activity, communication support, exercise and cardiovascular prevention are tailored to goals and capacity. Vascular risk factors should be treated for their ordinary cardiovascular indications, not with a promise to reverse established dementia. FTD may need behavioural and communication strategies; DLB plans address falls, autonomic symptoms, sleep and visual misperception; Alzheimer's care supports memory and navigation. Diagnose and treat depression, pain, sensory loss and sleep disorder across all subtypes.
Antipsychotic caution is greatest in DLB and Parkinson's disease dementia because medicines can markedly worsen parkinsonism and provoke severe sensitivity reactions. Before treating hallucinations, ask whether they are distressing; pleasant or neutral experiences may need explanation and environmental adaptation rather than suppression. Across dementia, antipsychotics are considered only for risk of harm or severe distress after structured assessment and psychosocial or environmental measures. Specialist advice is prudent when Lewy-body disease is possible.
Explain that subtype diagnosis may evolve. Mixed Alzheimer's and vascular pathology is common, and late-stage profiles converge. Record the evidence, uncertainty and medicine implications, not just a label. Reassess when progression is unexpectedly rapid, new focal signs appear, hallucinations follow a medicine change or behaviour changes acutely. Support the person to plan early, address driving and work appropriately, and involve family or another chosen supporter within consent and confidentiality boundaries.
Key points
Alzheimer's disease often begins with progressive difficulty learning and recalling recent information, but language, visuospatial or executive variants occur and mixed pathology is common.
Vascular dementia may follow a stroke or evolve gradually through small-vessel disease; early slowing, executive difficulty, gait change and focal signs can outweigh memory loss.
Dementia with Lewy bodies commonly combines fluctuating cognition, recurrent well-formed visual hallucinations, REM-sleep behaviour and spontaneous parkinsonism, with falls and autonomic symptoms as supportive clues.
Frontotemporal dementia often presents earlier with disinhibition, apathy, loss of empathy, compulsive behaviour, altered eating or progressive language impairment while episodic memory is relatively preserved initially.
Use validated clinical subtype criteria and expect overlap; vascular imaging burden or one characteristic symptom cannot establish a diagnosis alone.
NICE recommends structural imaging for reversible structural causes and subtype support unless dementia is already well established and the subtype is clear.
When DLB is suspected and diagnosis is uncertain, use iodine-123 FP-CIT SPECT; a normal result does not independently exclude DLB.
When vascular dementia is suspected but subtype remains uncertain, use MRI if possible or CT if MRI is unavailable or
Aetiology
01
Alzheimer protein pathology
Amyloid and tau-related synaptic and neuronal injury spreads through vulnerable memory and association networks, producing progressive cognitive loss.
02
Cerebrovascular injury
Large infarcts, strategic strokes, haemorrhage and small-vessel disease damage or disconnect cognitive networks through varied temporal patterns.
03
Lewy-body disease
Alpha-synuclein pathology affects cortical and subcortical networks involved in attention, perception, autonomic function, sleep and movement.
04
Frontotemporal degeneration
Tau, TDP-43 and other pathologies injure frontal and temporal systems, with genetic causes particularly relevant in some families.
Pathophysiology
1
Episodic memory network failure
Medial temporal and connected association-system dysfunction impairs durable encoding and retrieval of recent experience in typical Alzheimer's disease.
2
Cortical-subcortical disconnection
Vascular damage slows processing and disrupts executive, gait and emotional-control circuits according to lesion location and cumulative burden.
3
Perceptual-attentional instability
Lewy-body network and neurotransmitter dysfunction produces fluctuating cognition, visual misperception, parkinsonism and vulnerability to dopamine-blocking medicines.
4
Frontal and temporal network loss
Degeneration alters inhibition, motivation, social cognition, semantic knowledge or speech production before broader cognition becomes affected.
Clinical features and red flags
Alzheimer amnestic profile
Gradual impaired learning and retention of recent information leads to repetition, disorientation and later broader cognitive and functional loss.
Vascular executive profile
Processing speed, attention, planning, gait and focal neurological function may change abruptly, stepwise or gradually according to vascular injury.
Lewy-body profile
Cognitive fluctuation, detailed visual hallucinations, REM-sleep behaviour and spontaneous parkinsonism cluster with falls and autonomic dysfunction.
Frontotemporal behavioural profile
Early disinhibition, apathy, empathy loss, compulsive routines or eating change precedes widespread memory and self-care impairment.
Frontotemporal language profile
Progressive effortful speech, grammar loss, impaired word meaning or naming dominates while other abilities may initially remain stronger.
Mixed dementia pattern
Features and pathology from more than one disease coexist, commonly Alzheimer's and vascular injury, making single-label certainty inappropriate.
Red flags requiring action
An abrupt focal neurological syndrome is a possible stroke even in established vascular dementia and requires emergency assessment from the last-known-well time.
New fluctuating inattention or altered arousal over hours or days suggests delirium superimposed on dementia, not an ordinary subtype fluctuation.
Investigations
01Longitudinal domain and function historyFirst step
Why
Identify the first affected cognitive domain, progression pattern, neurological symptoms, behaviour and daily consequences.
Interpretation and limitations
Characteristic clusters guide subtype hypotheses but overlap and mixed disease require corroboration rather than checklist diagnosis.
Acute attention or focal change triggers urgent assessment; chronic signs help specialist subtype formulation.
03Structural MRI or CT
Why
Exclude structural mimics and identify regional atrophy, infarction, haemorrhage and small-vessel patterns relevant to subtype.
Interpretation and limitations
Use MRI for uncertain suspected vascular dementia where possible; no structural pattern independently proves or excludes a degenerative subtype.
04Iodine-123 FP-CIT SPECT
Why
Support an uncertain specialist diagnosis when dementia with Lewy bodies is suspected and the result would change management.
Interpretation and limitations
Reduced striatal uptake supports Lewy-body disease, but a normal scan alone does not rule it out.
05
Differential diagnosis
01
Delirium
Acute fluctuating attention and arousal may be superimposed on any subtype and always requires immediate physiological cause assessment.
02
Depression or primary psychosis
Mood, motivation, belief and perceptual symptoms can mimic cognitive disease, while late onset also raises neurological and medical concern.
03
Medicine or sensory effect
Dopaminergic drugs, anticholinergics, sedatives, impaired vision and hearing can worsen hallucinations, attention and everyday functional performance.
04
Other neurodegenerative syndrome
Parkinson's disease dementia, corticobasal degeneration, progressive supranuclear palsy and motor neurone disease may overlap with common subtype features.
05
Structural or inflammatory disease
Tumour, subdural collection, hydrocephalus, encephalitis and other neurological disorders require targeted exclusion when phenotype or speed is atypical.
Management
01Subtype formulationMatch chronology, domains and neurologyFirst stepSpecialist assessment confirms dementia but the disease subtype or combination remains uncertain.+
1Map first symptoms, course, function, hallucinations, sleep, parkinsonism, focal signs, behaviour and language with person and collateral accounts.
2Apply validated subtype criteria and structural imaging, treating delirium, depression, sensory and medicine contributors in parallel.
3Use additional biomarker or functional imaging only when uncertainty remains and the result would change medicines, counselling or planning.
02Lewy-body possibilityProtect against neurological medicine harmFluctuation, visual hallucinations, REM-sleep behaviour or spontaneous parkinsonism raises concern for DLB.+
1Exclude acute delirium, medicine and sensory causes and assess falls, syncope, autonomic symptoms, sleep and hallucination distress.
Complications
01
Subtype-specific medicine harm
Antipsychotic sensitivity in Lewy-body disease and ineffective cognitive medicines in FTD make an inaccurate label clinically consequential.
02
Falls and autonomic injury
Parkinsonism, visuospatial impairment, syncope and orthostatic hypotension combine to cause falls, fractures and loss of mobility.
03
Communication and nutrition loss
Language degeneration, executive dysfunction, dysphagia and altered eating behaviour can impair consent, nutrition and social connection.
04
Vascular recurrence
Further stroke or cardiovascular disease may create abrupt additional disability on top of chronic cognitive impairment.
05
Family and identity disruption
Behavioural, perceptual and personality change can strain relationships when symptoms are interpreted as intentional or morally meaningful.
Monitoring and follow-up
Track the dominant cognitive domains, daily function, neurological signs, mood, sleep and person-defined goals rather than a total score alone.
Ask at each review about delirium, falls, syncope, hallucination distress, REM-sleep behaviour, medication sensitivity and new focal events.
Review vascular risk treatment, anticholinergic burden, sedatives and cognitive medicines for indication, benefit, tolerability and adherence support.
In suspected DLB, document every antipsychotic exposure and monitor urgently for rigidity, sedation, dysphagia, autonomic change and cognitive worsening.
Reopen the diagnosis for rapid progression, seizures, motor neurone features, unexpected age, strong family history or imaging-clinical mismatch.
Review driving, work, nutrition, medication management, communication, carer support, capacity and advance preferences as function changes.
Special situations
Memory is not universal onset
Executive, visuospatial, behavioural or language change can precede amnesia and still represent a progressive dementia syndrome.
Fluctuation has timescale
Lewy-body cognition varies chronically, but a new hours-to-days attentional change remains delirium until acute causes are addressed.
Images support phenotypes
Vascular lesions, atrophy and functional patterns gain meaning only when they fit chronology, examination and real-world impairment.
Hallucinations need impact assessment
A well-formed visual experience that is not distressing may require explanation and environmental adjustment rather than dangerous suppression.
Mixed pathology is ordinary
Overlapping Alzheimer's, vascular and Lewy-body processes often explain apparently inconsistent features better than forcing one pure subtype.
Common pitfalls
01
Calling every dementia Alzheimer's disease because memory is impaired, without examining executive, visuospatial, neurological, behavioural and language features.
02
Diagnosing vascular dementia solely from white-matter change or infarcts on imaging without a compatible cognitive and clinical relationship.
03
Treating chronic Lewy-body fluctuation as proof that an acute inattention change is not delirium.
04
Giving haloperidol or another antipsychotic reflexively for hallucinations in possible DLB without assessing distress, causes and severe sensitivity risk.
05
Offering cholinesterase inhibitors or memantine for frontotemporal dementia despite NICE advice against their use.
06
Using APOE genotype or routine EEG to diagnose Alzheimer's disease.
07
Dismissing early FTD behaviour as bad character or primary relationship conflict and delaying neurological assessment.
08
Presenting a provisional subtype as pathologically certain or failing to revisit it when the course diverges.
contraindicated
;
do not
diagnose from lesion burden alone.
AChE inhibitors and memantine have subtype-specific indications: do not offer either for frontotemporal dementia and use them in vascular dementia only when relevant comorbid dementia is suspected.
Antipsychotics can worsen motor symptoms and cause severe sensitivity in Lewy-body and Parkinson's disease dementia; analyse distress causes and seek specialist advice before use.
Repeated syncope, severe autonomic hypotension, falls, REM-sleep behaviours and visual hallucinations with parkinsonism support Lewy-body assessment and increase medicine risk.
Marked rigidity, sedation, dysphagia, fever or autonomic instability after antipsychotic exposure in possible Lewy-body dementia needs urgent cessation and medical review.
Rapid progression over weeks or a few months, seizures, myoclonus, ataxia or unusual neurological signs requires an urgent rapidly progressive dementia pathway.
Early major behavioural or language change, especially before age sixty-five, should prompt frontotemporal and young-onset specialist assessment rather than a moral or psychiatric label.
FDG-PET or perfusion SPECT
Why
Clarify uncertain Alzheimer's or frontotemporal disease through specialist regional metabolic or perfusion patterns.
Interpretation and limitations
Testing is selective and interpreted with phenotype; normal functional imaging does not independently exclude frontotemporal dementia.
06Specialist cerebrospinal-fluid biomarkers
Why
Assess specified amyloid and tau measures when Alzheimer's disease remains uncertain and clarification would change care.
Interpretation and limitations
Age and comorbidity affect specificity; use alongside clinical evidence and do not substitute APOE testing or routine EEG.
2
When diagnosis remains uncertain and management would change, arrange specialist FP-CIT SPECT and interpret a normal result cautiously.
3Avoid reflex antipsychotic use, seek specialist advice for severe distress or danger and consider NICE-directed cognitive treatment by stage and tolerance.
03Subtype-specific careLink diagnosis to useful actionA high-confidence Alzheimer's, vascular, Lewy-body, frontotemporal or mixed formulation is available.+
1PreferredExplain the evidence, overlap and uncertainty in the person's preferred language and record subtype-specific medicine cautions and treatment options.
2Offer cognitive medicines only for NICE-supported subtype and stage, and manage vascular risks for their established cardiovascular indications.
3Tailor communication, mobility, sleep, autonomic, behaviour, occupational, carer and advance-planning support and revisit subtype if the course changes.