Synopsis
Recognise the Lewy-body cognitive, visual, sleep, motor and autonomic phenotype, use chronology to distinguish DLB from Parkinson disease dementia, prevent neuroleptic harm and balance cognitive, mobility, function and carer priorities.
- Core DLB features are recurrent well-formed visual hallucinations, marked cognitive fluctuation, spontaneous parkinsonism and REM-sleep behaviour disorder.
- Use the one-year convention: DLB when dementia precedes or occurs within one year of parkinsonism; Parkinson disease dementia when cognitive decline follows established Parkinson disease by more than one year.
- Early attention, executive and visuoperceptual deficits may dominate while memory storage appears less impaired than in typical Alzheimer disease.
- Supportive clues include severe antipsychotic sensitivity, autonomic dysfunction, falls, syncope, hyposmia, depression and relative medial-temporal preservation.
- First-line diagnosis remains clinical with collateral; dopamine-transporter SPECT supports DLB when parkinsonism or subtype remains uncertain.
- Treat acute change as possible delirium and review anticholinergics, dopamine blockers, sedatives and Parkinson medicine timing.
- NICE recommends donepezil or rivastigmine for mild-to-moderate DLB; consider them in severe DLB and for Parkinson disease dementia under specialist care.
- Rivastigmine oral treatment begins 1.5 mg twice daily with food and increases no more often than every two weeks according to tolerance.
- Levodopa may improve disabling motor symptoms but can worsen hallucination or posture; use a low specialist dose against a functional goal.
- Avoid haloperidol. Antipsychotic use is exceptional, specialist-led, lowest-dose and shortest-duration because all options retain serious risk.
Key red flags
Haloperidol and other potent dopamine blockers can cause severe or fatal sensitivity and should be avoided in DLB and Parkinson disease.
Acute inattention, drowsiness or new immobility still requires 4AT and a delirium cause search despite baseline cognitive fluctuation.
Syncope, recurrent falls, postural hypotension and bradycardia may reflect autonomic disease, AChE treatment or interacting medicines.
Dream enactment can injure the person or bed partner and requires environmental safety and specialist sleep assessment.
New dysphagia, weight loss, aspiration or medication-timing failure requires urgent swallowing, nutrition and Parkinson-team review.
Sudden focal deficit or rapid progression is atypical for routine Lewy-body course and needs alternative neurological assessment.
Severe rigidity, dysphagia, somnolence or autonomic decline follows dopamine blockade and is an emergency.
Postural hypotension, syncope, constipation, urinary dysfunction and falls interact with treatment and function.
Investigation priorities
Apply phenotype and one-year convention.
Management branches
Lewy-body disease is suspected. within the current clinical context.
- Obtain collateral on core features and one-year chronology and exclude delirium, visual and medicine mimics.
- Complete cognitive, neurological, autonomic, blood and structural imaging assessment.
- Use dopamine-transporter SPECT or polysomnography when specialist uncertainty would change diagnosis or care.
Mild-to-moderate DLB or Parkinson dementia is diagnosed.
- Check pulse, syncope, posture, weight, GI and interaction risk and agree cognitive, functional or distress targets.
- Start donepezil or rivastigmine at the licensed initial dose and titrate slowly under specialist or shared care.
- Review cognition, hallucination, ADLs, falls, pulse and weight and consider memantine only when AChE treatment is unsuitable.