Phys · geriatric
Dementia
Also known as major neurocognitive disorder · cognitive impairment · Alzheimer disease · vascular dementia · dementia with Lewy bodies · frontotemporal dementia · mixed dementia · primary progressive aphasia · behavioural variant frontotemporal dementia · mild cognitive impairment · pseudodementia
Consultant-physician-depth guide to dementia for FRACP DWE and DCE — DSM-5 major neurocognitive disorder definition, the five major subtypes (Alzheimer, vascular, Lewy body, frontotemporal, mixed), mild cognitive impairment, cognitive assessment with MoCA and ACE-III, the reversible-cause workup, cholinesterase inhibitors and memantine, the BPSD escalation ladder, the antipsychotic contraindication in Lewy body dementia, driving and capacity, and the differentiation from delirium and depression.
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Red flags
- Rapidly progressive dementia over weeks to months — exclude Creutzfeldt-Jakob disease, autoimmune encephalitis, paraneoplastic limbic encephalitis, and rapidly progressive Alzheimer; this is a different differential and demands urgent MRI and CSF
- Acute or subacute worsening in a patient with known dementia — assume superimposed delirium until proven otherwise; search for infection, drugs, metabolic disturbance, and pain
- New visual hallucinations, fluctuating cognition, or parkinsonism in a patient labelled as Alzheimer — reconsider the diagnosis; dementia with Lewy bodies carries an absolute contraindication to antipsychotics
- Personality change, disinhibition, or language decline with relative memory sparing in a patient under 65 — think frontotemporal dementia, not Alzheimer; cognitive enhancers do not work and may worsen behaviour
- Gait disturbance, urinary incontinence, and cognitive decline in the same patient — think normal pressure hydrocephalus; it is partially reversible and is missed when attributed to Alzheimer or Parkinson
- Cognitive decline with a low B12, low folate, or abnormal TSH — these are reversible or partially reversible causes that must be identified and treated before labelling the patient as having dementia
Dementia
The answer first
Dementia is progressive decline in cognition across multiple domains, sufficient to interfere with independence, that is not delirium and not depression. It is not one disease but a syndrome with at least five underlying pathologies, each with a different course, a different drug, and a different trap. Alzheimer disease is the commonest, at 60 to 70 percent of cases.[1]
Five rules run the topic. First, it is a clinical diagnosis, anchored by the collateral history — no blood test or scan makes it; you prove a decline from a documented baseline across several domains, confirmed by a carer, having excluded delirium, depression, and the reversible mimics. Second, the subtype matters more than the label — it decides which drug helps (cholinesterase inhibitors help Alzheimer and Lewy body, not frontotemporal) and which drug kills (antipsychotics in Lewy body). Third, exclude the reversible causes before you settle — B12, TSH, depression, normal pressure hydrocephalus, subdural, and drug burden. Fourth, management is mostly non-pharmacological — cognitive enhancers give a modest symptomatic gain, not a cure. Fifth, antipsychotics are dangerous, and in Lewy body dementia they are absolutely contraindicated.[1]
The classic trap: when asked "best initial management of behavioural and psychological symptoms of dementia," the answer is almost always search for a precipitant (pain, infection, constipation, environment, drug), fix it, and use non-pharmacological strategies — not an antipsychotic. Risperidone is the only agent subsidised for this use, and only for severe aggression, time-limited to 12 weeks.[1]
References11ShowHide
- [1]Livingston G, Huntley J, Sommerlad A, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission Lancet, 2020.PMID 32738937
- [2]Nasreddine ZS, Phillips NA, Bédirian V, et al. The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment J Am Geriatr Soc, 2005.PMID 15817019
- [3]Petersen RC Clinical practice. Mild cognitive impairment N Engl J Med, 2011.PMID 21651394
- [4]Birks J Cholinesterase inhibitors for Alzheimer's disease Cochrane Database Syst Rev, 2006.PMID 16437532
- [5]McShane R, Westby MJ, Roberts E, et al. Memantine for dementia Cochrane Database Syst Rev, 2019.PMID 30891742
- [6]Schneider LS, Dagerman KS, Insel P Risk of death with atypical antipsychotic drug treatment for dementia: meta-analysis of randomized placebo-controlled trials JAMA, 2005.PMID 16234500
- [7]McKeith IG, Boeve BF, Dickson DW, et al. Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium Neurology, 2017.PMID 28592453
- [8]Rascovsky K, Hodges JR, Knopman D, et al. Sensitivity of revised diagnostic criteria for the behavioural variant of frontotemporal dementia Brain, 2011.PMID 21810890
- [9]Hsieh S, Schubert S, Hoon C, et al. Validation of the Addenbrooke's Cognitive Examination III in frontotemporal dementia and Alzheimer's disease Dement Geriatr Cogn Disord, 2013.PMID 23949210
- [10]Ngandu T, Lehtisalo J, Solomon A, et al. A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomised controlled trial Lancet, 2015.PMID 25771249
- [11]Mitchell SL, Teno JM, Kiely DK, et al. The clinical course of advanced dementia N Engl J Med, 2009.PMID 19828530