Dementia and major NCD — structured clinical viva

Nosology. Functional loss in IADLs (finances/medications) with progressive cognitive decline supports major NCD, not mild NCD. Stepwise course, executive problems, gait, and vascular history suggest vascular cognitive disorder / major vascular NCD (VASCOG framing), possibly mixed with AD pathology — common in this age group.[1]

Acute agitation. Assume delirium contributors until excluded (infection, metabolic, drugs, pain, environment). Do not accept "regular risperidone for dementia behaviours" as a default plan.[2]

Assessment. Collateral + MSE + MoCA/MMSE limitations + neurologic exam + bloods/imaging once + NPI-style BPSD description. MoCA is more sensitive for mild deficits but still a screen.[7]

BPSD. DICE/person-centred care first; treat medical triggers; antipsychotics last-line only for severe risk, lowest dose, short duration.[2]

Antipsychotic evidence honesty. Schneider 2005: increased mortality vs placebo. CATIE-AD: modest effectiveness offset by adverse effects. DART-AD: continuing antipsychotics linked to higher long-term mortality than withdrawal when withdrawal feasible. Counsel black-box-style risk.[3][4][8]

Cognitive enhancers. If substantial AD phenotype, discuss donepezil 5→10 mg and memantine titration for moderate–severe disease (DOMINO/Tariot/Reisberg evidence base). Pure vascular disease has weaker AChEI evidence — still optimise vascular risk factors.[5]

Capacity (finances). Appelbaum: understand, appreciate, reason, communicate choice for that financial decision; supports and timing matter; substitute decision-making if lacking capacity — jurisdiction-specific mechanisms.[6]