Discuss dementia in the elderly and its management

Dementia is a clinical syndrome of sustained, acquired loss of intellectual function and memory, severe enough to cause dysfunction in daily living, occurring in clear consciousness. Loss of functional ability due to impaired cognition is the key feature separating dementia from mild cognitive impairment.

Its cardinal features are a gradually progressive course (months to years) and no disturbance of consciousness — the two features that distinguish it from delirium. DSM-5 renamed dementia “major neurocognitive disorder” and introduced “mild neurocognitive disorder” for the MCI range.

Dementia is broadly grouped into reversible or partially reversible and non-reversible types. Reversible dementia accounts for under 4% of cases, but concurrent treatable medical conditions causing mild cognitive disturbance are far commoner.

Alzheimer’s disease (AD) and vascular dementia account for the vast majority in older people and frequently coexist in the same patient (mixed dementia). Dementia with Lewy bodies contributes 15–25% in autopsy and clinical series. Approximately 6–8% of persons over 65 have AD, with prevalence doubling every 5 years so that nearly 30% of those over 85 are affected.

Indian data: the LASI-DAD nationally representative study estimates dementia prevalence at 7.4% in adults aged 60+, equating to about 8.8 million Indians, projected to reach 16.9 million by 2036. Prevalence is higher in women than men and in rural than urban areas, with wide state variation (Delhi 4.5% to Jammu & Kashmir 11.0%).

Non-reversible causes are grouped as degenerative (AD, Lewy body disease, Parkinson’s disease, Pick’s disease, Huntington’s disease, PSP), vascular (multi-infarct, Binswanger’s disease, arteritis, post-anoxic), traumatic (including dementia pugilistica) and infective (HIV, Creutzfeldt–Jakob disease, progressive multifocal leukoencephalopathy, post-encephalitic).

Age and family history are the primary risk factors for AD. The apolipoprotein E ε4 allele on chromosome 19 is the strongest genetic linkage with late-onset AD (relative risk ~2.5 in whites), but it is neither sensitive nor specific and is not recommended as a screening test. Rare mutations on chromosomes 1, 14 and 21 cause early-onset familial AD.

In AD, progressive neuronal degeneration produces neurotransmitter abnormalities, with a combined cholinergic and glutamatergic dysfunction underlying the symptomatology — this is the rationale for all currently licensed symptomatic drugs. Amyloid-β deposition and hyperphosphorylated tau (neurofibrillary tangles) are the defining neuropathological lesions.

Vascular pathology acts additively or synergistically with AD pathology: vascular lesions lower the threshold of AD pathology needed to produce dementia, and AD pathology increases the risk of dementia after stroke. Hence in a patient with AD plus cerebrovascular disease, both conditions require treatment even if the vascular component seems trivial.

Patients most commonly present with memory loss, poor concentration, depression, behavioural change or language difficulty. Questioning both the patient and an informant is vital to gauge impact on usual activities, lifestyle, history of the cognitive disorder and the key issue of functional decline.

Severity is graded with the Global Deterioration Scale (GDS), the Clinical Dementia Rating (CDR) and the MMSE — mild 20–24, moderate 10–19, severe below 9. The MMSE is dependent on sociocultural level and shows a ceiling effect; the Severe Impairment Battery (SIB) is used when impairment is too severe for standard testing.

Neuropsychiatric symptoms occur in 90–98% of people with dementia over the disease course and may precede the diagnosis; they drive caregiver burden and institutionalisation.

Recommended baseline studies: complete blood count, glucose, blood urea, electrolytes (sodium mEq/L, potassium mEq/L), calcium and phosphorus (mg/dL), liver function tests, TSH (µIU/mL), vitamin B12 (pg/mL), and serology for syphilis and HIV if suspected, together with CT or MRI of the head. Neuropsychological testing is reserved for selected patients.

Imaging is done to exclude treatable structural causes — subdural haematoma, tumour, normal-pressure hydrocephalus. Cerebral atrophy alone does not establish AD. Functional imaging aids differentiation: HMPAO-SPECT shows temporoparietal hypoperfusion in AD, anterior hypoperfusion in FTD, multiple focal deficits in VaD; FP-CIT SPECT distinguishes DLB and parkinsonian syndromes from AD.

General principles: treat any reversible or partially reversible cause; optimise therapy of comorbid conditions; counsel families about the stages of dementia, drugs to avoid and excessive alcohol; discuss behavioural symptom strategies, advance directives and future planning early. Treat hypertension to prevent further lacunar infarcts, provided side effects are avoided.

Four pharmacological approaches (Kane’s framework): (i) avoid drugs that worsen cognition, principally those with strong anticholinergic activity; (ii) agents that enhance cognition and function; (iii) treat coexisting depression; (iv) treat complications — paranoia, delusions, psychosis, agitation.

Cholinesterase inhibitors — donepezil (1996), rivastigmine (2000), galantamine (2001) — increase available acetylcholine; approved for mild to moderately severe AD, with donepezil also approved for severe AD. Pooled benefit is a mean improvement of −2.7 points (95% CI −3.0 to −2.3) on the 70-point ADAS-Cog.

Memantine, a voltage-dependent, low-affinity, uncompetitive NMDA receptor antagonist, blocks pathologically elevated glutamate and is approved for moderate to severe AD. Combination of a ChEI with an NMDA antagonist gives better symptomatic effect. In the DOMINO trial, continuing donepezil in moderate-to-severe AD gave cognitive and functional benefit over 12 months.

Vascular dementia: cholinesterase inhibitors are not recommended for pure VaD but should be used in mixed dementia once both AD and vascular components are demonstrated. Antithrombotics need caution when lobar microbleeds are present on MRI because of amyloid angiopathy and haemorrhage risk. Levodopa may help apraxic gait in subcortical ischaemic vascular disease.

Non-pharmacological management is central: physical exercise is the single most efficient strategy for dementia prevention, with multicomponent aerobic plus strength protocols reducing cortical atrophy in executive-control areas; cognitive interventions build cognitive reserve. Caregiver education and support, structured routine, meaningful activity, task simplification and environmental safety form the backbone of behavioural management.