Quick Answer
Dementia is a NEET PG psychiatry, neurology and medicine crossover topic — the four types, treatments and reversible causes are recurrent MCQ themes. Fix these:
- DSM-5 uses major and mild neurocognitive disorder instead of dementia.
- Alzheimer disease — 60 to 70 percent; amyloid plaques (Abeta-42) and tau tangles; hippocampal atrophy.
- Vascular dementia — 15 to 20 percent; stepwise decline; CV risk factor control.
- Lewy body dementia (DLB) — 5 to 10 percent; fluctuating cognition, visual hallucinations, parkinsonism, RBD; neuroleptic sensitivity.
- Frontotemporal dementia — early personality change, disinhibition, hyperorality; memory relatively preserved; onset 45 to 65.
- NPH triad — gait, urinary incontinence, dementia; VP shunt.
- Cholinesterase inhibitors — donepezil, rivastigmine, galantamine (mild-moderate AD, DLB).
- Memantine — moderate-severe AD.
- Lecanemab, donanemab — anti-amyloid monoclonal antibodies; ARIA risk requires MRI.
- Never haloperidol in DLB — quetiapine or clozapine only if antipsychotic essential.
Dementia is a compulsory read for NEET PG psychiatry and medicine — the four major types, treatments, reversible causes and DSM-5 terminology are tested in every recent paper. This deep dive walks through diagnosis, the four subtypes, disease-modifying anti-amyloid therapy, reversible causes and Indian dementia care realities.
Definition and DSM-5 framework
- DSM-5 replaced the term dementia with major neurocognitive disorder (major NCD) and mild NCD to reduce stigma and capture earlier disease.
- Major NCD — significant cognitive decline from a previous baseline in one or more of six domains (complex attention, executive function, learning and memory, language, perceptual-motor, social cognition), objective testing, deficits impair independence, not delirium, not another mental disorder.
- Mild NCD — modest decline but preserved independence with greater effort or compensation.
- Distinguished from delirium — acute onset, fluctuating course, disturbance of attention and awareness, reversible with cause treated.
- Distinguished from depression pseudodementia — patient's memory concern often exceeds objective deficit, abrupt onset, prominent low mood, normalises with antidepressant.
Bedside cognitive assessment
- MMSE (Mini-Mental State Examination) — score out of 30; less than 24 abnormal; language- and education-biased.
- MoCA (Montreal Cognitive Assessment) — better sensitivity for MCI; less than 26 abnormal.
- Clock Drawing Test — quick screen of visuospatial and executive function.
- Abbreviated Mental Test Score (AMTS) — 10-item bedside.
- Formal neuropsychological testing — comprehensive domain-by-domain profile; distinguishes dementia subtypes.
The four major dementias
1. Alzheimer disease (AD) — 60 to 70 percent
- Neuropathology — extracellular amyloid-beta (Abeta-42) plaques, intracellular neurofibrillary tangles of hyperphosphorylated tau, hippocampal and cortical atrophy.
- Risk factors — age (strongest), family history, APOE epsilon-4 allele, autosomal-dominant early-onset mutations (APP, PSEN1, PSEN2), Down syndrome (trisomy 21 carries extra APP gene, near-universal AD by age 60), traumatic brain injury, cardiovascular risk factors.
- Clinical course — insidious short-term memory decline, word-finding difficulty, spatial disorientation, executive impairment, apraxia and agnosia, eventual functional dependence and terminal bed-bound frail phase; MMSE declines about 3 points per year.
- Diagnosis — clinical, supplemented by MRI (hippocampal and cortical atrophy) to exclude reversible causes, CSF biomarkers (low Abeta-42, high tau), amyloid-PET and tau-PET at specialist centres.
- Symptomatic treatment — cholinesterase inhibitors (donepezil, rivastigmine, galantamine) modestly slow decline in mild to moderate disease; memantine (NMDA antagonist) added for moderate to severe.
- Disease-modifying therapy — lecanemab (2023) and donanemab (2024) anti-amyloid monoclonal antibodies FDA-approved for early symptomatic AD; modestly slow cognitive decline; require MRI monitoring for amyloid-related imaging abnormalities (ARIA — cerebral oedema and microhaemorrhage); Indian access limited by cost and infrastructure.
2. Vascular dementia (VaD) — 15 to 20 percent
- Neuropathology — multi-infarct dementia, strategic single infarct (thalamus, angular gyrus), Binswanger disease (subcortical white matter ischaemia), or CADASIL (autosomal-dominant NOTCH3 mutation).
- Clinical course — classically stepwise decline with focal neurological signs (contrasted with the smooth decline of AD), executive dysfunction more prominent than memory, gait and urinary changes early.
- Diagnosis — MRI shows multiple infarcts, strategic infarct, or extensive white matter disease.
- Treatment — aggressive control of cardiovascular risk factors (hypertension, diabetes, hyperlipidaemia, smoking cessation, atrial fibrillation anticoagulation) is the mainstay; cholinesterase inhibitors have modest benefit; mixed AD-VaD is very common.
3. Dementia with Lewy bodies (DLB) — 5 to 10 percent
- Neuropathology — alpha-synuclein Lewy bodies in cortex and brainstem.
- Core clinical features — fluctuating cognition, recurrent well-formed visual hallucinations, spontaneous parkinsonism, REM sleep behaviour disorder (RBD, dream enactment).
- Supportive features — severe neuroleptic sensitivity, autonomic dysfunction, repeated falls, reduced dopamine transporter uptake on DAT-SPECT.
- One-year rule — DLB if cognitive decline precedes or occurs within 12 months of parkinsonism onset; Parkinson disease dementia if cognitive decline emerges over 1 year after established PD (same underlying pathology).
- Treatment — cholinesterase inhibitors (particularly rivastigmine and donepezil) are effective for cognition and hallucinations; carbidopa-levodopa cautious for parkinsonism (may worsen hallucinations); avoid conventional antipsychotics (haloperidol) because of severe neuroleptic sensitivity; if antipsychotic essential, quetiapine or clozapine only; melatonin or low-dose clonazepam for RBD; manage orthostatic hypotension, constipation and urinary symptoms.
4. Frontotemporal dementia (FTD, Pick disease) — 5 to 10 percent
- Common cause of early-onset dementia (age 45 to 65).
- Three clinical variants — behavioural variant FTD (bvFTD, early personality change, disinhibition, apathy, loss of empathy, perseverative or ritualistic behaviour, hyperorality with dietary changes, executive dysfunction), semantic variant PPA (loss of word meaning and object knowledge, preserved fluency), and non-fluent agrammatic PPA (effortful non-fluent speech, agrammatism).
- Memory and visuospatial function relatively preserved early on.
- Molecular pathology heterogeneous — TDP-43 (half of bvFTD, most sv-PPA), tau (Pick bodies, MAPT mutations), rare FUS.
- Familial in 10 to 20 percent (MAPT, GRN, C9orf72 expansions — the last also causes ALS).
- MRI — frontal and temporal atrophy in a pattern matching the clinical variant.
- Treatment — no disease-modifying therapy; SSRIs for behavioural symptoms; avoid antipsychotics (extrapyramidal sensitivity); trazodone or carbamazepine for behavioural symptoms; cholinesterase inhibitors are not helpful and may worsen behaviour; caregiver support and safety planning central.
Reversible causes — always exclude
Mnemonic DEMENTIAS:
- D — Drugs (anticholinergics including diphenhydramine, oxybutynin, tricyclics; benzodiazepines; opioids; sedatives).
- E — Emotional (depression pseudodementia).
- M — Metabolic (hypothyroidism, hyponatraemia, hypercalcaemia, hepatic and renal failure).
- E — Eyes and Ears (uncorrected sensory loss mimics cognitive impairment).
- N — Nutritional (vitamin B12, folate, thiamine — chronic alcoholism, Wernicke-Korsakoff).
- T — Tumour (frontal meningioma, subdural haematoma).
- I — Infection (neurosyphilis, HIV dementia, tuberculous meningitis particularly in India, cryptococcal, Lyme in endemic areas).
- A — Alcohol (chronic use, thiamine).
- S — Sleep and Stroke (obstructive sleep apnoea, silent infarct, small vessel disease).
Normal-pressure hydrocephalus (NPH) — the Hakim triad of gait disturbance (magnetic gait), urinary incontinence and cognitive decline; MRI shows ventriculomegaly out of proportion to sulcal atrophy; positive high-volume lumbar tap test predicts response to ventriculoperitoneal shunting.
Diagnostic workup
- Full blood count, urea and electrolytes, calcium, glucose, liver and renal function.
- Thyroid function; vitamin B12 and folate.
- Syphilis serology; HIV testing where risk is present.
- MRI brain (or CT if MRI contraindicated).
- Lumbar puncture in atypical, rapidly progressive or infectious presentations.
- Formal neuropsychological testing.
- Rapidly progressive dementia (weeks to months) — urgent workup for Creutzfeldt-Jakob disease (CSF 14-3-3, RT-QuIC, MRI cortical ribbon on diffusion-weighted imaging), autoimmune encephalitis (LGI1, NMDA-R and other antibodies; steroid-responsive), paraneoplastic syndromes, CNS lymphoma.
Non-pharmacological management
- Cognitive stimulation, physical exercise, social engagement.
- Reality orientation and validation therapy in later stages.
- Structured routine, environmental adaptation, safety proofing.
- Driving cessation once significant impairment is established.
- Advance care planning while decision-making capacity remains.
- Caregiver education, respite, support groups.
Behavioural and psychological symptoms of dementia (BPSD)
- Non-pharmacological approaches first — identify triggers (pain, hunger, boredom, environment), redirect, activity-based interventions.
- Antipsychotics only for severe agitation or danger; FDA black-box warning for increased mortality in elderly dementia; risperidone and olanzapine used cautiously; quetiapine or clozapine preferred in DLB and PDD.
- SSRIs for depression.
- Trazodone for insomnia.
- Melatonin for sleep-wake disturbance and RBD.
- Memantine may modestly reduce agitation in AD.
India-specific context
- Rising burden — India's ageing population and improving longevity have driven dementia prevalence up sharply; estimates suggest over 8 million Indians with dementia and rising.
- Under-diagnosis — most dementia in India remains undiagnosed or diagnosed late because of limited memory clinics, workforce shortages and cultural framing of cognitive decline as normal ageing.
- Tertiary memory clinics — NIMHANS Bengaluru, AIIMS Delhi, CMC Vellore, PGI Chandigarh, and Christian Fellowship centres offer multidisciplinary assessment and follow-up.
- Family caregiving — the extended family model remains a strength but caregiver burden and burnout are high; Alzheimer's and Related Disorders Society of India (ARDSI) provides advocacy, support groups and daycare centres.
- Dementia India Strategy Report 2010 and subsequent national initiatives call for training primary-care physicians and integrating dementia into non-communicable disease programmes.
- Access to disease-modifying therapy — lecanemab and donanemab are not yet widely available in India due to cost, infrastructure for infusion and MRI monitoring, and regulatory status.
- Cost of care — largely out-of-pocket; Mental Healthcare Act 2017 mandates insurance parity; enforcement for dementia inpatient and daycare remains uneven.
- Rural and tuberculous meningitis — TB meningitis is a treatable cause of subacute cognitive decline in India that must not be missed.
NEET PG MCQ traps
- DSM-5 major NCD replaced dementia.
- AD 60 to 70 percent of dementias.
- AD pathology — amyloid-beta plaques and tau tangles.
- APOE epsilon-4 — commonest risk allele for late-onset AD.
- Down syndrome — extra APP gene, near-universal AD by age 60.
- VaD stepwise decline with focal neurology.
- DLB core — fluctuating cognition, visual hallucinations, parkinsonism, RBD.
- DLB one-year rule distinguishes from Parkinson disease dementia.
- Never haloperidol in DLB — severe neuroleptic sensitivity; use quetiapine or clozapine.
- FTD onset 45 to 65 with early personality change and disinhibition; memory preserved.
- NPH triad — gait, incontinence, dementia; VP shunt.
- Cholinesterase inhibitors — donepezil, rivastigmine, galantamine.
- Memantine — moderate-severe AD (NMDA antagonist).
- Lecanemab, donanemab — anti-amyloid monoclonal antibodies; ARIA on MRI.
- Rapidly progressive dementia — think CJD (14-3-3, RT-QuIC), autoimmune encephalitis, paraneoplastic.
- CJD MRI — cortical ribbon on diffusion-weighted imaging.
- B12 deficiency — reversible cognitive decline plus subacute combined degeneration.
- Neurosyphilis — reversible dementia; general paresis; VDRL and FTA-ABS.
- TB meningitis — subacute cognitive decline in India; do not miss.
- Antipsychotic black-box — increased mortality in elderly dementia patients.
Frequently asked questions
What is the DSM-5 definition of dementia and how is it distinguished from delirium and depression?
DSM-5 replaced the term dementia with major neurocognitive disorder (major NCD) and mild neurocognitive disorder (mild NCD) to reduce stigma and to capture earlier disease. Major NCD requires (A) significant cognitive decline from a previous level in one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) based on both the concern of the patient or informant and objective neuropsychological or bedside testing, (B) cognitive deficits that interfere with independence in everyday activities, (C) deficits that do not occur exclusively in the context of delirium, and (D) deficits that are not better explained by another mental disorder. Delirium is distinguished by its acute onset (hours to days), fluctuating course, disturbance of attention and awareness, and reversibility once the underlying cause (infection, hypoxia, drugs, electrolyte disturbance) is treated. Depression can mimic dementia (pseudodementia) with poor concentration, memory complaints, apathy and slowed cognition; clues to depression include the patient's own concern about memory (often exceeds objective deficit), an abrupt onset, low mood as the dominant symptom, and normalisation with antidepressant treatment. Bedside cognitive screens include MMSE (score out of 30, less than 24 abnormal, culturally biased and heavily language- and education-dependent) and MoCA (Montreal Cognitive Assessment, better sensitivity for mild cognitive impairment, less than 26 abnormal). Clock drawing and Abbreviated Mental Test Score are quicker screens; full neuropsychological testing is definitive.
What are the neuropathology and clinical features of Alzheimer disease and what are the current treatment options?
Alzheimer disease (AD) accounts for 60 to 70 percent of dementias. Neuropathology is characterised by extracellular amyloid-beta (Abeta-42) plaques, intracellular neurofibrillary tangles of hyperphosphorylated tau protein, and cortical atrophy that begins in the entorhinal cortex and hippocampus and spreads through the temporal, parietal and eventually frontal cortex. Risk factors include age (the strongest), family history, the APOE epsilon-4 allele, autosomal-dominant familial early-onset mutations (APP, PSEN1, PSEN2), Down syndrome (trisomy 21 carries an extra APP gene and near-universal AD by age 60), traumatic brain injury and cardiovascular risk factors. Clinical presentation is insidious short-term memory decline followed by word-finding difficulty, spatial disorientation, executive impairment, apraxia, agnosia, and eventual complete functional dependence, with terminal bed-bound frail phase. MMSE typically declines about 3 points per year. Diagnosis is clinical, supplemented by neuroimaging (MRI showing hippocampal atrophy) to exclude reversible causes, and increasingly by CSF biomarkers (low Abeta-42, high tau) and amyloid- or tau-PET at specialised centres. Symptomatic treatment — cholinesterase inhibitors (donepezil, rivastigmine, galantamine) modestly slow decline in mild to moderate disease; memantine (NMDA-receptor antagonist) is added for moderate to severe disease. Disease-modifying anti-amyloid monoclonal antibodies (lecanemab, donanemab) were FDA-approved in 2023 to 2024 for early symptomatic AD; they modestly slow cognitive decline and carry a risk of amyloid-related imaging abnormalities (ARIA — cerebral oedema and microhaemorrhage) requiring serial MRI monitoring; Indian access is currently very limited by cost and infrastructure. Cardiovascular risk factor control and cognitive, social and physical engagement reduce risk and slow decline.
How does dementia with Lewy bodies differ from Parkinson disease dementia and Alzheimer disease?
Dementia with Lewy bodies (DLB) accounts for 5 to 10 percent of dementias and shares underlying alpha-synuclein pathology (Lewy bodies) with Parkinson disease. DLB is defined clinically by the core features — fluctuating cognition with pronounced variation in attention and alertness, recurrent well-formed visual hallucinations, spontaneous parkinsonism, and REM sleep behaviour disorder (RBD, dream enactment). Supportive features include severe neuroleptic sensitivity (life-threatening rigidity, autonomic dysfunction and mental status change), autonomic dysfunction, repeated falls, and reduced dopamine transporter uptake on DAT-SPECT. The DLB one-year rule distinguishes DLB (cognitive decline before or within one year of parkinsonism onset) from Parkinson disease dementia (cognitive decline emerging more than one year after established Parkinson disease); the underlying pathology is essentially the same. Compared with AD, DLB has less severe memory impairment early on, more visuospatial and executive dysfunction, prominent visual hallucinations from the start, parkinsonism, and RBD. Management — cholinesterase inhibitors (rivastigmine and donepezil) are particularly effective for cognition and visual hallucinations; carbidopa-levodopa can help parkinsonism but is used cautiously as it may worsen hallucinations; conventional antipsychotics (haloperidol) are contraindicated because of severe neuroleptic sensitivity; if antipsychotic is unavoidable, quetiapine or clozapine are preferred; melatonin or low-dose clonazepam for RBD; treat co-morbid REM behaviour disorder, orthostatic hypotension, constipation and urinary symptoms.
What is frontotemporal dementia and how is it distinguished from Alzheimer disease?
Frontotemporal dementia (FTD), historically Pick disease, accounts for about 5 to 10 percent of dementias but is a common cause of early-onset dementia (typical age 45 to 65). It comprises three clinical variants — behavioural variant FTD (bvFTD, the most common, with early personality change, disinhibition, apathy, loss of empathy, perseverative or ritualistic behaviour, hyperorality with dietary changes, and executive dysfunction), semantic variant primary progressive aphasia (sv-PPA, with loss of word meaning and object knowledge, semantic paraphasias, and preserved fluency and repetition), and non-fluent agrammatic variant primary progressive aphasia (nfv-PPA, with effortful, non-fluent speech and agrammatism). Memory and visuospatial function are relatively preserved early on, in stark contrast to AD. Underlying molecular pathology is heterogeneous — TDP-43 in about half of bvFTD and most sv-PPA, tau in the remainder including Pick bodies and MAPT mutations, and rare FUS pathology. About 10 to 20 percent are familial (MAPT, GRN, C9orf72 expansions — the last also causes ALS). MRI shows frontal and temporal atrophy in a pattern matching the clinical variant. There is no disease-modifying therapy. SSRIs are used for behavioural symptoms (disinhibition, compulsive behaviour, hyperorality); antipsychotics are best avoided because of extrapyramidal sensitivity; carbamazepine or trazodone may help behavioural symptoms; cholinesterase inhibitors do not help and may worsen behaviour. Caregiver support and safety planning are central. Onset before 65, prominent personality or language change, and preserved memory should always prompt consideration of FTD.
What are the reversible causes of cognitive decline that must be excluded in every dementia workup?
Before diagnosing an irreversible dementia, exclude reversible or partially reversible causes because treatment restores or arrests cognitive decline. The mnemonic DEMENTIAS is useful — Drugs (anticholinergics including diphenhydramine, oxybutynin and tricyclics, benzodiazepines, opioids, chronic sedative use), Emotional (depression pseudodementia), Metabolic (hypothyroidism, hyponatraemia, hypercalcaemia, hepatic and renal failure), Eyes and Ears (uncorrected sensory loss), Nutritional (vitamin B12 and folate deficiency, thiamine — chronic alcoholism, Wernicke-Korsakoff), Tumour (frontal lobe meningioma, subdural haematoma), Infection (neurosyphilis, HIV dementia, tuberculous meningitis particularly in India, chronic Lyme in endemic areas), Alcohol, and Sleep and Stroke (obstructive sleep apnoea, silent infarct). The classic non-drug reversible cause is normal-pressure hydrocephalus (Hakim triad — gait disturbance, urinary incontinence, and cognitive decline — treated by ventriculoperitoneal shunt after positive tap test). Standard workup includes full blood count, urea and electrolytes, calcium, liver and renal function, thyroid function, vitamin B12 and folate, syphilis serology, HIV testing where risk is present, MRI of the brain, and lumbar puncture in atypical, rapidly progressive or infectious presentations. Formal neuropsychological testing complements bedside screening. Rapidly progressive dementia (weeks to months) prompts an urgent workup for Creutzfeldt-Jakob disease (CSF 14-3-3, RT-QuIC, cortical ribbon on MRI diffusion), autoimmune encephalitis (LGI1, NMDA receptor and other antibodies with a strong steroid response), paraneoplastic syndromes and CNS lymphoma.
This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
Written by: NEETPGAI Editorial Team
Reviewed by: Pending SME Review
Last reviewed: September 2026
