← All EducationNABR Medical Group — Staff Education
Where to start

A structured approach to cognitive assessment

Dementia diagnosis at the bedside requires layering three types of information: a validated screening tool (MoCA), a condition-specific history, and targeted bedside tests that probe specific cognitive networks implicated in different dementia syndromes.

Clinical principle
Dementia is a clinical diagnosis. No single test makes it. The MoCA screens — it does not diagnose. Diagnosis requires history, cognitive testing, functional assessment, and often neuroimaging.

The 4-step bedside workflow

Step 1 — Establish baseline & history

Onset (acute vs. insidious), trajectory (stepwise vs. gradual), domains affected, functional impact. Corroborate with informant. Review vascular, sleep, metabolic, medication, and psychiatric history.

Step 2 — Administer the MoCA

10–15 minutes. Screens across 6 cognitive domains. Score ≤25 warrants further workup. Add 1 point for ≤12 years of education. Adjust for language, hearing, and motor impairments.

Step 3 — Targeted bedside tests

Based on your leading hypothesis: naming for FTD, clock draw for visuospatial/executive, gait assessment for NPH, primitive reflexes for FTD, finger-nose for LBD, serial 7s for attention/delirium.

Step 4 — Synthesize & classify

Pattern the deficits: amnestic (AD), frontal-predominant (FTD), visuospatial (LBD/PCA), stepwise (VaD), reversible (NPH, B12, thyroid, depression, medications). Refer or investigate accordingly.

Cognitive domains at a glance

Domains commonly assessed

  • Memory — encoding, storage, delayed recall
  • Attention/concentration — sustained, divided
  • Language — fluency, naming, comprehension
  • Executive function — planning, abstraction, set-shifting
  • Visuospatial — construction, perception, navigation
  • Orientation — time, place, person

Red flags requiring urgent workup

  • Acute onset (<days) → delirium / stroke
  • Rapid progression (<weeks) → prion disease, autoimmune encephalitis
  • Focal neurological signs → structural lesion, vasculitis
  • Personality change as first symptom → FTD
  • Visual hallucinations early → Lewy body dementia
  • Falls, gait disturbance, incontinence triad → NPH
Montreal Cognitive Assessment

MoCA Administration

The MoCA takes 10–15 minutes, requires only a printed form and pencil, and has 90% sensitivity for mild cognitive impairment. Expand each domain for verbatim instructions and scoring rules.

Interpreting the total score (max 30 points)
016212530
0–15
Moderate–severe impairment
16–25
MCI or mild dementia
26–30
Normal (≥26)
Education correction: Add 1 point if the patient has ≤12 years of formal education. Maximum adjusted score is still 30.
Click each domain to expand instructions
5 pts Visuospatial / Executive

Tests frontal-parietal networks. Three sub-tasks: Trail-making, clock draw, and 3D cube copy.

Trail-making alternating (1 pt)

Say to patient
"I'm going to give you a sheet with numbers and letters. Draw a line, going from a number to a letter in ascending order. Start at number 1 [point], and draw a line from 1 to A [point], then from A to 2 [point], and so on. End here [point to E]."
✓ 1 pt — correct sequence (1→A→2→B→3→C→4→D→5→E) ✗ 0 — any sequence error not self-corrected

Clock draw (3 pts)

Say to patient
"Draw a clock. Put in all the numbers and set the hands to 10 past 11."
1 pt — contour (circle, no significant distortion) 1 pt — numbers (all 12 present, correct order/position) 1 pt — hands (both present, correct time, minute hand longer)

3D cube copy (1 pt)

Say to patient
"Copy this drawing as accurately as you can."
✓ 1 pt — 3D, all lines drawn, no extra lines, sides parallel and roughly equal ✗ 0 — does not meet all criteria
3 pts Naming

Tests semantic memory and language. Three line drawings are presented: lion, rhinoceros, camel.

Say to patient
"Tell me the name of each animal." (Point to each drawing in sequence.)
1 pt each — correct name (lion, rhinoceros/rhino, camel/dromedary)
Clinical note: Naming errors (anomia) are non-specific but prominent in Alzheimer's, semantic variant PPA, and advanced LBD. Normal naming with other deficits suggests executive-first presentation (FTD-behavioral variant).
5 pts Memory (Delayed Recall)

The most diagnostically powerful domain for Alzheimer's disease. Words are presented twice, scored only on delayed free recall at ~5 minutes.

Encoding (no points at this stage)

Say to patient (read at 1 word/second)
"This is a memory test. I am going to read you a list of words that you will have to remember now and later on. Listen carefully. When I am through, tell me as many words as you can remember. It doesn't matter in what order you say them."
FACE — VELVET — CHURCH — DAISY — RED

Record which words recalled. Read list a second time. Tell patient they will need to recall these words later.

Delayed recall (~5 min later — after attention, language, abstraction tasks)

Say to patient
"Tell me as many of the words I read earlier as you can remember."
1 pt each — word recalled spontaneously (free recall) Optional: offer category cue if not recalled (no points) Optional: offer multiple choice if cue fails (no points)
Alzheimer's pattern: Failure on free recall AND failure with semantic cueing (e.g., "It was a color" for RED) suggests an encoding/storage deficit — the hallmark of hippocampal-predominant AD. Patients who recall with cues have a retrieval deficit, more typical of subcortical or frontal disease.
6 pts Attention

Three sub-tasks: digit span forward/backward, vigilance (tap on A), and serial 7s. Critical for distinguishing delirium from dementia.

Forward digit span (1 pt)

Say to patient (read 1 digit/second)
"I am going to say some numbers and when I am through, repeat them in the same order I said them." 2 — 1 — 8 — 5 — 4

Backward digit span (1 pt)

Say to patient
"I am going to say some more numbers, but when I am through, you must repeat them in the backwards order." 7 — 4 — 2 Correct answer: 2 — 4 — 7

Vigilance / Tap on A (1 pt)

Say to patient
"I am going to read a sequence of letters. Every time I say the letter A, tap your hand once. If I say a different letter, do not tap." F B A C M N A A J K L B A F A K D E A A A J A M O F A A B
1 pt — ≤1 error (miss or false positive) ✗ 0 — ≥2 errors

Serial 7s (3 pts)

Say to patient
"Now I will ask you to count by subtracting 7 from 100, and then to keep subtracting 7 from your answer until I tell you to stop."
3 pts — 4–5 correct subtractions 2 pts — 2–3 correct 1 pt — 1 correct 0 pts — none correct

Correct sequence: 93 — 86 — 79 — 72 — 65. Each subtraction scored independently.

3 pts Language

Sentence repetition (2 pts) and verbal fluency (1 pt). Sensitive to aphasia, PPA, and word-finding difficulties.

Sentence repetition (2 pts)

Say to patient
"I am going to read you a sentence. Repeat it after me, exactly as I say it [pause]: 'I only know that John is the one to help today.'" "Now I'll read you another sentence. Repeat it after me, exactly as I say it [pause]: 'The cat always hid under the couch when dogs were in the room.'"
1 pt each — exact verbatim repetition only. No partial credit.

Verbal fluency (1 pt)

Say to patient
"Tell me as many words as you can think of that begin with the letter F. I will tell you to stop after one minute. Proper nouns such as Fred or France are not allowed, and you cannot use the same word twice with a different ending, for example, eat and eating. Ready? Begin."
1 pt — ≥11 words in 60 seconds ✗ 0 — <11 words
Letter vs. category fluency: In AD, category fluency (animals) is typically more impaired than letter fluency. In FTD, both degrade — but letter fluency often falls first. This distinction has diagnostic value beyond the MoCA.
2 pts Abstraction

Tests conceptual thinking and frontal lobe function. Failure on abstraction with spared memory suggests FTD or vascular disease affecting frontal networks.

Say to patient
"I am going to tell you two words and I would like you to tell me in what way they are similar — what do they have in common?" "How are a train and a bicycle alike?" "How are a watch and a ruler alike?"
Train/bicycle: "vehicles" / "means of transport" = 1 pt Watch/ruler: "measuring instruments" = 1 pt ✗ Concrete answers: "both have wheels" = 0 pts

If the patient gives a concrete answer on the first pair, give no credit but say: "Yes, and they are both a means of transportation." Do not help on the second pair.

6 pts Orientation

Typically preserved until moderate-severe dementia. Loss of date/month orientation before day/year is a common early Alzheimer's pattern.

Say to patient
"Tell me today's date." [If incomplete, prompt: "Can you also tell me the month? The year? The day of the week?"] "Now, can you tell me the name of this place, and what city it is in?"
1 pt each: date, month, year, day of week, place, city
Tip: Date orientation is the most sensitive of the 6 items. A patient who consistently misses the date by >3 days warrants further evaluation even with a normal total MoCA score.
After the MoCA
A score ≤25 warrants: informant interview, functional ADL assessment, laboratory workup (CBC, CMP, TSH, B12, folate, RPR ± HIV), and neuroimaging (MRI brain preferred over CT). Refer to neuropsychology or geriatrics if diagnosis remains uncertain.
Diagnosis-specific history

History Deep-Dives

The history identifies reversible causes, points to specific dementia syndromes, and quantifies vascular and metabolic risk. Expand each condition for targeted questions and clinical pearls.

Always interview an informant separately. Patients with anosognosia (especially FTD, moderate AD) underreport symptoms. The informant often provides the most clinically useful information.
Vascular disease & cerebrovascular history

Vascular dementia (VaD) is the second most common dementia. It is characterized by a stepwise or abrupt-onset course, focal neurological findings, and prominent executive dysfunction with relatively spared early memory.

Key history questions

  • History of stroke, TIA, or "mini-strokes"? Timing relative to cognitive decline?
  • Stepwise decline vs. gradual? Any plateau periods?
  • Hypertension — duration, control, adherence?
  • Atrial fibrillation — anticoagulation status?
  • Diabetes — HbA1c trend, hypoglycemic episodes?
  • Hyperlipidemia — treated? Statin use?
  • Smoking history (pack-years), current status
  • Carotid artery disease — any prior imaging or intervention?
  • Peripheral vascular disease — claudication, prior bypass?
  • Family history of early stroke or vascular dementia?
Clinical pattern — VaD: Executive dysfunction first (planning, multitasking, slowed processing speed). Memory may be relatively spared early. Gait often impaired. Pseudobulbar affect (inappropriate laughing/crying) may be present. MRI shows white matter hyperintensities, lacunar infarcts, or cortical infarcts.

CADASIL note

Consider CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) in patients with early-onset vascular dementia, migraines with aura, psychiatric symptoms, and a family history of stroke — especially without traditional vascular risk factors. NOTCH3 gene testing is available.

Obstructive sleep apnea (OSA)

OSA is strongly associated with cognitive impairment and is often underdiagnosed in older adults. It is a potentially reversible contributor to cognitive decline — CPAP treatment may improve cognitive performance.

Key history questions

  • Witnessed apneas? Ask the bed partner directly.
  • Loud snoring, gasping, or choking during sleep?
  • Excessive daytime somnolence (Epworth Sleepiness Scale ≥10)?
  • Morning headaches on waking?
  • Nocturia ≥2×/night (nocturnal hypoxia-mediated)?
  • Prior sleep study or CPAP prescription? Current adherence?
  • BMI, neck circumference (high-risk: ≥17 inches F, ≥17.5 inches M)
  • Alcohol use (relaxes upper airway musculature)?
  • Hypothyroidism (associated with OSA)?
Clinical pearl: Cognitive complaints dominated by attention, processing speed, and daytime fatigue in an overweight patient with snoring should prompt a sleep study before attributing symptoms to primary dementia. CPAP-responsive "pseudodementia" is a satisfying clinical diagnosis.
Metabolic and reversible causes

Always exclude reversible causes before diagnosing a primary neurodegenerative dementia. Up to 10% of apparent dementia presentations have a treatable underlying cause.

Thyroid disease

  • Hypothyroidism: fatigue, cold intolerance, constipation, hair loss, bradycardia
  • Check TSH — even subclinical hypothyroidism can impair cognition
  • Hyperthyroidism (less common): anxiety, agitation, rapid AF, heat intolerance

Vitamin B12 deficiency

  • Diet (vegans, elderly with poor intake), malabsorption (metformin use, PPI use, gastric surgery, pernicious anemia)
  • Subacute combined degeneration: cognitive decline + posterior column signs (vibration/proprioception loss)
  • Check B12 level; methylmalonic acid if borderline

Normal pressure hydrocephalus (NPH)

  • Classic triad: gait disturbance (magnetic, wide-based), urinary incontinence, cognitive decline
  • Gait abnormality is the first and most prominent feature
  • MRI: ventriculomegaly out of proportion to sulcal atrophy
  • Treat: serial LPs or VP shunt (gait responds best)

Other reversible causes

  • Neurosyphilis (RPR/VDRL + FTA-ABS)
  • HIV-associated neurocognitive disorder
  • Chronic subdural hematoma (trauma history, anticoagulation)
  • Autoimmune encephalitis (anti-NMDA, anti-LGI1 — rapid onset, psychiatric features)
  • Medication toxicity (benzodiazepines, anticholinergics, opioids)
  • Alcohol-related (Wernicke-Korsakoff — thiamine history)
Standard reversibility workup: CBC, CMP (glucose, renal, hepatic), TSH, B12, folate, RPR, HIV (if at risk), UA. Consider LP if rapid onset, young patient, atypical features, or autoimmune suspicion. MRI brain preferred over CT.
Psychiatric history and depressive pseudodementia

Depression in older adults mimics dementia and frequently co-occurs with it. A psychiatric history is essential in every cognitive assessment.

Key history questions

  • PHQ-9 or GDS-15 — screen for current depression
  • Prior depressive episodes, anxiety disorders, psychosis?
  • History of ECT — can cause persistent memory deficits
  • Current antidepressant use — type, dose, duration, response?
  • Onset of cognitive vs. mood symptoms — which came first?
  • Patient complaints about memory vs. informant-observed impairment?
  • Motivation and effort during testing — does performance improve with encouragement?
  • Sleep disturbance, anhedonia, appetite change?
  • Social withdrawal, loss of former interests?
  • Alcohol or substance use (self-medication pattern)?
Depressive pseudodementia clues: (1) Patient loudly complains about memory, informant notes preserved daily function. (2) "I don't know" responses predominate over near-miss errors. (3) Cognition fluctuates with mood. (4) History of depression predating cognitive complaints. (5) Responds to antidepressant trial.
Medication review and polypharmacy

Medications are among the most common and correctable contributors to cognitive impairment in older adults. Perform a full medication reconciliation at every visit.

High-risk agents (Beers Criteria / ACB scale)

Highest anticholinergic burden
DiphenhydramineOxybutyninTolterodineAmitriptylineHydroxyzineChlorpheniramine
CNS depressants / sedatives
BenzodiazepinesZ-drugs (zolpidem)GabapentinOpioidsFirst-gen antipsychotics

Key questions

  • Any OTC sleep aids, allergy meds, pain relievers? (Often not volunteered)
  • Metformin ≥5 years? B12 malabsorption risk.
  • PPIs long-term? B12 malabsorption, Mg depletion.
  • Any new medication started 1–6 months before cognitive change?
  • Any recent dose increase in existing medications?
  • Diuretics — chronic dehydration → confusion?
  • Statins — rare but reported cognitive side effect (reversible on discontinuation)
Family history and genetic risk

Key history questions

  • First-degree relatives with dementia — age of onset, type?
  • Early-onset dementia in family (<65 years) → consider EOAD, FTLD-related mutations (GRN, MAPT, C9orf72)
  • Family history of Parkinson's disease → LBD spectrum?
  • Family history of ALS + dementia → C9orf72 expansion
  • Ethnic background (Ashkenazi Jewish → higher APOE ε4 prevalence; African American → higher vascular risk)
Genetic testing: APOE ε4 genotyping is available but not recommended for routine clinical use — it is a risk modifier, not diagnostic. APOE ε4/ε4 confers ~10x lifetime risk of AD. Genetic counseling should precede testing, especially in early-onset cases.
Targeted bedside assessment

Bedside Tests by Cognitive Domain

These tests take 2–5 minutes each, require no equipment beyond a pen and paper, and provide domain-specific information beyond the MoCA to narrow the differential diagnosis.

Naming & Semantic Memory Object naming & semantic battery

Naming is impaired in several dementia syndromes. The pattern of errors is as diagnostically useful as the number of errors.

Confrontation naming (Boston Naming Test — short form)

Show line drawings of objects ranging from common to uncommon (pencil → abacus → sphinx). Ask patient to name each. If failed, offer a semantic cue ("It's an animal") then a phonemic cue ("It starts with 'ab-'").

Error typeExampleSuggests
Semantic paraphasia"horse" for camelSemantic degradation (AD, svPPA)
Phonemic paraphasia"canel" for camelPhonological processing disorder (lvPPA)
Circumlocution"the thing you write with"Word retrieval difficulty — non-specific, AD, FTD
No response / "don't know"Severe anomia — svPPA, advanced AD
Responds to phonemic cue onlyKnows it's "ab-" somethingRetrieval deficit > storage (subcortical, frontal)

Category fluency (animals in 60 seconds)

Say to patient
"Tell me as many different animals as you can think of. You have one minute. Begin."
Normal: ≥15 animals in 60 sec MCI/AD: typically 10–14 Concern: <10 (especially if letter fluency better than category)
Key pattern: In AD, category fluency degrades more than letter fluency (semantic memory > phonological access). In FTD, both degrade; in severe svPPA, category fluency may be nearly absent. Compare with the MoCA F-letter fluency score.
Executive Function Frontal lobe battery — FTD screen

Luria sequences (motor sequencing)

Tests frontal motor programming. Ask patient to imitate and then perform independently: Fist → Edge → Palm (repeat 6 times without verbal cuing). Perseveration or inability to alternate is a frontal sign.

Say to patient
"Watch me. Fist — Edge — Palm. Now do it with me... Now you do it on your own, as quickly as you can."
Normal: Independent performance after 2–3 imitation trials Abnormal: Perseveration, arrest, or mirroring — frontal impairment

Primitive / frontal release reflexes

Present in FTD and advanced dementia; absent in normal aging and early AD.

ReflexTechniqueSignificance if present
Grasp reflexStroke patient's palm from wrist to fingers — abnormal if patient grasps involuntarilyFrontal lobe dysfunction; bvFTD, advanced AD
PalmomentalStroke thenar eminence briskly → watch for chin muscle contraction ipsilaterallyNon-specific but sensitive for frontal pathology
Snout reflexTap upper lip — abnormal if lip protrudes/puckersPrefrontal dysfunction; any advanced dementia
Glabellar tapTap forehead between eyebrows repeatedly — normal = blink extinguishes after 2–3 tapsPersistent blinking = frontal/basal ganglia disease

Go/No-Go task (inhibition)

Say to patient
"When I tap once, you tap twice. When I tap twice, don't tap at all." [Practice 3 rounds] "Ready? Do not tap when I tap twice."

Normal = correctly inhibits on double tap. Failure to inhibit (echoing the examiner) = significant frontal disinhibition, strongly associated with bvFTD.

Visuospatial Visuospatial tests — LBD & PCA screen

Intersecting pentagons

Draw two intersecting pentagons and ask the patient to copy them exactly. Both pentagons must have 5 sides and the overlap must form a quadrilateral for full credit. Impaired in AD (constructional apraxia) and especially in LBD and PCA.

Number location test (perceptual)

Say to patient
"I'm going to point to a number on this clock face. Tell me which number I'm pointing to." [Cover face, point to various positions] "Now, if this clock shows 10 past 11, which position would the big hand be in?"

PCA patients fail spatial analysis tasks even when naming and memory are relatively intact — a characteristic pattern.

Counting embedded figures

Show overlapping line drawings (e.g., Poppelreuter figures — a cube, scissors, and cup overlaid). Ask patient to identify all three objects. Failure on figure-ground discrimination is a specific sign of posterior cortical dysfunction (PCA, LBD).

Lewy body dementia visuospatial pattern: Severe visuospatial dysfunction early, often with clock draw showing markedly distorted spatial arrangement despite intact number recall. Combine with history of visual hallucinations, REM sleep behavior disorder, parkinsonism, and cognitive fluctuations.
Gait & Motor Gait assessment — NPH, LBD, VaD screen

Timed Up and Go (TUG)

  1. Patient sits in a standard chair with arms.
  2. Instruct: "When I say go, stand up, walk to that line [3 meters], turn around, walk back, and sit down again — as quickly and safely as you can."
  3. Time with a stopwatch from "go" to re-seated.
Normal: <12 sec Increased fall risk: >12 sec High fall risk / frailty: >20 sec

Gait observation — NPH vs. Parkinsonism

FeatureNPHParkinsonism / LBDVascular
BaseWide-basedNarrow-basedWide-based
StrideShort, shuffling, "magnetic"Short, festinatingShort, cautious
InitiationStart hesitation, feet "stuck"Freezing, start hesitationMay have start hesitation
Arm swingNormal or mildly reducedAsymmetric, reducedVariable
TurnsEn bloc ("all at once")En blocVariable
Improves with promptsSometimesVisual cues helpUnlikely
NPH tap test: After an LP removing 30–50 mL of CSF, reassess gait within 2–4 hours. Objective improvement in gait speed (TUG) predicts shunt responsiveness with good specificity.
Memory Free and cued selective reminding — AD memory profile

The Free and Cued Selective Reminding Test (FCSRT) is the most sensitive bedside test for hippocampal (Alzheimer's-type) memory impairment. A simplified version can be administered in 5 minutes.

Simplified FCSRT protocol

  1. Show patient a card with 4 pictures (e.g., a dog, a chair, a hammer, an apple). For each, ask: "Point to the [animal / piece of furniture / tool / fruit]." This ensures encoding.
  2. Perform a ~2-minute distractor task (serial 7s or forwards digit span).
  3. Ask: "Tell me all the pictures you saw." Record free recall (FR).
  4. For any missed item, give the category cue: "What was the [animal]?" Record cued recall (CR).
Normal: FR ≥3/4; CR = 4/4 AD pattern: FR impaired AND cues do not help (CR also impaired) Frontal/subcortical: FR impaired, CR normalizes with cues
Critical distinction: A patient who recalls none of 4 words on free recall but recalls 4/4 with cuing has a retrieval deficit — consistent with depression, vascular disease, or subcortical pathology. A patient who fails both free AND cued recall has an encoding/storage failure — the hallmark of hippocampal-predominant AD.
Differential diagnosis

Dementia Syndromes at a Glance

Select a syndrome to review its characteristic clinical profile, cognitive signature, and key distinguishing features.

Alzheimer's Disease
Most common · Amnestic · Insidious
Frontotemporal Dementia
Frontal-predominant · Early personality change
Lewy Body Dementia
Fluctuating · Hallucinations · Parkinsonism
Vascular Dementia
Stepwise · Executive-first · Focal signs
Normal Pressure Hydrocephalus
Reversible triad · Gait first
Posterior Cortical Atrophy
Visuospatial · Usually AD pathology

Alzheimer's Disease

Core features

  • Insidious onset, gradual progression (years)
  • Episodic memory most impaired first (encoding failure)
  • Semantic memory impairs with progression (naming)
  • Visuospatial and executive dysfunction mid-stage
  • Orientation (date/time) lost relatively early
  • Personality changes: apathy, later agitation

Bedside signature

  • FCSRT: fails free AND cued recall
  • MoCA: delayed recall lowest domain score
  • Category fluency (< letter fluency)
  • Clock draw: preserved outline, impaired hand placement
  • Orientation: date fails before day/year
Key distinguisher from FTD: Memory impairment is prominent and early in AD. Personality and behavior are relatively spared until mid-to-late stages. FTD presents with frontal/behavioral changes first, with memory relatively spared.

Frontotemporal Dementia (bvFTD)

Core features

  • Onset often <65 years (earlier than AD)
  • Personality and behavior change as first symptom
  • Disinhibition, impulsivity, socially inappropriate behavior
  • Apathy, loss of empathy, emotional blunting
  • Compulsive/ritualistic behaviors, dietary change (carbohydrate preference)
  • Language variants: svPPA (naming), nfvPPA (motor speech)

Bedside signature

  • Primitive reflexes: grasp, snout, palmomental
  • Go/No-Go: fails inhibition (echoes examiner)
  • Luria sequences: perseveration
  • Naming: impaired in svPPA variant
  • Category fluency severely impaired in svPPA
  • Memory: relatively spared in early bvFTD
Clinical pearl: Family history of FTD, ALS, or parkinsonism in a first-degree relative + early behavioral change should prompt genetic testing (C9orf72, GRN, MAPT). FTD-ALS overlap is the C9orf72 hexanucleotide repeat expansion phenotype.

Lewy Body Dementia

Core features (McKeith criteria)

  • Fluctuating cognition with episodes of pronounced confusion
  • Recurrent, detailed visual hallucinations (people, animals)
  • Spontaneous parkinsonism (not drug-induced)
  • REM sleep behavior disorder (acts out dreams — ask bed partner)
  • Severe neuroleptic sensitivity (may precipitate crisis)

Bedside signature

  • Visuospatial: severely impaired (worst on clock, pentagon copy)
  • Attention markedly fluctuating — may vary within single visit
  • Memory: impaired but less severely than AD early on
  • Parkinsonism: UPDRS assessment; finger-nose for tremor type
  • Orthostatic hypotension (autonomic dysfunction)
AVOID antipsychotics in LBD. Conventional (haloperidol) and many atypical antipsychotics can cause severe, potentially fatal neuroleptic sensitivity reactions in LBD — irreversible worsening, rigidity, altered consciousness. Quetiapine at low dose is the safest option if needed.

Vascular Dementia

Core features

  • Stepwise or abrupt onset following vascular events
  • Focal neurological signs: asymmetric reflexes, pseudobulbar palsy
  • Executive dysfunction disproportionate to memory loss
  • Gait disturbance early (small vessel disease)
  • Emotional lability / pseudobulbar affect
  • Vascular risk factor burden (HTN, DM, AF, dyslipidemia)

Bedside signature

  • MoCA: attention and executive domains most impaired
  • Memory: improves with cueing (retrieval deficit, not storage)
  • Processing speed: markedly slowed
  • Neurological exam: focal signs, hyperreflexia, Babinski
  • Gait: wide-based, short-stepped, cautious
Management is secondary stroke prevention: antiplatelet therapy (or anticoagulation for AF), aggressive BP control (target <130/80), statin therapy, smoking cessation. No FDA-approved dementia-specific treatment for pure VaD.

Normal Pressure Hydrocephalus

Classic triad (Hakim's triad)

  • Gait — "magnetic" gait; wide-based, shuffling, feet barely leave floor
  • Urinary incontinence — urgency incontinence; follows gait impairment
  • Cognitive decline — executive and attention; memory relatively spared

Gait is always first. If cognition is the primary complaint, reconsider diagnosis.

Workup and treatment

  • MRI: ventriculomegaly disproportionate to sulcal atrophy; callosal angle <90°
  • LP tap test: remove 30–50 mL CSF; assess gait/TUG before and 2–4 hr after
  • Gait improvement after LP predicts shunt response
  • VP shunt: gait responds best, cognition variable, incontinence least responsive
  • Complications: shunt infection, overdrainage, subdural hematoma

Posterior Cortical Atrophy

Core features

  • Early visuospatial and visuoperceptual impairment
  • Difficulty reading (alexia), writing (agraphia)
  • Dressing apraxia, limb apraxia
  • Difficulty navigating familiar environments
  • Balint syndrome (simultagnosia, ocular apraxia, optic ataxia) in severe cases
  • Relatively spared memory and language early

Bedside signature

  • Clock draw: severely distorted spatial arrangement
  • Pentagon copy: unable to capture spatial relationships
  • Fails overlapping figure identification (Poppelreuter)
  • Letter/number cancellation tasks impaired
  • Normal or near-normal naming and verbal memory early
  • Ophthalmologic exam: normal (primary visual processing deficit)
Pathology: ~80% of PCA cases have underlying Alzheimer's pathology (amyloid + tau) on biomarker or autopsy — just with a different regional distribution (posterior cortex > hippocampus). Lewy body pathology accounts for most of the remainder. Important for prognosis and treatment planning.
Rapid reference

Quick Reference Tables

Dementia differential — pattern recognition

Feature AD FTD (bvFTD) LBD VaD NPH
OnsetInsidiousInsidious, often <65InsidiousStepwise / abruptMonths–years
First symptomMemory lossPersonality/behaviorVisuospatial / fluctuationExecutive dysfunctionGait
MemorySevere early, encoding failureRelatively spared earlyImpaired, less than ADRetrieval deficitMild, retrieval
LanguageNaming lateFluency early; svPPA = namingMild anomiaMildPreserved
VisuospatialMid-latePreserved earlySeverely impaired earlyMildMild
HallucinationsLateUncommonEarly, vivid visualUncommonAbsent
GaitLateLate (FTD-PSP overlap)ParkinsonismAffectedMagnetic, early
IncontinenceLateLateAutonomic lateLateEarly (follows gait)
Reversible?NoNoNo (some features)Risk modificationPartially (shunt)
MRIHippocampal atrophyFrontal/temporal atrophySubstantia nigra signalWMH, lacunesVentriculomegaly

MoCA domain breakdown

DomainPointsSub-tasksMost impaired in
Visuospatial/Executive5Trail alternating, clock draw, cube copyLBD, VaD, PCA, AD (mid)
Naming3Lion, rhino, camelAD (late), svPPA (early)
Memory55-word delayed recallAD (earliest impaired)
Attention6Digit span F/B, Vigilance-A, Serial 7sDelirium, VaD, LBD (fluctuating)
Language3Sentence repetition ×2, F-fluencyAD, nfvPPA, LBD
Abstraction2Train/bicycle, watch/rulerFTD, VaD (frontal)
Orientation6Date, month, year, day, place, cityAD (date first), moderate–severe dementia

Reversible causes — workup checklist

CauseTestClue in history
HypothyroidismTSH, free T4Fatigue, cold intolerance, bradycardia, hair loss
B12 deficiencyB12; MMA if borderlineVegan diet, metformin, PPI, pernicious anemia, posterior column signs
NeurosyphilisRPR/VDRL → FTA-ABS if +Prior STI history, psychiatric features, CSF VDRL if LP done
HIV neurocognitiveHIV Ab/AgRisk factors, CD4 history, subcortical pattern
Normal pressure hydrocephalusMRI, LP tap testGait first, incontinence, mild cognitive decline
Chronic subdural hematomaCT/MRI headFalls, head trauma, anticoagulation
Autoimmune encephalitisAnti-NMDA, anti-LGI1, etc. (serum + CSF)Rapid onset, psychiatric features, seizures, young patient
OSAPolysomnographySnoring, witnessed apneas, daytime somnolence, morning headaches
Medication toxicityMedication reconciliation + trial deprescribingAnticholinergics, benzodiazepines, opioids, gabapentin
DepressionPHQ-9, GDS-15Mood change precedes cognition, complains of memory, "I don't know" responses
Thiamine deficiencyThiamine level; empiric replacementAlcohol use disorder, malnutrition, post-bariatric surgery

Bedside tests — when to use

TestTargetsUse when suspectingTime
FCSRT (simplified)Encoding vs. retrieval memoryAD vs. subcortical/frontal disease~5 min
Animal fluencySemantic memoryAD, svPPA — compare with F-letter fluency1 min
Confrontation namingSemantic/lexical accessAD, svPPA, LBD2–3 min
Luria sequencesFrontal motor programmingFTD, VaD with frontal involvement2 min
Go/No-GoResponse inhibitionbvFTD (disinhibition)1 min
Primitive reflexesFrontal release signsFTD, advanced any dementia2 min
Pentagon copyVisuospatial constructionLBD, PCA, AD (mid-stage)1 min
Poppelreuter figuresFigure-ground perceptionPCA, LBD1 min
TUG testGait speed, fall riskNPH, LBD, VaD, fall risk assessment2 min
Gait observationGait pattern classificationNPH vs. Parkinsonism vs. vascular2 min