Dementia assessment and reversible causes

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Start with the person's concerns and permission for collateral. Ask for concrete episodes rather than yes-or-no memory complaints: repeated questions, missed payments, medication errors, navigation, cooking, appliance use, word-finding, visual misjudgement and personality change. Establish onset, rate, steps or fluctuation and effect on chosen roles. Family disagreement is resolved by dates and examples, not by accepting the loudest account.

Separate current state from baseline. New inattention, altered alertness or hour-to-hour variability needs 4AT and delirium investigation. Cognitive assessment during infection or immediately after surgery may document need but should not create a permanent dementia label. Arrange follow-up after recovery when baseline remains uncertain.

Optimise testing conditions. Supply hearing aids, glasses, interpreter and accessible written material; treat pain and fatigue and explain the purpose. GPCOG combines a patient screen with informant questions. A normal brief test does not exclude executive or high-premorbid decline, and a low result can reflect language, education, sensory or motor barriers.

Functional history gives scores clinical meaning. Record whether the person safely manages medicines, finances, shopping, transport, telephone, meals, appointments and home hazards, and what cueing or hidden carer input is required. Loss of a culturally unfamiliar task is not decline. OT assessment can test real-life executive and environmental safety.

Review mood, anxiety, sleep, alcohol and medicines. Calculate anticholinergic and sedative exposure conceptually rather than treating a scale as an order to stop. Taper withdrawal-prone drugs and monitor target cognition and symptoms. Correct confirmed thyroid or nutritional abnormality, but explain that treating a contributor may improve function without reversing coexisting neurodegeneration.

Examine pulse, blood pressure including posture where relevant, cardiovascular system, gait, balance, focal neurology, tone, bradykinesia, tremor, eye movements, praxis and cortical sensory function. Formed hallucinations, REM-sleep behaviour and parkinsonism point toward Lewy-body disease; focal and stepwise features support vascular contribution; early behavioural or language change raises frontotemporal disease.

Use targeted blood tests and structural imaging. Non-contrast CT or MRI can identify tumour, subdural, hydrocephalus, major infarction and burden or pattern of atrophy; MRI better characterises vascular and regional change when feasible. Functional imaging or CSF biomarkers belong to specialist uncertainty when subtype distinction would change management, not routine screening.

After diagnosis, assess driving, medicines, cooking, finances, falls, nutrition and safeguarding while preserving autonomy. A dementia diagnosis never determines capacity automatically. Assess each material decision with support, encourage lasting power of attorney and advance care planning while capacity permits and identify what the person still does well.

Offer the person and carers a named contact, dementia adviser or equivalent, information about subtype and prognosis, carers assessment, community support and review. Revisit cognition, function, mood, sensory needs, medicine tolerance and carer capacity. New rapid decline triggers delirium and medical reassessment, not assumed progression.

Key points

Dementia is acquired cognitive decline that interferes with everyday function; a low score without functional change does not establish it.
First establish chronology and baseline through the person and collateral: memory, executive, language, visuospatial, behaviour, IADLs and ADLs.
Exclude delirium first with 4AT when change is acute or fluctuating and reassess after acute illness, pain and communication barriers improve.
Use a validated brief tool such as GPCOG in primary care, but do not exclude dementia solely because a normal score conflicts with convincing history.
Check hearing, vision, language, education, motor and speech impairment before interpreting performance and record the test conditions.
Review anticholinergic, sedative and opioid medicines, alcohol, sleep and mood and make cautious monitored changes when they plausibly contribute.
Core examination includes neurological and gait assessment, parkinsonism, eye movements, focal signs and cardiovascular risk; function and home safety are equally important.
Routine blood work commonly includes FBC, renal, liver, calcium, glucose or HbA1c, thyroid, B12 and folate, adapted to the clinical picture.
Structural imaging is usually offered to exclude reversible lesions and support subtype unless dementia is already established and the result would not change care.
Refer for specialist subtype assessment; discuss diagnosis, driving, advance planning, capacity, carer assessment, support and review in accessible language.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Neurodegenerative disease

Alzheimer, Lewy-body, Parkinson-related and frontotemporal pathologies produce characteristic but overlapping cognitive, behavioural, motor and functional trajectories.

Cerebrovascular injury

Large or small infarcts, haemorrhage and chronic small-vessel disease cause executive, gait and focal deficits and often coexist with Alzheimer pathology.

Secondary cognitive disorders

Depression, sleep disorder, alcohol, medicines, thyroid dysfunction, nutritional deficiency, infection, tumour, subdural and normal-pressure hydrocephalus can mimic or compound dementia.

Mixed pathology and vulnerability

Most very old adults have several pathologies; sensory loss, low education, frailty and social isolation influence presentation and test performance without being dementia causes alone.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Progressive network loss
Synaptic dysfunction and neuronal death disrupt memory, executive, visuospatial, language and social-cognitive networks according to disease distribution.
2
Reduced cognitive reserve
Prior brain injury, vascular burden and lower reserve make functional symptoms appear earlier for a given pathological load.
3
Executive-functional coupling
Planning and sequencing failure impairs medicines, money, cooking and navigation before basic self-care, making collateral IADLs central to diagnosis.
4
Stress-sensitive cognition
Illness, sleep loss, pain and unfamiliar environment can transiently expose impairment or provoke delirium without proving a permanent stage change.
5
Behaviour-environment interaction
Distress arises from cognition interacting with unmet needs, communication and care environment rather than from pathology alone.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Amnestic pattern

Repetition and impaired learning of new information with later orientation and navigation difficulty supports Alzheimer-type disease.

Executive-functional pattern

Money, medicines, planning and multitasking fail early despite relatively preserved casual conversation.

Fluctuating visual-motor pattern

Formed hallucinations, cognitive fluctuation, REM-sleep behaviour and spontaneous parkinsonism suggest Lewy-body disease.

Vascular pattern

Stepwise decline, slowed processing, gait disorder and focal signs with vascular history support cerebrovascular contribution.

Rapid or focal changeRed flag

Weeks-to-months progression, seizure or new focal finding requires expedited alternative-disease investigation.

Functional safeguarding signalRed flag

Scams, wandering, unsafe cooking or medication errors require immediate risk mitigation while diagnosis proceeds.

Red flags requiring action

Rapid progression over weeks, seizures, focal deficits, early gait disorder, severe headache or systemic illness requires expedited neurological and medical investigation.
Acute fluctuation or inattention is delirium until assessed, even when family has noticed longer memory difficulty.
Getting lost, unsafe cooking, medication duplication, scams, driving incidents or self-neglect requires immediate functional and safeguarding risk mitigation.
Depression with suicide intent, psychosis, starvation or profound withdrawal needs same-day mental-health and medical review.
A screening score must not be used to infer global incapacity, mandate residential care or remove control of finances.
Strong anticholinergic or sedative burden, alcohol dependence and sensory loss may materially worsen cognition and must be addressed without promising full reversal.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
4AT when acute change existsFirst step
Why
Identify superimposed delirium before dementia interpretation.
Interpretation and limitations
A positive or clinically suspected syndrome triggers urgent cause treatment; repeat persistent cognition after recovery.
02
Collateral cognitive and functional history
Why
Establish decline and phenotype. within a safe older-adult assessment.
Interpretation and limitations
Document onset, trajectory, memory, executive, language, visuospatial, behaviour, IADLs, ADLs and carer input.
03
Validated cognitive tool
Why
Objectively sample cognitive domains. within a safe older-adult assessment.
Interpretation and limitations
Use a complete approved instrument under accessible conditions and interpret with premorbid ability, language, education and function.
04
Medication, mood and sensory assessment
Why
Find modifiable contributors and test barriers.
Interpretation and limitations
Review anticholinergics, sedatives, alcohol, sleep, depression, hearing and vision and change treatment cautiously with follow-up.
05
Blood investigations
Why
Detect common reversible or compounding disease.
Interpretation and limitations
Use FBC, renal, liver, calcium, glucose or HbA1c, thyroid, B12 and folate routinely where appropriate and targeted infection tests by risk.
06
Structural brain imaging
Why
Exclude lesions and support subtype.
Interpretation and limitations
CT or MRI is usual unless established dementia and no management impact; urgent imaging follows rapid, focal, traumatic or pressure features.
07
Specialist biomarker testing
Why
Resolve clinically important subtype uncertainty.
Interpretation and limitations
FDG-PET, dopamine-transporter imaging, CSF or other biomarkers are selected by specialists when the result changes diagnosis or care.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Delirium

Acute onset, fluctuation, inattention and altered arousal indicate an urgent physiological syndrome that may sit on top of chronic dementia.

Depression and anxiety

Low motivation, slowed thinking, rumination and subjective memory concern can mimic cognitive disease; chronology, function and mood assessment separate and identify coexistence.

Sensory or communication impairment

Hearing, vision, aphasia, literacy and language mismatch depress test scores and can create apparent withdrawal or misunderstanding.

Medication, alcohol and sleep effects

Anticholinergics, sedatives, opioids, intoxication, withdrawal and sleep apnoea impair attention and memory and may be partially reversible.

Structural and medical causes

Subdural, tumour, hydrocephalus, thyroid, B12 or folate deficiency, HIV and neurosyphilis are investigated when history, examination or risk supports them.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-line diagnostic sequenceExclude delirium, establish decline and test functionFirst stepFirst linePersistent cognitive concern is raised by the person, carer or clinician.

1Optimise communication, use 4AT if acute change exists and obtain collateral cognition and function chronology.
2Complete validated cognitive, mood, medicine, sensory, neurological and targeted blood assessment.
3Arrange structural imaging and specialist subtype diagnosis unless results would not alter care.

02Reversible-contributor routeTreat without overpromising reversalMedicine, depression, sensory, metabolic or sleep factors may compound decline.

1Confirm the contributor and its plausible functional effect rather than attributing all impairment to one abnormal result.
2Treat or taper safely with monitoring and maintain support for coexisting neurodegenerative disease.
3Repeat cognition and function after an appropriate interval and continue subtype assessment if decline persists.

03Safety and support routeProtect function while preserving autonomyDiagnosis or suspected decline affects real-world tasks.

1Assess medicines, meals, driving, finances, falls, wandering and safeguarding with the person and chosen supporters.
2Use decision-specific capacity assessment, least-restrictive adaptation and carer assessment rather than blanket removal of control.
3Provide a named service contact, advance-planning opportunity and planned review with urgent-change triggers.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Loss of independent function

Medication, finance, transport, meal and personal-care failure increases risk of injury, malnutrition and crisis admission. Anticipatory multidisciplinary prevention and review are therefore important.

Delirium and medical harm

Dementia raises delirium, falls, aspiration and treatment-error risk, especially when pain and illness are communicated atypically.

Safeguarding vulnerability

Scams, exploitation, wandering, self-neglect and dependence on potentially abusive care relationships require proportionate protection. Anticipatory multidisciplinary prevention and review are therefore important.

Carer strain and breakdown

Progressive supervision, sleep loss and behavioural distress affect carer health and can precipitate unsafe crisis placement.

Decision and driving risk

Capacity becomes decision-specific and variable, while navigation, reaction and judgement impairment may require driving cessation and DVLA action.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Follow cognition together with IADLs, ADLs, nutrition, mobility, mood, sensory access and medicine burden; scores alone do not define progression.
Ask carers privately about supervision, sleep and strain and revisit formal support before crisis develops.
Repeat delirium and medical assessment for any abrupt or fluctuating deterioration rather than bringing forward a routine memory review.
Track safety adaptations for medicines, cooking, driving and finances and remove restrictions when capacity or function supports it.
Review diagnostic confidence and subtype when new parkinsonism, hallucination, focal signs or unexpectedly rapid change emerges.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Function makes decline diagnostic

A test result becomes dementia only when acquired cognitive change materially interferes with ordinary life.

Reversible does not mean sole cause

Hearing loss, depression or B12 deficiency may improve while Alzheimer or vascular pathology remains.

Collateral requires specificity

Dated examples of money, medicines and navigation are stronger evidence than a global statement that memory is worse.

Normal screening can mislead

High premorbid ability or executive-predominant disease may produce important decline despite a brief score above threshold.

Dementia is not incapacity

Understanding and weighing are tested for one decision with support, not inferred from diagnosis.

Older brains often have mixed pathology

Subtype labels guide treatment, but vascular and neurodegenerative mechanisms commonly coexist.

11Common pitfallsFrequent interpretation and management errors.

01
Diagnosing dementia from a single screen during delirium, grief or sensory failure.
02
Calling every abnormal blood result the reversible cause and stopping subtype assessment.
03
Using next of kin as an automatic consent proxy or removing finances without capacity assessment.
04
Ignoring IADL decline because basic washing and feeding remain intact.
05
Starting a cognitive enhancer before an indicated subtype and safe prescribing assessment are established.
06
Treating rapid focal deterioration as ordinary progression and delaying neurological investigation.