05 · Cognitive disorders and older adults

5.1 What counts as cognitive impairment?

Cognitive domains

A person may remember a conversation yet be unable to organise a meal or recognise an object. Identify which ability has changed, then its effect on daily life.

Instrumental activities (finances, shopping, cooking, transport and medicines) usually deteriorate before basic activities such as washing, dressing, feeding and toileting. Apparent independence may conceal a partner quietly taking over.

Ageing, mild impairment or dementia?

Memory loss is not compulsory in ICD-11 dementia. Establish acquired cognitive decline and its effect on independence. Delirium, substances and other disorders must be considered as explanations.

MCI may improve, remain stable or progress. Its cause and trajectory matter more than a single annual conversion percentage. Cholinesterase inhibitors and memantine are not routine treatment for undifferentiated MCI.

5.2 Distinguishing delirium, dementia and depression

“Don't know” does not diagnose depression; a confident wrong answer does not diagnose dementia. Depression can coexist with neurodegeneration. Normal blood results do not exclude delirium, and a normal mood questionnaire does not exclude depression.

Delirium: vulnerability plus a precipitant

Dementia, frailty, age and sensory impairment lower the threshold. Common precipitants include infection, hypoxia, dehydration, pain, constipation, urinary retention, metabolic disturbance, surgery, drug toxicity and withdrawal.

• Hyperactive: agitation and restlessness.

• Hypoactive: slowing, withdrawal, poor intake and drowsiness; easily mistaken for depression.

• Mixed: alternation between the two.

Sleep–wake reversal, frightening misperceptions and brief normal-looking periods fit delirium. The 4AT covers alertness, orientation, attention and acute change/fluctuation. It supports clinical diagnosis; CAM-ICU or ICDSC are used in critical care and postoperative recovery. When dementia and delirium are difficult to separate, treat delirium first. Recovery may outlast the precipitating infection; persistence warrants reassessment.

Treatment and drug risks

Treat the precipitant and support hydration, pain control, orientation, sensory input, mobility and sleep. Benzodiazepines may worsen confusion and falls; alcohol or benzodiazepine withdrawal is an important exception.

Haloperidol has a limited role for severe distress or danger when other measures fail. Remember QT prolongation/arrhythmia, parkinsonism, akathisia and dysphagia with aspiration risk. Check ECG and correct electrolyte disturbances. It is contraindicated in Parkinson's disease and DLB.

5.3 The main dementia syndromes

Alzheimer's disease

Failure to learn new information is the usual early pattern: repeated questions, forgotten conversations and poor retention of recent events. Remote memories may survive longer. Language, orientation, recognition, visuospatial skills and personal care deteriorate as disease advances.

Amyloid-beta plaques and tau tangles are the principal pathology. Clinical symptoms and function still determine the syndrome; mixed Alzheimer and vascular pathology is common.

Most cases are not single-gene disorders. Rare familial disease involves APP, PSEN1 or PSEN2, often with young onset across generations. Family history increases risk without making dementia inevitable; a strong young-onset pedigree warrants genetic counselling.

Risk reduction

Control blood pressure, diabetes and cholesterol; address smoking, harmful alcohol use, inactivity and hearing loss; maintain social contact. These support brain health without guaranteeing prevention. Smoking, alcohol, supplements and commercial “memory boosters” are not preventive treatments.

Vascular cognitive impairment

The cognitive syndrome must be plausibly related to cerebrovascular injury. Small-vessel changes on a scan alone do not establish vascular dementia. Decline may follow a stroke, occur in steps or develop gradually.

Executive dysfunction and slowed processing often outweigh early amnesia. Focal signs, gait difficulty, emotional lability and urinary symptoms support a subcortical pattern. Hypertension, diabetes, smoking, atrial fibrillation and previous stroke are risk factors, not proof of causation.

Manage vascular disease and rehabilitation needs. Antiplatelets, anticoagulants and statins require their usual vascular indications. Cognitive medicines are considered for relevant coexisting neurodegenerative disease, not automatically for pure vascular dementia.

Dementia with Lewy bodies

Alpha-synuclein is the pathological association. The four core clinical features are:

• Fluctuating cognition.

• Recurrent, well-formed visual hallucinations.

• REM sleep behaviour disorder: acting out dreams because normal REM paralysis is lost.

• Spontaneous parkinsonism.

Constipation, orthostatic hypotension, syncope and falls are useful supporting clues.

Probable DLB, under the 2017 consensus framework, requires two core features, or one with an indicative biomarker. Reduced striatal dopamine-transporter uptake is one such marker; a normal scan does not conclusively exclude DLB.

The one-year convention: dementia before, alongside or within one year of parkinsonism is DLB; dementia after more than one year of established Parkinson's disease is Parkinson's disease dementia. This classifies closely related disorders rather than defining a biological boundary.

Neuroleptic sensitivity may cause profound rigidity, sedation, reduced consciousness and serious deterioration. Dopaminergic drugs can worsen hallucinations, while reducing them can worsen mobility. Quetiapine and clozapine have selected specialist uses; neither is an uncomplicated “safe” choice.

Frontotemporal dementia

Behavioural-variant FTD causes progressive personality and social-conduct change, often before obvious memory loss. Its six characteristic areas are disinhibition, apathy, loss of empathy, stereotyped/repetitive behaviour, hyperorality/dietary change, and executive impairment with relative early preservation of episodic memory and visuospatial skills.

Under the Rascovsky framework, possible bvFTD requires progression and at least three of these features. Probable bvFTD adds functional decline and supportive imaging. Younger age and preserved memory do not rule dementia out. Mania is more episodic, with altered mood/energy and reduced need for sleep.

Language-led presentations include semantic loss of word/object meanings and non-fluent/agrammatic effortful or grammatically impoverished speech. FTD can overlap with motor neurone disease. Remember C9orf72, GRN and MAPT.

5.4 What investigations can establish

History, change from baseline and lost function establish the clinical problem. MMSE, MoCA and ACE-III describe performance; a score is not a diagnosis. Education, language, sensory loss, anxiety, intellectual disability and acute illness affect results. A high total may conceal executive or focal language impairment.

Blood tests identify contributors such as thyroid dysfunction, vitamin deficiency, anaemia and renal, hepatic or metabolic disease. Structural imaging identifies strokes, atrophy, tumour or subdural collections. Neuropsychology, functional imaging and biomarkers are useful when they resolve meaningful uncertainty. A normal structural scan does not exclude early dementia.

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5.5 Cognitive medicines: mechanism and adverse effects

Before a cholinesterase inhibitor, consider slow pulse, conduction disease, other rate-lowering drugs and falls. New collapse needs assessment. These drugs may improve or stabilise symptoms temporarily; they do not restore lost brain tissue.

APOE testing is not a stand-alone diagnostic or predictive test in routine memory assessment. It can, however, affect anti-amyloid treatment eligibility and safety. Lecanemab is licensed for selected early Alzheimer's with confirmed amyloid and appropriate APOE status. Amyloid-related oedema and haemorrhage are important risks. Licensing and NHS funding are separate; this is not a cure or treatment for every form of MCI.

5.6 Agitation, wandering and hoarding

New behaviour needs a cause. Pain, delirium, constipation, urinary retention, sensory loss, drug effects, frightening care or an unfamiliar environment may explain agitation, aggression, hallucinations or disturbed sleep.

Wandering may follow disorientation, a familiar routine, searching, restlessness or unmet needs. Hoarding can accompany cognitive illness, psychosis or primary hoarding disorder. The latter involves difficulty discarding and distress about disposal, with accumulation compromising living space. Fire, falls, blocked exits, poor nutrition and exploitation are relevant consequences.

Antipsychotics increase stroke and mortality risk in dementia, alongside sedation, postural hypotension, movement and metabolic effects.

Reserve them for risk of harm or severe distress after addressing causes and non-drug measures. Risperidone's licence covers up to six weeks for persistent aggression in moderate–severe Alzheimer's under specified conditions. Review ongoing need at least six-weekly; stop without clear benefit. Valproate is not a treatment for dementia-related agitation unless separately indicated.

5.7 Depression, self-neglect and late-onset mania

Older-adult depression may present as physical complaints, anxiety, slowing, poor appetite, functional loss or hopeless refusal of care. Delusions of guilt, poverty or bodily decay suggest psychotic depression. Passive death wishes and severe self-neglect matter despite denial of active suicidal intent. Bereavement does not exclude depression; apathy does not establish it.

Drug vulnerabilities: SSRIs can cause hyponatraemia, bleeding and falls. Tricyclics can worsen cognition, urinary retention and postural hypotension. New confusion after an antidepressant requires an adverse-effect assessment.

First mania in later life prompts a search for neurological, endocrine or drug causes, including corticosteroids, dopamine agonists and levodopa. Reduced need for sleep, increased activity, pressured speech, grandiosity and expansive/irritable mood support mania. Insomnia with exhaustion alone does not. Delirium adds fluctuating attention/awareness; FTD generally progresses. Coordinate changes to steroids or Parkinson's medicines with the prescribing team.

Dementia does not automatically remove capacity: assess the decision at the time. Notify the DVLA of dementia. Fitness to drive is assessed individually, not decided by a screening score.