Clinical literacy companion

Dementia and Cognitive Change

Recognition, differentiation and liaison context

Dementia in brief

Dementia describes cognitive and behavioural symptoms caused by diseases affecting the brain. It is not one disease and is not an inevitable part of ageing.

It can affect memory, reasoning, communication, perception, mood, behaviour and the ability to manage everyday activities. Dementia is progressive, but its pattern and pace vary.

Main presenting types

  • Alzheimer’s disease
  • Vascular dementia and vascular cognitive impairment
  • Dementia with Lewy bodies
  • Frontotemporal dementia

Mixed presentations

More than one disease process can be present. Alzheimer’s disease with vascular disease is a common mixed pattern.

Subtype patterns help recognition; they are not fixed diagnostic rules.

Sources: NICE NG97 — About this guideline; NHS — Symptoms of dementia; NHS — Causes of dementia.

Ageing, dementia and delirium

PresentationPattern that may be seenWhat keeps the picture open
Ordinary ageingTaking longer to learn something new, occasionally losing a word or misplacing an item and later retracing the steps.A sustained change from previous ability that increasingly affects familiar daily tasks is more concerning than an isolated lapse.
DementiaProgressive cognitive or behavioural change with functional effect; the particular pattern varies by disease and person.Mood, anxiety, physical illness, medicines, sensory needs and social context may influence the presentation.
DeliriumRecent change over hours or days, fluctuation, altered attention or arousal, perceptual change, restlessness or unusual withdrawal.Dementia and delirium can coexist. One cognitive score does not reliably separate delirium superimposed on dementia.
Resolving deliriumConfusion and cognitive difficulty may persist while the acute episode improves.Persistence after the most obvious acute features settle does not by itself confirm dementia. Baseline and trajectory remain central.

These are illustrative patterns, not diagnostic thresholds.

Sources: Alzheimer’s Society — Memory problems and dementia; NICE CG103 — Delirium; NICE NG97 — Recommendations.

Alzheimer’s disease

What is happening in the brain

Alzheimer’s disease is associated with abnormal amyloid protein forming plaques around brain cells and tau protein forming tangles within them. These changes disrupt communication between nerve cells and progressively damage brain tissue. The exact trigger is not known, and the process begins years before symptoms become obvious.

Source: NHS — Causes of Alzheimer’s disease.

Onset, presentation and distinguishing pattern

The onset is usually insidious and the change develops gradually over years. Recent-event memory and difficulty learning new information are often prominent early features because memory-related brain regions are commonly affected first.

Possible presentation includes repeated questions, losing track of recent events, word-finding difficulty, difficulty organising familiar tasks, disorientation in unfamiliar places and increasing difficulty with numbers or money. Other presentations occur and the rate and sequence vary between people.

Compared with vascular dementia, decline is more often steadily progressive than abrupt or stepwise. Early recurrent visual hallucinations, marked fluctuations or Parkinsonian movement are more characteristic of dementia with Lewy bodies; early personality, behavioural or language change is more characteristic of frontotemporal dementia. Mixed Alzheimer’s and vascular disease is common.

Sources: NHS — Symptoms of Alzheimer’s disease; NHS — Symptoms of vascular dementia; NHS inform — Dementia with Lewy bodies.

Treatment context

There is currently no cure. Donepezil, galantamine and rivastigmine are acetylcholinesterase inhibitors used for mild to moderate Alzheimer’s disease. They slow the breakdown of acetylcholine, allowing this chemical messenger to remain available for longer and improving communication between surviving nerve cells. For some people this temporarily helps symptoms such as recent forgetfulness, confusion, slowed thinking, difficulty following familiar tasks or difficulty understanding more complicated information.

Memantine is used in specified moderate or severe Alzheimer’s disease circumstances. It blocks the effects of excessive glutamate, which can further damage vulnerable nerve cells. For some people it can help memory, confusion, thinking speed, anxiety or coping with daily activities. Response varies, and neither medicine type stops the underlying disease process.

Sources: NICE NG97 — Pharmacological management; NHS — Treatment of Alzheimer’s disease; NHS — How donepezil works; NHS — How memantine works.

Vascular dementia and post-stroke cognitive change

What it is
Cognitive change related to disease or injury affecting the brain’s blood supply. It may follow small-vessel disease, one stroke or several strokes.
Onset and course
Change may be sudden after a stroke, gradual with small-vessel disease, or progress in distinct steps or “step downs” as further vascular injury occurs.
Possible presentation
Attention, processing speed, planning, reasoning and concentration may be more prominent than memory early on.
Associated features
Mood change, altered gait or focal neurological change may coexist.
Distinguishing pattern
A close relationship to stroke or vascular disease, focal neurological features and abrupt or stepwise change support a vascular pattern more than the steadily progressive recent-memory pattern commonly seen in Alzheimer’s disease.
Treatment context
Management is centred on vascular disease and stroke prevention. NICE limits consideration of acetylcholinesterase inhibitors or memantine in vascular dementia to situations where comorbid Alzheimer’s disease, Parkinson’s disease dementia or dementia with Lewy bodies is suspected.

Sources: NHS — Symptoms of vascular dementia; Stroke Association — Memory and thinking after stroke; NICE NG97 — Pharmacological management.

Dementia with Lewy bodies

What it is
Lewy bodies are abnormal clumps of alpha-synuclein protein that develop inside nerve cells. They disrupt chemical signalling and connections in brain areas involved in thinking, perception, movement and sleep. The reason they form is not fully understood, and Lewy body and Alzheimer-type changes can coexist.
Onset and course
Symptoms usually develop gradually and worsen over time, but day-to-day or hour-to-hour variation can be much more marked than in Alzheimer’s disease.
Cognitive pattern
Marked variation in alertness or confusion may occur alongside other cognitive difficulty.
Perception
Recurrent visual hallucinations are a recognised feature.
Physical context
Slowed or stiff movement, falls or fainting and disturbed sleep may be present.
Overlap
Fluctuation and hallucinations also occur in delirium and other conditions, so time course and context remain important.
Medication relevance
Antipsychotics can worsen motor features and can sometimes cause severe sensitivity reactions in dementia with Lewy bodies. Their presence on a medication chart does not necessarily mean the diagnosis has been overlooked: where agitation, hallucinations, delusions or risk are severe, prescribers may have weighed the possible benefit against those additional harms in the context of the individual presentation.

Sources: NHS inform — Dementia with Lewy bodies; Alzheimer’s Society — What is dementia with Lewy bodies?; NICE NG97 — Recommendations.

Frontotemporal dementia

What it is
Frontotemporal dementia is caused by progressive damage to the frontal and temporal lobes. Abnormal proteins accumulate within brain cells, disrupting their function and eventually causing cell loss. These regions are strongly involved in behaviour, personality, decision-making and language.
Onset and course
The change is usually gradual. It commonly begins at a younger age than Alzheimer’s disease, although it can occur later in life.
Typical early pattern
Behaviour, personality, social awareness, motivation or language may change before memory becomes prominent.
Behavioural features
Loss of tact or inhibition, apathy, altered eating patterns or repetitive behaviour may occur.
Language features
Difficulty producing speech or understanding words may be central to the presentation.
Distinguishing pattern
Early behavioural disinhibition, apathy, loss of empathy, repetitive behaviour or progressive language difficulty is more characteristic than the early recent-memory pattern of Alzheimer’s disease.
Treatment context
There is no medicine that slows frontotemporal degeneration. NICE does not recommend acetylcholinesterase inhibitors or memantine for frontotemporal dementia.

Sources: NHS — Symptoms of dementia; NHS — Frontotemporal dementia.

BPSD, distress and personhood

BPSD is an umbrella term for psychological experiences and observable behaviours that can occur in dementia. These include agitation, anxiety, low mood, apathy, disturbed sleep, wandering, calling out, aggression, hallucinations, delusions and changes in eating or sexual behaviour. The term describes a presentation; it does not identify its cause.

Context and meaning

Distress or behavioural change can reflect the dementia itself, but can also be shaped by pain, delirium, medicine effects, communication difficulty, sensory impairment, fear, an unfamiliar environment, disrupted routine or an unmet physical or emotional need. The same outward behaviour can therefore have different meanings in different people.

Source: NICE NG97 — Managing non-cognitive symptoms.

Seeing distress from the person’s perspective

Dementia educator Teepa Snow demonstrates how behaviour that appears challenging can be reconsidered by recognising distress, communication and unmet need from the person’s point of view.

Video: Teepa Snow — Challenging Behaviors and Dementia.

Medication evidence

Medication does not provide a general solution to BPSD. NICE reserves antipsychotic treatment in dementia for situations involving risk of harm or severe distress linked to agitation, hallucinations or delusions. Trial evidence shows modest benefit for some symptoms alongside increased risks, including stroke and death. People with dementia with Lewy bodies can have particularly severe sensitivity reactions to antipsychotics.

Sources: NICE NG97 — Antipsychotic medicines in dementia; NICE — Antipsychotic decision aid evidence.

What the Memory Assessment Service does

Memory Assessment Services are specialist multidisciplinary services for people with cognitive concerns. Their role can include specialist assessment, diagnosis and subtype clarification, relevant investigations, access to treatment and post-diagnostic information or support.

Diagnosis is not restricted to one named clinic

NICE describes referral to a specialist dementia diagnostic service, which may be a memory clinic, community old age psychiatry service or another appropriately configured specialist service. Dementia specialists can include psychiatrists, geriatricians, neurologists and other clinicians with specialist expertise in dementia assessment and diagnosis, including appropriately skilled GPs, nurse consultants and advanced nurse practitioners. The central requirement is specialist dementia expertise, not the title “Memory Assessment Service”.

Source: NICE NG97 — Dementia diagnosis and specialist services.

Typical multidisciplinary team

Local teams vary, but commonly include:

  • Consultant psychiatrists or other specialist doctors
  • Specialist nurses or advanced practitioners
  • Clinical psychologists
  • Occupational therapists
  • Support workers or psychology assistants
  • Administrative staff

Some services also include geriatric, neurological, speech and language, social-care or third-sector input.

Sources: NHS England — Dementia implementation guide; Birmingham and Solihull Mental Health NHS Foundation Trust — Memory Assessment Service; Humber Teaching NHS Foundation Trust — Memory Assessment Service team.