dementia Flashcards

1
Q

definition

A
  • Chronically impaired cognition that affects multiple cognitive domains: memory, attention, language, non-cognitive symptoms: agitation, aggression, apathy
  • No impairment of consciousness
  • Acquired and progressive
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2
Q

epidemiology

A

↑s w/ age >80y - 20%

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3
Q

Differentiating dementia from delirium and depression as causes of cognitive impairment

A

Differentiating dementia from delirium and depression as causes of cognitive impairment

Dementia

Delirium

Depression

Conscious state

Alert

Impaired

Alert

Onset

Insidious/gradual

Abrupt

Variable

Course tempo

Gradually progressive

Fluctuant – may be circadian disruption

Fluctuant

Orientation

Initially preserved

Early prominent disorientation

Variable

Hallucinations

Late feature

Prominent

Rare (auditory typically)

Behaviour

Depends on cause

Restless

Withdrawn

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4
Q

classification of dementia

A

young-onset dementia – formerly known as “pre-senile dementia”, refers to patients who develop dementia before the age of 65 years

late-onset dementia – previously known as “senile dementia”, refers to patients who develop dementia after the age of 65 years

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5
Q

non modifiable risk factors

A
  • age – advancing age is the most important risk factor in developing dementia
  • learning disabilities – in people with Down’s syndrome, dementia develops 30–40 years earlier than in a normal person
  • gender – rate of dementia is higher in women than in men (specially for Alzheimers disease)
  • genetic factors
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6
Q

modifiable risk factors

A
  • alcohol consumption
  • smoking – particulary for Alzheimers
  • obesity
  • hypertension
  • hypercholesterolaemia
  • head injury
  • education and mental stimulation
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7
Q

aetiology of dementia

A

The most common causes of dementia are age-related neurodegenerative processes.

Dementia is becoming an increasing problem as the population ages

  • Infection
  • Viral: HIV
  • syphilis
  • Vascular
  • Chronic subdural haematoma
  • Inflammation
  • SLE
  • Sarcoid
  • Neoplasia: meningioma
  • Nutritional
  • Thiamine deficiency (EtOH)
  • B12 and folate deficiency
  • Pellagra (B3 / niacin deficiency)
  • Hypothyroid
  • Hydrocephalus (normal pressure)

Whipple disease

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8
Q

what assessment tools can be used to assess dementia?

A

assessment tools include the

  1. Abbreviated mental test score (AMTS),
  2. 6-Item cognitive impairment test (6CIT),
  3. General practitioner assessment of cognition (GPCOG) and the
  4. mini-mental state examination (MMSE) is widely used.
  • A MMSE score of 24 or less out of 30 suggests dementia
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9
Q

what qs would you ask in a dementia hx

A

he history should be gathered from a person who has known the patient for a period of six months at least and if possible directly from the patient and includes:

  • age
  • medical and psychiatric history of the family e.g. - dementia or other mental health problems (1)
  • origin and progression of condition
  • associations:
  • myoclonus
  • seizures
  • depression, anxiety
  • past and present medical and psychiatric history - e.g. diabetes, hypertension, cerebrovascular accident

exposure to toxins:

  • alcohol
  • lead
  • drugs e.g. barbiturates
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10
Q

how would you examine a pt with dementia?

A

Examination of the demented patient should:

🍭 exclude dysphasia as a cause for apparent dementia

🍭 find information about the patient’s social functioning which would not be normal in dementia

🍭 physical examination – to recognize physical disorders which may be responsible for cognitive impairment

  • cardiovascular system – for evidence of CVA
  • neurological examination – to detect focal deficits, gait abnormalities, speech abnormalities
  • endocrine system – signs of hypothyroidism

🍭 mental state examination – to identify other psychiatric disorders (e.g. – depression) or non-cognitive symptoms that may be associated with dementia (e.g. – delusions, hallucinations) (1)

🍭 cognitive examination – to estimate the extent of how different cognitive domains are affected and should include examination of attention and concentration, orientation, short and long-term memory, praxis, language and executive function. Standardised screening tests used for this purpose include (2)

  • 30-item Mini Mental State Examination (MMSE) – commonly used
  • 6-item Cognitive Impairment Test (6-CIT)
  • the General Practitioner Assessment of Cognition (GPCOG)
  • 7-Minute Screen
  • the clock drawing test – to assess praxis and executive function (1)

🍭 investigations

  • FBC
  • urea and electrolytes
  • blood sugar
  • thyroid and liver function test
  • B12 and folate levels
  • lipid profile (3)
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11
Q

screening ix in dementia

A

Perform a midstream urine test if delirium is a possibility.

🍬 Blood tests:

  • FBC, ESR, CRP - anaemia, vasculitis
  • T4 and TSH - hypothyroidism
  • biochemical screen - hypercalcium or hypocalcaemia
  • urea and creatinine - renal failure, dialysis dementia
  • glucose
  • B12 and folate - vitamin deficiency dementia
  • clotting and albumin - liver function

🍬 Other possible blood tests (though not routinely requested in primary care) include:

  • syphilis serology
  • HIV - if in young person
  • caeruloplasmin - Wilson’s disease

🍬 Conduct investigations such as chest X-ray or (ECG) as determined by clinical presentation.

🍬 Other possible specialist investigations include:

  • Genetic testing – can be offered to patients or to their unaffected relatives if a genetic cause is suspected
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12
Q

mx of dementia

A

A valid consent should be obtained from the patient before starting management. If the patient lacks the capacity to make any decisions on their own, the provisions of the Mental Capacity Act 2005 should be followed

It is sometimes desirable to admit the patient for observation and investigation with blood tests, CSF analysis and brain imaging. The tests can be performed as an outpatient but several visits should be arranged to permit repeated assessment.

Also patients should be offered written information and advice about

  • signs and symptoms of dementia
  • course and prognosis of the disease
  • treatments
  • local care and support services
  • support groups
  • sources of financial and legal advice and advocacy
  • medico-legal issues, including driving
  • local information sources, including libraries and voluntary organizations

Interventions in dementia can be aimed at

  • cognitive symptoms
  • noncognitive symptoms and challenging behavior
  • reduction of comorbid emotional disorders
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13
Q

alzheimer’s

A

Epidemiology

  • Slightly more common in females.
  • The most common cause of dementia in the UK, accounts for about half of all dementia diagnoses.

Pathophysiology

  • REMEMBER THESE TWO: Amyloid plaques + Neurofibrillary tangles.
  • Amyloid plaques: clumps of beta amyloid and degenerating bits of neurons and other cells which lurk in between nerve cells.
  • Neurofibrillary tangles: bundles of twisty filaments within neurons, mostly made from tau protein.
  • The accumulation of these leads reduction in transmission of information, and eventually to death of brain cells, with abnormal depositions remaining post-mortem.

Symptoms

  • Usually begin after the age of 60 (though there are “early-onset” cases, most of which involve genetics).
  • Can affect all areas of the brain: many functions and abilities can be impacted upon and eventually lost.
  • Most common presenting symptom is memory loss, with evidence of varying changes in planning, reasoning, speech and orientation.

General progression

  • Alzheimer’s dementia tends to progress steadily over time.
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14
Q

vascular dementia

A

Epidemiology

  • More common in males, generally thought to be due to their increased risk of vascular disease.
  • Second most common type of dementia. Increased prevalence in those who have had a stroke (9x higher than the general population).

Pathophysiology

  • There are several subtypes of vascular dementia, the most common of which are multiple (commonly small) cerebrovascular infarcts, small vessel disease and a single cerebrovascular accident.
  • The most commonly affected areas of the brain are the white matter of both cerebral hemispheres, grey nuclei, thalamus and the striatum.
  • Hypertension is a major risk factor for diffuse vascular dementia. Other general “vascular” risk factors increase the chances of developing vascular dementia and can increase cognitive decline – smoking, diabetes mellitus, hyperlipidaemia, obesity, hypercholesterolaemia etc.

Symptoms

  • Single infarct vascular disease: classically cognitive impairment (acutely or subacutely) following the event.
  • Functional deficits are often seen before memory impairment.
  • Mood disturbances and mood disorders are common in vascular dementia
  • Psychosis, delusions, hallucinations and paranoia can often be seen, especially in later stages.
  • Patients should be screened for depression and for signs of psychomotor retardation (often a more common feature than positive signs of depression).
  • Emotional lability can be prominent.

General progression

  • ‘Stepwise’ – often shows a period of stability at one level of functioning, before an acute decline progression, followed by another period of stability. There is little way to predict how quickly (or when) these declines will occur.
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15
Q

Lewy-Body dementia

A

Epidemiology

  • Appears to affect slightly more men than women. Mostly affects those over the age of 50.

Pathophysiology

  • Spherical “Lewy Body” proteins are deposited in the brain (alpha-synuclein for those who love the science words). These Lewy Bodies are also present in Parkinsons – the difference being that in Parkinsons they are mainly deposited in the substantia nigra, whereas they are more widespread in Lewy-Body dementia.

Symptoms

  • Often involves visual hallucination and Parkinson-like symptoms.
  • If physical symptoms precede cognitive decline by more than a year, the diagnosis is often Parkinsons, with superimposed cognitive decline.
  • Fluctuation in cognitive ability is common.
  • At presentation, problems multitasking and performing complex cognitive actions are more likely to be issues than memory.
  • Sleep disorders are a common manifestation.

General progression

  • Fairly rapidly progressive, with death most commonly in the first 7 years post-diagnosis.
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16
Q

Mixed

A

Mixed dementia is exactly what it says on the tin.

This is diagnosed when patients have evidence of more than one type of dementia (often Alzheimers and vascular dementia) based upon clinical or neuroimaging evidence.

17
Q

Frontotemporal dementia (including Pick’s)

A

Epidemiology

  • Much less common type, but responsible for a significant number of diagnoses of dementia in under 65s.
  • Tends to affect both sexes equally.
  • There are several types of frontotemporal dementia, one of which is Pick’s disease, but often all frontotemporal dementias are mislabelled Pick’s.

Pathophysiology

  • Neuron damage and death in the frontal and temporal lobes (funnily enough…). The atrophy is due to deposition of abnormal proteins (often tau protein) within the lobes. There is thought to be a genetic component in about a quarter of cases.

Symptoms

  • Tend to present with one of three clinical pictures (or an overlap): changes in personality and behaviour (which may be labelled psychiatric), or as progressive language difficulty and aphasia.
  • Behavioural presentation
  • Altered emotional responsiveness, apathy, disinhibition, impulsivity. Progressive decline noted in interpersonal skills. Changes in food preference, more childlike amusements. Obsessions and rituals may also be noted.

Semantic presentation

Progressive decline in the understanding of word meanings. Speech may still be fluent, but there is difficulty in name-retrieval and use of less precise terms. Are unable to determine the meanings of common words when asked. This tends to develop into the inability to recognise objects, or familiar faces (prosopagnosia).

Non-fluent presentation

Progressive breakdown in the output of language. Speech takes effort and is not fluent. Generally display speech apraxia (poor articulation) or disorders of speech sound. There also tends to be impaired comprehension of sentences and an impact on literacy skills.

Over time, all three initial presentations tend to emerge and worsen. There is also evidence for the development of motor disorders either before or alongside these symptoms.

General progression

There is great variation in progression, but average life expectancy is 8 years post-diagnosis.

18
Q

Quick notes on some differentials!

A

Prion Protein Diseases (focussing on Creutzfeldt-Jakob Disease)

Infectious prion proteins cause diseases such as Creutzfeldt-Jakob disease (CJD).

This can be sporadic or ‘variant’. Sporadic CJD tends to affect over 40s and is a one in a million occurrence. Variant CJD is caused by eating meat infected by bovine spongiform encephalopathy through eating infected cattle meat.

The disease can be indolent for many years. To begin with it may present as minor memory lapses, mood disturbance and loss of interest. This quickly (over weeks) becomes more prominent and is followed by unsteadiness and physical clumsiness. Progression then involves stiffness, jerking movements, incontinence and aphasia. Death usually occurs within 6 months of symptom presentation.

HIV-related Cognitive Impairment/Dementia

Almost half of all people with HIV experience some symptoms relating to their brain, which can include mild cognitive impairment and dementias.

With the use of antiretrovirals around 2% will still go on to develop dementia.

Milder cognitive impairment can be caused indirectly (by a weakened immune system leaving the brain more vulnerable) or directly by the virus.

Symptoms can include short-term memory problems, issues with concentration, thinking and language skills. Mood disturbance is very common and makes the diagnosis more difficult to differentiate from depressive episodes.

Normal Pressure Hydrocephalus

Pathophysiology

Abnormal build-up of cerebrospinal fluid in the ventricles causes pressure to increase in the brain tissue, producing symptoms of cognitive impairment.

Can occur at any age, but more common in the elderly. Other factors which increase the likelihood of development include head trauma, infection or inflammation in the brain, tumour, subarachnoid haemorrhage.

Symptoms

Progressively worsening memory lapses, personality and mood disturbances, difficulties with walking, dementia, urinary incontinence.

Management

To treat normal pressure hydrocephalus, a shunt is surgically placed to drain excess CSF into the abdomen. This relieves the pressure on the brain. Success of treatment depends on prompt diagnosis and treatment; some may make an almost complete recovery.

Severe Depression

Severe depression can involve cognitive impairment, and can masquerade as the early stages of dementia.

“Mild Cognitive Impairment”

The term given to people with problems with memory or higher cortical thinking, not severe enough to interfere with everyday life.

Mild cognitive impairment can be caused by a range of circumstances and conditions. Each year, 10-15% will go on to develop a form of clinical dementia. Other causes of cognitive impairment can include stroke, depression, stress, physical illness and drug side-effects – due to this, many with mild impairment may never go on to develop dementia, and some may even completely recover.

19
Q

Part of brain: Associated function

A

Frontal lobe: Problem-solving, emotions, reasoning, planning, personality. Site of many inhibitory functions.Primary Motor Cortex: generates voluntary movements of muscles.Broca’s area: (usually left) postero-inferior part of frontal cortex, involved with motor aspects of speaking.

Temporal lobe: Perception/recognition of auditory stimuli, memory, speech.Contains Wernicke’s area – helps formulation/understanding of speech.

Parietal lobe: Recognition, movement, orientation, perception.Primary Sensory cortex: processes sensory stimuli.

Occipital lobe: Visual processing

Cerebellum: Posture, balance and co-ordination of movement