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PSYCHIATRY > MEMORY PROBLEMS AND CONFUSION > Flashcards

MEMORY PROBLEMS AND CONFUSION Flashcards

1
Q

What is cognition?

A

all the mental activities that allow us to perceive, integrate and conceptualise the world around us. These include attention, concentration, memory, orientation, reading, writing, calculation, comprehension, learning, language, judgement, reasoning and visuospatial ability.

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2
Q

What is conciousness?

A

to be conscious is to be aware, both of objects that are perceivable and of oneself as a subjective being. It’s said to be normal, heightened or lowered

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3
Q

What can cause heightened conciousness?

A

psychoactive stimulants, hallucinogens or it may be seen in early mania.

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4
Q

Outline the continuum of conciousness?

A

Clear conciousness
Clouding of conciousness
Coma

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5
Q

What is confusion?

A

when thinking lacks normal clarity and coherence and it can occur in a state of normal or impaired conciousness.

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6
Q

What is stupor?

A

clinical presentation of akinesis, mutism and extreme unresponsiveness in an otherwise alert patient

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7
Q

What can cause stupor?

A

Schizophrenia, depression, mania, dissociative stages, dementia, delirium, cerebral tumours or cysts, neurosyphilis, encephalitis, post-ictal states.

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8
Q

What is sensory/immediate memory?

A

held fro less than a second, unprocessed, in the form that it was perceived by the sense organ. This allows the brain time to process the vast amount of visual (iconic), auditory (echoic) and touch (haptic) input it receives every second.

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9
Q

What is primary memory?

A

Short term - once immediate memory has been attended to it may be transferred to a temporary memory store which has a limited capacity for 7+/- 2 items at a time. This will be forgotten in 15-30 seconds if it is not rehearsed or converted to long term memory. This is tested clinically with the digit span test.

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10
Q

What is secondary memory?

A

can be recent that refer to memories stored minutes/hours/days/weeks/months ago, or remote which refers to memories stored years/decades ago. Long term memory stored may be explicit (stored memory which the individual is conciously aware of and can declare to others) or implicit (material stored without the individuals conscious awareness e.g. ability to ride a bike).

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11
Q

How do we test remote memory?

A

ask about important events that occurred decades ago and correlate with collateral history

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12
Q

How do you test recent memory?

A

ask patients about events over the past few days e.g. what they had for breakfast

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13
Q

How do you test anterograde memory?

A

ask patients to commit an unfamiliar name and address to memory; test and recall 3-5 minutes later after interposition of other cognitive tests.

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14
Q

What is amnesia?

A

loss of the ability to store new memories or retrieve memories that have previously been stored.

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15
Q

What is anterograde amnesia?

A

occurs after an amnesia-causing event and results in the patient being unable to store new memories and from the event outwards, although the ability to retrieve memories stored before the event may remain unimpaired.

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16
Q

Damage to which area of the brain usually causes anterograde amnesia?

A

medial temporal lobes, especially the hippocampal formation.

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17
Q

What is retrograde amnesia?

A

occurs after an amnesia-causing event and results in the patient being unable to retrieve memories stored before the event, although the ability to store new memories from the event onwards may remain unaffected.

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18
Q

Which area of the brain is usually damaged in retrograde amnesia?

A

frontal or temporal cortex.

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19
Q

What is dementia?

A

An acquired syndrome characterised by a global impairment of one or more cognitive functions without an impairment of conciousness.
It’s irreversible and chronic in course. T
here needs to be an impact on daily functioning related to a decline in the ability to judge, think, plan and organise.
There is an associated change in behaviour such as emotional lability, irritability, apathy or coarsening of social skills.
There must be evidence of decline over time (months or years rather than days or weeks) to make a diagnosis of dementia.

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20
Q

Whats the epidemiology of dementia?

A

5% over 65 and 20% over 80s.

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21
Q

What is mild cognitive impairment?

A

Mild cognitive impairment (MCI) is a condition in which someone impairment in 1 cognitive functioning but it is not severe enough to interfere with their daily life

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22
Q

Whats the incidence of mild cognitive impairment?

A

5-25% of those over 65

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23
Q

What 3 general categories of impairment occur in dementia?

A

Cognitive impairment
Behavioural and psychological impairment
Diffiuclties with ADLs

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24
Q

What cognitive impairments occur in dementia?

A

Memory loss
Problems with reasoning and communication
Difficulty in making decisions
Dysphasia
Difficulty in carrying out coordinated movements e.g. dressing
Disorientation and unawareness of time and place
Impairment of executive function e.g. planning, judgement, problem solving

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25
Q

What behaviours and psychoglocial impairments occur in dementia?

A

Psychosis — the person may have delusions (which may be persecutory) and/or hallucinations (visual and auditory).
Agitation and emotional lability
Depression and anxiety
Withdrawal or apathy.
Personality changes
Disinhibition (socially/sexually)
Motor disturbance — wandering, restlessness, pacing, and repetitive activity may be reported.
Sleep cycle disturbance or insomnia.
Tendency to repeat phrases or questions.

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26
Q

When is depressiona. Warning sign for dementia?

A

When the onset of depression is later in life

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27
Q

Outline how dementia can affect ADLs?

A

In the early stages of dementia this may lead to difficulty carrying out complex household tasks.
In the later stages, basic ADLs such as bathing, toileting, eating, and walking become affected.

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28
Q

What is dysphasia?

A

a condition that affects your ability to produce and understand spoken language. Dysphasia can also cause reading, writing, and gesturing impairments.
(The areas of the brain responsible for turning thoughts into spoken language are damaged and can’t function properly)

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29
Q

Whats the most common cause of brain damage that leads to dysphasia?

A

Strokes

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30
Q

What is aphasia?

A

complete loss of speech and comprehension abilities.
Dysphasia, on the other hand, only involves moderate language impairments.

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31
Q

What is echolalia?

A

The repetition or echoing of words or sounds that you hear someone else say

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32
Q

What is palilalia?

A

Spontaneous repetitions of ones own words

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33
Q

What is apraxia?

A

Loss of ability to carry out skilled motor movements despite an intact motor and sensory functions

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34
Q

What is agnosia?

A

Loss of ability to recognise or identify previously familiar objects or people despite intact sensory functioning

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35
Q

What is senile dementia?

A

Late onset
When it presents over the age of 65

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36
Q

What is pre-senile dementia?

A

When it presents <65

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37
Q

What are non-modifiable risk factors for dementia?

A

• older age
• Mild cognitive impairment
• Learning disabilities - particularly Down’s syndrome
• Genetics
• CVD / risk factors for cardiovascular disease
• Cerebrovascular disease
• Parkinson’s disease

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38
Q

What proportion of those with mild cognitive impairment will go on to develop dementia within 3 years?

A

1/3rd

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39
Q

What proportion of those with LD over 65 will meet the diagnostic criteria for dementia?

A

20%

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40
Q

What proportion of those with Down syndrome over 60 will meet the criteria for dementia?

A

75%

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41
Q

Whats the risk of dementia in Parkinson’s disease patients?

A

5 x higher
75% after 10 years diagnosis

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42
Q

What are modifiable risk factors for dementia?

A

• lower educational attainment - high levels of education, more mentally damaging jobs and cognitive stimulation are associated with a lower risk of developing dementia
• Hypertension
• Hearing impairment - cognitive decline through reduced cognitive stimulation
• Smoking
• Obesity
• Depression
• Physical activity
• Diabetes in middle/later life increases risk by 50%
• Low social engagement and support
• Moderate alcohol consumption may protect but high alcohol consumption has increased risk
• TBI
• Air pollution

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43
Q

How much does smoking increase the risk of dementia?

A

50-80% increase

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44
Q

What are the types of dementia?

A

Alzheimers
Frontotemporal
Lewy body
Vascular
Mixed
Secondary dementia

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45
Q

What can cause secondary dementia?

A

Parkinson’s, huntington’s and MS
Structural lesion - normal pressure hydrocephalus, subdural haematomas, brain tumours
Trauma
Infections - HIV, neurosyphilis, viral encephalitis
Endocrine diseases - Hypothyroidism, hypoparathyroidism, adrenal and pituitary gland diseases and Insulinoma
Nutritional deficiencies - thiamine, B12, folate or niacin deficiency
Alcohol and drugs
Infectious diseases - meningitis, cerebral abscesses, neurosyphilis, whipples disease, Lyme disease and AIDS, Creutzfeldt-Jakob disease
vascular diseases - SLE, vasculitis and sarcoidosis
Cognitive disorders due to psychiatric diseases, particularly depression and late-onset schizophrenia.
Medication side effects

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46
Q

How do we diagnose dementia?

A

History
Collateral history
Assess cognition using a cognitive assessment tools
Physical examination to look for possible causes/ focal neurological signs/ vision and auditory signs/ CVD signs
Blood tests/urine microscopy/ U&Es/ECG/syphilis serology/HIV testing
Imaging - CT/MRI
CSF examination

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47
Q

What blood tests should you order when considering dementia?

A

FBC, ESR, CRP, U&E, calcium, HBA1c, LFT, TFT, serum B12 and folate

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48
Q

What are examples of cognitive assessment tools?

A

10 point cognitive screener
6-item cognitive impairment test
6 item screener
Memory impairment screen
Mini-cog
Test your memory self-administered test

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49
Q

What are typical CT appearances of the brain in normal ageing?

A

Progressive cortical atrophy and increasing ventricular size

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50
Q

What are typical CT appearances of the brain in alzheimers?

A

Generalized cerebral atrophy
Widened sulci
Dilated ventricles
Thinning of the width of medial temporal lobe

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51
Q

What are typical CT appearances of the brain in vascular dementia?

A

Single/multiple ares of infarction
Cerebral atrophy
Dilated ventricles

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52
Q

What are typical CT appearances of the brain in Frontotemporal dementia?

A

Greater relative atrophy of frontal and temporal lobes
Knife-blade atrophy

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53
Q

How do we manage mild cognitive impairment?

A

discuss diagnoses, arrange regular follow-up visit to monitor possible progression and if symptoms deteriorate refer for specialist assessment and management.
Suggest brain activities e.g. word games and regular exercise

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54
Q

What should you do if you suspect rapidly progressive dementia?

A

Refer to neurological service
They can test for CJD and similar conditions

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55
Q

When should you admit someone with dementia/

A

If they are severely disturbed

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56
Q

When should you refer someone to a specialist diagnostic service e.g. a memory clinic or community old age psychiatry service?

A

If Reversible causes of cognitive decline have been investigated and dementia is still suspected

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57
Q

What are the rules of driving when you have dementia?

A

must notify DVLA when you have mild cognitive impairment, dementia, any organic syndrome affecting cognitive functioning. DVLA will decide if you can drive or not.

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58
Q

How do you manage dementia non-pharmacologically?

A

• cognitive stimulation therapy - a range of activities and discussions (usually in a group) that are aimed at general improvement of cognitive and social functioning.
• Group reminiscence therapy - this uses objects from daily life to stimulate memory and enable people to value their experiences
• Cognitive rehab or occupational therapy to support functional ability - the aim is to addresses the disability resulting from the impact of cognitive impairment on everyday functioning and activity by identifying goals that are relevant to the person

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59
Q

What are pharmacological treatment options for mild-moderate alzheimers?

A

Acetylcholinesterase inhibitors
Memantine if above not possible

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60
Q

How should you treat severe alzheimers pharmacologically?

A

Memantine

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61
Q

How should you treat Lewy body dementia?

A

Non-pharmacologically as no pharm methods are licensed
But some use Acetylcholinesterase inhibitors or memantine

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62
Q

When do we use acetylcholinesterase inhibitors and memantine for vascular dementia?

A

I if the person has suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia or dementia with Lewy bodies (unlicensed)

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63
Q

How is alzheimers classified as mild, moderate and severe?

A

mild Alzheimer’s disease: MMSE 21–26
moderate Alzheimer’s disease: MMSE 10–20
moderately severe Alzheimer’s disease: MMSE 10–14
severe Alzheimer’s disease: MMSE < 10.

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64
Q

When can antipsychotics or benzodiazepines be used to treat dementia?

A

When the pt has disturbed behaviour e.g. aggression

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65
Q

Why should benzodiazepines be used with caution in pt with dementia?

A

due to their vulnerability to adverse side effects such as sedation, increased risk of falls, worsening cognition and marked confusion

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66
Q

When should antipsychotics or antidepressants be used in dementia?

A

When there is psychosis or concurrent depression

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67
Q

Why do you have to be careful giving antipsychotics to pt with Lewy body dementia?

A

They have severe neuroleptic sensitivity - 50% of patients with low body dementia will have a catastrophic reaction to antipsychotics precipitating worsening irreversible parkinsonism, sedation, immobility, or even neuroleptic malignant syndrome and a 2-3x increased risk of mortality

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68
Q

What is neuroleptic maligannt syndrome?

A

a life-threatening neurologic emergency caused by an adverse reaction to medications with dopamine receptor-antagonist properties or the rapid withdrawal of dopaminergic medications.

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69
Q

What are the symptoms of neuroleptic maligannt syndrome

A

very high fever, irregular pulse, tachycardia, tachypnea, muscle rigidity, altered mental status, autonomic nervous system dysfunction resulting in high or low blood pressure, profuse perspiration, and excessive sweating.

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70
Q

Whats the pathology behind neuroleptic maligannt syndrome?

A

Disruption of the regulatory systems in the brainstem has been linked to the systemic hypermetabolic syndrome
central dopamine blockade has been linked to hyperthermia and signs of dysautonomia
nigrostriatal dopamine blockade has been linked to rigidity and tremor

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71
Q

What can cause neuroleptic malignant syndrome

A

Potent typical neuroleptics such as haloperidol, fluphenazine, chlorpromazine, trifluoperazine, and prochlorperazine have been most frequently associated with NMS and thought to confer the greatest risk.
Although atypical neuroleptics appear to have reduced the risk of developing NMS compared to typical neuroleptics, a significant number of cases have been reported with most atypical neuroleptics including risperidone, clozapine, quetiapine, olanzapine, ariprazole and ziprasidone.

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72
Q

Which dementia has the worst prognosis?

A

Creutzfeldt-Jakob disease - 70% die within a year

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73
Q

Whats the prognosis of alzheimers?

A

8-10 years

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74
Q

Whats the prognosis of vascular dementia?

A

About 5 years

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75
Q

Whats the prognosis of frontotemporal dementia?

A

8-11 years

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76
Q

How does alzheimers present?

A

Loss of recent memory first and difficulty with executive function and/or nominal dysphasia
Loss of episodic memory - memory loss for recent events
repeated questioning and difficulty learning new information
Cognitive deficits may include aphasia, apraxia and agnosia

(Amnesia, apraxia, agnosia, aphasia and anomia)

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77
Q

How does vascular dementia present?

A

Stepwise increases in severity of symptoms
Symptoms are affected cortical area-dependant:
- frontal - executive functions
- left parietal - aphasia, apraxia and agnosia
- right parietal - hemineglect, confusion, agitation, visuospatial difficulty
- temporal - anterograde amnesia

Deficits due to subcortical infarcts aka small vessel disease:
- Focal neurological signs e.g. hemiparesis or visual field defects
- Gait disturbances
- urinary frequency and urgency
- personality and mood change
- relatively mild memory deficit

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78
Q

How does Lewy body dementia present?

A

Fluctuating cognition
recurrent visual hallucinations
REM sleep behaviour disorder
one or more symptoms of parkinsonism: disorder; bradykinesia, rest tremor, or rigidity.
Memory impairment may not be apparent in early stages

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79
Q

How does frontotemporal dementia present?

A

Personality change and behavioural disturbance (such as apathy or disinhibition) may develop insidiously.
Language and speech problems
Other cognitive functions (such as memory and perception) may be relatively preserved.

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80
Q

What age does Alzheimer’s disease usually present?

A

> 65 if senile
30-60 if presenile

81
Q

What age does Frontotemporal dementia usually present?

A

45-64

82
Q

What age does Lewy body dementia usually present?

A

> 50

83
Q

What age does vascular dementia usually present?

A

> 65

84
Q

What are the 4 types of alzheimers as classified by ICD10?

A

Dementia in Alzheimer’s disease
Dementia in Alzheimer’s disease with early onset
Dementia in Alzheimer’s disease with late onset
Dementia in Alzheimer’s disease atypical or mixed type

85
Q

What are examples of cortical dementia?

A

Alzheimer’s disease
frontotemporal lobe dementia
Lewy body dementia
Creutzfeldt-Jakob disease

86
Q

Whats are examples of subcortical dementia?

A

Huntington’s disease
Parkinson’s dementia
vascular dementia

87
Q

Whats the pathology of Alzheimer’s disease?

A

The two key pathological changes in AD are extracellular beta amyloid plaques and formation of intracellular neurofibrillary tangles

88
Q

What are senile plaques?

A

deposits of beta-amyloid leading to the formation of beta-amyloid plaques outside neurones
Amyloid precursor protein is found in the cell membrane of neurones. α-secretase and β-secretase are enzymes involved in the breakdown of amyloid plaques. α-secretase breaks down the protein into soluble remnants that are easily taken away by the blood and lymphatics. β-secretin produces non-soluble remnants the end up being deposited as beta-amyloid plaques. These plaques often accumulate between synapses and affect nerve transmission
They can also deposit around blood vessels in the brain (amyloid antipathy) which weakens blood vessel walls and can increase the risk of haemorrhage

89
Q

What are neurofibrillary tangles?

A

Aggregations of hyperphosphorylated tau proteins.

The Tau protein is integral in the structure of microtubules
It is thought that beta-amyloid plaques outside the cell, leads to increased activation of kinase within the cell
Kinase transports phosphate groups to the Tau protein – which causes structural changes in Tau proteins, causing them to dissociate from the microtubule, and TANGLE with other similarly affected tau proteins within the cell
The lack of tau proteins in the microtubules also weakness the microtubules and they breakdown
As a result of tangles and non-functioning microtubules, some neurones can’t function and undergo apoptosis

90
Q

Which areas of the brain are affected by alzheimers?

A

Hippocampus - memory loss
Amygdala affected later - So a person with Alzheimer’s will often recall emotional aspects of something even if they don’t recall the factual content
As Alzheimer’s disease damage spreads through the brain, additional areas and lobes become affected
-left hemisphere = problems with semantic memory and language
- temporal lobes = difficulty recognising familiar faces and objects
-right parietal lobe = problems with judging distances in three dimensions
- frontal lobes = difficulty with decision-making, planning or organising

91
Q

What is atypical Alzheimer’s disease?

A

There are rarer forms of Alzheimer’s in which the first parts of the brain affected may not be in or near the hippocampus. This means that memory problems are often not the earliest symptoms.

92
Q

What is posterior cortical atrophy?

A

One form of atypical alzheimers where early damage is mainly to the occipital lobes and parts of parietal lobes = difficulty processing visual information, difficulty with eyesight and dealing with spatial awareness

93
Q

What are the clinical features of alzheimers?

A

Cognitive impairment: poor memory, disorientation, language problems
Behavioural and psychological symptoms of dementia: agitation, depression, sleep cycle disturbance, motor disturbance
Disease-specific features: AD is characterised by early impairment of memory. This manifests as short-term memory loss and difficulty learning new information
Activities of daily living: an increasing reliance on others for assistance, problems with high-level functioning (e.g. work, finance), problems with basic personal care

94
Q

What are the stages of alzheimers?

A

Preclinical AD
Mild cognitive impairment due to AD
Mild AD
Moderate AD
Severe AD

95
Q

How is alzheimers classified?

A

As pre-senile or senile
And as familial or sporadic

96
Q

Whats the most common form of Alzheimer’s?

A

Late onset/senile sporadic AD
>90% of cases

97
Q

Whats the risk of AD if a first-degree relative is a sufferer?

A

3x increased

98
Q

Whats the most important gene found for the development of late-onset alzheimers?

A

ApoE - codes a protein involved in cholesterol metabolism called apolipoprotein E

99
Q

What mutations have been identified in early-onset familial AD?

A

Amyloid precursor protein - chromosome 21
Presenilin 1 - Chromosome 14
Presenilin 2 - Chomosome 1

100
Q

How can early onset AD be inherited?

A

Some cases in an autosomal dominant fashion

101
Q

When does autosomal dominant AD present?

A

30-60

102
Q

Why are those with Down syndrome at an increased risk of AD?

A

As Down syndrome is trisomy 21
And chromosome 21 carries a gene that produces amyloid precursor protein which is involved with changes in the brain associated with Alzheimer’s = triplication and over expression

103
Q

Whats the cholinergic hypothesis in AD?

A

many of the cognitive, functional and behavioural symptoms in AD are due to a reduction in brain acetylcholine activity, secondary to the degeneration of cholinergic neurones in nuclei projecting to the hippocampus and medial temporal region. Evidence for this theory comes from studies of physostigmine which inhibits acetylcholinesterase and was shown to improve memory in healthy individuals.

104
Q

What are risk factors for AD?

A

Age over 65
FHx
Downs syndrome
Head injury
CVD risk factors
Depression
Low educational attainment
Low social engagement and support

105
Q

What investigations are needed for alzheimers? Why are they important?

A

Full blood count
Erythrocyte sedimentation rate (ESR)
Urea and electrolytes
Bone profile
HbA1c
Liver function tests
Thyroid function tests
Serum B12 and folate levels
ECG
Virology (e.g. HIV)
Syphilis testing
CXR
Neuroimaging - CT or MRI

Important to rule out other differential diagnoses

106
Q

What would you see on CT/MRI in AD?

A

diffuse cortical atrophy (particularly hippocampus), Gyri narrowing, sulci widening and ventricle enlargement

107
Q

How do we manage alzheimers?

A

Assess capacity and advanced care planning to be done whilst memory is still good
Consideration of advance decisions and appointment of lasting power of attorney.
Manage physical and mental health
Consider delirium if any acute deterioration.
Driving: must inform the DVLA.
Pharmacological
Non-pharmacological
Managing behavioural and psychological symptoms
Consider referral to old-age psychiatry if difficult to control.
Care plans
End-of-life care:

108
Q

How do we manage alzheimers pharmacologically?

A

Mild-to-moderate AD: acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine).

Moderate-to-severe AD: NMDA receptor antagonist (e.g. memantine). May be used in combination with acetylcholinesterase inhibitors.

109
Q

What age does frontotemporal dementia typically affect?

A

<65 younger

110
Q

What is pick disease?

A

An old clinical term that now refers to a pathological finding of pick bodies which contain tau protein inclusions
These may be seen in certain subtypes of FTD

111
Q

What are the variants of FTD?

A

Behavioural variant
Primary progressive aphasia - non-fluent PPA and semantic PPA

112
Q

Whats the most common variant of FTD?

A

Behavioural variant

113
Q

How is behavioural variant FTD characterised?

A

By progressive personality and behaviour change

114
Q

How is primary progressive aphasia variant FTD characterised?

A

characterised by insidious onset of progressive language defects (e.g. word finding, aphasia)

115
Q

Whats the difference between non-fluent PPA and semantic PPA?

A

Non-fluent PPA: characterised by articulatory difficulty
Semantic PPA: characterised by impaired single-word comprehension

116
Q

Whats the pathology behind FTD?

A

characterised by tissue deposition of aggregated proteins including phosphorylated tau or transactive response DNA-binding protein 43 (TDP-43) in the frontal or temporal lobes = atrophy and neuronal loss

117
Q

Whats the inheritance pattern in FTD?

A

10-25% of cases autosomal dominant - genetic
Sporadic

118
Q

which area of brain affected in behavioural variant ftd

A

Prefrontal cortex and anterotemporal lobes (mostly frontal lobes)

119
Q

What are the typical features of behavioural variant FTD?

A

Disinhibition
Loss of empathy
Apathy
Hyperorality (oral exploration of objects, increased consumption of alcohol/cigarettes, altered food preference)
Compulsive behaviour

120
Q

What are the typical features seen in primary progressive aphasia?

A

Effortful speech
Halting speech
Speech-sound errors
Speech apraxia
Word-finding difficulty
Surface dyslexia or dysgraphia: mispronouncing difficult words

As the conditions progresses, patients develop more behavioural symptoms and overtime memory impairment. However, language dysfunction remains a dominant feature.

121
Q

What are 3 clinical syndromes that can occur as a result of Frontotemporal lobar degeneration?

A

FTD with motor neuron disease
Corticobasal syndrome
Progressive supranuclear palsy

122
Q

What is FTD with motor neuron disease?

A

Features of FTD and upper and lower motor neurone symptoms e.g. spasticity, weakness, atrophy and fasciculations
A SUBTYPE OF FTD

123
Q

What is corticobasal syndrome?

A

a rare neurodegenerative disorder with significant overlap with FTD. Characterised by abnormal tau deposition. Usually begins with cognitive or behavioural disturbance with development of characteristic motor features. Classical motor features include asymmetrical akinesia, dystonia, ideomotor apraxia or alien-limb phenomenon.
A DIFFERENTIAL DIAGNOSIS WITH SIMILAR FEATURES TO FTD

124
Q

What is progressive supranuclear palsy?

A

a rare neurogenerative disorder characterised by postural instability and falls, impairment of vertical gaze, parkinsonism and frontal lobe dysfunction.

A DIFFERENTIAL DIAGNOSIS WITH SIMILAR FEATURES TO FTD

125
Q

How do we investigate FTD?

A

Baseline investigations - blood tests
Clinical assessment
Neuroimaging

126
Q

What are the typical features on Neuroimaging seen in bvFTD?

A

frontal and temporal atrophy in up to 65%. Particularly anterior insula, anterior cingulate cortex, and amygdala. May be asymmetrical

127
Q

What are the typical features on Neuroimaging seen in nonfluent PPA?

A

early atrophy and hypoperfusion in the left posterior fronto-insular cortex.

128
Q

What are the typical features on Neuroimaging seen in semantic PPA?

A

significant anterior temporal atrophy. Often asymmetric.

129
Q

How do we manage FTD?

A

No specific treatments for FTD so management is aimed at improving ADLs
E.g. financial advice, supervision if behaviour is problematic, encouraging regular exercise, adapting home, speech and language therapist, behaviour charts

130
Q

What can be used to manage difficult behaviour symptoms in FTD?

A

SSRI or second line atypical anti-psychotics
They can decrease disinhibition, anxiety, impulsivity and repetitive behaviours

131
Q

Which variant of FTD has the shorter prognosis?

A

BvFTD

132
Q

Whats the second most common form of dementia in the UK?

A

Vascular dementia

133
Q

What is ‘mixed dementia’?

A

Features of more than one type of dementia (usually a combination of Alzheimer’s disease and Vascular Dementia.)

134
Q

What is vascular cognitive impairment?

A

a syndrome of all cognitive disorders which are due to cerebrovascular disease

135
Q

Whats the most severe form of vascular cognitive impairment?

A

Vascular dementia

136
Q

What are the 3 main types of vascular dementia?

A

Subcortical
Stroke-related
Single or multi-infarct

137
Q

What is subcortical VD?

A

Dementia caused by disease affecting the small vessels of the brain which predominantly supply the subcortical white matter.

138
Q

What is stroke-related VD?

A

Development of dementia following a large cortical stroke. Up to 20% develop this within the next 6 months.

139
Q

What is single/multi-infarct VD

A

Development of dementia following a single, or multiple small strokes. It is the collective burden of cerebrovascular disease from these strokes that precipitates development of dementia.

140
Q

Whats the pathology of VD?

A

Any condition that affects the brain parenchyma by impairing cerebral blood flow)or haemorrhage can lead to vascular cognitive impairment, and therefore, VD
Causes include ischaemic stroke, small vessel disease, haemorrhage, cerebral amyloid etc

141
Q

Whats the autosomal dominant inherited type of vascular dementia called?

A

cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
CADASIL

142
Q

What causes CADASIL?

A

mutation in the NOTCH3 gene and leads to arterial thickening and occlusion.

143
Q

What is CADASIL characterised by?

A

recurrent migraine-type headaches, multiple strokes and progressive dementia.

144
Q

What are the 2 classic presentations of VD?

A

Post-stroke dementia: stepwise cognitive decline following a clinically diagnosed stroke.
Vascular dementia without recent stroke: stepwise cognitive decline without history of a symptomatic stroke.

145
Q

What are the typical features of vascular dementia?

A

Stepwise decline in cognitive function - poor memory, disorientation, language problems
Gait abnormalities
Personality changes
Behavioural and psychological symptoms of dementia
May have focal neurological signs e.g. due to previous stroke
Affects ADLs

146
Q

How do we manage VD?

A

Optimising cardiovascular risk factors as VD is modifiable and preventable e.g. give anti-hypertensives, diabetic medications, anti-lipid therapy

147
Q

How can vascular dementia be managed pharmacologically?

A

Acetylcholinesterase inhibitors such as donepezil may be used in VD if the cognitive decline cannot solely be attributed to cerebrovascular disease. This is because a significant proportion of patients with dementia with have mixed AD/VD, which may show a small amount of benefit.

Limited efficacy

148
Q

What are risk factors for vascular dementia?

A

History of stroke or TIA
AF
Hypertension
Diabetes mellitus
Hyperlipidaemia
Smoking
Obesity
Coronary heart disease
A FHx of stroke or cardiovascular

149
Q

Whats the epidemiology of dementia with Lewy bodies?

A

Third most common cause of dementia - accounts for 20%
Prevalence increases with age. Average age is 75
Male:female 4:1

150
Q

What is Parkinson’s disease dementia?

A

This is defined as having Parkinson’s disease for more than one year before the onset of dementia.

151
Q

What is dementia with Lewy body?

A

This is defined as developing dementia within one year of Parkinsonism features

152
Q

What are the main differences between Parkinson’s disease dementia and dementia with Lewy body?

A

Parkinson’s disease dementia is when you have parkinsons for >1 year before the onset of dementia and DLB is when you develop dementia in <1 year of onset of Parkinsonism features
DLB usually has an older age of onset, faster cognitive decline and reduced responsiveness to anti Parkinson medications

153
Q

Whats the pathophysiology of DLB?

A

The exact cause of DLB remains unknown but it is characterised by the presence of Lewy bodies. These are intracytoplasmic inclusions of alpha-synuclein that may be found throughout the cerebral cortex and brainstem. Alpha-synuclein is suspected to play a role in neurotransmitter release and vesicle turnover. Interestingly, dopaminergic neurones are found to be more susceptible to dysfunction of alpha-synuclein.

Some studies have shown that the specific location and density of Lewy bodies correlate with specific features (e.g. visual hallucinations associated with Lewy bodies in areas of the temporal lobes).

154
Q

What are the clinical features of DLB?

A

Fluctuating cognition with pronounced variations in attention and alertness
Recurrent visual hallucinations that are typically well formed and detailed
REM sleep behaviour disorder
One or more spontaneous cardinal features of parkinsonism

155
Q

What are examples of parkinsonism features?

A

tremor, rigidity, bradykinesia, postural instability

156
Q

What are some supportive clinical features of DLB?

A

Severe sensitivity to antipsychotic agents
Postural instability and repeated falls
Syncope or other transient episodes of unresponsiveness
Severe autonomic dysfunction (eg, constipation, orthostatic hypotension, urinary incontinence)
Hypersomnia
Hyposomnia

157
Q

How is DLB diagnosed?

A

Probable DLB: ≥2 core clinical features OR one core clinical feature with ≥1 biomarker

Possible DLB: only one core clinical feature and no biomarker OR ≥1 biomarker and no core clinical features

Less likely DLB: the presence of another that could account for symptoms OR parkinsonian features are the only core clinical feature and appear for the first time at a stage of severe dementia

158
Q

How is DLB managed pharmacologically?

A

Cholinesterase inhibitors: generally offered as first-line treatments for patients with DLB and troublesome cognitive/behavioural symptoms
Memantine for severe dementia with Lewy bodies
Melatonin: may be used in refractory REM sleep disorders
Levodopa: this is an antiparkinson medication that may be used for severe, disabling Parkinsonism features

159
Q

Why should neuroleptics be avoided in DLB?

A

precipitate severe reactions e.g. irreversible parkinsons/confusion/autonomic dysfunction and may double or triple the rate of mortality due to neuroleptic maligannt syndrome (they have a severe neuroleptic sensitivity)

160
Q

Why should anticholinergic medications be avoided in Lewy body dementia?

A

They exacerbate symptoms of dementia

161
Q

What is Huntingtons disease?

A

an autosomal-dominantly inherited, neurodegenerative condition characterised by chorea, dystonia and cognitive changes.

162
Q

When do symptoms of Huntingtons tend to develop?

A

Between the ages 20-40

163
Q

Whats the prognosis of Huntingtons?

A

It is a progressive disorder that often results in death within 20 years of onset.

164
Q

What causes Huntingtons?

A

an increased number of cysteine-adenosine-guanine (CAG) trinucleotide repeats within the huntingtin gene on chromosome 4 (usually >40 repeats)

165
Q

What are the clinical features of huntingtons?

A

Choreiform movements, parakinesia, dysphagia, speech difficulties, dystonia, parkinsonian features, akinetic-rigid syndrome
Psychiatric features
Cognitive decline

166
Q

What is Parkinson’s disease?

A

Parkinson’s disease is the most common form of parkinsonism. Parkinsonism describes the presence of bradykinesia and at least one of the following:
Resting ‘Pill rolling’ tremor
Cogwheel rigidity
Postural instability

May also have an expressionless face, micrographics, soft voice, drooling of saliva, shuffling gait, glabella tap, depression, bowel and bladder symptoms, sleep disorder, sexual dysfunction

167
Q

Whats the pathophysiology of Parkinson’s?

A

Loss of dopaminergic neurons of the substantia nigra pars compacts

168
Q

What is the cause of Creutzfeldt-Jakob disease?

A

Rapidly progressive, invariably fatal neurological condition caused by prion proteins (abnormal isoform of a cellular glycoprotein).
These proteins induce the formation of amyloid folds resulting in tightly packed beta-pleated sheets resistant to proteases.

169
Q

How does Creutzfeldt-Jakob disease present?

A

dementia (rapid onset) and myoclonus

170
Q

How is new-variant CJD thought to be acquired?

A

ingestion of bovine-spongiform-encephalopathy-infected beef products.

171
Q

Whats the prognosis of CJD?

A

Death within 1 year of onset of illness

172
Q

How can HIV cause dementia?

A

infection with HIV can cause direct damage to the brain in addition to HIV complications such as opportunistic infections (cerebral cytomegalovirus infection, cryptococcosis toxoplasmosis, TB, syphilis) and cerebral lymphoma. HIV encephalopathy presents clinically as a subcortical dementia and neuropathologist examination shows diffuse multi focal destruction of white matter and subcortical structures.

173
Q

Whats the short Confusion Assessment Method (short-CAM) criteria for delirium?

A
  • Confusion that has developed suddenly and fluctuates, and
  • Inattention and either
    1. Disorganised thinking or
    2. Altered level of consciousness — ask about changes in level of consciousness from alertness to: lethargy; stupor; comatose; or hypervigilant
174
Q

Whats the difference between lethargy, stupor, comatose and hypervigilant

A

lethargy (drowsy, easily aroused)
stupor (difficult to arouse)
Comatose (unable to be aroused)
hypervigilant (hyper-alert).

175
Q

Whats the 4 As test?

A

This is a short, four-item tool designed for use in clinical practice to assess delirium
The four items are alertness, cognition (a short test of orientation), attention (recitation of the months in backwards order), and the presence of acute change or fluctuating course.

176
Q

How should delirium be managed?

A

Correct any precipitating factors e.g. infections, drugs, constipation, dehydration, pain, sensory impairment
Optimise treatment of comorbidities
Advise family/carers to try reorientation staretegies, maintain safe mobility and normalise sleep-wake cycle
Explain diagnosis
Arrange follow up

177
Q

When might specialists suggest pharmacological measures for delirium?

A

Verbal and non-verbal de-escalation techniques are inappropriate or have failed, and
The person is a danger to themselves or others, and
The cause of delirium is known and being treated, and
The benefit outweighs the risk to the person, and
There is enough care in place for the person to be continually monitored.

178
Q

What medication may be offered in severe cases of delirium?

A

Short term low-dose haloperidol
Avoid antipsychotics in Parkinson’s disease and Lewy body dementia!

179
Q

What are symptoms of delirium?

A

Fluctuations in mood and alertness
Agitation
Drowsiness
Hallucinations
Delusions

180
Q

Whats the prevalence of delirium in hospitals?

A

10-30%

181
Q

Who’s at risk of delirium?

A

Older people, those with dementia, cognitive impairments, severe illness or hip fractures.

182
Q

What is delirium?

A

an impairment of conciousness with a reduced ability to focus or maintain attention. It develops over a short period of time and is transient. It causes impaired conciousness, impaired cognitive function with impaired short term memory but preserved remote memory, perceptual disturbances ranging from misinterpretations-> illusions -> hallucinations (esp visual), psychomotor abnormalities, sleep-wake cycle disturbances and mood disturbances.

183
Q

What are the variants of delirium?

A

Delirium can be hypoactive or hyperactive but some people show signs of both (mixed). People with hyperactive delirium have heightened arousal and can be restless, agitated and aggressive. People with hypoactive delirium become withdrawn, quiet and sleepy. Hypoactive and mixed delirium can be more difficult to recognise.

184
Q

What can cause delirium?

A

Pain/post surgical
Infection
Nutrition
Constipation
Sleep
Hydration
Medication + mobility + metabolic (hypercalcaemia, hypoglycaemia, hyperglycaemia)
Environmental

Change of environment in those with cognitive impairments

185
Q

How are delirium and dementia differentiated?

A

Delirium has acute onset and dementia is more gradual
Delerium lasts hours-weeks and dementia months-years
Delirium has a fluctuating course whilst dementia is a progressive deterioration
Impaired conciousness in delirium but normal in dementia
Perceptual disturbances are more common in delirium
Sleep-wake cycle is impaired in delirium and usually normal in dementia
Delirium is reversible and dementia is usually not

186
Q

What is Amnesic syndrome?

A

A syndrome of prominent impairment of recent and remote memory while immediate recall is preserved, with reduced ability to learn new material and disorientation in time. Confabulation may be a marked feature, but perception and other cognitive functions, including the intellect, are usually intact.

187
Q

How is Amnesic syndrome characterised?

A

• anterograde and retrograde amnesia
• No impairment of attention or conciousness or global intellectual functioning (no defect of short term memory) - but may be disorientated to time and have confabulations, lack of insight and apathy.
• Strong evidence of a brain disease known to cause Amnesic syndrome

188
Q

What are examples of Amnesic syndrome?

A

Korsakoff syndrome
Stroke
Brain inflammation e.g. due to herpes simplex virus encephalitis
Brain hypoxia e.g. CO poisoning, cardiac arrest, complications of general anaesthesia, choking, drowning, strangling
Tumours in brain
Alzheimers
Seizures
Certain meds e.g. benzos which act as sedatives

189
Q

What medications should be stopped in the elderly (>65) due to the risk of confusion?

A

Antidepressants amitrptyline and imipramine
Anti-Parkinson drug trihexyphenidyl
Products containing antihistamines
IBS drug dicyclomine
Sleeping pills
Benzodiazepines
Muscle relaxants

190
Q

What is normal pressure hydrocephalus?

A

a reversible cause of dementia seen in elderly patients.
It is thought to be secondary to reduced CSF absorption at the arachnoid villi.
These changes may be secondary to head injury, subarachnoid haemorrhage or meningitis.

191
Q

How does normal pressure hydrocephalus present?

A

A classical triad of features is seen:
• urinary incontinence
• dementia and bradyphrenia
• gait abnormality (may be similar to Parkinson’s disease)

192
Q

How can you distinguish between depression and dementia?

A

The main symptoms that point to depression here are:
• Recent loss of a spouse
• Loss of appetite
• Early morning wakening
• Poor concentration

As a rule of thumb, when performing a mini mental state examination on a patient with depression they will answer with ‘I don’t know’, whereas patients with Alzheimer’s will try their best to answer your questions, but answer incorrectly. They also have global memory loss (pseudo dementia) rather than short term memory loss.

193
Q

What are the specialist nurses for dementia?

A

Admiral nurses

194
Q

What other health professionals are involved with managing dementia?

A

Occupational therapists and physiotherapists for mobility
Optometrists, audiologists and speech and language therapists for vision, hearing and speech therapy
Music therapy can help with restlessness and help you reminisce
Social workers

195
Q

What are pros and cons of being in a care home vs own home?

A

Staying on own home - familiar place, feel safe, independence, happier
Staying in care home - regular meals and hydration, medication prompts, prompts with person care, physical safety improved, improves dignity, staff available 24/7, releases strain on family members, company of others

196
Q

What are deprivation of liberty safegaurds?

A

A set of checks as part of MCA
It protects a person recieving care whose liberty has been limited. It checks the care is appropriate and in their best interests

197
Q

What are some home safety tips for people with dementia?

A

Install locks on interior doors out of sight
Keep walkways and rooms well lit. Night lights
Place meds in a locked cabinet or use a pill box organiser
Remove tripping hazards
Watch temperature of water and food - e.g. automatic thermometer for water temp
Closely monitored use of electric products
Secure large furniture to prevent tripping
Consider small appliances with automatic shut-off features in case a person forgets to tur it off
Install smoke and CO alarms
Stop signs on doors leading to outside to prevent people leaving unescorted

198
Q

How do you reduce the risk of developing delirium?

A

Orientation and ensure pt have their glasses and hearing aids
Promote sleep hygiene
Early mobilisation
Pain control
Prevention/early identification and treatment of postoperative complications
Maintain optimal hydration and nutrition
Regulation of bladder and bowel function
Medication review

199
Q

What drugs can cause delirium?

A

Benzos
Anticonvulsants
Antiparkinsonian agents
Analgesics
Narcotics - opiates
NSAIDs
Antihistamines
GI agents e.g. antispasmodics, H2 blockers, antiemetics
Antibiotics
TCA
Lithium
Cardiac - antiarrhythmics, digitalis, antihypertensives
Steroids

PSYCHIATRY (20 decks)

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