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Neurology > Cognitive function > Flashcards

Cognitive function Flashcards

1
Q

How is cognitive attainment and dementia risk influenced?

A

Mixture of environmental and genetic factors starting at early life

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2
Q

What can be used to predict dementia risk and cognitive attainment

A

Educational attainment

Occupational status

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3
Q

What are the risk factors that increase dementia risk in early life

A

Less education

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4
Q

What are the risk factors that increase dementia risk in middle life

A 
Hearing loss
Traumatic brain injury
Hypertension
Alcohol 
Obesity
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5
Q

What are the risk factors that increase dementia risk in later life

A 
Smoking 
Depression
Social isolation
Physical inactivity 
Air pollution
Diabetes
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6
Q

What is the frontal lobe responsible for?

A

Executive function/ Behavioural control

Speech output

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7
Q

What is the left lateral temporal lobe responsible for?

A

Speech comprehension

Semantic knowledge

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8
Q

What is the occipital/parietal lobe responsible for?

A

Visuoperceptual/spatial processing;

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9
Q

What is the left parietal lobe responsible for?

A

calculation

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10
Q

What are symptoms of disease in the left inferior area of the frontal lobe

A

Hesitant, effortful telegraphic speech

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11
Q

What are symptoms of problems with the left lateral temporal lobe

A 
sometimes confused with deafness, 
 fluent empty speech
specific naming 
 problems reliance on jargon or high 
 frequency words
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12
Q

What is the right lateral temporal lobe responsible for?

A

Memory for sounds shapes and faces

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13
Q

What are symptoms of problems with the occipital/parietal lobe

A

Neglect - Ignores half of space (usually left half) e.g misses food on plate
ignores people on left
Difficulty laying the table.
Fails to recognise objects
Difficulty navigating surroundings-bangs into doorframes etc
Hemianopia- visual loss of one half of space
Dyspraxia: difficulty carrying out practical tasks-dressing, washing

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14
Q

What is predominately in the medial temporal lobe?

A

Hippocampus

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15
Q

What are symptoms of problems with the occipital/parietal lobe

A

Neglect - Ignores half of space (usually left half) e.g misses food on plate
ignores people on left
Difficulty laying the table.
Fails to recognise objects
Difficulty navigating surroundings-bangs into doorframes etc
Hemianopia- visual loss of one half of space
Dyspraxia: difficulty carrying out practical tasks-dressing, washing

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16
Q

What is the medial temporal lobe responsible for

A

Memory and navigation

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17
Q

What are symptoms of problems with the medial temporal lobes

A

Classically cannot recall recent events
Will not retain new information
Difficulty navigating surroundings

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18
Q

How do we assess cognitive decline (early)?

A

Patient present to their GP initially with mild symptoms

GP will perform tests to look for a reversible cause of cognitive impairment —
such as B12 , thyroid function — and screen for alcohol use

GP will do a brief memory check

Referred to memory clinic of there is a SIGNIFICANT decline

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19
Q

What stages will a patient go through before having dementia

When are they diagnosed

A

Cognitively normal
Mild symptoms
Dementia
Early stages, pathological proteins already affecting patients
Diagnosis- Once dementia hits or even later in dementia

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20
Q

What are the pathological proteins that cause dementia

A

Ammyloid Beta form plaques

Tau- medicated neural injury and dysfunction

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21
Q

What are the pathological proteins that cause dementia

A

Amyloid Beta

Tau

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22
Q

What does Amyloid beta do

A

Forms plaques in Alzheimer’s disease

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23
Q

What does tau do ?

A

Forms tangles in Alzheimer’s disease

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24
Q

Damage to what part of the brain causes Alzheimer’s disease

A

Hippocampus

Medial temporal lobe

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25
Q

How is Alzheimer’s disease caused?

A

Amylose beta forms around hippocampus then tau tangles clusters around which cause neuronal injury and dysfunction
Problems start only when tau accumulates

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26
Q

What treats Alzheimer’s disease?

A

Nothing

Treatment of slow progression of disease at later mild stages

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27
Q

How is Alzheimer’s disease diagnosed before A beta start coming in?

A

Genetic risk
Rare genetic mutations
polygenic risk

28
Q

How is Alzheimer’s disease diagnosed before A beta start coming in?

A

Genetic risk
Rare genetic mutations
polygenic risk

29
Q

What genes cause alzheimers disease?

A

PSEN 2 - presenilin 2
PSEN 1- presenilin 1
APP- amyloid precursor protein
Rare

30
Q

What genes from high to low risk can cause alzheimers disease

A

APOE4- Apolipoprotein E4 - 2 copies pose the highest risk
TREM2- Triggering Receptor Expressed On Myeloid Cells 2- mediun risk
APOE4- 1 copy

31
Q

How is Alzheimer’s disease diagnosed after A beta start coming in but before any
symptoms emerge?

A

Evidence of amyloid

32
Q

Why is evidence of amyloid not advised for patients to diagnose Alzheimer’s

A

Evidence of amyloid will not determine at what stage of getting dementia they are
Might be at start or close to getting Alzheimer’s

33
Q

How is evidence of amyloid tested?

A

Lumbar puncture

PET scan

34
Q

How is Alzheimer’s disease diagnosed when clinical signs show before dementia stage?

A

Cognitive change

Functional impairment

35
Q

What assessment tests cognition

A

Montreal cognitive assesment

36
Q

What are the different parts of the Montreal cognitive assessment

A 
Orientation
Memory
Delayed recall
Attention
Visuospatial and executive function
Language ( this is assessed through all areas however)
37
Q

What does orientation part need from the patient? (Montreal cognitive assessment)

A

Non specific

Requires intact memory, attention, comprehension and expression language

38
Q

What does memory part test (Montreal cognitive assessment)

A

Immediate (working memory) <1 minute
Short term memory (a few minutes)
Long term memory (over 20 minutes)
Very long term memory (over night).

39
Q

What does attention part need from the patient? (Montreal cognitive assessment)

A

Non-specific

requires intact language, concentration, executive function.

40
Q

What is done in the Visuospatial and executive function part (Montreal cognitive assessment)

A

Follow the dots in the order given by the assesor

41
Q

What do people with Alzheimer’s do with the Visuospatial and executive function part (Montreal cognitive assessment)

A

They follow the dots in the way they see it works

42
Q

What does the Montreal cognitive assessment not test?

A

Behaviour

43
Q

How can behaviour be tested (Alzheimer’s disease)

A

Taking a history

44
Q

What can cause cognitive decline?

A 
Acute illness (delirium)
Fatigue including sleep disorders
Metabolic disturbance
Thyroid/Liver disease
Vitamin deficiencies e.g. B1 (thiamine)
Dementia (in later life)
Alzheimer's disease
Vascular dementia
Lewy body dementia
Frontotemporal dementia
45
Q

What is the role of B1

A

Combines with ATP to form thiamine pyrophosphate

46
Q

What is thiamine pyrophosphate

A

Co-enzyme

47
Q

What is the role of thiamine pyrophosphate

A

Carbohydrate metabolism

48
Q

What causes B1 deficinecy

A

-Global health issue:
Rice-based diets can be low in thiamine.
When food is then rationed (refugee populations or drought), thiamine reserves are low and people quickly become deficient.
Alcohol intake leads to thiamine deficiency.
Fad diets that are high in carbohydrates and low in thiamine cause deficiency.

49
Q

What are some thiamine containing foods

A

Beef, liver, nuts, oats, oranges, pork, eggs, seeds, Fegunnes, peas and yeast

50
Q

Name syndromes caused by B1 deficiency

A

Wernicke-Korsakoffs

Wet Beri Beri

Dry Beri Beri

51
Q

What are common symptoms of Wernicke’s encephalopathy

A

Ocular abnormalities- double vision, cant move their eyes

Mental status changes

Incoordination of gait and trunk ataxia

52
Q

What are uncommon symptoms of Wernicke’s encephalopathy

A

Stupor
Hypotension and tachycardia
Hypothermia
Bilateral visual disturbances and papilloedema
Epileptic seizures
Hearing loss
Hallucinations and behavioural disturbances

53
Q

What are late-stage symptoms of Wernicke’s encephalopathy

A

Hyperthermia
Increased muscular tone and spastic paresis
Choreic dyskinesias
Coma

54
Q

What happens if a patient has thiamine deficinecy

A

Replace thiamine

Use IV tap

55
Q

What is Korsakoff’s syndrome

A

Chronic neurological sequelae of thiamine deficiency — can follow
Wernicke’s
AKA alcohol-related brain disease

56
Q

What are the signs of Korsakoff’s syndrome

A

Behavioural and cognitive change — amnesia and confabulation

57
Q

How is Korsakoff’s syndrome treated?

A

iv/im thiamine (pabrinex)
Can check red cell transketolase
Do not give dextrose alone

58
Q

When treating Korsakoff’s syndrome why Do not give dextrose alone?

A

Metabolising dextrose uses thiamine

59
Q

What is Dry Beri- Beri

A

peripheral nerve damage-neuropathy

Can accompany Korsakoff’s syndrome

60
Q

Symptoms of Dry Beri- Beri

A 
Confusion
Wrist drop
Inability to speak
Great weakness
Numbness of feet
Loss of tendon reflex
Painful, tender muscles
Foot/Wrist drop
Burning of tingling
61
Q

What is wet Beri Beri

A

Peripheral vasodilation occurs, leading to a high cardiac output state,
retention of salt and water and edema (swelling).

62
Q

What does wet Beri Beri cause

A

Injury to leading chest pain

63
Q

What is the term for rapid form of wet Beri Beri

A

Acute fulminant cardiovascular beriberi, or Shoshin beriberi.

64
Q

Why can treatment with thiamine cause low-output cardiac failure

A

systemic vasoconstriction is reinstated before the heart muscle recovers.

65
Q

What to do if treatment with thiamine causes low-output cardiac failure

A

With support, recovery is usually fairly quick and complete if treatment is
initiated promptly. However, if no treatment is available, death occurs just
as rapidly (within hours or days).

66
Q

What is the Montreal cognitive assessment abbreviated to

A

MOCA

Neurology (14 decks)

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