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Baz Y2 Semester 1 > Week 2 Neurology Dementia And Tremor > Flashcards

Week 2 Neurology Dementia And Tremor Flashcards

1
Q

An 82-year-old man is being investigated for a cognitive impairment and concerns about a movement disorder. As part of the assessment he is referred for a number of scans.

The results are as follows:

MRI head normal age-related changes
SPECT scan reduced dopaminergic activity in the substantia nigra

Given the above information, what is the likely diagnosis?

A

Parkinson’s disease

Parkinson’s Disease is a neurodegenerative disorder involving death of neurones in the substantia nigra. The substantia nigra contains dopaminergic cells

There is no noticeable atrophy on a CT such as with Alzheimer’s

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2
Q

What are the two main components of Alzheimer’s pathophysiology

A

Amaloid plaques (A-beta)

Tau tangles

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3
Q

Regarding memory, learning and emotion which part of the brain does Alzheimer’s effect?

A

The hippocampus

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4
Q

Main Alzheimer’s treatment

A

Cholinesterase inhibitors prevent the breakdown of ACh. There is a shortage of ACh in Alzheimer’s patients particularly in the hippocampus

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5
Q

What are the risk factors for vascular dementia?

A

Same of for CV disease and stroke

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6
Q

How does the progression of vascular dementia differ to that of Alzheimer’s

A

Vascular gets worse in steps each time there is a vascular event e.g. tia

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7
Q

What is the focus of vascular dementia treatment?

A
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8
Q

Main differences between Alzheimer’s and frontotemporal dementia?

A

AD primarily affects the medial temporal and parietal lobes, especially the hippocampus, which is involved in memory and learning

FTD primarily affects the lateral frontal and temporal lobes, areas involved in behavior, personality, and language

Both have a build up of Tau, only Alzheimer’s has the amaloid plaques.

Age of onset is younger is frontotemporal dementia 45-65

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9
Q

What is lewy-body dementia

A

Pathophysiology is a build up of alpha-synuclein

Affects temporal, midbrain and parietal

Motor symptoms of Parkinson’s but with added dementia symptoms including sleep disorders

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10
Q

How do MRIs of the hippocampus and dopamine scans of the basal ganglia vary between between those suffering from Alzheimer’s and LBD

A
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11
Q

Fill in the blanks

A
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12
Q

What are the four symptoms collectively known as parkinsonism?

A
  • Bradykinesia - slow movement
  • Rigidity
  • Tremor
  • Postural instability
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13
Q

What are 6 non motor symptom of Parkinson’s disease?

A
  • Cognitive impairment
  • Depression
  • Anxiety
  • REM sleep behaviour disorder
  • Constipation
  • Pain
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14
Q

Which of these genes have links to parkinson’s?

  • PTCH1
  • SNCA(encoding alpha-synuclein)
  • Parkin
  • APC
  • PINK1
  • Amyloid precursor protein (APP)
  • SUFU
  • DJ-1
  • LRRK2
  • Presenilin 1 (PSEN1)
  • Presenilin 2 (PSEN2)

Bonus: which is responsible for late onset parkinsons?

A
  • SNCA(encoding alpha-synuclein)
  • Parkin
  • PINK1
  • DJ-1
  • LRRK2

LRRK2 is responsible for late onset parkinson’s

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15
Q

Average age of onset of Parkinson’s?

A

60

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16
Q

Is Alzheimer’s genetic?

A

Mostly no.

However half of early onset Alzheimer’s is caused by these three genes:

  • Amyloid precursor protein (APP):
  • Presenilin 1 (PSEN1)
  • Presenilin 2 (PSEN2)
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17
Q

Where do Lewy bodies begin in Parkinson’s?

A

Lewy body progression
Lewy bodies first appear in the medulla & olfactory bulb and then progressively spread to the pons, midbrain, limbic lobe and neocortex

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18
Q

What happen’s at stage 6?

A

You get all the symptoms of Lewy Body dementia

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19
Q

Lack of which neurotransmiter is responsible for parkinsonism?

A

Dopamine

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20
Q

Build of Lewy Bodies in which part of the brain is specifically causes parkinsonism?

A

Substantia Nigra

21
Q

How does dopamine from the substantia nigra involved in the direct and indirect pathways?

And how does a lack of dopamine cause parkinsonism?

Draw out pathways

A

Dopamine form the substantia nigra favours the direct pathway which promotes movement

When dopamine is diminished indirect pathway is favoured causing the bradykinisia and stiffness. The tremor comes because there isn’t enough dopamine to decide which one to take resulting in both and tremor

22
Q

When it comes to the motor cortex -> basal ganglia -> thalamus axis what does the direct pathway promote?

A

Movement

Hint -> to move somewhere take the most direct route

23
Q

Breif overview of parkinson’s medication (all focus on dopamine)

A
24
Q

What is the suffix for dopamine precursers?

A

“Dopa”

Levadopa
Carbidopa

25
Q

What is the suffix for MAO-B inhibitors?

What do they do?

A

Line

“Gis us a line” MAO-B inhibitors cause drugs to work wayyyyy better

Inhibit the enzyme monoamine oxidase B which breaks down dopamine

e.g.

Rasagiline
Selegiline

26
Q

What do COMT inhibitors do?

What is the suffix?

A

Block breakdown of dopamine precursors like levadopa

“Capone”

Al capone like comte cheese

27
Q

Fill in this table on the types of tremor

A
28
Q

What is the main cause of physiological tremor?

A

Often due to over-activity of sympathetic nervous system ‘fight or flight’

Often postural/action

Occurs with anxiety, caffeine, β-2-agonists, hyperthyroidism

29
Q

Common characteristics of essential tremor?

A

Autosomal in 50 % of cases

Often an action tremor

Relieved with alcohol

30
Q

Common features of Parkinson’s tremor?

A

Slow and corse

“Pill rolling”

Most prominant at rest but present during walking

31
Q

What is intention tremor and what is it a sign of?

A

Often a sign of cerebella disease

Ask to point nose to finger, if intention tremor present amplitude will increase (become corse) as it approaches the target.

Can also miss target completely

32
Q

Terms for amplitude of tremor

A

Fine: low amplitude
Corse: large amplitude

33
Q

In MND what is the typical features of a degenerating cell?

A

A degenerating cell containing eosinophilic ‘Bunina bodies’ which are typical of classical MND.

Ends up with aggregates of missformed TDP-43 protein (brown)

34
Q

Motor cortex features in MND?

A

Motor cortex atrophy

35
Q

What is the protein found missformed and which then aggregates in MND?

A

TDP-43

Hint: At 43 Teedee Peeded (due to MND)

36
Q

What spinal chord features do you get in MND?

A

Thinning of atrophic anterior roots (arrows).

37
Q

What is an anterior horn cell?

A

Anterior horn cells are large motor neurons in the spinal cord that trigger muscle responses

38
Q

What is this?

A

C is a normal anterior horn cell

D is a degenerated one with a bunina body (arrow)

39
Q

What is the difference between ALS and MND?

A

ALS is a subtype on MND and is the most common occuring in 60-70% of MND cases

40
Q

What does ALS stand for?

A

Amyotrophic lateral sclerosis

Myo - muscle
A-Trophic - without nourishment (no nerve orders)
Lateral - because you see atrophy of the spinal roots?

41
Q

What is ALS also known as?

A

Spinal onset MND

42
Q

What is the second most common form of MND?

A

Progressive bulbar palsy 10-20%

This just affects speech and swallowing

43
Q

Third most common form of MND?

A

Progressive muscular atrophy 10%

This only effects the LMN

44
Q

What form of dementia has an overlap with MND?

A

Frontotemporal dementia

(this covers whent he motor neurons are)

45
Q

What is tounge atrophy a common feature of?

A

MND

46
Q

Two biggest genes involved in autosomal MND?

A

1: C9orf72
2: SOD1

Hint: I wanted to go to Corfu but sod’s law I got MND

47
Q

First line of treatment for essential tremor?

A

Propanolol

48
Q

What type of scan might you need to diagnose parkinsons?

A

SPECT (uses radioactive tracer like a PET)

You don;t get niticable signs of atrophy on a CT or MRI like you would with alzheimer’s

49
Q

A 54-year-old man presents with progressive weakness over the past couple of months. The weakness is mainly affecting his legs which results in him struggling to climb his stairs at home. The weakness is also now affecting his right hand and has led to him dropping objects. On examination, you note thenar muscle atrophy and fasciculations. There is also increased tone in the lower limbs and hyperreflexia of the knee and ankle jerks. No sensory deficit is identified.
What is the most likely diagnosis?

  • Primary lateral sclerosis
  • Bulbar amyotrophic lateral sclerosis
  • Multiple sclerosis
  • Spinal amyotrophic lateral sclerosis
  • Progressive muscular atrophy
A

D

Primary lateral sclerosis is usually characterised by purely upper motor neuron features at the onset and may later on progress to lower motor neuron symptoms.

Bulbar ALS is the same as progressive bulbar palsy and is characterised by bulbar symptoms such as slurred speech and difficulty swallowing at the onset and on examination there might also be evidence of fasciulations and muscle wasting of the tongue.

MS would present with a mixture of motor and sensory deficits and only affects upper motor neurons

Patient has presented with symptoms purely affecting his motor function. Examination findings show a mixture of upper motor neuron signs (hyperreflexia and increased tone) and lower motor neuron signs (fasciculations and muscle atrophy). This is highly suggestive of spinal amyotrophic lateral sclerosis (ALS) - the most common variant of motor neuron disease which presents with a mixture of upper and lower motor neuron signs.

This variant of MND only presents with lower motor neuron features and does not correspond with this patient as he has hyperreflexia and increased tone which are upper motor neuron signs.

Baz Y2 Semester 1 (17 decks)

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