MedEd Neuro Lecture Flashcards

1
Q

MS- where and what?

A

Affects braiin and spinal cord
Immunological attack on myelin
Causes oligodendroglial and axonal pathology

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2
Q

Symptoms of MS

A

optic neuritis
motor weakness
sensory disturbance
fatigue

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3
Q

Optic neuritis

A

Meylin in optic nerve is being destroyed

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4
Q

DANISH symptoms (not necessarily MS)

A
dysdiadochokinesis.
ataxia (cerebellar)
nystagmus.
intention tremor.
scanning dysarthria.
heel-shin test.
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5
Q

Epidemiology of MS

A

The more vit d you get the less likely you are to get MS - so more common in places like Norway and less common around equator
More common in women
More likely in those already affected by AI conditions

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6
Q

MS MRI

A

Demyelinated plaques - different people are affected in different ways
Light plaques - recent
Dark plaques - old

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7
Q

MS diagnosis

A
  1. absense of alternative diagnosis
  2. dissemination in time (DIT)*
  3. dissemination in space (DIS)**
  • (2 attacks of MS - if you have one you might be fine. The second increases probability that the pt has MS)
  • *(Location of the plaques - i.e. optic neuritis and then something else is affected and not optic neuritis again)
Based on:
history and exam
Scan - MRI
Lab - CSF 
Electrophysiology - VEPs
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8
Q

Oligoclonal bands

A

CSF/plasma antibodies
Oligoclonal bands appear in infection - if the infection gets into the brain you get bands as well in CSF
If present in plasma and in CSF then probably
If only in CSF (inflammation confined to brain) then MS probable

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9
Q

VEPs

A

Visual evoked potentials - helps with MS diagnosis e.g when pt has not noticed visual disturbance?

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10
Q

Myaesthenia gravis

A

Fatiguable with use - if you look up long enough –> ptosis.

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11
Q

Symptoms of MG

A
ptosis 
diplopia
dysarthria
dysphagia 
\+/- SOB
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12
Q

Aetiology MG

A

antibodies against ACh receptors in neuromuscular junction

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13
Q

Associations with MG

A

Thymic hyperplasia

Thymoma

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14
Q

Investigations MG

A

bloods - anti-AChR and anti-MuSK
EMG - amplitude of action potentials goes down
AT/MRI

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15
Q

Lambert-Eaton myaesthenic syndrome vs MG

A

Opposite of MG
The more you use the muscle the better it gets
VGCC Ab - some cancers (esp lung) can release these antibodies

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16
Q

Motor neuron disease

A

5-8/100,000

Progressive destruction of muscle and motor neurons

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17
Q

MND symptoms (how do you distinguish from stroke)

A

dysphagia
SOB
progressive muscle weakness

SENSATION NOT AFFECTED

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18
Q

Wasting in MND

A

thenar muscle

tongue

19
Q

Is MND upper or lower MN ?

A

BOTH

20
Q

Investigations for MND

A

rule out everything else

21
Q

MND onset

A

gradual

22
Q

What type of gait in Parkinson’s?

A

Shuffling

23
Q

Parkinsonism Triad

A

Bradykinesia
Rigidity
Resting Tremor (pill-rolling)

24
Q

6Ms

A

Monotonous
Micrographia
HypomiMesis

25
Q

Rigidity in Parkinson’s

A

Cog-wheel rigidity - tremor imposed on rigidity

26
Q

Parkinsonism vs Parkinson’s

A

Parkinson’s - substantia niagra (dopamine) gets destroyed

Parkinsonism - can result from drugs, Lewy bodies etc, PD, atypical parkinsonism

27
Q

Aetiology PD

A

alpha synuclein deposition so neuron doesn’t function properly and neuron dies

28
Q

Epidemiology of PD

A

Farmers - pesticide?

Age

29
Q

PDD

A
Amnestic, language deficits 
Visuospatial dysfunction - can't draw clock 
Hallucinations - little people 
Fluctuations 
Aggression/anxiety

Lewy body dementia - later onsent between motor and

30
Q

hemiplegic
scissoring
choreiform

A

stroke
cerebral palsy
huntington’s - dance-like/involuntary movements

31
Q

Dementia definition

A

severe loss of memory and other cognitive abilities which leads to impaired daily function, regardless of underlying casuse

32
Q

Effects of dementia

A

cognition and memory
affect
motivation and attention
personality and behaviour

33
Q

Alzheimer’s - 5As

A
amnesia 
anomia
apraxia
agnosia
aphasia
\+/- depression
34
Q

Aetiology of AD

A

Hippocampus most affected - encodes memories - short term memory affected first

Amyloid precursor protein (APP) usually helps neurons function - as body ages it can’t process APP well so APP is moved out of cells, deposits and damages neurons

Tau - stabilises microtubules but in AD falls off and forms neurofibrillary tangles (hyperphosphorylated tau)

35
Q

Down’s syndrome

A

APP is found on Chr21 - since those with Down’s syndrome have 3 of these there is extra –>

36
Q

AMTS

A

Questions in the AMTS (1 point each):

  1. Age
  2. Current time (to the nearest hour)
  3. Recall: Ask the patient to remember an address (e.g. 42 West Register Street) - ensure they are able to say it back to you immediately, then check recall at the end of the test
  4. Current year
  5. Current location (e.g. name of hospital or town)
  6. Recognise two people (e.g. relatives, carers, or if none around, the likely profession of easily identified people such as doctor/nurse)
  7. Date of birth
  8. Years of the first (or second) world war
  9. Name of the current monarch (or prime minister)
  10. Count sequentially backwards from 20 to 1

A score of less than 8 in the AMTS implies the presence of cognitive impairment

37
Q

Vascular dementia

A
Like AD 
location specific 
emptional and personality changes 
focal neurology 
Older 
vasculopaths 
sudden onset 
stepwise deterioration
38
Q

VD on MRI

A

fluffy areas in several parts on MRI

39
Q

Pick’s disease

A
Tau  +  frontal lobe
Personality change 
disinhibition 
overeating, preference for sweet foods 
emotional blunting 
YOUNGER
40
Q

Wernicke’s encephalopathy - classic ACE

A

Ataxia
confusion
Eye signs - ophthalmoplegia
(ACE)

41
Q

Signs Wernicke’s

A

ataxia

malnourished

42
Q

Is Wernicke’s damage reversible?

A

No - MRI later will show little reversibility

43
Q

Wernicke’s investigation

A

bloods - B1 especially

others

44
Q

Korsakoff

A

Chronic
Alert
Amnesia and confabulation(brain makes stuff up to fill in gaps of what they have forgotten)
Irreversible (?)

(VS Wernicke’s = acute, confusion, cerebellar and eye signs, reversible)