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 ?

20
Q

Investigations for MND

A

rule out everything else

21
Q

MND onset

22
Q

What type of gait in Parkinson’s?

23
Q

Parkinsonism Triad

A

Bradykinesia
Rigidity
Resting Tremor (pill-rolling)

24
Q

6Ms

A

Monotonous
Micrographia
HypomiMesis

25
Rigidity in Parkinson's
Cog-wheel rigidity - tremor imposed on rigidity
26
Parkinsonism vs Parkinson's
Parkinson's - substantia niagra (dopamine) gets destroyed | Parkinsonism - can result from drugs, Lewy bodies etc, PD, atypical parkinsonism
27
Aetiology PD
alpha synuclein deposition so neuron doesn't function properly and neuron dies
28
Epidemiology of PD
Farmers - pesticide? | Age
29
PDD
``` Amnestic, language deficits Visuospatial dysfunction - can't draw clock Hallucinations - little people Fluctuations Aggression/anxiety ``` Lewy body dementia - later onsent between motor and
30
hemiplegic scissoring choreiform
stroke cerebral palsy huntington's - dance-like/involuntary movements
31
Dementia definition
severe loss of memory and other cognitive abilities which leads to impaired daily function, regardless of underlying casuse
32
Effects of dementia
cognition and memory affect motivation and attention personality and behaviour
33
Alzheimer's - 5As
``` amnesia anomia apraxia agnosia aphasia +/- depression ```
34
Aetiology of AD
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
Down's syndrome
APP is found on Chr21 - since those with Down's syndrome have 3 of these there is extra -->
36
AMTS
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
Vascular dementia
``` Like AD location specific emptional and personality changes focal neurology Older vasculopaths sudden onset stepwise deterioration ```
38
VD on MRI
fluffy areas in several parts on MRI
39
Pick's disease
``` Tau + frontal lobe Personality change disinhibition overeating, preference for sweet foods emotional blunting YOUNGER ```
40
Wernicke's encephalopathy - classic ACE
Ataxia confusion Eye signs - ophthalmoplegia (ACE)
41
Signs Wernicke's
ataxia | malnourished
42
Is Wernicke's damage reversible?
No - MRI later will show little reversibility
43
Wernicke's investigation
bloods - B1 especially | others
44
Korsakoff
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)