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Phase 3a > Neuro > Flashcards

Neuro Flashcards

1
Q

What are the possible causes of unilateral vision loss?

A 
Vascular 
-amaurosis fugax
-central retinal vein occlusion 
-anterior ischaemic optic neuropathy (GCA)
NON-Vascular 
-Optic neuritis 
-retinal detachment
-acute angle closure glaucoma 
-vitreous haemorrhage
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2
Q

What’s the difference between vascular changes in vision compared to inflammatory causes?

A
  • Vascular reaches height of problem quickly
  • Vascular would be associated with CVD risk factors such as smoking, diabetes & obesity
  • inflammatory causes blurring/loss of acuity w/ pain opposed to abrupt loss of vision
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3
Q

What would you see on examination of a n optic neuritis eye?

A
  • reduced direct and indirect pupillary response
  • decreased visual acuity and colour vision in one eye
  • normal fundoscopy and movements
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4
Q

What is papilloedma generally a sign of?

A

-raised intracranial pressure

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5
Q

What may exacerbate symptoms of someone with multiple sclerosis?

A
  • heat
  • exercise
  • infection
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6
Q

What is the epidemiology of MS?

A
  • F>M predominance - effects more and earlier
  • onset 20-40
  • 30% of MS risk genetic
  • closer to the equator risk lower
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7
Q

what’s the 3 stage model of MS pathophysiology?

A
  1. initiation
  2. propagation
  3. resolution
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8
Q

What happens during the initiation phase of MS pathophys?

A

T cells become primed to being autoreactive

  • increased genetic risk
  • environmental triggers - infectious agents similar to CNS antigens prime T cells to be autoreactive to oligodendrocytes
  • leaky gut hypothesis - increased inflammation in gut may lead to increased activation of T cells that then pass the BB
  • traumatic insult - 2x more likely to get MS if had a TBI
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9
Q

What happens during the propagation stage of MS pathophys?

A

once T cells are autoreactive

  • BBB loss due to inflammation m
  • plaque formation - killer cells, helper cells, B cells and microglia proliferate and aggregate
  • plaques cause - demyelination, conduction block and axonal loss.
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10
Q

What happens during the resolution stage of MS?

A
  • remyelination
  • neuroplasticity
  • axonal redundancy
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11
Q

Define relapse in terms of MS?

A
  • acute onset Sx that must be experienced by patient (not incidentally found)
  • confirmed by neuro exam
  • lasts longer than 48 hours
  • reaches nadir in subacute pattern - days to weeks
  • plateaus - weeks to months
  • complete resolution
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12
Q

What is uthoff’s phenomena?

A

Sx of MS get worse with heat i.e. bath, exercise, holidaying

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13
Q

What are common sites for plaques in MS? and what Sx would they cause?

A
  • periventricular -
  • spinal cord - parathesiae, weakness, numbness, bowel and/bladder incontinence
  • brainstem - dysarthria, vertigo, hemiplegia (if massive lesion)
  • cerebellar - ataxia, nystagmus, intention tremor
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14
Q

What is Lhermitte’s sign?

A

Electric shock felt through the body. indicative of spinal cord MS lesion.

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15
Q

What criteria would you use to diagnose MS? what are it’s requirements?

A

Macdonalds Criteria.
evidence of at least 2 lesions disseminated in time and space.
can be 2 clinical ones, can be 1 clincal + MR evidence of second lesion, can be 1 clinical + historical suggestion of previous episode of demyelination. bit of a maccies pic n mix.

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16
Q

What investigations would you do in suspected MS?

A
  • MRI
  • lumbar puncture - looking for oligoclonal bands
  • maybe neurophysiology - VEP, NCS.
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17
Q

What MRI changes would be suggestive of MS?

A
  • dawson’s fingers (corpus callosom)

- multiple sites of hyperintense lesions on T2 or multiple gadolinium enhancing lesions on T1

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18
Q

Describe the progression of MS?

A
  • separate pathophys to inflammation
  • not complete remyelination post relapse
  • leads to steady decline in function over 10-15 years
  • oligodendrocytes die so can no longer tropically support neurons that then subsequently die themselves.
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19
Q

What are the 4 types of MS?

A
  • relapsing remitting (85%)
  • secondary progressive - 10-15 years after onset of R&R
  • progressive relapsing
  • primary progressive - worsening of disease from onset minor improvements, plateaus maybe
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20
Q

What is the treatment for an acute MS rekapse?

A
  • oral methylpred - if not to bad

- IV methylpred - if severe

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21
Q

When would an MS patient be eligible for immunomodulation therapy? What are the pros and cons of this?

A
  • needs to have had 2 or more relapses within a 24 month period
  • drugs decrease recovery time and reduce number of lesions
  • drugs don’t slow progression of disability
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22
Q

What is the first line treatment for active MS? what is it’s MOA?

A

-interferon beta 1b - anti-inflammatory cytokine that reduces active inflammation

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23
Q

Name a second line biologic drug used to treat more active MS? briefly describe MOA.

A
  • nataluzimab - monoclonal antibody that targets integrin on lymphocytes
  • alemtuzumab - targets and kills T regulatory cells.
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24
Q

What is the definition of a TIA?

A

The rapid onset of focal neurological symptoms caused by a vascular injury that resolve completely within 24 hours (usually an hour) with no evidence of neuronal loss

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25
Q

What are risk factors for a TIA?

A
  • atrial fibrillation
  • Known Carotid stenosis
  • smoking Hx
  • Age
  • high systolic BP
  • diabetes
  • CVD
  • obesity
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26
Q

What investigations would you do for a suspected TIA?

A
  • Carotid doppler
  • ECG - 24 hour tape
  • BP
  • bloods - lipid profile
  • Echo
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27
Q

What management would you do for a TIA?

A

Treat underlying risk factors

  • anti-HTN
  • if AF - rivaroxaban or warfarin if contraindicated
  • carotid endarterectomy
  • PFO closure if clinically significant
  • statins probs anyway
  • aspirin anyway
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28
Q

What must you tell a patient who has had a TIA?

A

No driving for a month

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29
Q

What is the definition for a complete ischaemic stroke?

A

An acute onset of focal neurological symptoms lasting longer than 24 hours due a disturbance in cerebral blood flow that has led to neuronal death!

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30
Q

What are some non-modifiable risk factor for having a stroke?

A
  • Gender (M>F)
  • Age
  • genetic predisposition
  • Previous stroke or TIA
31
Q

What is a penumbra?

A

Brain tissue that surrounds the necrotic core of a stroke that remains viable for hours after the original vascular insult. Saving this is the target of acute stroke therapies like thrombolysis or thrombectomy.

32
Q

How would you differentiate between an embolic stroke vs a carotid stroke?

A

-embolic stroke is more likely to have infarctions that cross vascular territories because the source of the clot is lower than the carotids.

33
Q

What are the 3 pathophysiologic mechanisms for an ischaemic stroke?

A
  • carotid disease
  • embolic disease
  • hypoperfusion
34
Q

How does AF cause an increase risk of stroke? by how much?

A

5x increase risk
3x more likely to be severe
-incoordination of contraction of the atria
-causes blood stasis and clot formation (usually in the left atrial appendage)
-micro clots break off thrombus and go tot he brain

35
Q

What are the causes of embolic stroke?

A
  • AF
  • suboptimal anticoagulation of mechanical heart valves
  • LV thrombus post MI
  • PFO ????
  • subacute bacterial endocarditis vegetative growth
36
Q

What are the 2 carotids diseases that can cause stroke?

A
  • MAINLY atherosclerotic disease

- carotid dissection

37
Q

What can cause cerebral hypo-perfusion and thus stroke?

A
  • iatrogenic
  • sepsis
  • vasculitis
  • major carotid stenosis predisposes
38
Q

What are the 4 sub groups of stroke dependent on the Bamford classification? What is groups criteria?

A
  1. Total Anterior Circulation Stroke (TACS)
    3/3 - unilateral weakness of arms and legs, hemianopia, higher cortical dysfunction
  2. Partial Anterior Circulation Stroke (PACS)
    2/3 unilateral weakness of arms and legs, hemianopia, higher cortical dysfunction
  3. Lacunar syndrome (LACS)
    -pure sensory, pure motor, pure sensori-motor or ataxic hemiparesis
  4. Posterior Circulation Stroke (PACS)
    1/4 - cranial nerve palsy + contralateral sensory or motor deficit, cerebellar dysfunction, bilateral sensory/motor dysfunction, isolated homonymous hemianopia.
39
Q

What is thrombolysis?

A
  • a recanalising treatment that aims to restore blood from to brain tissue surrounding the ischaemic core of a stroke.
  • Done with Alteplase - tissue plasminogen activator (0.9mg/kg over 60 mins) 0 thrombolytic
40
Q

What are the indications for thrombolysis?

A
  • CONFIRMED (by CT) ischaemic stroke (rule out haemorrhagic acutely)
  • presents to hospital within 4.5 hours of onset of symptoms or last seen well
41
Q

What are contraindications for thrombolysis?

A
  • BP <185
  • on warfarin INR<1.7 or any NOAC or recent LMWH
  • stroke is too severe or not severe enough
  • prior ICH or known active cancer
  • known bleeding source/coagulopathy
  • really low or high BM
  • stroke within last 6 weeks
  • unsecured brain aneurysm
42
Q

What’s the outcomes of thrombolysis?

A

1/10 - better outcome
1/20 - outcome is no better that it would have been without
1/30 - worse outcome

43
Q

Other than thrombolysis what is the other acute stroke therapy?

A
  • thrombectomy
  • available up to 6 hours post onset or symptoms or last seen well
  • must be functioning well before stroke and be a severe stroke
  • however, it’s a limited resource
44
Q

What’s the most important factor to manage in stroke primary and secondary prevention?

A

BLOOD PRESSURE

  • 130/80 or less
  • 120 if DM
  • 140-50 if bilateral carotid stenosis
45
Q

what 3 responses are measured using the GCS?

A 
Eye /4
verbal /5
motor /6
lowest score 3 
normal = 15
46
Q

What meds would you give someone post stroke?

A
  • 300mg aspirin for 2 weeks then clopidogrel life long
  • anti-coag if AF HASBLED/CHADSVASC score
  • Anti-HTN - long term target of 130/80
  • Statin therapy - 40% reduction in non-HDL
47
Q

What are the reversal agents for what anti-coagulants?

A
  • Vitamin K for Warfarin
  • Protamine for Heparin (artially for LMWH)
  • Beriplex for NOACs
  • Idarucizumab for Dabigatran
48
Q

What is the classical triad of Parkinson’s disease?

A
  • Cog-wheel rigidity
  • Bradykinesia
  • resting tremor

ALL ASYMMETRICAL
All PRESENT
IMPORTANT

49
Q

Other than the classical triad, what other symptoms may people with parkinson’s disease have?

A
  • cognitive and mood changes
  • sleep disorders (20 years receding REM SD)
  • later autonomic dysfunction
50
Q

What is thought to be the main causative protein in parkinson’s disease?

A

Alpha Synuclein

51
Q

What environmental exposures increase your risk of having PD?

A
  • head injury, emotional stress, shy and depressed personality type
  • rural living: farming activity, well water drinking, exposure to pesticide, herbicide, insecticide
  • heavy metal exposure - lead, maganese, mercry

ALL EXHIBIT A DOSE EFFECT

52
Q

What are some protective factors of PD?

A
  • Smoking
  • Alcohol
  • Coffee
  • measles as a child
  • NSAID usage CCB
53
Q

What is the basic pathophysiology of parkinson’s disease?

A
  • degeneration of the dopaminergic neurones in the substantia nigra reducing the ability/stopping completely an individual with parkinson’s ability to initiate movement
  • degeneration is caused by cytoplasmic proteinaceous inclusions of alpha synuclein in these neurones
54
Q

Describe the tremor seen in parkinson’s.

A
  • 4-6Hz pill rolling tremor
  • present mainly at rest
  • worse on destraction
  • can affect upper and lower limbs
55
Q

Describe the Bradykinesia of parkinson’s.

A
  • Decrements over usage
  • has to be asymmetrical
  • Variable in nature
56
Q

Describe the rigidity seen in Parkinson’s.

A
  • increased tone across the whole ROM

- worse on activation manoeuvres - get them to tap other hand and testing limb becomes more rigid.

57
Q

Describe the gait seen in parkinson’s.

A
  • Stooped posture
  • short stride length
  • shuffling
  • Poor turning
  • Freeze in doors
58
Q

What are some complications of PD?

A
  • sleep disturbances - could be dopamine side effects, could be PD meds wearing off over night, could be insomnia due to concurrent anxiety
  • Psychosis - Dopamine therapy could trigger psychotic Sx, proving factors UTI, new drug (anticholinergic, MOAi, dopamine agonist)
  • Impulse control disorder - spectrum from pathological gambling to punding
59
Q

What things in a history would make you think it was likely PD?

A

Asymmetrical
Slowly progressive
Display excellent response to Levodopa
Average age of onset around 60 (but wide range)

60
Q

What things in a history would make you think it wasn’t PD?

A
  • Neuropsychiatric disorders when they present - LBD
  • Prominent falls and postural instability early on - MSA
  • Have abnormal eye movements -PSP
  • Have early onset autonomic features - MSA
  • Have ataxia - unequivocal cerebellar abnormalities
  • Have a structural abnormality explain their symptoms le a fatty stroke of their basal ganglia - vascular Parkinson’s won’t have decrement in movements
  • PD Sx restricted to the legs for <3 years - NPH
61
Q

What investigations would you perform in suspected PD?

A
  • L-dopa trial - if good response probably PD, if bad or responds and tails off probs not PD
  • DAT Scan - Dopamine Active Transported - visualises how much dopamine is getting transported around the brain - good for young people with odd Px
62
Q

What medication treatment would you give for PD?

A

FIRST LINE
-Levo-dopa - needs to be given with a dopamine decarboxylase inhibitor - Co-benaldopa/co-careldopa to prevent peripheral L-dopa metabolisation causing dopamine side effects
SECOND LINE ADJUNCTS
-Dopamine agonists - ropinerol - higher risk of Hallucinations, most improvement with off time & Motor Sx & ADL
-MAO-Bi- rasagiline
-COMT

63
Q

What causes dyskinesia PD?

A
  • post synaptic hypersensitivity to dopamine due to chronic dopamine deficiency
  • involuntary fidgety movements (dyskinesia) seen at the height of dopamine transmission
64
Q

What non-pharmacological treatment is available for PD?

A
  • Psychological support - PD A&D + life adjustment for chronic illness for family as well as pt
  • Deep brain stimulation of the sub nig
  • OT - Cueing for walking assistance - bypasses needs for basal ganglia activation of movement by accessing premotor, parietal and cerebellar corticies
65
Q

How do you treat trigeminal neuralgia?

A

-carbamazepine

66
Q

How do you manage migraine acutely?

A
  • Triptan - as soon as recognise one coming on
  • NSAIDS
  • Coedine
  • Anti-emetics
67
Q

What can you give to prophylatically treat migraine?

A
  • Beta blockers
  • topiramate
  • amitriptiline
68
Q

Tx for a partial seizure?

A

-Carbamazepine

2nd line - lamotrigine

69
Q

Tx for GTCS?

A
  • Valporate

- give carbamazepine if child bearing age

70
Q

Tx for Absence?

A

Ethosuximide

valporate

71
Q

Tx for myoclonic?

A

-Valporate or Keppra (leviteracetam)

72
Q

When does a seizure become status?

A

1 seizure lasts for 15 mins
or
multiple seizures without recovery in between

73
Q

What is the management for status?

A
  • ABCDE
  • O2, airways + IV access
  • buccal midaolam or rectal diazepam
  • IV lorazepam/diazepam
  • IV phenytoin if seizures continue
74
Q

What in MG is the pathophysiology and Tx?

A
  • autoimmune destruction of nicotinic acetylcholine receptors
  • pyridostigmine - 1st
  • prednisolone to induce remission - 2nd
  • may need chronic immunosuppresion from mycophenelate- 3rd
  • Thymectomy if indicated

Phase 3a (15 decks)

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