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3a neurology > Stroke And TIA > Flashcards

Stroke And TIA Flashcards

1
Q

What is a cerebrovascular accident (aka stroke)

A

Focal neurological deficit lasting over 24 hours caused by infarction

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2
Q

State the 2 types of stroke and how common each are

A
  • Ischaemic - 80%
  • Haemorrhagic - 20%
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3
Q

What is an ischaemic stroke

A

decrease in blood flow due to arterial occlusion/stenosis

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4
Q

Give 3 causes of an ischaemic stroke

A
  • thrombosis
  • embolus
  • Plaque
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5
Q

Give 5 RFs of an ischaemic stroke

A
  • HTN
  • Smoking
  • T2DM
  • AFib
  • TIA
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6
Q

How would an anterior cerebral artery stroke present

A
  • Contralateral weakness and numbness of LOWER limbs
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7
Q

How would a middle cerebral artery stroke present

A
  • Dysphasia
  • Contralateral weak and numb UPPER limbs
  • Face droop
  • Forehead sparing
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8
Q

How would a posterior cerebral artery stroke present

A
  • Vision loss - contralateral homonymous hemianopia
  • macular sparing
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9
Q

How would a vertebrobasilar artery stroke present

A
  • Cerebellar signs (Vanished)
  • reduced consciousness
  • balance disorders
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10
Q

How are ischaemic strokes diagnosed

A
  • Non contrast CT head
  • ECG - AFib?
  • Serum electrolytes and glucose
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11
Q

What would you expect to see on a non contrast CT of someone who has had an ischaemic stroke

A

darkness of brain parenchyma
(exclude haemorrhagic)

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12
Q

Why are serum electrolytes and glucose investigated for ischaemic strokes

A

To exclude stroke mimics such as hypoglycaemia and hyponatraemia

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13
Q

How is an ischaemic stroke treated

A
  • <4.5h since Sx onset = thrombolysis - IV alteplase
  • 300mg oral aspirin for 2 weeks
  • Thrombectomy
  • Maintain bp, glucose and hydration
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14
Q

What pharmacological interventions are used as prevention for ischaemic strokes

A

Clopidogrel
Atorvastatin after 48h

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15
Q

Hypoglycaemia and hyponatraemia are examples of ‘stroke mimics’, give 2 more examples

A
  • Hepatic encephalopathy
  • Brain tumours
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16
Q

What is a transient ischaemic attack (TIA)

A

Sudden and temporary episode of focal neurological dysfunction without infarction that resolves spontaneously within 24h

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17
Q

What is the most common cause of a TIA

A

Thrombo-emboli in the internal carotid artery

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18
Q

Give 5 ways a TIA may present

A
  • Amaurosis fugax
  • Dysphasia
  • Focal neurology - dependent on location ACA, PCA, MCA
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19
Q

What is amaurosis fugax

A

sudden and temporary loss of vision in one eye due to reduced blood flow to the retina

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20
Q

What investigations should be ordered for a suspected TIA

A
  • Blood glucose
  • FBC
  • PTT, INR
  • Serum electrolytes
  • ECG
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21
Q

If a TIA is suspected, when should an urgent CT head be requested and why

A

patient is taking anticoagulation or had a bleeding order
Exclude haemorrhage

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22
Q

How is a confirmed TIA managed

A
  • Dual antiplatelet therapy:
    aspirin AND clopidogrel - 300mg oral loading, then 75mg OD for 21 days (each)
  • Immediately start atorvastatin (oral OD)
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23
Q

What is an extradural haemorrhage (EDH)

A

Haemorrhage between the dura mater and the inner surface of the skull

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24
Q

What causes EDH

A

Typically bleeding from the middle meningeal arteries caused skull trauma

25
Q

Why is the middle meningeal artery susceptible to bleeding following a skull fracture

A
  • The pterion is where the parietal, frontal, sphenoid and temporal bones fuse
  • Bone at this location is relatively thin so vulnerable to fracture
  • MMA lies underneath pterion therefore fracture can result in rupture of the MMA
26
Q

What age group is at a higher risk of an EDH

A

Young adults 20-30

27
Q

Why does the risk of an EDH reduce as we age

A

Dura is more firmly adhered to skull as you age

28
Q

Describe the typical symptoms of an EDH

A
  • Headache
  • N+V
  • Confusion
  • LOC after head injury followed by a period of lucidity
  • Progressively decreasing level of consciousness
29
Q

Describe the pathophys of an EDH

A
  • bleeding into ED space
  • Increased intracranial pressure
  • brain compression and midline shift
30
Q

What imaging should be done for a EDH

A
  • GS = CT head
  • Xray - fracture
31
Q

What are features of an EDH that may be seen on a CT

A
  • Bi-convex (lemon) haematoma
  • midline shift
  • brainstem herniation
32
Q

Treatment of an EDH

A
  • ABCDE
  • IV mannitol to reduce ICP
  • Craniotomy - burr hole or trauma
33
Q

What is a subdural haemorrhage (SDH)

A

Collection of blood between the dura mater and arachnoid mater

34
Q

What is the most common cause of a SDH

A

trauma rupturing the bridging cranial veins

35
Q

Give 4 RFs of a SDH

A
  • Recent trauma - fall, blow to the head
  • Over 65
  • Coagulopathy or anticoagulant use
  • Brain atrophy - dementia, alcohol abuse
36
Q

What is classed as a subacute SDH

A

3-21 days

37
Q

Give 4 typical symptoms of a SDH

A
  • Physical signs of trauma
  • Headache
  • Confusion
  • N+V
38
Q

What clinical signs may be seen in a SDH

A
  • Cranial nerve abnormality
  • Seizures
  • LOC
  • Limb weakness/ sensory disturbance
39
Q

What imaging should be done for a SDH and describe a positive finding

A
  • Non contrast CT head
  • Crescent shaped (Concave) collection of blood
40
Q

How would a CT differ in acute, subacute and chronic SDHs

A
  • Acute - hyperdense (bright white)
  • subacute - hyperdense or isodense
  • Chronic - hypodense (black/grey)
41
Q

When is surgery considered for a SDH that is >10mm/ expansile/ causing significant neuro dysfunction

A
  • > 10mm size
  • expansile
  • significant neuro dysfunction
  • Chronic
42
Q

What is pharmacological management of a SDH

A
  • Antiepileptics - phenytoin or levetiracetam
  • Correction of coagulopathy
43
Q

What is a subarachnoid haemorrhage

A

Spontaneous bleeding between the arachnoid and pia mater most commonly due to rupture of a cerebral aneurysm

44
Q

What is the most common cause of a SAH

A

Rupture of a cerebral aneurysm - mainly communicating branches of the circle of willis

45
Q

Give 5 RFs for a SAH

A
  • HTN
  • Smoking
  • FHx
  • Coarctation of aorta
  • Genetic conditions
46
Q

Give 2 genetic conditions that increase the risk of having a SAH

A
  • Polycystic kidney disease
  • CT disorders - Marfans, ehlers danlos
47
Q

Give 4 symptoms of a SAH

A
  • Severe and sudden thunderclap occipital headache
  • N+V
  • LOC
  • Photophobia
48
Q

Give 4 signs of a SAH

A
  • 3rd nerve palsy
    Meningism:
  • neck stiffness
  • kernig’s and brudzinski +ve
49
Q

What investigations are done for a suspected SAH

A
  • CT head - star shaped
  • Lumbar puncture - 12h after CT
  • CT angiography - locate source of bleeding
50
Q

When investigating a SAH why is the lumbar puncture done at least 12h after the onset of Sx

A

With a SAH, CSF will show:
* raised red cell count
* Xanthochromia - yellowcolour due to bilirubin
It takes time for bilirubin to accumulate in the CSF hence the delay in the LP

51
Q

How is a SAH treated

A
  • IV fluids - cerebral perfusion
  • Nimodipine (CCB)
  • Surgery:
  • endovascular coiling
  • surgical clipping
52
Q

Why is Nimodipine prescribed for a SAH

A

Prevent vasospasms which result in brain ischaemia

53
Q

Give 2 complications of a SAH

A
  • Vasospasm
  • Hydrocephalus (increased CSF)
54
Q

What is a intracerebral haemorrhage (ICH)

A

Sudden bleeding into brain tissue due to rupture of blood vessels

55
Q

Give 5 RFs of a ICH

A
  • Uncontrolled HTN - mc
  • Alcohol
  • DM
  • Smoking
  • Anticoagulation
56
Q

Describe the presentation of a ICH

A

Presents the same as an ischaemic stroke - numbness/ weakness, speech disturbances
* more likely to lose consciousness
* more likely to have a headache

57
Q

How is a ICH investigated

A
  • NCCT head
  • midline shift if large
  • acute bleed within brain
58
Q

How is a ICH treated

A
  • BP control - 140mmHg aim
  • Reduce ICP - IV mannitol
  • Stop anticoagulants immediately
  • Neurosurgical referral
59
Q
A

3a neurology (13 decks)

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