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3a neurology > Stroke And TIA > Flashcards

Stroke And TIA Flashcards

1
Q

What is a cerebrovascular accident (aka stroke)

A

sudden onset neurological symptoms caused by interruption in the vascular supply of the brain

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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
  • Atrial fibrillation
  • TIA
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6
Q

What are total anterior circulation infarcts and how do they present

A
  • involves middle and anterior cerebral arteries
    Presents with all 3 of the following:
    1. contralateral hemiparesis and/or hemisensory loss of the face, arm & leg
    2. homonymous hemianopia
    3. higher cognitive dysfunction e.g. dysphasia, apraxia, agnosia
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7
Q

What are partial anterior circulation infarcts and how do they present

A
  • involves smaller arteries of anterior circulation
  • Presents with 2 of the following
    1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
    2. homonymous hemianopia
    3. higher cognitive dysfunction e.g. dysphasia, visuospatial disorder
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8
Q

How would a stroke in the anterior cerebral artery present

A
  • Contralateral hemiparesis and sensory loss
  • Lower limbs more affected than upper limbs
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9
Q

How would a stroke affecting the middle cerebral artery present

A
  • Aphasia/ dysphasia
  • Contralateral hemiparesis and sensory loss
  • Upper limbs> lower limbs
  • Contralateral homonymous hemianopia
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10
Q

What are lacunar infarcts and how would they present

A
  • involves perforating arteries around the internal capsule, thalamus and basal ganglia
  • presents with 1 of the following:
    1. clumsy hand and dysarthria
    2. pure hemisensory stroke
    3. pure motor hemiparesis
    4. sensori-motor stroke
    5. ataxic hemiparesis
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11
Q

What are posterior circulation infarcts and how do they present

A
  • involves vertebrobasilar arteries
  • presents with 1 of the following:
    1. cerebellar dysfunction - DANISH
    2. loss of conscioussness/ sleepiness (reduced GCS)
    3. isolated homonymous hemianopia
    4. Brainstem: bilateral sensory/motor deficit
    5. ipsilateral CN palsy and contralateral limb weakness
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12
Q

How would a stroke affecting the posterior cerebral artery present

A
  • Vision loss - contralateral homonymous hemianopia
  • macular sparing
  • visual agnosia - impairment in recognition of visually presented items
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13
Q

How would a vertebrobasilar artery stroke present

A
  • Cerebellar signs (Vanished)
  • reduced consciousness
  • balance disorders
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14
Q

How are ischaemic strokes diagnosed

A
  • Non contrast CT head
  • glucose and electrolytes
  • CT angiography - for candidates for thrombectomy
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15
Q

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

A
  • immediate: brightness in artery indicates clot within lumen
  • Late: darkness of brain parenchyma, loss of grey matter-white matter differentiation
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16
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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17
Q

How is an ischaemic stroke treated

A
  • <4.5h since Sx onset + haemorrhage excluded = thrombolysis (IV alteplase) + thrombectomy
  • 300mg oral/ rectal aspirin should be given ASAP if haemorrhagic stroke has been excluded
  • Maintain glucose, oxygen and hydration
  • HTN should not be treated in the initial period following a stroke (unless prior to thrombolysis)
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18
Q

What is the standard target treatment time for thrombolysis in acute ischaemic stroke

A
  • within 4.5 hours of symptom onset
  • within 9 hours of onset (or midpoint of sleep in ‘wake up’ stroke) if there’s salvageable brain tissue on MRI/ CT perfusion imaging
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19
Q

What is the standard target treatment time for thrombectomy in acute ischaemic stroke

A
  • within 6 hours of symptom onset
  • within 24 hours post-stroke onset if imaging shows salvageable brain tissue
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20
Q

Give 4 absolute contraindications to thrombolysis

A
  • Uncontrolled hypertension >200/120mmHg
  • intracranial neoplasm
  • stroke < 3 months
  • aortic dissection
  • recent head injury
  • active bleeding
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21
Q

Give 3 relative contraindications to thrombolysis

A
  • pregnancy
  • Concurrent anticoagulation
  • Major surgery / trauma in the preceding 2 weeks
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22
Q

What pharmacological interventions are used as prevention for ischaemic strokes

A
  • Clopidogrel monotherapy
  • if clopidogrel not tolerated/ contraindicated then give aspirin + dipyridamole lifelong
  • Atorvastatin after 48h
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23
Q

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

A
  • Hepatic encephalopathy
  • Brain tumours
  • seizures
  • vestibular neuritis
  • spinal cord lesion
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24
Q

What is a transient ischaemic attack (TIA)

A

a sudden transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.

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25
Q

What is the most common cause of a TIA

A

Thrombo-emboli in the internal carotid artery

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26
Q

Give 5 ways a TIA may present

A
  • visual loss: Amaurosis fugax, diplopia, homonymous hemianopia
  • aphasia or dysarthria
  • ataxia, vertigo, or loss of balance
  • unilateral weakness or sensory loss
  • typically resolves within 1 hour
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27
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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28
Q

What investigations should be ordered for a suspected TIA

A
  • MRI brain with diffusion weighted imaging
  • Blood glucose - exclude hypoglycaemia
  • FBC, PTT, INR
  • Serum electrolytes
  • ECG
  • All TIA patients should have an urgent carotid doppler unless they are not a candidate for carotid endarterectomy
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29
Q

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

A

should only be done if the patient is taking anticoagulation or has a bleeding disorder, admit urgently to exclude haemorrhage

30
Q

How is a confirmed TIA managed

A
  • Dual antiplatelet therapy:
    clopidogrel (initial dose 300 mg followed by 75 mg od) + aspirin (initial 300 mg followed by 75 mg od for 21 days) followed by monotherapy with clopidogrel 75 mg od
  • if DAPT not suitable: clopidogrel monotherapy
  • start atorvastatin (oral OD)
31
Q

What is an extradural haemorrhage (EDH)

A

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

32
Q

What causes EDH

A

Typically bleeding from the middle meningeal arteries typically caused by low-impact trauma

33
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
34
Q

What age group is at a higher risk of an EDH

A

Young adults 20-30

35
Q

Why does the risk of an EDH reduce as we age

A

Dura is more firmly adhered to skull as you age

36
Q

Describe the typical symptoms of an EDH

A
  • Headache
  • N+V
  • Confusion
  • fixed and dilated pupil
  • initially loses, briefly regains and then loses again consciousness after low-imapct head injury (lucid interval)
  • Progressively decreasing level of consciousness
37
Q

Describe the pathophys of an EDH

A
  • bleeding into extradural space causes raised ICP
  • results in brain compression and midline shift
38
Q

What imaging should be done for a EDH

A
  • GS = CT head
  • Xray - fracture
39
Q

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

A
  • Bi-convex (lemon) hyperdense collection
  • midline shift
  • limited by suture lines of skull
  • brainstem herniation
40
Q

Treatment of an EDH

A
  • ABCDE
  • IV mannitol to reduce ICP
  • Craniotomy and evacuation of haematoma
41
Q

What is a subdural haemorrhage (SDH)

A

Collection of blood between the dura mater and arachnoid mater

42
Q

What is the most common cause of a SDH

A

trauma rupturing the bridging veins

43
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
44
Q

What is an acute subdural haemorrhage

A

where symptoms develop within 48 hours of a high-impact injury, characterised by rapid neurological deficit

45
Q

What is classed as a subacute SDH

A

3-21 days post-injury, with a gradual progression

46
Q

What is a chronic subdural haemorrhage

A

Common in the elderly, developing over weeks to months. Patients may not recall a specific head injury.

47
Q

Presentation of a subdural haemorrhage

A
  • Fluctuations in the level of consciousness and confusion
  • Headache: Often localised to one side
  • Focal Neurological Deficits: unilateral weakness, aphasia or visual field defects
  • seizures
  • signs of raised ICP - bradykinesia, hypertensions and respiratory irregularities (cushing’s triad)
48
Q

Give 4 physical exam findings of a subdural haemorrhage

A
  • Papilloedema - raised ICP
  • Pupil Changes: Unilateral dilated pupil - compression of 3rd cranial nerve
  • Gait Abnormalities: ataxia or weakness in one leg
  • Hemiparesis
49
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
  • not limited by suture lines
  • midline shift
50
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)
51
Q

How is a subdural haemorrhage managed

A
  • surgical decompression with craniotomy
  • conservatively : observe, monitor and follow-up
  • Correction of coagulopathy
  • phenytoin or levetiracetam if Hx of seizures
52
Q

When is surgery considered for a subdural haemorrhage

A
  • > 10mm size
  • expansile
  • significant neurological dysfunction
53
Q

What is a subarachnoid haemorrhage

A

Spontaneous bleeding between the arachnoid and pia mater

54
Q

What is the most common cause of a subarachnoid haemorrhage

A

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

55
Q

Give 5 RFs for a subarachnoid haemorrhage

A
  • HTN
  • Smoking
  • FHx
  • Coarctation of aorta
  • Genetic conditions
56
Q

Give 2 genetic conditions that increase the risk of having a spontaneous subarachnoid haemorrhage

A
  • Polycystic kidney disease
  • CT disorders - Marfans, ehlers danlos
57
Q

Give 4 symptoms of a subarachnoid haemorrhage

A
  • Severe and sudden thunderclap occipital headache, peaking in intensity within 1-5 mins
  • N+V
  • seizures/ coma
  • meningism (photophobia, neck stiffness)
58
Q

Give 4 signs of a subarachnoid haemorrhage

A
  • 3rd nerve palsy
    Meningism:
  • neck stiffness
  • kernig’s and brudzinski +ve
59
Q

What is the first line investigation for a suspected subarachnoid haemorrhage

A

non-contrast CT head - hyperdense blood in a star pattern

60
Q

When suspecting a subarachnoid haemorrhage, if CT head is done within 6 hours of symptom onset and is normal what should be done next

A
  • do not do a lumbar puncture
  • consider alternative diagnosis
61
Q

When suspecting a subarachnoid haemorrhage, if CT head is done more than 6 hours after symptom onset and is normal what should be done next

A
  • do a lumbar puncture to confirm/ exclude diagnosis
  • lumbar puncture should be done at least 12 hours after the start of the headache
62
Q

What CSF findings are consistent with a subarachnoid haemorrhage

A
  • xanthochromia
  • normal or raised opening pressure
63
Q

When investigating a subarachnoid haemorrhage, why is the lumbar puncture done at least 12h after the onset of the headache

A

to allow the development of xanthochromia (the result of red blood cell breakdown)

64
Q

After spontaneous subarachnoid haemorrhage is confirmed, what investigation should be done to identify the causative pathology

A

CT intracranial angiogram - identify vascular lesion

65
Q

How is a subarachnoid haemorrhage managed

A
  • immediate referral to neurosurgery as soon as CT confirms SAH
  • Supportive - bed rest, analgesia, VTE prophylaxis, discontinue antithrombotics
  • oral Nimodipine (CCB)
  • Surgery within 24h:
  • endovascular coiling by interventional neuroradiologists (mc) or
  • craniotomy and clipping by a neurosurgeon
66
Q

Why is Nimodipine prescribed for a subarachnoid haemorrhage

A

Prevent vasospasms which result in brain ischaemia

67
Q

Give 4 complications of a subarachnoid haemorrhage

A
  • Re-bleeding (high mortality)
  • Vasospasm (typically 1-2w after onset)
  • Hydrocephalus (increased CSF)
  • hyponatraemia due to SIADH
68
Q

What is an intracerebral haemorrhage

A

Sudden bleeding into brain tissue due to rupture of blood vessels

69
Q

Describe the presentation of an intracerebral haemorrhage

A

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

70
Q

How is an intracerebral haemorrhage investigated

A

NCCT head:
- midline shift if large
- acute bleed within brain

71
Q

How is an intracerebral haemorrhage treated

A
  • BP control - 140mmHg aim
  • Reduce ICP - IV mannitol
  • Stop anticoagulants immediately
  • Neurosurgical referral
72
Q

What tool is used to assess stroke symptoms in an acute setting

A

ROSIER (‘Recognition Of Stroke In the Emergency Room’)

3a neurology (16 decks)

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