Neurology: Strokes Flashcards

1
Q

Remind yourself of the blood supply to the brain

A
  • Anterior cerebral artery: medial aspect of frontal lobe, medial aspect of parietal lobe, corpus callosum
  • Middle cerebral artery: lateral parts of frontal & parietal lobe, superior temporal lobe, deep grey matter structures via lenticulostriate arteries
  • Posterior cerebral artery: occipital lobe, inferior temporal lobe, thalamus, midbrain
  • Cerebellum:
    • Superior: superior cerebellar artery
    • Anterior inferior: anterior inferior cerebellar artery
    • Posterior inferior: posterior inferior cerebellar artery
  • Brainstem:
    • Midbrain: superior cerebellar artery & branches from PCA
    • Pons: anterior inferior cerebellar artery & pontine arteries from basilar artery
    • Medulla: posterior inferior cerebellar artery
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2
Q

State some potential sites of strokes and features of each

A
  • Lacunar strokes: stroke affecting lenticulostriate arteries supplying deep grey matter structures e.g. basal ganglia, thalamus, internal capsule. Strong association with hypertension. Present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
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3
Q

What else are strokes known as?

A

Cerebrovascular accidents

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4
Q

Define a stroke

A
  • Stroke is a clinical syndrome of presumed vascular origin characterized by rapidly developing signs of focal or global disturbance of cerebral functions which lasts longer than 24 hours or leads to death. (CKS NICE)
  • Neurological deficit lasting more than 24hrs caused by cerebrovascular aetiology (BMJ)
  • Serious life threatening condition in which blood supply to part of brain is disrupted. Symptoms persist for more than 24 hours
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5
Q

State, and describe, the two main types of stroke (include what % of strokes each accounts for) and any subtypes of each

A
  • Ischaemic stroke (85%)
    • Thrombotic
    • Embolic (important cause to remember is AF)
    • Systemic hypoperfusion (e.g. due to cardiac arrest)
    • Cerebral venous sinus thrombosis (causes back pressure which reduces perfusion)
  • Haemorrhagic stroke (10%)
    • Intracerebral
    • Subarachnoid
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6
Q

State some risk factors for ischaemic strokes

A
  • Increasing age
  • Previous stroke or TIA
  • Cardiovascular disease
  • Hypertension
  • Smoking
  • Hyperlipidaemia
  • Diabetes
  • AF (for embolism)
  • Carotid artery disease
  • Vasculitis
  • Thrombophilia
  • COCP
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7
Q

State some risk factors for haemorrhagic strokes

A
  • Increasing age
  • Hypertension
  • Anticoagulation
  • Coagulation disorders
  • AV malformations
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8
Q

Comparison of ischaemic and haemorrhagic strokes

A
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9
Q

Outline possible features of a stroke

A

Sudden onset of:

  • Weakness of limbs
  • Facial weakness
  • Dysphasia
  • Visual disturbance
  • Sensory disturbance
  • Balance problems

Symptoms & signs depend on where in brain the stroke is

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10
Q

State the classes of stroke based on the Oxford/Bamford stroke classification

A
  • Total anterior circulation infarct (TACI) 15%
  • Partial anterior circulation infarct (PACI) 25%
  • Posterior circulation infarct (POCI) 25%
  • Lacunar infarct (LACI) 25%
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11
Q

For a total anterior circulation infarction (TACI), discuss:

  • Which artery commonly involved
  • Features
A
  • Middle & anterior cerebral arteries resulting in large cortical stroke
  • ALL THREE OF THE FOLLOWING:
    • Unilateral hemiparesis and/or hemisensory loss of face, arm & leg
    • Homonymous hemianopia
    • Higher cognitive dysfunction (e.g. dysphasia)
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12
Q

For a partial anterior circulation infarct (PACI), discuss:

  • What artery usually involved
  • Features
A
  • Only part of anterior circulation compromised e.g. could be upper or lower division of MCA
  • TWO OF THE FOLLOWING MUST BE PRESENT:
    • Unilateral hemiparesis and/or hemisensory loss of face, arm & leg
    • Homonymous hemianopia
    • Higher cognitive dysfunction (e.g. dysphasia)
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13
Q

For a lacunar infarct (LACI), discuss:

  • Which artery commonly involved
  • Features
A
  • Subcortical stroke due to small vessel disease involving perforating/lenticulostriate arteries (which supply deep grey matter structures e.g. internal capsule, thalamus, basal ganglia)
  • ONE OF THE FOLLOWING:
    • Unilateral weakness and/or sensory deficit of face & arm, arm and leg or all three
    • Pure sensory stroke
    • Ataxic hemiparesis

Lacunar infracts can be:

  • Pure sensory stroke
  • Pure motor stroke
  • Sensori-motor stroke
  • Ataxic hemiparesis
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14
Q

For a posterior circulation infarct (POCI), discuss:

  • Which artery commonly involved
  • Features
A
  • Disruption to posterior circulation (posterior cerebral artery, vertebral artery, basilar artery)
  • ONE OF THE FOLLOWING:
    • Cerebellar or brain stem syndromes
    • Loss of consciousness
    • Isolated homonymous hemianopia

*NOTE: brainstem or cerebellar syndromes could include:

  • Cranial nerve palsy and a contralateral motor/sensory deficit
  • Bilateral motor/sensory deficit
  • Conjugate eye movement disorder (e.g. horizontal gaze palsy)
  • Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
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15
Q

Other than those included in the Oxford/Bamford stroke classification there are other recognised patterns of stroke; state 2

A
  • Lateral medullary syndrome/Wallenberg’s syndrome
  • Weber’s syndrome
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16
Q

For lateral medullary syndrome/Wallenberg’s syndrome, discuss:

  • Which artery is affected
  • Features (and why these features are seen)
A
  • Posterior inferior cerebellar artery (supplies lateral medulla
  • Features:
    • Ipsilateral limb ataxia (inferior cerebellar peduncle)
    • Nausea, vomiting, vertigo, nystagmus (CNVIII nuclei)
    • Dysphagia, dysarthria, loss of gag reflex (nucleus ambiguus)
    • Contralateral pain/temp loss on body (spinothalamic- remember decussate at level they enter spine)
    • Ipsilateral pain/temperature loss on face (spinal trigeminal tract)
    • Ipsilateral Horner’s syndrome (descending hypothalamics)
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17
Q

For Weber’s syndrome, discuss:

  • What artery is affected
  • Features (and why these features are seen)
A
  • Branch of posterior cerebral artery interrupting blood supply to the part of midbrain (crus cerebri and CNIII)
  • Features:
    • Ipsilateral CNIII palsy
    • Contralateral weakness (motor fibres run in crus cerebri then decussate at medulla)
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18
Q

Symptoms alone CANNOT be used to differentiate between ischaemic and haemorrhage strokes; however, some features are more likely in patients with haemorrhagic stroke. State some of these features

A
  • Decreased level consciousness (up to 50%)
  • Headache
  • Nausea & vomiting
  • Seizures (up to 25%)
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19
Q

What tool is used to identify stroke in the community?

A

FAST Campaign

  • Face - ‘Has their face fallen on one side? Can they smile?’
  • Arms - ‘Can they raise both arms and keep them there?’
  • Speech - ‘Is their speech slurred?’
  • Time - ‘Time to call 999 if you see any single one of these signs.’
  • *NOTES:*
  • Positive predictive value of 78%
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20
Q

What tool is used for recognition of stroke in the emergency room?

Briefly outline this tool

A

Stroke is likely is >0

21
Q

What investigations are done for a suspected stroke and why?

A
  • First line: Immediate non-contrast CT Head (to determine if ischaemic or haemorrhagic stroke)
  • Serum glucose (hypoglycaemia can mimic stroke)
  • U&E’s
  • FBCs
  • ECG (exclude cardiac arrhythmia- particularly AF)
  • Coagulation (see if coagulopathy but don’t delay tx waiting for results)
  • Troponin I/T (see if MI also)
22
Q

What might you see on non-contrast CT head In:

  • Acute ischaemic strokes
  • Acute haemorrhagic strokes
A

Acute ischaemic stroke:

  • Low density/hypodensity (dark)
  • Hyperdense artery sign (corresponding with the responsible arterial clot)

Acute haemorrhagic stroke:

  • Hyperdense (bright) material (blood) surrounded by low density (oedema)
23
Q

Discuss the immediate management of ischaemic strokes (ensure you include information about when treatments can and cannot be offered)

A

Immediate emergency admission to specialist stroke unit:

  • Exclude hypoglycaemia (hypoglycaemia can mimic stroke)
  • Immediate non-contract CT brain (exclude haemorrhagic stroke)
  • Aspirin 300mg (PO or PR) STAT after CT, continue for 2/52
  • Thrombolysis with IV alteplase can be used if:
    • Pt has presented within 4.5hrs of stroke symptoms
    • AND haemorrhage definitely been excluded (had CT head)
  • Thrombectomy:
    • Within 6hrs of symptom onset if pt has confirmed proximal anterior circulation occlusion (if within 4.5hrs can also have thrombolysis)
    • Within 24hrs of symptom onset if pt has confirmed proximal anterior circulation occlusion AND imaging shows there is potential to salvage brain tissue
    • Can consider within 24hrs of symptom onset it have confirmed proximal posterior circulation occlusion AND imaging shows there is potential to salvage brain tissue
  • Supportive (blood glucose, oxygen saturation, temperature, BP kept in normal ranges, SALT assessment & alternative feeding arrangements if required)
24
Q

Summarise when thrombolysis can be offered for stroke

Summarise when thrombectomy can be offered for stroke

A
  • Thrombolysis with IV alteplase: presented within 4.5hrs of stroke symptoms
  • Thrombectomy:
    • Within 6hrs of symptom onset if pt has confirmed proximal anterior circulation occlusion (if within 4.5hrs can also have thrombolysis)
    • Within 24hrs of symptom onset if pt has confirmed proximal anterior circulation occlusion AND imaging shows there is potential to salvage brain tissue
    • Can consider within 24hrs of symptom onset it have confirmed proximal posterior circulation occlusion AND imaging shows there is potential to salvage brain tissue

*Zero to finals says generally not used 24hrs since start of symptoms

25
Q

State some absolute contraindications to thrombolysis

A
26
Q

Discuss the immediate management of haemorrhagic strokes

A
  • Urgent neurosurgical consultation for advice on further management
  • Most pts not suitable for surgical intervention hence management is usually supportive:
    • Stopping anticoagulants and antithrombotic to minimise further bleeding
    • Reverse anticoagulation if possible
    • Lower BP (trials shown improved outcomes)
27
Q

Discuss the secondary prevention management of stroke

A
  • Treat modifiable risk factors (e.g. diabetes, hypertension [antihypertensive usually initiated by secondary care] obesity, AF [see separate FC]. Note that antihypertensive will be started in secondary care)
  • Clopidogrel 75mg once daily (alternative is MR dipyridamole 200mg twice daily & aspirin 75mg once daily. Can have just aspirin if both Clopidogrel and dipyridamole contraindicated)
  • Atorvastatin 80mg once daily (don’t start immediately)
  • Carotid endarterectomy or stenting (in patients with carotid artery disease. Different criteria vary: pts must have between 50-70% stenosis)
28
Q

Discuss what supportive care may be required for stroke pts

A

Fluid Management

  • Important to maintain normovolaemia (hypovolaemia can worse ischaemia & increase risks of other complications e.g. DVT, constipation. Hypervolaemia can lead to complications such as cerebral oedema, heart failure, hyponatraemia etc…)
  • Oral hydration preferred if safe swallow
  • IV fluids may be required otherwise

Glycaemic Control

  • Many pts will be NBM, at least until seen by SALT and others in MDT so that management plan put in place
  • Hence, must monitor (and even more important if diabetic)
  • NICE recommend blood sugar between 4 and 11mmol/L (hyperglycaemia associated with increased mortality, hypoglycaemia can cause neuronal damage)
  • If pt on insulin, NICE suggest using sliding scale

Blood Pressure

  • MUST BE CAUTIOUS about lowering BP as may compromise collateral blood flow and worsen perfusion & ischaemia. NICE only recommend anti-hypertensives if there is a hypertensive emergency or other serious issues (e.g. aortic dissection, pre-eclampsia etc…)
  • Always seek advice as must be careful

*

29
Q

What tool can be used to measure stroke severity?

A

National Institute of Health Stroke Scale: an assessment tool which gives a quantitative measure of stroke-related neurological deficit. It can be used as a measure of stroke severity.

It assess 11 key components:

  • Level of consciousness & communication
  • Eye movements
  • Visual fields
  • Facial palsy
  • Upper limb motor
  • Lower limb motor
  • Limb ataxia
  • Sensation
  • Language/aphasia
  • Dysarthria
  • Extinction/inattention

Score ranges from 0 to 42

  • 0= no stroke symptoms
  • 1-4= minor stroke
  • 5-15= moderate stroke
  • 16-20= moderate to severe stroke
  • 21-42= severe stroke
30
Q

What score is often used to measure disability post-stroke?

A

Barthel index (BI)

**10 tasks/ADLs scored according to amount of time or assistance required. Score is from 0 to 100 (worst). Should be used post-stroke and during ongoing rehabilitation to monitor improvement

31
Q

Who will be involved in the rehabilitation process post stroke?

A
  • Nurses
  • Speech and language (SALT)
  • Dieticians
  • Physiotherapy
  • Occupational therapy
  • Social services
  • Optometry and ophthalmology
  • Psychology
  • Orthotics
32
Q

What is the stroke pathway?

A

Document that details the core components of optimal service for someone who has suffered a stroke

33
Q

Summarise the stroke pathway

A
  • Pre-hospital
    • Hopefully patient will recognise signs of stroke (FAST) and ring 999
    • Priority 1 call for paramedics
    • Paramedics quickly assess patient
    • Paramedics use’ bat phone’ to alert hospital that they have a pt who may be having acute stroke
    • Stroke team is pre-alerted to be ready
  • Acute response and treatment on HASU
    • Stroke team meet pt in A&E and do the following:
      • Brief focused history
      • IV acess to get bloods
      • ECG
      • Baseline observations
      • NOTE: some of this may happen on route to CT
    • CT scan is interpreted there and then
    • Determine immediate treatment (thrombolysis [start giving whilst in CT scanner], bp lowering, thrombolectomy)
    • Pt transferred onto stroke unit for up to 72 hours
  • Life after HASU
    • Options: home, discharge at home with intensive therapy at home, rehabilitation, transfer to acute stroke ward
34
Q

State some potential complications following a stroke

A
  • Pneumonia (Sit up? Safe swallow?)
  • Seizures
  • Pressure sores
  • Dehydration/malnutrition
  • Constipation
  • Incontinece/retention
  • Depression
  • Spasticity
  • Venous thromboembolism
35
Q

What is a TIA?

A

Transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction

*NOTE: features are similar to those of a stroke but they resolve within ~1 hour usually

36
Q

What is crescendo TIA?

A

Two or more TIAs within 1 week

37
Q

How long do symptoms of a TIA usually last?

A

Typically ~1hr or less

38
Q

What score is used to risk stratify patients with a suspected TIA?

A

ABCD2 prognostic score (estimates risk of stroke after suspected TIA)

**NOTE: PassMed says no longer recommended by NICE as it performs poorly

39
Q

Discuss the immediate and further management/prevention of TIAs

A

Immediate Management

  • 300mg aspirin IMMEDIATELY unless:
    • Pt has bleeding disorder or is taking anticoagulant (needs immediate admission for imaging to exclude haemorrhage)
    • Pt already taking low dose aspirin; continue current dose until reviewed by specialist
    • Aspirin contraindicated; discuss with specialist
  • Urgent carotid doppler
    • All pts should have unless not a candidate for carotid endarterectomy
  • Diffusion weighted MRI
    • Detect vascular territory affected (ideally done same day as specialist assessment/or at least before)
  • Organise specialist review:
    • >1 TIA (crescendo TIA) or suspected cardioembolic source or severe carotid stenosis discusss need for admission & observation urgently with stroke specialist
    • TIA in last 7 days; arrange urgent assessment within 24hrs
    • TIA occurring >7 days ago arrange ASAP within 7 days
  • Advise person not to drive till seen by specialist (if TIA need to avoid driving for 1 month)

Further Management/Prevention

  • Treat modifiable risk factors (e.g. diabetes, hypertension [antihypertensive usually initiated by secondary care] obesity, AF [see separate FC]. Note that antihypertensive will be started in secondary care)
  • Clopidogrel 75mg once daily (alternative is MR dipyridamole 200mg twice daily & aspirin 75mg once daily. Can have just aspirin if both Clopidogrel and dipyridamole contraindicated)
  • Atorvastatin 80mg once daily (don’t start immediately)
  • Carotid endarterectomy or stenting (in patients with carotid artery disease. Different criteria vary: pts must have between 50-70% stenosis)
40
Q

What are NICE guidelines regarding management of patients with AF who develop a stroke or TIA

A
  • Following an ischaemic stroke or TIA, pts should be given warfarin or direct thrombin or factor Xa inhibitor as anticoagulant of choice
  • Anticoagulation should be started after 2 weeks (or even longer if very large infarct)
41
Q

What are the rules surrounding driving after a stroke or TIA?

A
  • Stroke or TIA: 1 month off driving, do not need to inform DVLA if no residual neurological deficit
  • Multiple TIAs over short period of times: 3 months off driving and inform DVLA
  • If there is residual neurological deficit after 1 month following stroke: inform DVLA and await guidance
42
Q

Put the following in order of density starting with lowest density first:

  • CSF
  • Water
  • Grey matter
  • White matter
  • Bone
  • Air
  • Coagulated blood
A
  • Air
  • Water
  • CSF
  • White matter
  • Grey matter
  • Coagulated blood
  • Bone
43
Q

What framework/mnemonic can you use to help you structure basic interpretation of head CT scan?

A

Blood Can Be Very Bad:

  • Blood
  • Cisterns
  • Brain
  • Ventricles
  • Bone

**Obviously usual intro as with all imaging… Head CT of ___ aged ___ taken ____ for _____.

44
Q

How does an acute bleed/haematoma appear on head CT?

How does chronic bleed/haematoma appear on head CT?

A
  • Acute: hyperdense (lighter)
  • Chronic: hypodense (darker)
45
Q

What is sulcal effacement and what does it suggest?

A
  • Loss of normal gyral-sulcal pattern of brain
  • Typically associated raised ICP
46
Q

What is loss of grey-white matter differentiation and what does it suggest?

A
  • Loss of distinction between grey & white matter
  • Suggests oedema which may be secondary to hypoxic brain injury, infarction, tumour or cerebral abscess
47
Q

State some potential causes of hypodense foci on head CT scans

A
  • Air
  • Oedema
  • Fat
48
Q

State some potential causes of hyperdense foci on head CT scans

A
  • Blood
  • Thrombus
  • Calcification

**Hyperdense MCA is sometimes seen in TACS and indicates large thrombus in vessel

49
Q

How can you distinguish between a T1 and T2 weighted head MRI?

A

Based on density of grey and white matter you expect white matter to appear darker (as it is hypodense) and grey matter to appear lighter (hyperdense):

  • T1: grey matter darker than white matter
  • T2: grey matter is lighter than white