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Neurology > Stroke > Flashcards

Stroke Flashcards

1
Q

Pathophysiology of stroke

A

**Atherosclerotic
**Large vessel, small vessel
**Artery to artery embolism
**Extracranial vessel stenosis
Dissection
**Cardioembolic
Paroxysmal embolism
Intracerebral bleed
**Lobar or deep
**Subarachnoid
Epidural
Subdural

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2
Q

Stroke risk factors

A

**Ischaemic
**Age (strongest independent risk factor for stroke)
Hypertension
AF
Tobacco
Diabetes
Dyslipidaemia
Life-style
Ethnicity
PFO
Hypercoaguable state

**Haemorrhagic
**Hypertension
Cerebral amyloid angiopathy
Antithrombotic therapy
Heavy ETOH use
Hypocholesterolaemia
Underlying structural pathology

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3
Q

Subtypes of ischaemic stroke - patterns

ACA, MCA, LACUNAR

A

Left MCA
○ Right hemiparesis (face/arm >leg as leg represented mostly in anterior artery circulation), aphasia, right sensory/visual inattention, right hemianopia

Right MCA
○ Left hemiparesis (face/arm>leg in MCA), dysarthria, left sensory/visual inattention, left hemianopia

Lacunar infarct
○ Isolated face/arm/leg weakness or numbness with dysarthria, clumsy hand, ataxic hemiparesis

Posterior circulation (particularly basilar)
○ Diplopia, vertigo, dysarthria, dysphagia, ataxia, hemi/tetraparesis, ipsilateral face/contralateral body numb/weak
- Posterior cerebral artery - homonymous heminaopia, behavioural change
- Diplopia most telling of a basilar occlusion

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4
Q

Notes on bleeds on CT Head and causes

A

Lobar haemorrhage - inolder person usually due to amyloid angiopathy
□ Other causes - bleeding metastases

Deeper haemorrhage often hypertensive

Cerebellar haemorrhages usually hypertensive

Subdural haemorrhage

Aneurysmal subarachnoid haemorrhage
□ Can also get focal subarachnoid haemorrhages as a manifestation of amyloid angiopathy

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5
Q

Notes on suspicious locations for a haemorrhage

A

**Anterior cranial fossa
**Suspect anterior communicating artery aneursym - need cta

**In contact with Sylvian fissure
**Suspect MCA aneursym - CTA

**Hyperdensity in sagital sinus with nearby haemorrhage
**Suspect venous sinus thrombosis - get a CTV

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6
Q

Notes on TIAs

A
  • Untreated 10% have a stroke in the first week after a TIA
  • If patient still has symptoms when they are seen in ED more likely a stroke (average duration TIA is 10 minutes)
  • Need to look for carotid stenosis, AF
  • DAPT, antihypertensives, statins
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7
Q

Investigations for ischaemic stroke mechanism

A

Investigation for arterial pathology
○ CTA (aortic arch to cerebral vertex) (or carotid ultrasound)
§ Atherosclerosis
§ Dissection
§ Vasculitis
Investigations for cardiac source embolism
○ ECG, Holter, TTE/TOE
§ AF
§ Akinetic LV segment
§ Endocarditis/vegetation
§ PFO - TTE with bubble study if age <60 and no other cause

Investigations for rare causes
Blood tests for thrombophilia (antiphospholipid etc.), vasculitis, Fabry’s disease

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8
Q

Investigations for ICH mechanisms

A
  • CT Angiography (most patients) - underlying vascular malformation
    • CT venography (selected patients) - cerebral venous sinus thrombosis
    • Catheter angiography (selected) - subtle AVMs or dural AV fistulas
    • Delayed MRI (around 8 weeks) for most patients - underlying mass lesion, cavernoma, AVM
      ○ Evidence of microangiopathy - hypertensive (deep), amyloid (lobar)
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9
Q

Notes on interventions available in stroke

A
  • Stroke unit admission reduces morbidity and mortality for all stroke subtpes and severity
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10
Q

Notes on thrombolysis

A
  • TPA cleaves plasminogen to plasmin which breaks up fibrin clot
  • No statidically significant benefit after 4.5 hours of onset

**Extended window thrombolysis
**CT perfusion or MRI selected patients benefit from alteplase 4.5-9 hours after onset, or within 9 hours of midpoint of sleep for wake up stroke
- Improved functional outcomes
- Similar ICH risk to 0-4.5 hr thrombolysis

100 patients within 3 hours of onset treated with thrombolysis
- 1/3rd better off, 2/3rds no differences, 2 worse off - bleed

**Notes on orolingual angioedema
**2% overall, 5% is taking ACEI
- Usually unilateral, contralateral to brain lesion
- 10-105 minutes post bolus (differential tongue haematoma)
- Traditionally give hydrocortisone
- Usually don’t required intubation
- Bradykinin mediated ?icatibant

**Chance of early recanalization after IV alterplase in large vessel occlusion
**See slide

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11
Q

Notes on symptomatic ICH after thrombolysis

A

Damaged blood brain barrier (which is a function of hypoperfusion intensity x time) plus reperfusion

Note haemorrhagic transformation is nearly universal in large infarcts
- Inconsequential (some studies associated with favourable prognosis as correlates with reperfusion)

Parenchymal haematoma with mass effect beyonf the infarct is harmful -1.7% and more common with increasing stroke severity
- Imaging risk factors - CT hypdensity, severe leukoaraiosis, large core and severe hypoperfusion, delayed reperfusion

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12
Q

Notes on thrombectomy

A

**Vessels which benefit
**ICA and M1
Tandem disease (cervical and intracranial) = benefit
?M2 - less common, highly variable anatomy, less territory at risk, greater tPA response, pooled meta analysis equivocal
Should consider if basilar occlusion but no clear evidence of benefit currently

  • **Benefit levels off after 6 hours
  • DEFUSE TRIAL
  • **Demonstrated benefit 6-12 hours from onset in ICA/M1 occlusions and cores < 70ml

**?To thrombolyse
**All trials have given thrombolysis
Tenecteplase improves reperfusion prior to thrombectomy vs alteplase
Also a benefit for endovascular therapy in those inegilible for IV thrombolysis

Need good pre-morbid function to be eligible

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13
Q

Management of intracerebral haemorrhage

A

Intensive BP lowering
○ 140mmHg but not substantially lower, ideally within 1 hour, no clear benefit after 6

Reverse anticoagulants
○ Prothrombinex + vitamin K
○ Idaraucizumab
○ Platelet transfusions associated with worse outcome

Stroke unit care

?Haemostatics - not using TXA currently

Surgery
○ Usually for posterior fossa if mass effect
○ Supratentorial = lifesaving, not routine
§ Ongoing research into ultra-early minimally invasive surgery

Determine underlying cause
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14
Q

Notes on carotid endaterectomy

A

**Strongest evidence for CEA within 2 weeks of stroke/TIA (including retinal ischaemia) in the relevant territory and a carotid stenosis of 70-99%
**Modest benefit for stenosis 60-69%
No benefit for asymptomatic carotid surgery (or in the setting on non-stroke presentations)

Carotid stenting often performed during acute thrombectomy (to allow access to intracranial circulation) - some emerging evidence for potential equipoise between endarterectomy and stenting in patients <70 years - not yet established

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15
Q

Notes on atrial fibrillation

A
  • If found DOACs. Warfarin only if mechanical heart valve, “valvular AF”, significant renal impairment
  • No head to head trials between different DOACs
  • LAA closure remains an option with absolute contraindications to anticoagulation

**Detection
**24 Holter +/- longer if not detected
The longer you look the more AF you will find

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16
Q

Notes on antiplatelet therapy

A

**DAPT - aspirin and clopidogrel (CHANCE & POINT Trials)
**For mild stroke (NIHSS <=3) or high risk TIA (ABCD2 >4)
Aspirin + load with clopidogerl 300mg and 75mg daily thereafterfor 3 weeks then one agent alone

**Ticagrelor + aspirin
**Potential benefit of ticagrelor is that it does not require hepatic activation (like clopidogrel which we know 60% of Asians are deficienct in).
One trial (THALES) comparing ticagrelor + aspirin to aspirin alone - small reduction in stroke/death risk but increased bleeding risk at 30 days
- CHANCE 2 trial in China - ticagrelor + aspirin compared to aspirin + clopidogrel - reduced strokes at 90 days

17
Q

Notes on hypertension management in stroke

A
  • Ideal long term target not well established - all patients with BP >140/90 should be started (on treatment intensified) in hospital
  • Benefit independent of agents in terms of stroke risk reduction
  • Long-term target not well established
18
Q

Notes on lipid lowering therapy post stroke

A
  • In patients with stroke or TIA of atherosclerotic origin, target LDL <1.8 is superior to target 2.3-2.8
  • Strongest evidence re lipid lowering from SPARCL trial 2006
  • Atorvastatin 80mg vs placebo in patients with stroke/TIA and LDL 2.6-4.9
  • Reduced risk of recurrent stroke over 5 years
  • Small increase in haemorrhagic stroke on post-hoc analysis - Statins generally not recommended after ICH
19
Q

Subtypes of dysphasia

A

Broca’s aphasia/expressive/non-fluent
○ Unable to name objects, poor comprehension, poor repitition
○ Localises to broca’s area in the L posterior inferior frontal gyrus
Wernicke’s aphasia/fluent/receptive
○ Able to perform correct grammatical sentences but language content is incorrect
○ Localises to dominent superior temporal gyrus
○ Poor comprehension and repitition
○ Fluent verbal output
Global aphasia
○ Almost mute patient
○ Poor verbal output, comprehension, repitition and understanding
Transcortical sensory aphasia
○ Good repitition but comprehension and fleuncy are poor
Transcortical motor aphasia
○ Good comprehension but poor verbal output w/ exception of repitiion
○ Writing usually impaired
○ Repitition spared - arcuate fasciculus not involved

20
Q

Notes on Gerstman Syndrome

A

**Location
**Inferior parietal lobule of dominant hemisphere
Angular and supramarginal gyri near the temporal and parietal junction

**Symptoms
**Dysgraphia/agraphia
Dyscalculia/acalculia
Finger agonsia
Left-right disorientation
+/- aphasia
+/- apraxia

21
Q

Notes on Lateral Medullary Syndrome

Wallenburg, PICA, vertebral artery syndromes

A

**Location
**Lateral medulla

**Vessels
**Vertebral artery
PICA
Superior middle and inferior medullary artery

**Symptoms
**C/L trunk/limb numbness to pain and temperature
Ipsilateral fical numbness (pain and temp), skew deviation, dysphagia/hoarseness/loss of gag, Horner’s syndrome, limb ataxia
Palatal myoclonus
Vertigo/nystagmus

22
Q

Notes on Top of the Basilar Syndrome

A

**Features
**Ptosis
Dilataed pupils
Ocular motor deficits
Somnolence, hallucinations, dreamlike behaviour
Moto function otherwise preserved

Can propagate -> locked in syndrome

If you get fixed dilated pupils, no upgaze and somnolent in a stem think brainstem problem

23
Q

Notes on Balint syndrome

A

Bilateral parietal/occiptial junction lesions e.g. watershed
Simultagnosia (inability to perceive more than one onject at a time)
Oculomotor apraxia
Optic ataxia

24
Q

Notes on Anton syndrome

A

Bilateral occipital lesions
Cortical blindness

25
Q

Benedikt syndrome

A

Midbrain stroke
Posterior cerebral artery or penetrating branches of basilar artery
CN III palsy
Ataxia/choreoathetosis

26
Q

Notes on Webber syndrome

A

Similar to Benedikt except more hemiplegia than limb ataxia

27
Q

Notes on anterior spinal artery infarct

Features

A

Loss of power distally
+/- loss of temp/pain
Posterior column unaffected

28
Q

Notes on subarachnoid haemorrhage

A
  • Thunderclap headache
  • Photophobia, neck stiffness, confusion, focal neurology, seizures
  • Main risk factors: aneursym, smoking, HTN, female, methamphetamines, cocaine

Work-up: Head CT ideally with CTA - 98.7% sensitive < 6 hours from onset. LP for xanthochromia (develops 12 hours post headache)
- MRI with SWI

Treatment
- ABC
- Lower BP to <140 to prevent rebleeding
- Clip/coil anuerysm to fix underlying issue
- Oral nimodipine to prevent vasospasm

Neurology (9 decks)

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