Stroke Flashcards
(28 cards)
Pathophysiology of stroke
**Atherosclerotic
**Large vessel, small vessel
**Artery to artery embolism
**Extracranial vessel stenosis
Dissection
**Cardioembolic
Paroxysmal embolism
Intracerebral bleed
**Lobar or deep
**Subarachnoid
Epidural
Subdural
Stroke risk factors
**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
Subtypes of ischaemic stroke - patterns
ACA, MCA, LACUNAR
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
Notes on bleeds on CT Head and causes
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
Notes on suspicious locations for a haemorrhage
**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
Notes on TIAs
- 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
Investigations for ischaemic stroke mechanism
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
Investigations for ICH mechanisms
- 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)
Notes on interventions available in stroke
- Stroke unit admission reduces morbidity and mortality for all stroke subtpes and severity
Notes on thrombolysis
- 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
Notes on symptomatic ICH after thrombolysis
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
Notes on thrombectomy
**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
Management of intracerebral haemorrhage
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
Notes on carotid endaterectomy
**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
Notes on atrial fibrillation
- 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
Notes on antiplatelet therapy
**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
Notes on hypertension management in stroke
- 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
Notes on lipid lowering therapy post stroke
- 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
Subtypes of dysphasia
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
Notes on Gerstman Syndrome
**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
Notes on Lateral Medullary Syndrome
Wallenburg, PICA, vertebral artery syndromes
**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
Notes on Top of the Basilar Syndrome
**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
Notes on Balint syndrome
Bilateral parietal/occiptial junction lesions e.g. watershed
Simultagnosia (inability to perceive more than one onject at a time)
Oculomotor apraxia
Optic ataxia
Notes on Anton syndrome
Bilateral occipital lesions
Cortical blindness
