What is the pathophysiology of stroke?
- Hypoperfusion in the endothelial lumen = depletion of available ATP and impairment of energy dependent cell processes
o Include membrane transport
o Membrane transport is vital to generating APs which drive neuronal transmission
o When available ATP in a vascular territory drops below the threshold that can sustain AP generation, there is a transition from AP activity to AP cessation in that area = absence of neuronal transmission
** this AP switch is binary
How does the pathophysiology of stroke correlate with the symptoms?
o sudden = the sudden transition into AP cessation phase
o Focal = only neurovascular areas in that vascular territory
o Predominantly negative = loss of function due to AP cessation
o All should fit within a vascular territory
What 3 features would make you think - stroke mimic
- Isolated presentations of dysarthria, vertigo or double vision
- Migration of symptoms doesn’t make sense with the AP cessation theory
- Stereotyping (episodic recurrence of neuro disturbance in an identical fashion with complete resolution in between) over weeks, months years typically is an indicator of stroke mimics eg. focal seizures, migraine auras etc
o Capsular warning syndrome can display fluctuating symptoms that recur over minutes to hours (can seem like stereotyping)
What are some post stroke complications?
- Extension of stroke = loss of ischaemic penumbra resulting from suboptimal physiology
- Raised ICP = haematoma expansion, malignant oedema, haemorrhagic transformation or hydrocephalus
- Infections = chest infections (aspiration), UTIs
- Immobility eg. VTE, constipation, bed sores
- Mood disorders (can then go on to affect compliance with rehab etc)
- Pain and fatigue eg. neuropathic pain, poor sleep, etc
- Spasticity, contractures and secondary epilepsy
What does stroke management entail? from the moment they present…
- Admission to stroke unit
- Revascularisation therapy (thrombolysis)
- Optimising physiology via surveillance, prevention, early intervention of complications, nutritional support
- Secondary prevention
- Rehabilitation and reablement
Describe the oxford community stroke project classification
Posterior Circulation Syndrome (POCS)
= cerebellar, vertebral, PCA, basilar arteries
- isolated homonymous hemianopia
- CN palsy and contralateral sensory/motor deficit
- bilateral sensory/motor deficit
- conjugate eye movement disorder
- cerebellar syndrome
Total Anterior Circulation Syndrome (TACS)
= proximal MCA, ICA
- homonymous hemianopia
- higher cerebral dysfunction like dysphasia
- unilateral motor/sensory deficit
Partial Anterior Circulation Syndrome (PACS)
= branch MCA
- 2/3 of TACS
- or just higher cerebral dysfunction
- unilateral sensory/motor deficit may be more focal ie may be confined to just one limb
Lacunar Syndrome (LACS) = lenticulostriate branches of MCA, etc - sensory deficit - motor deficit - sensory motor deficit - ataxic hemiparesis - clumsy hand dysarthria
What specific signs would lead you to an OCSP class
key if the stroke involves 2 or more contiguous somatic areas ie face/arm/leg, then consider LACS
Isolated homonymous hemianopia is a POCS as it can only happen with ischaemia in the occipital lobe
DANISH = POCS
CN + somatic motor/sensory dysfunction = POCS
quadrantinopias may be small occipital infarcts, but typically are PACS events (parietal or temporal lobes)
if motor/sensory is restricted to one somatic area ie just face, just arm, just leg. consider PACS
Why does stereotyping make you think mimic.
When is it not a mimic?
You would need to have repeated embolisation in the same blood vessel (symptoms would be different if another vessel was affected).
This is highly unlikely as blood flow is pretty random
However in focal cerebral hypoperfusion there can be a “stereotype” appearance
- Capsular warning syndrome
- Intracranial stenosis
What is Capsular warning syndrome
Basically when MCA flow is reduced, there is reduced flow into the lenticulostriate arteries.
However, there are so many branches that the perfusion can vary down each branch.
Results in intermittent or fluctuating impairments over mins-hours
(this is unlike vascular stereotyping which is over days/weeks/years)
It is also fluctuating symptoms, not complete resolution between each episode
These are typically LACS
How would intracranial stenosis present?
Basically happens because when an artery is stenosed, the downstream perfusion is disproportionately reduced throughout the vascular bed.
Stroke syndromes + markers of generalised hypoperfusion
ie palpitations, dizziness, pallor, clamminess, occur on standing in postural hypotension
Do target imaging with angiography to confirm
What are the 3 groups of stroke mimics?
1 = identifiable on brain imaging
(subdural haematomas, SOL like brain tumours, MS, brain abscesses)
2 = clear differentiating symptoms recognised on medical assessment.
(BPPV, vestibular neuronitis, transient global amnesia, bells palsy, syncope, etc)
3 = subtle differentiating symptoms
(migraine with aura, focal seizures, functional syndrome)
What toolswould you use to assess a patient presenting with stroke syndrome?
NIHSS = measure stroke related neuro deficit, choose therapies, chart recovery
ASPECTS =
10 point score on CT scan for patients with MCA stroke.
Deduct a point for every region involved.
Used to pick patients for revascularisation therapies and predict outcome
Modified Rankin = measure global disability and assess baseline function.
evaluate outcomes and treatment impact after interventions
Rosier scale for stroke mimics!!!
FAST to identify stroke
TOAST to identify cardioembolic source
ABCD2 for stroke risk assessment after TIA
What is a TIA?
brief episode of neuro dysfunction with clinical symptoms lasting <1 hour.
No evidence of acute infarction
How would you manage an ischaemic stroke?
exclude a haemorrhage first!!
- no contrast CT scan ASAP
(it is really sensitive for heamorrhages and identifies stroke mimics)
Other imaging = MRI, CTA, CTV, CTP/MRP
IV thrombolysis with alteplase = in 4.5 hour window
What would you see on an non contrast CT for an infarct?
- thrombus in vessels (clotted blood looks white so vessels look dense)
- effacement (swelling) and loss of grey/white matter distinction
Why would you do a perfusion CT?
Perfusion CT using iodinated CT contrast
It is worked out by calculating the Cerebral Blood Flow and the Mean Transit Time for blood to traverse a region.
areas with high MTT = hypoperfusion.
Subtract the infarcted tissue from the hypoperfused tissues to get your ischaemic penumbra.
We use it to distinguish ischaemia from infarction.
thrombolysis only benefits ischaemic penumbra. if there is a large core infarct, thrombolysis will only increase risk of secondary haemorrhage
What are the indications for alteplase thrombolysis?
Alteplase can be administered up to 4.5 hours.
Disabling impairments like NIH>4, dysphasia, inability to self care/mobilise independently, visual field defects, dysphagia
What are some absolute contraindications for alteplase thrombolysis
Absolute - bp >185/110 after 2 attempts to reduce - surgery/trauma in past 14 days - stroke in past 14 days active internal bleeding - severe haem abnormalities - INR>1.7, APTT>40 - on high dose lmwh - on rivaroxiban, epixaban, edoxaban - platelets <50x10 9/L - LP in last 7 days - SAH symptoms - infective endocarditis, pericarditis, etc - childbirth in past 4 weeks - acute pancreatitis - severe liver disease
What imaging would you do and why?
Pipes = blood vessels
= CT angiography
Parenchyma
= non contrast CT or MRI
Perfusion and Penumbra = at risk tissue
= CT Perfusion scan
When would you do a thrombectomy?
CT angiography showing good collateral circulation + a good ASPECTS score is good grounds
Indicated in large vessel occlusion stroke, pre stroke MRS0-1, NIHSS=5 or more
Do it in a 6 hour therapy window
What are some causes for haemorrhagic stroke
Primary (small vessel) haemorrhage
- hypertension
- cerebral amyloid angiopathy
Secondary haemorrhage
- tumour
- vascular eg. aneurysm, AVM, vasculitis
- coagulopathy, warfarin, aspirin
- cocaine, alcohol
How would you image a haemorrhagic stroke?
CT scan
- initially hyperdense
- then as blood clots, density increases
- then globin starts to break down, density starts to fall starting at periphery and going to centre
- eventually results in a residual haematoma cavity
MRI T1 and T2 for time course
Causes:
- haemorrhagic transformation of an infarct = Diffusion Weighted Imaging
- Venous Sinus Thrombosis = MRV
- Tumour = Contrast enhanced-MRI
- Aneurysm, AVM = MRA
What are some complications of a haemorrhagic stroke?
Mass effect
= effacement of ventricles, midline shift
Twisted ventricle
= occlusion contralateral foramen of munro.
twisted ventricle dilates as csf is trapped
Subfalcine herniation, midline shift
Uncal herniation
Transtentorial herniation (brain is forced down)
How would you manage intracranial haemorrhage?
within 6 hours of symptom onset:
- lower systolic bp to 130mmHg within 1 hour (first line IV LABETALOL)
- stop and reverse anticoagulants
- ventricular drain for hydrocephalus
- neurosurgery for haematoma removal or decompressive hemicraniectomy
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