hrhodes's version from 2015-11-03 00:52

CT anatomy



Question Answer
How can you remember the name of the middle of the lateral ventricles?LUCY. Septum Pellucidem
Where is the 4th ventricle?Between pons and cerebellum
What makes up the brainstem?Thalamus, Midbrain, pons, Medulla, cranial nerves
Whats the bit pup near the lateral ventricles and CC that is too high for third and 4th ventricles? Quadrigeminal cistern ( like trigeminal but quad
What are good websites form Brain anatomy and interpretation?,,

Epidemiology and demographics of stroke

Question Answer
How is TIA a good thing?early Ix and intervention can prevent 80% early CVA’s
How does CVA incidence change with age?incidence doubles every decade over 55yrs
Describe the economic impacts of CVAMASSIVE. 3rd largest killer in West. 20% need institutional care for >3/12; 20% remain permanently disabled; death 10%; 55% discharge home
Describe the incidence and demographics affected by ICHM >W, 30-50% die (80% if on warfarin); 33% discharge home; 30% 1yr survival
Lacunar infarct-die or disabled?death low; 30% long term disability


Question Answer
Define TIAFND lasting <24hrs usually lasting <1hr, without evidence of acute infarction
Define cerebral infarctThrombotic or embolic occlusion of major intracranial BV resulting in acute non-reversing loss of brain function due to vascular event
Few key words of CVAThrombotic/embolic occlusion. Major Intracranial BV. Non reversible vascular event. Permanent loss of brain function

Pathophysiology acute CVA

Question Answer
What % of cardiac output does the brain receive? 15% CO,
What % of pO2 used by brain?25% O2 consumption 70% glucose
At what blood flow level does permeant cell death in brain occur?<10ml/min/100g - cell death, ATP production ceased. (<20ml/min/100g = reversible ischaemia, absent EEG activity)

Risk factors

Question Answer
Name 12 risk factors for CVAHTN most important; also DM, smoking, incr chol, AF, endocarditis, MS, prosthetic heart valves, male, incr age, heart disease, cervical dissection
Where does thromboembolism most commonly occur?Bifurcation ICA
Where does atherosclerosis most commonly occur?Origin of ICA


Question Answer
Define TIAFND <24hours, usually less than 1 hour
What is the typical course of a TIA?sudden onset without warning, max in mins, last 2-15mins, rarely >1hr;
What findings do you get on TIA examination?Usually normal; look for evidence of cardiac / vascular disease; carotid bruit 75% sens and >75% spec for mod-high grade stenosis
What is the significant of finding a carotid bruit?90% carotid bruits are mod-high degree, 5-10% are surgically amenable - endarterctomy massively reduces RR of death from CVA - >80% stenosis, 50% decr RR of disabling CVA/death
What is the risk of having a CVA after having a TIA?20-25% will have CVA in next 1yr, 30% in next 5 years - 5% in 48hrs, 10% in 1/12, 10-20% in 90/7
How do you assess someone with a TIA?ABCD2 score
What does the ABCD2 score do?estimates the risk of subsequent stroke - essentially a risk stratification tool
What are the negatives of the ABCD2 score?May underestimate risk. Low accuracy when not a specialist doing it. developed for OP setting
What is the ABCD2 score?A age - 60 (1), B BP >140 triage (1), C - Clinical features - unilateral weakness(2), Speech impairment, no weakness (1) D - duration >1 hr (2) , 10-60mins (1)
What does the score mean?Admit anyone with score >4 for IP investigation, <4 can go home for OP investigation in <48hrs and specialist FU
What other reasons would cause toy to amit a TIA?>4 TIAs in a week, >3 72hrs, high grade carotid stenosis
What is the risk at 7 days with different ABCD2 scores?<5 = 5%, >=6 35-55% CVA
What treatment is required post TIA?Aspirin. Clopidogrel/assasantin/warfarin if AF (no benefit otherwise), stop smoking, BP control, carotid endartercotmy if mod-high stenosis
What is the single biggest factor affecting RRR? Stopping smoking - 66% RRR
Which studies showed aspirin was beneficial?CAST and IST - 30-50% reduction in CVA, mostly in 1st 2 weeks (50% reduction)

Ischaemic stroke

Question Answer
What are the two different "circulations" ?Anterior circulation - ACA, MCA, ICA and ophthalmic; Posterior circulation - PCA, Vertebral and basilar artery
What do the vertebrobasillar arteries supply?Cerebellum, brainstem and CNs. The PCA supplies the occipital lobe


Question Answer Column 3 Column 4 Column 5
MCA (80%)Contralateral weakness - face, arms>legscontralateral sensory losscontralat HH, eyes deviate TOWARD the lesionleft aphasia, right neglect
ACAContralateral weakness legs>armsno sensory loss abnormal conjugate gazepersonality change, incontinence, L speech, R neglect
PCANo motor losscontralateral loss of pain and tempcontralateral HH, pinpoint pupils if thalamic or pons, ipsilateral down and outdyslexia and memory changes
Vertebrobassilaripsilateral facial weakness, CN palsies, contralateral motor weaknessno sensory changeINO, diplopia nystagmus, vertigo ataxia, N+V


Question Answer
Why does the MCA affect face more than legs?the persons head starts at the sulcus and feet at front
In MCA stroke why do the eyes deviate toward the lesion?Because of the diagram. The contalateral hemisphere controls the ipsilateral pons to look away.
Why do you get contralateral pain and temp changes in PCA intact?Thalamus affected - Spinothalamic fibres decussate around level of entry
Why do you get ipsilateral facial changes in VB infarct?CN 7 in brainstem
What is lateral medullary syndrome?Horners syndrome and ipsilateral loss of pain and temp on face, contralateral pain and temp sensory loss on body, conjugate gaze palsy, nystagmus and cerebellar signs

Acute stroke treatment

Question Answer
How should a patient who has had a stroke be managed?Acute stroke unit or ICU where comprehensive services available for both timely neurosurgical intervention and rehab available. Head up, BP 140-160, Normoxia, normocarbia, normoglycaemia, normothermia (avoid hyperthermia), VTE prohylaxis, pressure area care
If a patent post CVA developes raised ICP how should they be managed?Maintain and secure airway, normoxia, normocarbia 35-40 - if blow pupil then can hyperventilate for short period, head up 30 degrees, strict BP control, , additional sedation, hypothermia 35-36, Glucose control 6-10, osmotic therapy = 3% NaCl, 100-200mls, if supratentorial consider craniectomy - esp if <60years
What is the evidence for craniotomy in supratentorial CVA (esp malignant MCA CVA)50% reduction in mortality but majority of patents are unable to manage their own affairs - Massive morbidity in survivors

BP in acute stroke treatment

Question Answer
What are the negatives of lowering BP in CVA?Aggressive BP lowering may decrease cerebral perfusion and worsen stroke Sx
When should you lower BP?Lower BP if consistently >220 / >120-140, or MAP >130
What are your goals for BP control?Aim 10-15% decr in BP within 24hrs
What does your BP have to be if you are hoping to thrombolyse?Need BP <185/110 to meet criteria

Antiplatelet in acute stroke rx

Question Answer
What is the anti platelet of choice and why?Aspirin (clopidogrel if CI’ed; delay 24hrs if thrombolysed) Decr risk of early death and recurrent CVA and beneficial as secondary prevention
What other anticoagulants can be used?Warfarin later if AF - not in 1st 24hrs, No evidence for heparin


Question Answer
What is the ultimate aim of thrombolysis?To salvage penumbra. THIS IS ONLY POSSIBLE <3 hrs
What is the agent and dose?tPA 0.9mg/kg (max 90mg), 10% as bolus, 90% over 60mins
Where should the patient be admitted if thrombolysis used?Admit stroke unit/HDU bed
How often does BP needs to be checked? Q15min for 2hrs - Q30mins for 6hrs - Q1hr for 16hrs. Intensive BP monitoring for 16hours. 2, 6, 16. 15, 30, 1hr
What are the contraindications for thrombolysis?unknown time of onset; improving Sx; minor (NIHSS <4); major (NIHSS >25); SBP >185; DBP >110; high risk CT findings (>1/3 MCA territory, multilobar infarction); seizure; plt <100; PT >15; BSL <2.7 / >22.2; Sx suggestive of SAH; heparin in last 48hrs, incr APTT; unable to consent; >3hrs; >80yrs; demonstrable perfusion
What is the NNT for positive outcome at 3/12? NNT 8 if <3hrs, <90mins NNT 4.5
After 3 hours should it be used?No. if 3- 4.5hrs, marginal benefit only and large morbidity risk
Why do we allow the neurologists to do this??Independent reviewers support use; small number of eligible patients so minimal disruption to ED function
What is the major negative of its use?Early mortality risk due to ICH

Thromobolysis and stroke trials

Question Answer
What are the main stroke trials?NINDS, ECASS I-III
What is the big pitfall of all of them?All industry sponsored and have some questionable reporting
Briefly outline NINDS studymulti-centre RCT; 600pts, tPA vs placebo. Outcome measures: NIHSS scores and mortality, and probability of favourable outcome. Showed no improvement at 24hrs, but improved outcome at 3-12/12 (OR 1.7) 2% reduction in dead or dependent patient at 3/12 - NNT 8
What are the major study design failures?Poorly matched groups, unrealistic time frames-therefore not generalisable to ED, No control of post thrombolysis care/stroke centre care, high number of cardioembolic strokes - unrealistic, not reported median NIHSS scores
What was the rate of ICH?6% ICH in tPA (0.6% in placebo) of which 50% were fatal
What was the overall mortality risk?3% mortality risk overall (vs 1% in MI) from ICH. 3/12 mortality 17% in tPA vs 21% in placebo
Which groups were more likely to have incr risk ICH? >80yrs and severe CVA


Question Answer
Briefly describe ECASSmulti-centre RCT; well matched; tPA vs placebo; <6hrs; 600 patients Post-hoc Analysis of <3hr group
Main findings of ECASSNon-significant improvement of all outcomes with tPA, increased haemorrhage with tPA, significant increase mortality with tPA
Briefly describe ECASS II multi-centre RCT; tPA vs placebo; <6hrs; 800 patients. No sts significant change in outcome or mortality, tPA have more ICH and cerebral oedema
Describe ECASS IIImulti-centre RCT; tPA vs placebo; 3-4.5hrs; excluded severe stroke. Better modified Rankin/NIHSS score at 90/7 in tPA group (approx 50% vs 45%), lower mortality at 90/7 in tPA (7.7% vs 8.4%); no change in Barthel Index/Glasgow Outcome score
Overall ECASS series demonstratedNeed to use tPA within <3hrs to get any demonstrable benefit, ICH always more likely in tPA group, but improve functional outcome and mortality at 3/12 if used early and in well selected group - i.e not a MASSIVE CVA


Question Answer
When should Interventional radiology be considered?if large vessel occlusion (esp basilar art / ICA / M1) + few morbidities and good prognosis, and <5hrs; important alternative as tPA poorly effective in large vessel lesions
Major advantages of Intra-arterial thrombolysis? trt window >6hrs, decr dose of drugs, possibility of mechanical clot disruption
Heparin use?Only if CVA with proven cardioembolic source, otherwise no improvement and people probably do worse

Haemorrhagic stroke

Question Answer
List causes of haemorrhagic strokeHypertension, amyloid antipathy, AVM, Bleed into tumour, haemorrhage transformation from ischaemic CVA
List risk factors for ICH HTN (DBP >95), XS ETOH and binge, aneurysm, anticoagulation, cocaine, intracranial SOL, amyloid angiopathy SCA most common cause of CVA in children
How does hypertension cause bleed?Charcout-Bouchard microaneurysms of penetrating arteries of MCA, basal, COW, haemorrhage evolves over few mins - will be central location on CT
Name the normal locations of Haemorrhagic CVAHTN: Putamen > thalamus > pons > cerebellum, upper brainstem, basal ganglia. Amyloid angiopathy: lobar = better prognosis
What percentage of CVAs are haemorrhagic? 25%
What is the death rate?30-50%, but if don't die do better as not immediate cell death. 50% deaths within 48hrs; >80% if on warfarin. 30% discharge rate
How do they present?more N+V+H; slow onset; LOC often impaired; 25% initially alert then deteriorate
Name 5 predictors of mortality in ICH?Blood in ventricles, Age > 80, GCS: on transfer from the ED to definitive to care, Location of bleed: supra vs infra tentorial, Volume of Bleed: < 30 mL or > 30 mL
Name 4 causes of deterioration in GCS post ICH1. extension of bleed, 2. Cerebral oedema, 3. Hydrocephalus 4. post ictal

Management of ICH

Question Answer
What is the biggest recommendation of National Stroke Foundation?manage in a stroke centre
What are the benefits of a stroke centre?decr death and disability, more adherence to key principles, more patients eligible for stroke unit than thrombolysis so more impact; interdisciplinary team, early mobilisation, avoid bed rest, active encouragement
Treatment of ICH?1. BP control, 2. Reverse anticoagulation, 3. ICP monitoring, 4. Craniotomy and evacuation 5. Intraventricular drain if blood in ventricles
Why and when do you actively manage BP in ICH?Reduces haematoma volume. Rx if >200 / >120 or MAP >150. Aim 160/90 or MAP 110, CPP 60-80 (if normal ICP)
What do you use for BP control?Labetalol 10-20mg IV over 1-2mins - repeat or double dose at 10mins (to max 300mg) or Sodium nitroprusside 0.5-10mcg/kg/min or GTN
3 indications for immediate OT1. <1cm from surface + <60yrs, 2. Hydrocephalus or marked mass effect 3. Cerebellar haem >3cm (Cerebellar is surgical emergency)
3 indications for ICP monitoring 1. GCS <8 2. Clinical evidence of transtentorial herniation 3. Significant intraventricular haemorrhage or hydrocephalus