2. Introduction
• Common encountered diagnosis and
very common differential
• Often initial presentation to A&E
– Or GP ushered
• Fairly rapidly evolving evidence base
• Still many unanswered questions
• Variable approach to
management/service provision
3. Topics
• Stroke and TIA diagnosis
• Risk assessment
• Service provision and investigation
• Secondary prevention
4. Case - Mr O
• 37 year old man
• PMH:
– Marfan’s syndrome
– Ulcerative colitis
• Presents with:
– Episode of memory loss 2/52 ago
• Could recall simple instructions at work
– Headache of gradual onset 3/7, more
prominent on left, intermittent
– 3-4 episodes of right arm weakness and
numbness
• Lasting 15 minutes
– 2 episodes of buttock numbness
5. Mr O
• Normal neurological examination
• Normal cardiovascular exam (BP
128/84)
• ECG – SR
• CTB ....
• What to do??
6. First question - Is it a stroke/TIA?
• Most important questions across
spectrum on acuity
• What are the common mimics and how
can you find them?
• Sudden onset
• Worse within minutes of onset
Hand , 2006
7. Collapse and TIA
• Consciousness disturbance indicates
pathology of reticular activating system
• Diffuse pathway – requires significant
vascular insult
– Likely to have focal deficits and CT changes
within hours if anterior
– Unlikely to recover rapidly – “never” a TIA
• Diagnosis – Syncope, seizure,
hypoglycaemia
• Pitfalls
– Focal neurology in seizure & hypoglycaemia
– Thalamic syndromes and secondary delirium
• Still likely to have subtle focal neurology in
neurologically robust patients
8. He’s vertiginous – it is a stroke
• Need to distinguish peripheral vs central
– Peripheral usually benign - no A&E
neuroimaging required
– Central - needs admission for MRI
• Key is examination if ongoing symptoms
– Focal neurology
– Nystagmus
• Central is multi-directional or up beating
• Peripheral is uni-directional and horizontal
– Eye ROM including skew test
– VOR – the head thrust test
– Application of these principles sensitivity
similar to MRI (HINTS study, Kattah, 2009)
• Other “red flags” - Headache & hearing
loss
• TIA very tricky!
10. Confusion
• Receptive dysphasia
– Can come in under the stroke radar
– Paraphasic errors and neologisms
– Attention key
• Transient global amnesia
– Profound but isolated inability to form
new memories
– loss of self-awareness and intact
higher functions excludes TGA
– Prominent perseveration
– Lasts less than 24 hours
11. Delirium
• Fluctuations in over time
• Attention is the key!
• Can be very difficult differential in a person
with an aged or demented brain
• Stroke diagnosis principles apply as delirium
complicates stroke in the aging brain
– As above - onset, focal deficits, vascular
territory
• Other acute medical condition
• Consider chronic medical condition prone to
delirium e.g. Decompensated cirrhosis
12. Functional
• Examination key here
– Gait
– Hoover’s sign
– Pronator drift
– Distraction & variability
– Give way weakness
• Beware of overlay and resolved
transient phenomenon
• Difficult to interpret psychological co-
morbidity
13. Migraine
• Headache often occurs after onset of
neurology
• Spotted by
• Gradual spreading of symptoms over
vascular territories
• Positive symptoms
– Scintilating scotoma
• Flashing lights
• Zigzagging
• Haze
– Strange sensory abnormalities - water
flowing down skin, paraesthesia still can be
stroke
• Hemiplegic migraine rare in onset over
14. Vision deficit
• Common presentation
• Transient painless visual loss is a stroke
case
– Most people don’t check if one or both eyes
involved
• Ophthalmology review however very
useful
– Retinal detachment/tear, venous occlusion
– Stroke aetiology
• Visualising an embolus very helpful
• ? Roth spots
• Similar stroke work up
– Less high risk however
15. TIA
• High risk of subsequent stroke
– Likely higher than completed stroke using
traditional definitions
• Witnessed population based success
– Treating TIAs urgently reduces the risk of
stroke by 80% (EXPRESS, 2007)
• In 2004, one in 10 TIAs led to a stroke
within a week in UK
• In 2012, about one in 20 TIAs led to a
stroke within a week
16. I think he’s had a TIA – what now?
• Do I need a scan in A&E?
– CT helpful
– Silent ischaemia
– Approx 1% in people will have non-
ischaemic scan
• Convexity SAH, SDH
• Tumour
• Scan the amaurosis?
17. MRI in TIA
• Acute MRI most helpful in clarifying
difficult cases
– 50% of traditional thought of TIA have DWI
abnormality
– Risk stratification significantly improved
– More common internationally
– Resultant tissue based definition
– Future: MRI perfusion
18. Other investigations
• Time critical (EXPRESS, 2007; SOS-TIA, 2007)
– Investigation to identify modifiable risk
factors
– Rapid initiation of stroke secondary
prevention
• Investigations
– Vascular anatomy
• Dopplers
– Early endarterectomy effective (NNT=6
at 2 years)
• CTA/MRA
– Dissections esp. young people
– Posterior circulation – high risk if
stenosis
19. Investigations
• Cardiac work up
– Up to ¼ have indication for anticoagulation
(broadly)
– ECG mandatory (and easy)
– Further telemetry/holter helpful
– Echocardiogram needed in most patients
20. In patient vs outpatient management?
• Risk stratification plays a (health
economic) role
• ABCD2
– use your app!
• Often quoted that if > 4 should be
admitted
Score 2 day stroke
risk
7 day stroke
risk
1-3 (low) 1.0% 1.2%
4-5 (moderate) 4.1% 5.9%
6–7 (high) 8.1% 11.7%
21. ABCD2
• Developed for 10
care
• External validation inconsistent
• Poorly performing in
– Hospitals (high risk group)
– Vs Specialist assessment
• Probably very difficult to simplify to
simple risk model
• Possible mimic exclusion?
• Possible role of diagnostics/treatments in
hospital
22. Other risk features
– Known carotid disease
– Multiple/fluctuating course
• Capsular warning syndrome
• Possible artery-artery embolism
– AF (?)
• Traditional thought of as high risk
population
– DWI hits
• Practical relevance
• May be even higher than traditional
defined stroke
– ? Related to sub-type e.g. artery to artery
– Needs more work
23. Service provision
• Risk front loaded
– Traditionally 50% of 30 day stroke risk
in 1st 24 hours
• Imaging revealing increasing
recognised dynamic process
• New stroke or evolution
• Collaterals & spontaneous re-
canalisation
– Is this relevant to clinical practice?
24. Service provision – who to admit?
• Where should rapid diagnostic work up be
done?
– A&E
– Clinic
– Inpatient
– GP
• Who should get admitted for monitoring
– Potential deterioration - who?
—High risk groups – how to identify?
—Hyper-acute treatment – is it cost effective?
—Investigations - telemetry
—At risk if alone
25. Medical management - Antiplatelets
• Dipyridamole out
– Bd dosing + side effects
• Aspirin
– Largest evidence base (CAST + IST)
– Stroke prevention - NNT = 111 in first 2
weeks
– Combined cardiovascular outcomes NNT 25-
30 over 2 years
– Various doses used (300mg in CAST)
• Clopidogrel
– Better than aspirin (but NNT=200) (CAPRIE, 1996)
– Not tested in TIA or acute stroke
monotherapy
26. Antiplatelets
• Combination
– In conventional stroke
• Worse outcomes (MATCH trial, 2004; SPS3 2011
CHARISMA, 2006)
– In high risk TIA or smaller stroke (CHANCE,
2013)
• 28 days combination
• 90 recurrent stroke 3.5% ARR
• Chinese population
• A/W subgroups analysis
– Non-clinical data supporting (CARESS, 2005;
CLAIR, 2010)
27. Antiplatelets
• Future
– Combination therapy in non-asian
populations (POINT)
– Different subgroups
–Large artery atherosclerosis
– Triple therapy (TARDIS)
– More potent anti-platelets
28. Anticoagulation
• Heparin higher risk of death than
aspirin in acute ischaemic stroke (Berge,
2002)
• However – certain subtypes may be
beneficial
– Cardiac mural thrombus
– Intra-arterial thrombus?
• Note aspirin as effective as warfarin
(WARSS, 2002)
• May not need aspirin in addition if another
anticoagulation requirement
29. Lipids
• Atorvastatin 80mg tested in stroke
group in SPARCL trial
– 1 to 6 months after stroke
– Combined ARR over 5 years was 3.5%
– Similar RRR whatever baseline LDL-
cholesterol
• Start low as SE occur
• Simvastatin?
• Fibrates or ezetimibe?
• Targets?
30. Blood pressure
• Most important secondary prevention option
• Often transiently elevated in acute stroke
– ? TIA
• However little acute trial data
• Influenced most by PROGRESS trial
– Perindopril/indapamide
– Similar RRR across very broad BP range
• Goal is 130/80
• Start in A&E ?
32. Mr O
• Readmitted, symptoms settled with
aspirin
• Readmitted again 2 months later with
recurrent symptoms
– Anticoagulated
• Due for follow up neuro-imaging in few
months
CT HEAD
CLINICAL DETAILS:
Three weeks history of intermittent altered sensation with upper and lower limb motor weakness. Severe headache, worse when coughing. One week history of vision blurriness intermittently. Unsteady on feet. History of Marfan’s with ulcerative colitis. Transient global amnesia. No obvious neurological deficit on examination.
FINDINGS:
No prior imaging available for comparison.
No intracranial haemorrhage or large vessel vascular territory infarct. Normal grey/white matter differentiation is seen. CSF spaces are prominent at the vertex. This may be due to the patient’s head shape or arachnoid cysts. No prior imaging available for comparison.
The ventricles and CSF spaces are symmetrical with no features to suggest hydrocephalus.
Pituitary fossa and contents are normal. The orbits and contents are unremarkable.
Left maxillary sinus mucosal retention cyst is noted.
CONCLUSION:
1. No acute intracranial haemorrhage or infarct.
2. Prominent CSF spaces at the vertex maybe due to the shape of the head, or alternatively may represent small arachnoid cysts.
Hand PJ, Kwan J, Lindley RI, Dennis MS, Wardlaw JM. Distinguishing between stroke and mimic at the bedside: The Brain Attack Study. Stroke. 2006; 37: 769–775.
Abstract/FREE Full Text
Ambitious project
Systolic blood pressure >150 mm Hg, atrial fibrillation, valvular heart disease, or absent peripheral pulses;
†respiratory, abdominal, or other abnormal signs
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Paraphasic errors are usually either whole word (semantic) substitutions, eg, "chair" for "table," or phonemic (literal) substitutions, eg, "cable" for "table." Neologisms are entirely new nonwords
Clin Med February 2013 13:80-83; doi:10.7861/clinmedicine.13-1-
Jon Stone
Functional neurological symptoms
The 90-day risk of recurrent stroke in the patients referred to the study clinic was 10.3% (32/310 patients) in phase 1 and 2.1% (6/281 patients) in phase 2 (adjusted hazard ratio 0.20, 95% CI 0.08-0.49; p=0.0001);
Lovett, J, Dennis, M et al (2003) The very early risk of stroke following a TIA Stroke 34: P138-140
Intercollegiate Stroke Working Party. National clinical guideline for stroke, 4th
Rothwell, P (2007) Major reduction in risk of early recurrent stroke by urgent treatment of TIA and minor stroke: EXPRESS Study Lancet 370: P1432- 1443
Risk 0.4 vs 7.1
Addition of brain infarction to the ABCD2 Score (ABCD2I): a collaborative analysis of unpublished data on 4574 patients. Giles MF, Albers GW, Amarenco P, Arsava MM, Asimos A, Ay H, Calvet D, Coutts S, Cucchiara BL, Demchuk AM, Johnston SC, Kelly PJ, Kim AS, Labreuche J, Lavallee PC, Mas JL, Merwick A, Olivot JM, Purroy F, Rosamond WD, Sciolla R, Rothwell PM. Stroke. 2010;41(9):1907.
particularly from the pooled analyses combining data from both trials (Rerkasem and Rothwell 2011)
There is accumulating evidence suggesting that the findings of acute infarction on diffusion-weighted MRI (DWI) [39,40,49-51] or acute or chronic ischemic lesions on CT [52] after a transient ischemic event are important predictors of stroke. In patients with an imaging-positive transient event, the 90 day risk of stroke appears to be as high as 14 percent [39,40,43,49]. In contrast, after an imaging-negative transient event, the corresponding risk is <1 percent
PROFESS, 2008 clopidorgel as good as ASA+ DIPY
In PROGRESS, the addition of two more BP-lowering drugs to people after stroke or TIA, 52% of whom were normotensive at entry (mean entry BP 136/79), reduced BP by 12/5 mmHg and resulted in a 42% reduction in recurrent stroke and 35% fewer major coronary events. NNT = 20 for hypertensives
36 year old gentleman with Marfan’s syndrome. Right brachial sensory motor disturbance last seven to ten days.
? left internal carotid artery dissection at the skull base and ? origin.
? other vascular pathology. (? Reversible cerebral vasoconstriction syndrome).
FINDINGS:
Multiple fairly widespread posterior left MCA external watershed and mid territory cortical infarcts, including the left arm homunculus (accounts for the patient’s symptoms).
No background ischaemic sequelae. A small non specific haemosiderin focus in the left subfrontal sulcus. There is no intracranial mass, hydrocephalus, surface collection or structural defect.
ANGIOGRAM:
Conventional left arch. No origin stenosis. Codominant vertebral arteries, with a patent vertebro-basilar system throughout.
Common and proximal to mid internal carotid arteries are normal. No atherosclerotic stenosis.
On the left hand side, there is a well delineated dissection involving the mid to distal internal carotid artery, affecting its ventro-medial wall, with in part mild luminal stenosis, normalising at its skull base entry site. No pseudoaneurysm at this stage.
The remainder of the right mid to distal internal carotid artery has a prominent tonsillar loop, but no dissection or flow abnormality.
Intracranial circulation has a conventional calibre and configuration.
CONCLUSIONS:
A well delineated mildly stenosing dissection involving a smooth 35mm segment of left ventro-medial mid to distal ICA, with multiple scattered cortical infarcts within a mid and posterior left MCA external watershed distribution.
The remainder of the angiogram and the brain findings are essentially unremarkable.
Suggest short term followup to assess stability / resolution of this dissection.