www.wales.nhs.

uk

Stroke & TIA

Dr Rebecca Chave-Cox Countdown 2 Finals, 2013

Objectives
Define & differentiate stroke & TIA

Cover the basic epidemiology & aetiology

Discuss clinical presentations

Correlate symptoms to anatomical location

Learn to assess the patient

Discuss management

Definition
Clinical diagnosis Stroke:

Focal, non-convulsive neurological deficit due to

vascular lesion with symptoms lasting over 24h (if pt survives)

Transient Ischaemic Attack:

Focal, non-convulsive, neurological deficit lasting
less than 24h with complete clinical recovery

Stroke
The most common presentation is hemiplegia
85% caused by thromboembolic vascular occlusion Haemorrhagic strokes are often secondary to chronic
HTN (leading to rupture of microaneurysms)

Late deterioration after a stroke can be due to

'haemorrhagic transformation' post the acute event

TIA
Symptoms are usually of sudden onset, often
recurrent & repeat episodes are often stereotypical

Maximum deficit reached in <1m Due to focal hypoperfusion in the brain Up to 20% patients will have a subsequent stroke
within 90 days (half of these in first 2 days)

Prompt investigation & management is essential

Epidemiology
Commonest cause of adult disability 12% all deaths 5% NHS budget Stroke incidence = 150-200 per 100,000/yr TIA incidence = 30 cases per 100,000/yr Incidence rates increase with advancing age

Prognosis of stroke

1/3 die, 1/3 recover well, 1/3 remain disabled

Mortality: 10% in first week 20% in first month 30% in first year

Worse prognosis:

coma defects in conjugate gaze with hemiplegia severe hemiplegia

Intracerebral haemorrhage has greater mortality but better functional recovery from acute, severe deficits

Common aetiologies
Atherosclerosis

Cardiac or carotid embolism

Arterial dissection Intracerebral haemorrhage Lipohyalinosis of small arteries

Risk Factors

H - Hypertension: major RF for both ischaemic & haemorrhagic stroke A - cArdiac: Cardiac causes (AF, Arrhythmias, cardiomyopathy, valve disease etc linked to embolism) & coronary Artery disease is marker for atherosclerosis elsewhere L - hyperLipidaemia: less significant than in coronary artery disease

T - Tobacco: quitting lowers risk of stroke

S - Sugar (diabetes mellitus): 2x increased cerebral infection risk & RF for atherosclerosis Homocysteine Family history: close family members at slightly increased risk, but DM & HTN also familial Obesity & diet: probably less important than in coronary artery disease

Oral contraceptive pill: may increase risk of thromboembolic stroke, central venous thrombosis & subarachnoid haemorrhage in the vulnerable

Primary intracerebral haemorrhage

Commonly due to chronic hypertension; small vessel disease,
aneurysms; AVMs; bleeding disorders & cerebral amyloid angiopathy

In the context of chronic hypertension >70% haemorrhages

occur in the internal capsule or basal ganglia due to CharcotBouchard aneurysms

But, can occur in any part of the cortex, pons or cerebellum Clinical signs vary by location but often associated with mass
effect with reduced consciousness

Otherwise, very hard to distinguish from an infarct

Localisation

Arterial supply
Posterior communicating artery Posterior cerebral artery Basilar artery Junction of vertebral arteries

External carotid Internal carotid Vertebral artery Common carotid

http://en.wikipedia.org/wiki/File:Vertebral_artery.png {Grays Anatomy plate}

Circle of Willis

www.meducation.net/encyclopedia/27006

Vascular territories

http://missinglink.ucsf.edu

Middle cerebral artery occlusion

MCA is the artery most commonly involved in stroke Largest branch of the internal carotid & supplies the largest area of cerebral cortex Wernicke's & Broca's are found in the dominant hemisphere, therefore in most individuals speech will only be affected by a left MCA occlusion Non-dominant lesions cause visuospatial problems eg inattention Initially limbs are flaccid & areflexic; then reflexes recover & exaggerate; plantar responses become extensor and spastic limb tone develops There is variable weakness over days, weeks or months

Middle cerebral artery

Contralateral hemiplegia

Contralateral hemisensory loss

Contralateral homonymous hemianopia

Dominant hemisphere: aphasia

Non-dominant hemisphere: neglect of contralateral
limb, dressing apraxia

Middle cerebral artery

Both sides Dominant Wernickes (speech comprehension) Brocas (speech expression) Non-dominant

Motor cortex

Visuospatial

Sensory cortex

Hemianopia

Visual field defects

http://medical-dictionary.thefreedictionary.com/homonymous+hemianopia

Anterior cerebral artery

Pure ACA stroke is uncommon Proximal occlusion is usually well tolerated with few symptoms Distal occlusion causes:
Contralateral weakness

Contralateral sensory loss in leg

Incontinence

Occasionally there is a contralateral grasp, or other primitive reflexes

Lacunar stroke
25% ischaemic strokes

Infarction of internal capsule

Pure hemiparesis

Hemisensory loss
Ataxic hemiparesis

Clumsy hand - dysarthria syndrome

Opthalmic artery

Amourosis fugax

Posterior cerebral artery occlusion

The PCAs are the terminal branches of the basilar
artery

The PCAs send cortical branches to the temporal lobe,

occipital lobe & visual cortex as well as perforating branches to the midbrain & thalamus

The effect of the occlusion depends on the site and is

associated with specific syndromes

Posterior cerebral artery occlusion

Homonymous hemianopia with macula sparring
(which is supplied by MCA)

Complete visual loss with reduced/no insight Ipsilateral third nerve palsy with contralateral
hemiplegia

Lateral medullary syndrome

Specific brainstem syndromes

Also known as posterior inferior cerebellar artery syndrome
The most widely recognised brainstem syndrome Sudden onset vertigo, vomiting & nystagmus Ipsilateral ataxia (cerebellar connections) Ipsilateral facial numbness (5th CN descending tract) Ipsilateral Horner's syndrome (sympathetic tract) Contralateral loss of pain & temperature sensation in limbs (ascending spinothalamic tract)

Dysarthria & dysphagia (10th CN)

'Locked-in' syndrome
Specific brainstem syndromes

Due to bilateral infarction of ventral pons with or

without medullary involvement

Patient is conscious

However they are mute & paralysed

Patients can often move their eyes due to sparing of
the 3rd & 4th CN nuclei in the midbrain

Assessment & Diagnosis

History
Onset - spread of symptoms; warning TIA? Focal symptoms - language/motor/sensory/visual

Headache? - if severe & progressive may indicate haemorrhage

Progressive consciousness impairment: suggests raised ICP secondary to haemorrhage; complete anterior circulation infarct or coning secondary to cerebellar haemorrhage Risk factors PMH: prev TIA/stroke, connective tissue disease, neoplasia, bleeding disorders, arrhythmias & cardiac disease DHx: especially for anticoagulants and oral contraceptive pill Normal functional levels: ADLs

Examination
CVS:
embolus (pulse for AF, bruits esp carotid, valve lesion, signs of endocarditis) hypertension (BP, lying & standing) stenosis (asymmetric brachial BPs, pulse delay)

Chest:
Neuro:

pneumonia standard (cranial nerves & vision; limbs) GCS swallow

Differential diagnosis for acute stroke

Stroke
Seizure Systemic infection Brain tumour Toxic-metabolic

Most likely

Least likely

Basic Investigations

FBC: polycythaemia, infection
ESR & CRP: inflammatory disease Urinalysis & blood sugar: diabetes mellitus Cholesterol Blood culture: if suspect endocarditis or superadded infection Autoantibodies & coagulation studies: in young patients connective tissue disorder or prothrombotic disorder ECG/echo: arrhythmia; myocardial infection/ischaemia

Chest X-ray: heart failure; neoplasia

Neuroimaging
All stroke patients should have a CT scan <24h to
differentiate ischaemia & haemorrhage

MRI needed if lesion clinically placed in posterior

fossa (ie brainstem & cerebellum)

MRI also better at detecting small strokes

Vascular imaging

Carotid doppler: Effective, non-invasive demonstration of internal carotid artery stenosis when carotid bruit heard or carotid thromboembolism suspected

CTA & MRA CT & MR angiography (CTA & MRA) can help visualise carotids & posterior circulation for atheromatous disease, dissections & aneurysms

Angiography: Used to locate intracerebral aneurysms and diagnose cerebral vasculitides which are poorly detected on MRA Do not consider in first 2 weeks after acute stroke

Management

Management of acute stroke

Establish initial diagnosis Admit directly to HASU Reopen artery (thrombolysis with alteplase) <4.5 hrs only

Prevent early recurrence

Aspirin 300mg for all ischaemic strokes Avoid anticoagulation (heparin) unless specifically indicated

Give clopidigrel instead of aspirin if there are co-morbidities

Protect from secondary brain damage Maintain physiology

Treat complications, including craniotomy for MCA oedema

Complications of acute stroke

Neurological:

Non-neurological:

Cerebral oedema
Completion of stroke Early recurrence Haemorrhagic transformation Obstructive hydrocephalus Seizures Incorrect diagnosis

Infection Metabolic Drugs Hypoxia/hypercapnia

Large 'malignant' MCA territory infarcts are the commonest cause of death in the first week (peaks at 24h & 4-5 days) Severe hemispheric stroke syndrome; hemiplegia; forced eye & head deviation; progressive deterioration within 1st 2 days CT signs of infarct within 12 hours 80% mortality

Transtentorial herniation & cerebral oedema

Steroids have no effect on outcome Mannitol has no effect on outcome but may stabilise rapidly deteriorating patient Early hemicraniectomy improves survival & functional outcome almost threefold (NNT=2)

Management of completed stroke

Prevent complications

Rehabilitation
Control hypertension if >220/120 Give aspirin (300mg)/dipyridamole or clopidogrel

Control cholesterol
Smoking cessation advice Good glycaemic control Remove/treat embolic source (nb no anticoagulation in 1st 7 days even if indicated for cardiac embolus) Treat inflammatory or connective tissue disorders

Stop thrombogenic drugs

Carotid endarterectomy
Disadvantages of a procedure: Significant risk of inducing stroke Risk of CN palsy or cardiac event Neck incision/haematoma

Cost & inconvenience

Criteria for intervention: 70% or more stenosis of internal carotid artery ipsilateral to affected cortex (contralateral to symptoms) 50-69% stenosis considered <50% stenosis not suitable for surgery

Management of TIA
Confirm diagnosis (history & examination) Refer immediately to A&E for any 1 of the following: Symptoms present at time of assessment ABCD2 score 4 or more & within 7 days of symptoms

Patient in AF
Patient with recurrent TIAs

ALL other patients should be seen in the Rapid Access TIA

clinics

ABCD2 Score
Criteria Age Qualifier 60 yrs + Points 1

Under 60
BP Over 140 Under 90 Clinical features Unilat weakness Speech disturbance only

0
1 0 2 1

Other
Duration of Sx Over 1 hour 10-59 mins Under 10 mins Diabetes

0
2 1 0 1

Management of TIA
Identify & treat risk factors
Aspirin/dipyridamole or clopidogrel Avoid anticoagulants (heparin/warfarin) in the short
term unless clear need eg AF

Investigate possible sites for primary lesion (eg

carotid stenosis, cardiac embolus 2ndry to AF)

Driving
Patients with suspected TIA or stroke must not drive
for 1 month

Can automatically resume driving if no residual

deficit at 1 month

Drivers with multiple TIAs in a short time may

require 3 months away from driving

Primary & secondary prevention

Primary prevention: stops a disease from happening

Secondary prevention: stops recurrence of a disease

Lifestyle interventions
Physical activity Weight reduction

Low salt, sugar, saturated fat diet

Less (or no) smoking or alcohol

Medical interventions
Aim for BP <130/80

Clopidogrel monotherapy or aspirin/dipyridamole

dual therapy

Statins Warfarin - for people in AF (major cause of stroke);

only start 2 weeks after stroke to avoid haemorrhage

Good glycaemic control

Summary
Stroke is a clinical diagnosis and the commonest cause of adult disability in the UK

1/3 die, 1/3 recover, 1/3 remain disabled

Prompt recognition and referral to HASU is key High dose aspirin/dipyridamole or clopidogrel Thrombolyse ischaemic strokes within 4.5 hours (if no CI) Modify risk factors

High risk of stroke in days/weeks following TIA

Refer straight to A&E if high risk All other TIA patients should be seen in Rapid Access TIA clinic

References

Oxford Handbook of Clinical Medicine
Pocket Essentials of Clinical Medicine 4th Ed, Ballinger & Patchett (Kumar & Clarke) SIGN: Management of patients with stroke or TIA: assessment, investigation, immediate management and secondary prevention (www.sign.ac.uk/guidelines/fulltext/108/index.html) NICE guidance CG68: Diagnosis and initial management of acute stroke and transient ischaemic attack (TIA) July 2008 (www.nice.org.uk/CG68) LTHT TIA guidelines (LGI/SJUH intranet) GP notebook (www.gpnotebook.co.uk DVLA (www.dvla.gov.uk) About.com (http://stroke.about.com) The Neurosurgeons Handbook, Samandouras

Questions?