Stroke

Both infarctions and bleeds can lead to rapid onset of signs and sx taking seconds to min
There are 4 main causes
1. Small vessel occlusions e.g. thrombosis in situ
2. Cardiac emboli e.g. AF, endocarditis, MI
3. Atherothromboembolism e.g. carotids
4. CNS bleeds e.g. HTN, trauma, aneurysm rupture, anticoagulation, thomboylsis

other causes include

 Watershed stroke – sudden drop of BP by >40mmHg e.g. in sepsis
 Carotid artery dissection
 Spontaneous
 Neck trauma
 Fibromuscular dysplasia
 Vasculitis
 SAH
 Venous sinus thrombosis
 Acute venous infarct
 Antiphospholipid syndrome
 Thrombophilia
 Fabry’s disease
 CADASIL
 Cerebral autosomal dominant arteriopathyy with subcortical infarcts and
leucoencepalopathy  TIA/stroke sx with migrane from 4th decade of life

Risk factors
 HTN
 Smopking
 DM
 CVD
 Valvular
 IHD
 AF
 Peripheral vascular disease
 Past TIA or stroke
 Increase PCV (packed cell volume aka Haematocrit)
 Carotid bruit
 OCP
 Hyperlipidaemia
 EtOH
 Hypercoagulability
 Increase plasma fibrinogen
 Decrease antithrombin III
 Increase homocysteine  hyperhomocysteinemia increases endothelial cell injury, vessel
inflammation which leads to atherogenesis and ischaemia. It is a homologue of amino acid
cysteine
 Syphilis

DDX
 Head injury
 Subdural haemorrhage
 Hypo or hyper glycaemia
 Intracranial tumours
 Hemiplegic migrane
 Epilepsy – Todd’s palsy
 CNS lymphomas
 Pneumocephalus (air entry via otitis, mastoid, trauma)
 Wernike’s encephalopathy
 Drug overdose if in coma
 Hepatic encephalopathy
 Mitochondrial cytopathies
 Herpes encephalitis
 HIV
 Toxoplasmosis
 Abscess e.g. typhoid
 Mycotic aneurysms
 Coccidiodes immitis
 Acanthamoeba
 Status epilepticus can cause infarcts

Sx
 Sudden onset with possible further progression over hrs(rarely days)
 Focal signs related to distribution of artery but there are collaterals
 Location of infarcts
 Cerebral haemisphere infarts
 These account for 50%
 Depends n site there may be contralateral hemiplegia
 Initially flaccid (floppy limb, falls) then spastic (UMN lesion)
 Contralateral sensory loss
 Dysphasia
 Homonymous hemianopia
 Visuo-spatial deficit
 Brain stem infarcts
 These accound for 25%
 Wide range of effects
 Quadriplegia
 Disturbance of gaze and vision
 Locked in syndrome  aware but unable to respond
 Lacunar infarcts
 These account for 25%
 Small infarcts around basal gangia, internal capsule, thalamus and pons
 The 5 lacunar syndromes are classically described
  Pure motor
 Ataxic hemiparesis
 Pure sensory
 Mixed sensorimotor
 Dysarthria/slumsy hand
 Cognition and consciousness remain intact except in thalamic lacunes
 While difference between haemorragic and ischaemic stroke not distinguishable clinically there
are some differences
 Haemorrhagic: meningism, severe headache, coma within hrs
 Ischaemic: carotid bruits, AF, past TIA, IHD

MX
 Acute
 ABCs
 Airways to avoid hypoxia or aspiration
 Blood glucose
 BP
 But treating even very high levels may harm unless there is encephalopathy or aortic
dissection
 A 20% fall may compromise perfusion as autoregulation is impaired
 Urgent CT/MRI
 If
 thrombolysis is considered
 cerebellar stroke (cerebella haematomas may need urgent referral for evacuation)
 unusual presentation or alterative dx is likely
 high risk of haemorrhage
 decreased GC scale
 signs of elevated ICP
 headache severe
 meningism
 progressive sx
 known bleeding tendency
 anticoagulation
 otherwise imaging can wait but still aim within <24hrs
 CT will rule out primary haemorrhage
 MRI diffusion weighted is most sensitive for acute infarct
 Thrombolysis
 18-80 yrs of age
 <4.5hrs since the onset of sx
 If the team is in place and there is no contraindications refer urgently for reperfusion
with recombinant tissue plasminogen activator tPA: alteplase 0.9mg/kg over 1hr
 Check if this is tenectaplase instead TNK-tPA
 All patients should then have a CT head scan 24hrs post to check for haemorrhage as
these are often very small and asymptomatic (the use of antiplatelets do not increase
the risk of haemorrhage in this case)
 Contraindications
  Major infarct or haemorrhage on CT
 Mild non-disabling deficits
 Recent surgery, trauma or obstetric delivery
 Past CNS haemorrhage
 AVM or aneurysm
 Severe liver disease, varices or portal HTN
 Seizures at presentations
 Recent arterial or venous puncture at a non-compressible site
 Anticoagulation or PTT>15s
 Plts <100 E9/L
 HTN >220/130
 Nil by mouth
 Until swallowing is assessed
 Keep hydrated
 Don’t over hydrate as there is a risk of cerebral oedema
 Educate
 Advanced care planning
 What has happened
 Carers and pt
 QoL changes and prognosis
 Antiplatelet
 Once haemorragic stroke is excluded, aspirin 300mg
 Admit to stroke unit
 Chronic
 Rehab

Primary prevention
 Control RFs
 HTN
 DM
 Lipids
 CVD
 Exercise
 Folate supplements
 Smoking
 Lifelong anticoagulation if left sided heart valve prosthetic or rheumatic
 Consider use of lifelong anticoagulation in AF

Secondary prevention – reducing risk of recurrence

 Primary prevention
 Lower BP and cholesterol
 Antiplatelet agents
 Unless primary haemorrhage
 Aspirin 300mg/d for 2weeks; 75mg/d
 Dipyridamole 200mg/12hrs with aspirin improves results
 Clopidogrel can also be used esp if aspirin sensitive
  Add PPI if aspirin intolerant
 Esp use antiplatelet compared to anticoagulant if risk of falls
 Anticoagulation
 Warfarin should be used instead of antiplatelets if embolic stroke or chronic AF and only
from 2 weeks after the stroke (7-10 days if small stroke)
 Use antiplatelet until anticoagulation works
 Aspirin + warfarin increases risks of falls without any benefits

Tests
 HTN
 Retinopathy
 Nephropathy
 CXR – cardiomegaly
 Cardiac source of emboli
 Holter monitor
 AF
 CXR – left atrial enlargement
 Echo – mural thrombus due to AF or hypokinetic segment of cardiac muscle post MI
 It can also show valvular lesions in infective endocarditis or rheumatic heart disease
 TOE >> TTE
 Carotid stenosis
 Carotid Doppler US +/- CT/MRI angiography
 Carotid endarterectomy shows a clear benefit in those >70% stenosis
 ?? stenting
 Metabolic state
 Glycaemia
 Lipidaemia
 Homocysteinaemia
 Vasculitis
 ESR raised
 ANA +ve
 Prothrombotic states
 Thrombophilia
 Atiphospholipid syndrome
 Hyperviscosity
 Polycytheaemia
 Sicklecell disease
 Thrombocytopenia and other bleeding disorders
 Genetic test

Prognosis
 Pressure sore
 Aspiration pneumonia
 Contracture
 Constipation
 Depression
 Stress of carer and pt

Rehab
 Swallow test
 Drink water and check for coughing or change in voice
 Speech therapy
 Avoid falls and damaging pts shoulders by lifting
 Good bladder and bowel movements through frequent toileting, avoid catheterisation
 Position the pt to avoid spasticity and get physiotherapy
 Botulimun toxins may aid to prevent spasm
 OT
 Emotional lability
 TCA
 Screen for depression
 End of life discussion

TIA
 Temporary occlusion of part of the circulation usually by an emboli
 Sx<24hrs  1hr
 15% of strokes preceeded by TIA
 Sx
 Attacks can be single or many
 Sx similar to those of strokes in that region
 Global events e.g. syncope and dizziness are not features of TIA
 Multiple highly stereotyped attacks suggest intracranial stenosis
 Often the superior division of MCA
 Amaurosis fugax  curtains descending
 Limb shaking TIA can be misinterpreted as focal motor seizure
 Cause
 Carotid atherothromboemboli
 Cardiac emboli – mural thrombus post MI or AF or valve disease
 Hyperviscosity e.g. polycythaemia
 Myeloma
 Vasculitis e.g. SLE, PAN
 DDx
 Hypoglycaemia
 Migraine aura  sx spread and intensify over min often with visual scintillations
 Focal epilepsy  sx spread over sec and incl. twitching and jerking
 Hyperventilation
 Retinal bleeds
 Malignant HTN
 MS – paroxysmal dysarthria
 Tumours
 Peripheral neuropathy
 Phaeochromocytoma
 Somatisiation
 Ix
 Determine the cause and vascular risk
 FBC
 ESR
 UEC
 Glucose
 Lipids
 CXR
 ECG
 Carotid Doppler w/w/o angio
 CT or MRI
 If bilateral, suggestive of cardiac  echo
 Tx
 CVD risk factors
 BP <140/85
 Lipids
 DM
 Smoking
 Antiplatelet
 Aspirin
 Dipyridamole
 Clopidogrel
 Warfarin
 Cardiac emboli
 AF
 Mitral stenosis
 Septal MI
 Carotid endartectomy if 70% stenosis
 Driving risk
 NOTE
 When should TIA lead to prompt or emergency referral
 ABCDD score >6
 Age >60 (1)
 BP >140/90 (1)
 Clinical
 Unilateral weakness (2)
 Speech disturbance without weakness (1)
 DM (1)
 Duration
 Sx >1hr (2)
 Sx 10-59min (1)
 s
 x