TIA
- what is it?
- when do they resolve?
- presentation
- Circulation - anterior; posterior; lacunar; carotid artery
- Ddx
- investigations
- management
- driving advice?
Transient episode of neurological dysfunction caused by focal brain/spinal cord/retinal ischaemic without acute infarction
- Majority of TIA resolve within 1hr
Without intervention, 1 in 12 will go on to have a stroke within a week ABCD2 score predicts risk of stroke following TIA • Age >60= 1 • Hypertension= 1 • Clinical features • Unilateral weakness=2 • Speech disturbance without weakness=1 • Duration • >60mins= 2 • 10-59mins=1 • Diabetes=1
> 4= high risk of early stroke, review within 24h
Presentation
Dictated by region of brain supplied by the obstructed vessel
May be
- Unilateral weakness affecting face, arm or leg in isolation or combination
- Unilateral sensory loss affecting face, arm or leg in isolation or combination
Anterior circulation
- Amaurosis fugax→ occlusion of retinal artery leading to unilateral progressive vision loss like curtain descending
- Aphasia or other language problems – dyslexia, dysgraphia
Posterior circulation→ homonymous hemianopia, dysarthria, ataxia, vertigo, incoordination, bilateral weakness or sensory loss
Lacunar→ isolated sensory/motor deficits
Carotid artery territory → speech disturbance
DDx: hypoglycaemia, migraine aura, focal seizure with Todd’s paralysis, MS (paroxysmal dysarthria)
IF LOC → consider other diagnosis
Investigations
- FBC→ polycythaemia, extreme thrombocytosis, high WBC can contribute to risk of cerebral hypoperfusion
- Thrombocytopaenia is risk factor for intracerebral haemorrhage, ci to tPa therapy if second stroke occurs
- ESR
- U&Es→ hyponatraemia can trigger seizures/generalised weakness
- BM→ rules out hypoglycaemia
- Fasting lipid profile
- ECG→ AF?
- Carotid doppler
- MRI diffusion-weighted/CT
- ECHO
- PTT, INR→ suspecting abnormal coagulation and thrombolytic therapy is considered
Management
- Control risk factors: optimise BP (aim for below 140/90), hyperlipidaemia, diabetes, smoking cessation
- Antiplatelet→ aspirin 300mg for 2 weeks, switch to clopidogrel 75mg
- If ci→ aspiring with slow release dipyridamole
Anticoagulation if cardioembolic e.g. DOAC/warfarin
Carotid endarterectomy→ if 70-99% stenosis
Driving→ prohibited for 1month
Circulation - anterior; posterior; lacunar; carotid artery
- what would be shown in each?
Anterior circulation
- Amaurosis fugax→ occlusion of retinal artery leading to unilateral progressive vision loss like curtain descending
- Aphasia or other language problems – dyslexia, dysgraphia
Posterior circulation→ homonymous hemianopia, dysarthria, ataxia, vertigo, incoordination, bilateral weakness or sensory loss
Lacunar→ isolated sensory/motor deficits
Carotid artery territory → speech disturbance
Are most strokes haemorrhagic or ischaemic?
80% ischaemic
Risk factors for haemorrhagic stroke
- Hypertension (both ischaemic & haemorrhagic)
- Vascular malformation
- Neoplasia
- Trauma
- Cerebral amyloid angiopathy (aging)
- Iatrogenic, other blood dyscrasias
Small vessel disease of white matter
• Associated with aging and hypertension
• Lipohyalinosis – degenerative process initiated by fibrinoid necrosis
• Arteriosclerosis – concentric hyaline wall thickening of small arteries and arterioles
- Smoking
- High waist:hip ratio
- Diabetes
- AF
RF for sagittal sinus thrombosis
oral contraceptives
dehydration
meningitis
If present more than 1 week post start, what investigation should be done?
MRI
NOT CT
Anterior cerebral circulation (via internal carotid artery)
- clinical features
- what side is affected?
Middle cerebral artery: hemiparesis (face and arm > leg); hemianaesthesia; Dysphasia (dominant hemisphere), dysparaxia, (non-dominant hemisphere), visual field defect
Anterior cerebral artery: leg weakness
Contralateral to lesion
Posterior cerebral circulation (via vertebrobasilar supply)
- clinical features
- what side is affected?
Visual field defect (hemianopia)
Ataxia, diplopia, nystagmus, dysarthria, dysphagia, facial weakness/numbness, loss of consciousness
Sensory symptoms
Ipsilateral to lesion
What circulation supplied the internal capsule?
- if there was lesion here, how would they present?
MCA
face, arm, leg weakness with no other deficits
usually unilateral
speech intact - may be slurred
MCA blocked in left vs right
Both - hemiplegia, hemianopia
Left - aphasia (loss of speech)
right - visuospatial problems
Total anterior circulation stroke (TACS)
Carotid or middle cerebral artery infarct; internal carotid disease; intracerebral haemorrhage
Hemiparesis
Hemisensory loss
HCD
Homonymous hemianopia
Partial anterior circulation stroke (PACS)
Branch of carotid or MCA
HCD or restricted hemiparesis/ sensory loss (+/- hemianopia)
Lacunar stroke (LACS)
Deep perforator artery; occlusion of small branches of anterior/posterior circulation
Hemiparesis
Hemisensory loss (Ataxic hemiparesis)
Posterior circulation stroke (POCS)
Vertebrobasilar circulation Cerebellar signs Cranial nerve palsy Bilateral motor/sensory loss Conjugate eye mvt Isolated hemianopia
Ischaemic stroke
• Acute neurological deficit lasting >24h, caused by cerebrovascular aetiology
o Vascular occlusion/stenosis
• Pathophysiology:
o Primary vascular
o Cardiac
o Haematological
Prognosis improves from TACS→ POCS
1. Dysphasia (higher cognitive dysfunction)
2. Hemiparesis
3. Hemianopia
• TACS: all of above
• PACS: 1 of above
• LACS: lenticulostriate arteritis/deep arteries in internal capsule→ only sensory/ motor
• POCS: cerebellar/brain stem/occipital lobe constellation of symptoms
o Cerebellar signs are ipsilateral to lesions
Investigations
• CT/MRI within 1h→ essential if thrombolysis considered, or if high risk of haemorrhage (reduced GCS, increased ICP, headache, meningism, progressive symptoms)
o Diffusion weighted most sensitive for ischaemic infarct
• BM
• U&Es
• Troponin
• ECG→ excludes arrhythmia
o ECHO may reveal mural thrombus/ hypokinetic segment of cardiac muscle post-MI
• FBC→ exclude anaemia/thrombocytopaenia (lack of platelets→ bleeding)
• Carotid doppler→ carotid endarterectomy
• Other risk factors:
o Vasculitis
o Thrombophilia/antiphospholipid syndrome
o dyslipidaemia
Management
• If <4.5h→ thrombolysis with alteplase
o 1 in 20 can lead to haemorrhage
o Contraindications
• Recent operation <2/52
• Recent ischaemic stoke <3/12
• Significant trauma
• INR >1.6
• On anticoagulants (e.g. apixaban, treatment dose heparin)
• If >4.5h→ aspirin 300mg for 2 weeks, change to clopidogrel
• Thrombectomy within 6h→ NNT 3-4
• Hemicraniectomy
Haemorrhagic strokes
• Intraparenchymal haemorrhage:
o lobar→ caused by cerebral amyloid angiopathy→ microhaemorrhages
o Deep (lacunar)→ small vessel disease
o primary:
• idiopathic; anticoagulation
o secondary:
• trauma/malignancy
• vascular malformation
• Extraparenchymal haemorrhage:
o sub-arachnoid
• symptoms: sudden onset headache (typically occipital), vomiting, collapse, seizures, meningism (Kernig’s sign), retinal/vitreous bleeds,
• causes: berry aneurysms 80%, AV malformation 15%, encephalitis/vasculitis/tumour
• risk: HTN, FHx, PCK, ED syndrome
• DDx: meningitis, migraine
• Management:
• Refer to neurosurgery
• Maintain cerebral perfusion→ but manage SBP <160
• Nimodipine→ reduces vasospasm
• Surgery→ endovascular coiling/surgical clipping
o sub-dural
• symptoms: usually bridging veins between cortex and venous sinuses, fluctuating conscious levels, insidious physical/intellectual slowing, sleepiness, personality change
• DDx: stroke, dementia, CNS masses
• Management:
• Reverse clotting abnormality
• >10mm clot/>5mm midline shift→ surgical evacuation via craniotomy/burr-hole washout
o extra-dural/epidural
• symptoms: increasingly severe headache, vomiting, confusion, seizures, hemiparesis with brisk reflexes
• DDx: epilepsy, carotid dissection, CO poisoning
• Management:
• Neurosurgical clot evacuation/ligation of bleeding vessel
Investigation
• CT/MRI
o Clot+midline shift/ crescent-shaped collection of blood over 1 hemisphere→ subdural haemorrhage
o Biconvex/lens-shaped→ extradural haemorrhage ci LP
• LP >12h→ xanthochromia in SAH if CT-ve
Venous thrombosis
Venous thrombosis
• Thrombosis of cerebral sinuses/veins causes cerebral infarction
o Causes: OCP, pregnancy, dehydration, tumours, malignancy, infection
• Dural venous sinus thrombosis
o Sagittal→ headache, vomiting, seizures, reduced vision, papilloedema
o Transverse sinus→ headache+mastoid pain, focal CNS signs
o Sigmoid→ cerebella signs
o Inferior petrosal sinus→ Vth/VIth cranial palsies with tempora/retro-orbital pain
o Cavernous sinus→ spread from facial pustules/folliculitis→ headaches, chemosis, oedematous eyelids, proptosis, painful ophthalmoplegia, fever
• Cortical vein thrombosis
o Usually occurs with sinus thrombus extending to cortical veins
o Gives rise to stroke-like focal features
Investigations
• Thrombophilia screen
• CT/MRI→ absence of sinus
• T2-weighted MRI can image thrombus directly
Management
• Anticoagulation with heparin/LMWH→ warfarin