Stroke & TIA

 

• Types and definitions

  Stroke:

  • Rapid onset neurological deficit(s) resulting from altered blood supply to the brain and lasting ≥24 hours.
  • In clinical practice, the term stroke is often used synonymously with ischaemic stroke, though technically haemorrhage causing deficit ≥24 hours is also a stroke.

  Ischaemic stroke:

  • 85% of strokes.
  • Ischaemia due to cerebrovascular thrombosis or embolus. Emboli typically originate from the heart (AF/MI/IE/valve disease), aortic arch, carotid artery (atheroma or dissection), or vertebral artery (dissection).

  Haemorrhagic stroke:

  • Intracerebral (intraparenchymal or intraventricular), subarachnoid.
  • Causes: vascular abnormality (aneurysm, AVM), HTN, coagulopathy, vasculitis, or amyloidosis.

  Transient ischemic attack (TIA):

  • Symptoms last <24 hours.
  • Stroke and TIA are collectively known as cerebrovascular events (CVE) or cerebrovascular accidents (CVA).

• Signs and symptoms

  • Focal neurological signs, usually 'negative' i.e. weak, numb (as opposed to 'positive' signs like pain). Onset is sudden, possibly waking from sleep, and symptoms worsen within hours.
  • Ischaemic stroke: there may also be signs of an embolic source e.g. murmur (valve disease), fever (infective endocarditis), carotid bruit (carotid artery disease). Loss of consciousness is rare.
  • Haemorrhagic stroke: meningism, headache, and often coma within hours.

  Oxford (Bamford) stroke classification

  Anterior circulation stroke

  Results from occlusion of the internal carotid (ICA), middle cerebral (MCA), or anterior cerebral arteries (ACA).

  Total anterior circulation stroke (TACS) is all 3 of the following, and partial anterior circulation stroke (PACS) is number 2 alone or any 2 of 3:

  1. Motor or sensory deficits – contralateral to the lesion – in 2 out of 3 of the face, arm, and legs. Initially weak, flaccid, and areflexic, later UMN signs and less weakness. These signs alone = lacunar stroke. Predominant leg symptoms suggest ACA stroke, while predominant arm and face symptoms suggest MCA stroke.
  2. Impaired higher function: aphasia (if in dominant hemisphere), apraxia, agnosia, hemispatial neglect (if in non-dominant hemisphere), altered level of consciousness. This alone = PACS.
  3. Visual field changes, especially homonymous hemianopia. This alone = POCS.

  Posterior circulation stroke (POCS)

  Results from occlusion in the vertebro-basilar system or posterior cerebral artery.

  Any of the following presentation(s):

  1. CN palsy plus contralateral motor or sensory deficits of body.
  2. Bilateral motor or sensory defect
  3. Eye movement problems.
  4. Isolated homonymous hemianopia.
  5. Cerebellar lesions.
  6. Locked-in-syndrome, due to occlusion of the basilar artery affecting the pons.
  7. Lateral medullary syndrome: posterior-inferior cerebellar artery occlusion leads to ipsilateral face signs – Horner's, loss of temperature and pain sensation, dysarthria, dysphagia, palatal paresis – and contralateral body signs – loss of temperature and pain sensation.

  Lacunar stroke (LACS)

  Results from small infarct in end artery, usually in the anterior circulation. There is no loss of higher function, but the motor symptoms may be profound as it affects an area of the brain through which many motor white matter tracts pass.

  Various presentations, including:

  1. Unilateral motor and/or sensory deficits.
  2. Ataxic hemiparesis: ipsilateral clumsiness and weakness, as opposed to cerebellar dysfunction (POCS) which is just clumsy.
  3. Dysarthria and clumsy hand.

• Risk factors

  Demographic and lifestyle:

  • Demographic: ↑age, male, non-white.
  • Lifestyle: smoking, alcohol, combined pill.

  Vascular risk factors:

  • Major CVD risk factors: HTN, diabetes, ↑cholesterol.
  • Existing CVD: heart disease (valvular, IHD, AF), PVD, previous stroke, carotid bruit.

  Abnormal clotting:

  • Thrombophilia (e.g. polycythaemia, APS) → ischaemic stroke.
  • Coagulopathy (e.g. warfarin, liver disease) → haemorrhagic stroke.

  Inflammatory and congenital:

  • Vasculitis: SLE, TA.
  • Homocystinuria
  • Amyloid angiopathy.
  • Mitochondrial disease.
  • Syphilis

• Differential diagnosis

  M8S:

  • Migraine
  • Sugar: hypoglycaemia.
  • Seizures, especially Todd's palsy.
  • Sepsis, encephalitis.
  • Syncope
  • SDH
  • Space occupying lesion.
  • Old Strokes with intercurrent illness.
  • Somatisation

• Investigations

  Imaging aids diagnosis, while most other tests look for risk factors and complications.

  Bloods:

  • FBC: polycythaemia, ↓platelets (potential cause of stroke and contraindication to some treatments).
  • ESR: vasculitis.
  • U&Es and LFTs: look for renal, electrolyte, or hepatic causes of neurological symptoms.
  • Coag: looking for stroke cause and prior to initiating thrombolysis or antiplatelets.
  • Glucose
  • Cholesterol

  CV tests:

  • ECG: AF.
  • CXR: may show LVF from HTN, large atria as source of embolus, or aspiration pneumonia.
  • Echo: if embolic source suspected.
  • Carotid duplex US for potential endarterectomy candidates i.e. TIA or non-disabling stroke.

  Neuroimaging:

  • CT: rules out haemorrhage and tumour, but initially may be normal in ischaemia. Allows thrombolysis to proceed if -ve.
  • CT angiography (CTA): detects large vessel occlusion to identify potential thrombectomy candidates.
  • MRI: shows infarct more clearly and is as sensitive as CT for bleed. However, less widely available.
  • In TIA, CT only indicated acutely if suspecting alternative diagnosis that CT can detect (e.g. bleed). If imaging considered necessary in TIA clinic (e.g. to define ischemic territory or rule out alternative diagnoses), MRI is preferred.

• Management

  Overall approach

  Acute stroke management:

  • Monitor to prevent ↓O2, ↓glucose, ↓BP, infection.
  • Imaging within 1 hour.
  • DVT prophylaxis if immobile. Intermittent pneumatic compression 1st line, plus LMWH only if very high risk.
  • Admit to specialist stroke ward.
  • MDT: speech and language therapy (SALT), physio, and OT.

  Acute TIA management:

  • Refer all patients with suspected TIA for specialist assessement within 24h.

  Specific therapies

  Reperfusion therapy for ischaemic stroke:

  • Thrombolysis: alteplase or tenecteplase IV for patients presenting within 4.5 hours of symptom onset.
  • Thrombectomy: consider for patients with large vessel occlusion (on CT/MR angiography) and non-infarcted tissue beyond the occlusion (an 'ischaemic penumbra', as seen on CT perfusion or diffusion-weighted MRI). Effective up to 24 hours post symptom onset, though only 10% eligible.

  Antiplatelets for ischaemic stroke and TIA:

  • Start aspirin 300 mg OD 24 hours after alteplase, or immediately if outside the treatment window or in TIA. Continue for 2 weeks then switch to long-term antiplatelet.
  • Consider dual-antiplatelet therapy (aspirin plus clopidogrel) for 3 weeks in high risk TIA (ABCD2 ≥4) or minor ischaemic stroke (NIHSS ≤3).

  Haemorrhagic stroke:

  • Neurosurgical referral. Few interventions for intracerebral bleeds, but SAH may be coiled or clipped.

  Secondary prevention

  • Antiplatelet: clopidogrel 1st line, aspirin plus modified-release dipyridamole 2nd line.
  • Anticoagulation (DOAC or warfarin) instead of antiplatelets if there is AF.
  • Statins for all.
  • Screen for and treat hypertension as per the normal pathway.
  • Carotid endarterectomy or stenting if there is ≥50% carotid artery stenosis. 5% perioperative stroke risk. More likely to be done post-TIA or non-disabling stroke, as after a disabling stroke it's essentially too late.
  • Lifestyle: improve diet, ↑exercise, ↓smoking, ↓alcohol. No driving for 1 month.

• Thrombolysis for ischaemic stroke

  Alteplase is the only licensed thrombolytic agent for ischaemic stroke in the UK. Tenecteplase is an alternative with similar mechanism, risks, and benefits.

  Mechanism

  A recombinant tissue plasminogen activator (tPA), catalysing plasminogen conversion to plasmin, which degrades fibrin.

  Risks and benefits in stroke

  • Increased risk of intracranial bleed and 7 day mortality (2% absolute increase). Repeat CT 24 hours after administration to look for haemorrhage.
  • Mortality difference (vs. placebo) evens out by 3-6 months, at which point it shows a 10% absolute increase in the number of people achieving a good functional outcome. This benefit is only achieved if given within 3 hours, and possibly up to 4.5 hours. However, there are questions about the methodological reliability and consistency of this beneficial finding in the literature.

  Contraindications

  Bleeding:

  • Ongoing bleeding (except menstruation).
  • History of CNS bleeding.

  Unstable:

  • Seizures at presentation.
  • Uncontrolled HTN >180/110.

  Recent medical history:

  • LP in the past week.
  • Ischaemic stroke or head injury within the last 3 months.
  • Surgery or major trauma within the last 2 weeks.

  Cautions:

  • Anticoagulated
  • Coagulopathy

• Complications and prognosis

  Complications:

  • Short-term: DVT, aspiration pneumonia, seizures, cerebral oedema and ↑ICP.
  • Long-term: persistent neurological deficits, epilepsy.

  Prognosis:

  • Most recovery happens in first 3 months.
  • Overall 20% mortality within 1 month.
  • TACS at 12 months: 50% mortality, 45% disabled, and 5% fine.
  • Non-TACS at 12 months: 15% mortality, 35% disabled, 50% fine.