Ischaemic stroke

Acute neurological deficit, lasting more than 24 hours, caused by ischaemia. Stroke presentations are:

Pathophysiology

Disruption of blood flow resulting in liquefactive necrosis of neural tissue. Histologically characterised by red neurons (<48hr), evidence of necrosis and neutrophilic infiltration (48hr-72hr), microglial activation (3-5 days), gliosis and scarring (1-2 weeks) creating a cystic space/cavitation.

If the cause of the disrupted flow reverses within days of the insult, recirculation may lead to haemorrhage and associated oedema = haemorrhagic transformation.

Aetiology:

  1. Thrombosis
    • Large vessel disease:
      • Intracranial
        • Classically atherosclerosis
        • Also… dissection, vasoconstriction (migraine)
        • Rarely… vasculitis, Moyamoya
      • Extracranial
        • Classically atherosclerosis
        • Also… dissection
        • Rarely… vasculitis (Giant cell and Takayasu) & fibromuscular dysplasia
    • Small vessel disease:
      • Hyaline arteriosclerosis due to hypertension blocks small vessels penetrating to basal ganglia nuclei, producing lacunar infarct
      • Rarely… CADASIL (notch3 mutation) producing stroke, vascular dementia, migraine with aura and pseudobulbar palsy
  2. Embolism
    • Cardiac/Aorta
      • potential for multiple sites within different vascular territories
      • classically AF with clots in the left auricular appendage of the LA, or LV thrombus post-MI
      • rarely… infective endocarditis, atrial myxoma, PFO
    • Unknown source
  3. Systemic hypoperfusion
    • Usually secondary to arrest/anything causing a reduced output (MI, PE, tamponade)
    • Affects “watershed areas”
    • Neuron types most susceptible are the Purkinje neurons of the cerebellum and the pyramidal neurons of the hippocampus
    • Presents clinically as symmetrical proximal weakness and cortical blindness or defects in higher cortical visual processing
  4. Blood disorders
    • Relatively rare, but to be considered in a young person

Epidemiology

  • Common. Very common.
    • UK: incidence ~ 100,000/year
    • US: incidence ~ 795,000/year
  • Mortality after 1st stroke: 12% at 2 months (UK)

Symptoms

Depends on the vascular territory affected, and the stroke aetiology.

Patients will usually present with acute weakness/sensory loss/visual loss/dysphasia.

On examination

If associated headache, meningism, and low GCS – have high suspicion for ICH

  • MCA
    • Dominant hemisphere
      • Dys/aphasia
      • Motor/sensory loss (face/UL > LL)
      • Homonymous hemianopia
    • Non-dominant hemisphere
      • Motor/sensory loss (face/UL > LL)
      • Homonymous hemianopia
      • Hemispatial neglect
      • Anosognosia (loss of self-awareness)
    • Either hemisphere – if internal capsule involved
      • Complete hemiplegia (UL = Face = LL)
  • ACA
    • Motor/sensory loss (LL > face > UL)
    • Apraxia/Gait apraxia
    • Frontal release signs – primitive reflexes (grasping)
    • Abulia (apathy/loss of motivated behaviour)
  • PCA
    • Peripheral branches (hitting occipital cortex)
      • Homonymous hemianopia (with macular sparing)
      • Visual agnosia (loss of recognition)
      • Alexia (loss of ability to read – dominant hemisphere)
      • Rarely… visual hallucinations
    • Central branches (hitting the thalamus, cerebral peduncle or midbrain)
      • Sensory loss
      • Central post-stroke pain syndrome (allodynia)
      • Hyperkinetic movement disorders (e.g. hemiballismus)
      • Weber’s syndrome
  • Vertebrobasilar
    • Syndromes involving cerebellar, CN and cord signs
    • See brainstem stroke syndromes
      • Lateral medullary (Wallenberg)
      • Medial medullary
      • Millard-Gubler
      • Foville’s
      • Benedikt’s
  • Penetrating vessels (“lacunar” strokes)
    • No cortical signs (aphasia, hemianopia, apraxia etc.)
    • Associated subcortical signs (coma, seizures)
    • Classic syndromes:
      • Pure motor hemiparesis (>45%)
      • Sensorimotor stroke (15-20%) – PL thalamus + internal capsule
      • Pure sensory stroke (7-18%)
      • Ataxic hemiparesis (3-18%)
      • Dysarthria-clumsy hand syndrome (<6%)

Full CVS history/examination should be included. Things that are especially relevant:

  • Irregular rhythm (AF/flutter)
  • Murmur (IE, MS)
  • Prosthetic valves
  • Carotid bruit
  • Patent foramen ovale
  • Ischaemic heart disease/CABG/CCF
  • SLE

Diagnosis

Imaging <1hr of arrival:

  • Non-contrast CT head
  • If proximal intracranial large vessel occlusion suspected, and clot extraction available <5hr of onset:
    • CT angiogram: aortic arch to skull vertex
    • This should not delay thrombolysis

Treatments

  • Secure airway – if low GCS, consider adjuncts
  • Oxygen
  • ECG – patients can have co-presenting MI…
  • Blood pressure – if ischaemic…
    • Cerebral autoregulation dysfunction associated with ischaemia, producing a transient increase in BP, thought to be protective – evidence of U-shaped relationship between admitting BP and outcomes
    • This could be on a background of chronic HTN
    • No good evidence for lowering blood pressure in the acute setting unless target-organ damage (if anything, associated with worse outcomes), however…
    • To be eligible for thrombolysis, BP should be <185/110 (RCP Guideline UK, 2016), so treat cautiously to target <185/110
  • Sliding scale insulin aiming 4-11mmol/L
  • Aspirin 300mg PO (if swallow safe)

Thrombolysis

The following is a summary of the RCP Guideline 2016:

  • General eligibility
    • Anyone <3 hours of known onset
    • <80yo between 3-4.5 hours of known onset
    • >80yo between 3-4.5 hours of known onset – case-by-case basis
  • Blood pressure
    • Treat to reduce to below 185/110 mmHg before treatment
  • Thrombolysis does not preclude intra-arterial clot extraction (if available), and those with contraindications to thrombolysis should be considered for intra-arterial clot extraction (if available and NIHSS>5)
  • Contraindications (check local guidelines):
    • Major infarct or haemorrhage on CT
    • Non-disabling deficit
    • Seizures at presentation
    • Anticoagulated or INR >1.7
    • PLT <100
    • Recent surgery/trauma/birth
    • History of CNS haemorrhage
    • History of AVM or aneurysm
    • Severe liver disease/varices/portal HTN

Intra-arterial clot extraction (thrombectomy)

 

Consider for those:

  • Proximal intracranial large vessel occlusion causing a disabling neurological deficit
  • NIHSS >5
  • if arterial puncture can occur <5 hours of known onset
  • if >5 hours, consider for
    • posterior circulation (<24 hours)
    • predicted good outcome (<12 hours)

Neurosurgery

Consider decompressive hemicraniectomy <48 hours of stroke onset in MCA infarcts with:

  • pre-stroke modified Rankin Scale <2
  • NIHSS >15
  • NIHSS 1a >0 (consciousness)
  • CT demonstrates infarct >50% MCA territory