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Artery of Percheron stroke


Learning objectives

  • To understand the pathophysiology of AOP stroke
  • To understand the Causes and clinical signs and symptoms of AOP stroke
  • To understand the Diagnostic tests for AOP stroke
  • To understand the Management of AOP stroke

About

  • Artery of Percheron first described in 1973 by French Neurologist Gerard Percheron.
  • Interesting as most vascular supply respects the midline.

Pathophysiology

  • This is a single vessel that supplies bilateral structures.
  • May have altered mental status, vertical gaze palsy, and memory impairment
Anatomy of AOP: There is an error in the graphic
Read Posterior cerebral artery and not posterior communicating artery.

Epidemiology

  • Acute Artery of Percheron infarcts represent 0.1 to 2% of total ischaemic stroke
  • A typical stroke centre with 1000 strokes PA may see 1-2 cases

Aetiology

  • The arterial supply of thalamus and midbrain is complex and is provided by perforating branches from the posterior cerebral artery and the posterior communicating artery.
  • Many numbers of significant variations in vascular supply of thalami and mesencephalon are seen.
  • The Artery of Percheron is a rare vascular variant in which a single dominant thalamo-perforating artery arises from one P1/2 segment of PCA and bifurcates to supply both paramedian thalami.
  • Occlusion of this uncommon vessel results in a characteristic pattern of bilateral paramedian thalamic infarcts with or without mesencephalic infarctions
  • Aetiology likely cardioembolic or artery to artery from aorta or vertebral

MRI appearance

Clinical

  • Result of bilateral damage patient is often degrees of acute coma.
  • Somnolescence - patient is unresponsive but may roll over and pull up bed clothes as if sleeping.
  • Coma in others even needing intubation.
  • Pinpoint pupils may be seen unless IIIrd nerve involved
  • Long term when awakens memory and cognition often affected
  • Midbrain involvement - may have hemiplegia, IIIrd nerve deficits

Differentials in Comatose patient with normal initial CT

  • Meningo-Encephalitis
  • Opiates or other sedatives
  • Pontine strokes
  • Post ictal
  • Hypoglycaemia
  • Post concussion

Investigations

  • FBC, U&E, LFTs. CRP. ESR. Cholesterol
  • ECG/24 hr tape for AF
  • Echo for cardioembolic cause
  • CT: usually normal but may show hypodensity with time
  • MRI: classical bilateral "butterfly" medial thalamic infarcts and may show some midbrain involvement. There may be the V sign of a hyperintense signal intensity on axial FLAIR and DWI images along the pial surface of the midbrain in the interpeduncular fossa in 67% in cases of AOP infarction with midbrain involvement.
  • CTA/MRA to look for vertebral dissection can be useful as a cause
  • LP may be normal mildly elevated protein but may help exclude infective process if suspected

Management

  • ABC, support acutely. Often delayed diagnosis as stroke as other non stroke diagnoses need exclusion
  • Consider thrombolysis and /or thrombectomy if appropriate. However often the presentation is difficult and diagnosis delayed and beyond window for thrombolysis.
  • Uncertainty means that one may give antibiotics, antivirals initially as ?? Meningitis/Encephalitis. LP may be normal or mildly elevated protein.
  • Can make good recovery. But there may remain memory and cognitive issues.
  • Manage as other ischaemic strokes. Look for embolic sources.
  • Standard Care: Antiplatelets, BP medications, Statin
  • Neurorehabilitation: cognitive issues may predominate so involve Neuropsychology

References

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