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Transient focal leukoencephalopathy with cerebral oedema as a presentation of cerebral amyloid angiopathy
  1. Martin Nicholas Michael Punter1,
  2. James Lilleker2,
  3. Joseph Vassallo3
  1. 1Department of Neurology, Greater Manchester Neurosciences Centre, Salford Royal NHS Foundation Trust, Salford, UK
  2. 2University of Manchester, Salford Royal NHS Foundation Trust, Manchester, UK
  3. 3Department of Elderly Care, Stockport NHS Foundation Trust, Stockport, UK
  1. Correspondence to Dr Martin Nicholas Michael Punter, Greater Manchester Neurosciences Centre, Salford Royal NHS Foundation Trust, Stott Lane, Salford M6 8HD, UK; Martin.punter{at}

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Cerebral amyloid angiopathy affects the small-to-medium-sized cerebral arteries most commonly resulting in asymptomatic microhaemorrhages and symptomatic lobar brain haemorrhages. More unusually, it may present as an acute or subacute leukoencephalopathy.

Its mechanism is unknown but probably relates to altered permeability of cerebral blood vessels that results from endothelial dysfunction secondary to β-amyloid accumulation in the vessel wall.1 ,2 There is sometimes associated vessel wall inflammation, termed ‘cerebral amyloid-related inflammation’.3

We describe a challenging case with a relapsing encephalopathic syndrome and discuss its implications.

Case presentation

A 72-year-old man presented to the emergency department having awoken that morning with confusion, disorientation and visual hallucinations. Thirty minutes later, he had a generalised tonic–clonic seizure followed by postictal agitation, during which he was non-cooperative and non-attentive.

On examination, there were no lateralising neurological signs although he was in a state of delirium, with a Montreal Cognitive Assessment score of 9/30. His blood pressure was 215/115 mm Hg.

CT scan of head is shown in figure 1. We made a working diagnosis of acute ischaemic stroke with symptomatic seizure and commenced aspirin and sodium valproate. His blood pressure fluctuated during his admission (systolic between 141 and 201 mm Hg and diastolic 79 and 145 mm Hg). His clinical status improved steadily over the subsequent 4 days and he was able to go home.

Figure 1

Axial CT brain scan demonstrating an area of hypodensity …

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  • Contributors JL collected the clinical information and imaging and formatted the imaging for presentation. MNMP wrote the drafts of manuscript and coordinated the production of the manuscript. JV, JL and MNMP reviewed the manuscripts and discussed the content to produce the final draft.

  • Competing interests None declared.

  • Patient consent Obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed. Reviewed by Tom Hughes, Cardiff, UK.

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