[A case of primary subarachnoid hemorrhage due to cerebral amyloid angiopathy]

Rinsho Shinkeigaku. 2007 Jan;47(1):42-6.
[Article in Japanese]

Abstract

A 77-year-old man who was suffering from an intracerebral hemorrhage of the left subcortex without hypertension was admitted to our hospital. The only neurological symptom was right arm monoparesis. Brain MRI demonstrated a subarachnoid hemorrhage (SAH) in the left frontal lobe. On the day of admission, conventional cerebral angiography revealed no abnormalities in brain arteries. His symptom was disappeared immediately after admission. He was discharged without neurological deficit on day 25. However, he was rehospitalized in our hospital on the same day because he experienced a right subcortical hemorrhage. The neurological symptoms were consciousness disturbance, aphasia and right hemiparesis. Brain CT disclosed a subcortical hemorrhage in the left temporal lobe. CT stereo-guided drainage was performed. Then, we examined tissue removed from the brain's surface. Histologically, beta-amyloid protein was deposited on the walls of the meningeal and cortical vessels, and it replaced all the layers of those walls. Therefore, a diagnosis of cerebral amyloid angiopathy (CAA) was made. His condition gradually improved, but CT showed an asymptomatic ICH in the right parietal lobe on day 36. On day 47, he had a symptomatic ICH in the left caudate nuclei and right frontal lobe. He died on day 66 because of pneumonia. Intracranial hemorrhages due to CAA have been reported and the majority of the lesions have been lober hemorrhage. To the best of our knowledge, few reports have been published regarding primary SAH caused by CAA. The cause of SAH should be considered as CAA when SAH appears without hypertension or in elderly patients.

Publication types

  • Case Reports
  • English Abstract

MeSH terms

  • Aged
  • Cerebral Amyloid Angiopathy / complications*
  • Humans
  • Magnetic Resonance Imaging
  • Male
  • Subarachnoid Hemorrhage / diagnosis
  • Subarachnoid Hemorrhage / etiology*