Cerebral amyloid angiopathy: multiple intracranial hemorrhages

Case contributed by RMH Neuropathology
Diagnosis certain


Previous history of left temporal hemorrhage 10 years ago. Thought to be vasculitis. Now presenting with two weeks of headache.

Patient Data

Age: 67
Gender: Male

A relatively stable ill-defined 2 cm area of gliosis/encephalomalacia and hemosiderin staining, compatible with old hemorrhage, remains centered posteriorly in the left inferior and middle temporal gyri.

There is no evidence of underlying tumor, vascular malformation or aneurysm. Of note, a linear focus of T2 hyperintensity and diffusion restriction, consistent with a recent small vessel infarct , is now noted to course obliquely through the posterior left parietal lobe subcortical white matter.

A stable 2-3 cm area of partly liquefied encephalomalacia/gliosis remains centered inferiorly in the left occipital lobe, with moderately extensive chronic small vessel ischemic change elsewhere in the white matter of both cerebral hemispheres and brainstem considered excessive even for a 62 year old patient.The remainder of the study is unremarkable.

A left cerebellar hemisphere acute hemorrhage is demonstrated, measuring 4 x 2.5 x 2.5 cm, with extension into the extra-axial space, with this component measuring 13 mm in depth. The overall effect is effacement of the posterior fossa basal cisterns and 4th ventricle, with enlargement of the 3rd and lateral ventricles consistent with developing hydrocephalus.

Extensive patchy white matter hypoattenuation is in keeping with chronic small vessel ischemic change.

CTA arch to vertex:

Intradural vessels demonstrate no focal abnormality, specifically no evidence of avascular malformation or aneurysm related to the aforementioned left cerebellar hemisphere hemorrhage. No evidence of arteriovenous shunting to suggest a malformation or dural arteriovenous fistula.

Incidental note is made a somewhat ectatic right extradural cavernous ICA, without defined aneurysm. Note is also made of both posterior inferior cerebellar arteries arising from the vertebral arteries at or just prior the entry through the dura.

The extracranial circulation is largely unremarkable, with only moderate stenosis of the left internal carotid artery origin (50-65%).

Minor multilevel degenerative change of the cervical spine is demonstrated, with no high-grade stenosis. Soft tissues of the neck are within normal limits.


1. Left cerebellar hemispheric hemorrhage with extra-axial extension in this clinical context (known poorly controlled hypertension) presumably represents a primary hypertensive hemorrhage. No underlying vascular abnormality evident.

2. developing hydrocephalus

3. moderate left ICA stenosis at it origin


MRI Brain (10 days later)


Image quality on some sequences are degraded by motion artefact.There is been recent left frontal craniotomy with expected changes in the overlying subcutaneous soft tissues. Thin extra-axial collection overlying the left frontal convexity measuring up to 4 mm in depth. Altered signal and cavity in the subjacent frontal lobe in keeping with partially evacuated left frontal parenchymal hematoma.

Very small volume residual intraventricular blood in the dependent portion of the right lateral ventricle.

Compared to previous MRI, lateral and ventricles are enlarged. Confluent T2 and FLAIR hyperintensity in the periventricular white matter.

Altered signal, encephalomalacia, and gliosis in the left cerebellar hemisphere, left temporal lobe, and left occipital pole in keeping with previous parenchymal hemorrhage in these locations.

Multiple foci of blooming susceptibility sensitive sequence in both cerebral hemispheres, with predilection for the grey-white matter junction. Allowing for differences in comparison between GRE (current study) and SWI (previous) these appear more numerous.

Sulcal hemosiderin staining, most notably at the vertex, in keeping with previous subarachnoid hemorrhage.

Susceptibility related signal loss in the left parietal lobe indicates location of the previous ventricular catheter.

Multiple foci of T2 and FLAIR hyperintensity in the subcortical white matter of both hemispheres have increased in size compared to previous MRI.

No abnormal contrast enhancement. Altered signal on DWI most likely a result of extensive blood products.

Time-of-flight MRA demonstrates a slightly bulky anterior communicating artery, but no intracranial aneurysm. No evidence of intracranial steno-occlusive disease other than the distal M3 left side branch narrowing which could represent mass effect or intrinsic disease - of doubtful relevance.


Appearance of left frontal lobe in keeping with recent intraparenchymal hemorrhage and subsequent evacuation.

Enlarged ventricles compared to previous MRI. Periventricular T2 and FLAIR hyperintensity suggestive of transependymal fluid shift. Small residual intraventricular blood is noted.

Distribution of punctate foci of blooming suggestive of amyloid angiopathy.

Marked progression of subcortical white matter disease compared to the previous study.

Prior left cerebellar hematoma, remote left occipital lobe hematoma.

5 days later - sudden drop GCS


New large left frontoparietal parenchymal hemorrhage (54 x 34 x 55 mm results in midline shift to the right of 6 mm (previously there was no midline shift). This appears separate to the previous left frontal hemorrhage. There is also further subarachnoid hemorrhage at the vertex. No CTA spot sign.

Normal aortic arch anatomy. Common carotid and internal carotid arteries are patent with no dissection. Vertebral arteries are patent with no dissection. Normal circle of Willis anatomy. No aneurysms, filling defects or vascular malformations are identified.

ETT positioned appropriately. Apical subpleural blebs. Nasogastric tube is noted.

Conclusion: Large left frontoparietal parenchymal hemorrhage with subarachnoid extension has developed since the CT at 09:56 this morning with new midline shift to the right. No basilar artery thrombus.


MICROSCOPIC DESCRIPTION: The sections contain cerebral cortex and white matter. There are areas of hemorrhage within both cortex and white matter. Some entrapped neutrophils are seen within the areas of blood. The leptomeningeal and cortical blood vessels appear to contain some amorphous eosinophilic material. B-amyloid immunostain is positive. Many amyloid plaques are also seen in the cortex. No vasculitis is seen. There are no perivascular CD3 or CD20+ lymphocytes. No tumor is identified.

DIAGNOSIS: Brain tissue: Amyloid angiopathy with areas of hemorrhage. No evidence of vasculitis. 

Case Discussion

This case demonstrates multiple brain hemorrhages due to cerebral amyloid angiopathy (CAA), which is a cerebrovascular disorder that tends to manifest in normotensive elderly patients. 

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