Cerebral Amyloid Angiopathy Related Hemorrhage Masquerading as SAH
Drs Kevin Petrecca, Grant Linnel, Marie-Christine Guiot, John Richardson & Denis Melançon

CASE REPORT

e present the case of a 77 year old man who presented with acute paresis of the left lower face and arm. The patient was otherwise neurologically intact. One week prior to admission he sustained a fall from his own height striking his occiput.
A plain CT revealed acute blood in the right central sulcus and inferior frontal sulcus (Fig. 1A). The presumptive diagnosis was vasospasm secondary to a traumatic subarachnoid hemorrhage (SAH). A diagnostic cerebral angiogram, performed to exclude an underlying vascular abnormality, was normal. The patient was started on Nimodipine resulting in a significant improvement in symptoms. One week later he developed more widespread symptoms including right arm weakness. A second plain CT revealed more extensive hemorrhage with acute blood in the right superior frontal sulcus, right precentral sulcus and left central sulcus (Fig. 1B).

 

 

 


Figure 1. A, CT plain. B, CT plain. C, T1-weighted MR. Arrows indicate hyperintense signals restricted to the cortex.

         The systemic work-up of a vasculitis was negative. A T1-weighted MRI (Fig. 1C) showed hyperintense signals corresponding to the CT images; however, the hyperintense signals appeared, in certain regions, to be cortical and not extracortical (Fig. 1C, arrows). An open left frontal biopsy was performed for diagnosis. The pathology revealed -amyloid deposition in blood vessel walls consistent with cerebral amyloid angiopathy.

 

 


Figure 2. A,
H&E stain showing a thickened vessel wall. B, Blood vessel immunolabelled with an anti-β-amyloid antibody revealing abundant β-amyloid deposition in the vessel wall.

DISCUSSION

       Cerebral amyloid angiopathy (CAA) is a common cause of primary spontaneous intracerebral hemorrhage. The pathogenesis of CAA involves b-amyloid deposition in the media and adventitia of cortical and leptomeningeal arteries, arterioles, capillaries and less often veins (1). As a result, vessels become more brittle and thus more susceptible to minor trauma and changes in blood pressure. As such, CAA-related hematomas are of cortical/subcortical origin; however, they are not restricted to these regions as they typically extend deeply into white matter. Here we present an unusual case of a CAA-related hemorrhage that is strictly confined to the cortex mimicking subarachnoid hemorrhage on plain CT.

REFERENCE

Qureshi AI, Tuhrim S, Broderick JP, Batjer HH, Hondo H, Hanley DF. New England Journal of Medicine. 2001;344:1450.

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