Elsevier

Surgical Neurology

Volume 68, Issue 4, October 2007, Pages 457-460
Surgical Neurology

Vascular
A restricted subarachnoid hemorrhage in the cortical sulcus in cerebral amyloid angiopathy: could it be a warning sign?

https://doi.org/10.1016/j.surneu.2006.11.028Get rights and content

Abstract

Background

Cerebral amyloid angiopathy is a well-known disease that is predominantly recognized in elderly people and repeatedly causes large subcortical hemorrhages. These hemorrhages may be derived from vessel wall weakness because of Aβ depositions in the wall of the cortical and leptomeningeal arteries. Although vessel ruptures in CAA have been thought to occur in cortical arteries, it was recently demonstrated that the primary hemorrhage occurs in the subarachnoid space, particularly the cerebral sulci, as a result of multiple ruptures of meningeal arteries in some cases of subcortical hematoma caused by CAA.

Case Description

Case patient 1 was a 74-year-old woman who presented with epileptic seizure. A restricted SAH in the right frontal lobe was observed on MRI. Thirty-three days later, left hemiparesis occurred suddenly and a huge subcortical hematoma was observed in the right frontal lobe on CT. The hematoma was removed, and the patient was pathologically diagnosed with amyloid angiopathy. Case patient 2 was a 73-year-old man who presented with epileptic seizure. A restricted SAH in the right frontal lobe was observed on MRI. Twenty days later, left hemiparesis occurred suddenly and a huge subcortical hematoma was observed in the right frontoparietal area on CT. Hematoma removal was performed on both patients, and they were diagnosed pathologically with amyloid angiopathy.

Conclusions

We report on the cases of 2 patients with CAA who presented with epileptic seizure and were found to have a restricted subarachnoid hematoma in the cerebral sulcus on MRI before their subcortical hemorrhages occurred. Both cases were diagnosed pathologically. This demonstrated that vessel ruptures in CAA can occur in the subarachnoid space, particularly the cerebral sulci, as a result of ruptures of meningeal arteries. A restricted SAH on CT/MRI could be a warning sign of a huge subcortical hemorrhage in CAA.

Introduction

Cerebral amyloid angiopathy is a well-known disease that is predominantly recognized in elderly people and repeatedly causes large subcortical hemorrhages. These hemorrhages may be derived from vessel wall weakness and are very difficult to anticipate or control.

We report on 2 cases of CAA with huge subcortical hematomas. The patients presented with epileptic seizure and were found to have a restricted subarachnoid hematoma in the cerebral sulcus on MRI before their subcortical hemorrhages occurred.

A restricted SAH with epileptic seizure could be a warning sign of a huge subcortical hemorrhage in CAA.

Section snippets

Case patient 1

A 74-year-old woman presented herself to the Hokkaido Neurosurgical Memorial Hospital because of transient left hemiparesis and sensory disturbance. Neurologic deficit disappeared 30 minutes later. On MRI, there was no abnormality; however, she noted numbness in the left side of her body 7 days after her first visit. Although the numbness disappeared after 15 minutes, a restricted SAH in the right frontal lobe was observed on MRI (Fig. 1).

Because epileptic waves were found on electric

Case patient 2

A 73-year-old man was admitted to the Hokkaido Neurosurgical Memorial Hospital because of repeated left hemiparesis that lasted for approximately 10 minutes. Neurologic examination disclosed slight left hemiparesis. On MRI, a restricted SAH was noted in the right frontal sulcus (Fig. 4).

Sodium valproate was prescribed, and the repeated episodes of left hemiparesis disappeared.

We thought the patient might have had CAA when he presented with a restricted SAH on MRI; therefore, we paid close

Discussion

Cerebral amyloid angiopathy is caused by the deposition of Aβ in the walls of cortical and leptomeningeal arteries. As a rule, veins and capillaries tend to be affected less frequently than arteries [3], [4]. Finally, the layers of smooth muscle cells disappear, resulting in vessel weakness.

Although the etiology of this condition remains unknown, Weller and Nicoll [6] suggested that Aβ  deposits in vessel walls because of a loss of function in the periarterial interstitial fluid drainage

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