Small Chronic Hemorrhages and Ischemic Lesions in Association With Spontaneous Intracerebral Hematomas
To the Editor:
Tanaka et al1 have cited my article2 concerning fibrinoid necrosis, miliary aneurysms and cerebral hemorrhage, in a misleading way. I did NOT, as their text suggests, offer support for the concept of “pseudoaneurysms” or “bleeding globes.” In fact, I reported no such lesions. Rather, one important finding in my paper was that the miliary aneurysms [ie, true aneurysms] can become fibrosed, rather than rupture, and then become fibrous balls. I pointed out that when cut in cross-section and thus isolated from their parent arteriole in histological section, these balls may not be recognized for what they are—healed, TRUE aneurysms. The proof of their identity was the presence of remnants of arteriolar wall elastic tissue at their margins. In longitudinal sections I clearly illustrated the continuity of this elastic tissue with the elastica of the parent arteriole at the point where the neck of the fibrosed aneurysm joined with the fibrous ball. As Tanaka et al point out, if there are pseudoaneurysms caused by organization of hemorrhages from nonaneurysmal sites of bleeding, these would have a completely different structure and would be, in their words, rimmed by fibrin and later supposedly transformed into masses of collagen (without remnants of elastica). This point remains extremely important as I pointed out elsewhere:3 the failure to recognize fibrous balls as true miliary aneurysms will lead to great underestimation of the incidence of miliary aneurysms in benign hypertension; the failure to use elastic stains to distinguish between healed aneurysms and “bleeding globes” (which are simply small hemorrhages adjacent to a vessel) will also lead to underestimation of the incidence of miliary aneurysms. Both errors continue to contribute to the failure of many persons to recognize the importance of miliary aneurysms as potential sources of cerebral hemorrhage.
- Copyright © 1999 by American Heart Association
In our article,R1 the term “fibrous ball” was used to mean an organized miliary pseudoaneurysm. This is not consistent with Dr Rosenblum’s definition of the term as a fibrosed true aneurysm with endothelium and internal elastic laminae, in patients with intracerebral hemorrhage.R2 Our diagnosis of pseudoaneurysm has been based on both light- and electron-microscopic observations of 7 miliary aneurysms that were found among 48 specimens of hypertensive intracerebral hemorrhage.R3 The aneurysmal walls invariably consisted of dense layers of fibrin and plasma protein admixed with a few hematogenous cells. Endothelial cells, however, were totally absent on the luminal surface. The wall of the aneurysm contained no remnants of arteriolar elements such as internal elastic laminae. Our findings of miliary aneurysms are completely consistent with the descriptions in the textbook Pathology of the Cerebral Blood VesselsR4 : “Vessels bearing miliary aneurysms usually exhibit a severe degree of arteriosclerosis. The aneurysmal wall consists of hyaline and collagenous tissue, the media and internal elastic lamina in most cases terminating near the entrance to the sac. In some aneurysms a considerable amount of fibrin occurs in the thickened aneurysmal wall, and red cells and remnants of a hyaline or collagenous tissue are recognizable within the fibrin laminations. A few leukocytes, macrophages and siderophages are not infrequent. The lesions could be false aneurysms if formed as the result of rupture of the wall. Miliary aneurysms undergo partial or complete thrombosis and eventually be replaced by a collagenous mass.”
As mentioned in our article, however, an abrupt breakage of the arterial wall is more common than microaneurysms at the site of rupture in hypertensive intracerebral hemorrhages. This is also consistent with the descriptions in the textbook, Greenfield’s NeuropathologyR5 : “The long-lived controversy about the role of microaneurysms is still unsettled. Challa and co-workers who presented strong evidence for microaneurysms being actually complex coils and twists of small arterioles regarded rupture of non-aneurysmal arteriolar wall damaged by hypertension as the likely cause of hypertensive haemorrhages.” Thus, we maintain our belief that hypertensive intracerebral hemorrhage is caused by a direct rupture of the arteriosclerotic arterial wall at the bifurcation, with or without a secondary formation of pseudoaneurysms.
Tanaka A, Ueno Y, Nakayama Y, Takano K, Takebayashi S. Small chronic hemorrhages and ischemic lesions in association with spontaneous intracerebral hematomas. Stroke.. 1999;30:1637–1642.
Rosenblum WI. Miliary aneurysms and “fibrinoid” degeneration of cerebral blood vessels. Hum Pathol.. 1977;8:133–139.
Takebayashi S, Kaneko M. Electron microscopic studies of ruptured arteries in hypertensive intracerebral hemorrhage. Stroke.. 1983;14:28–36.
Stehbens WS. Pathology of the Cerebral Blood Vessels. St Louis, Mo: CV Mosby Co; 1972:317–319.
Kalimo H, Kaste M, Haltia M. Hypertensive haemorrhage. In: Graham DI, Lantos PL, eds. Greenfield’s Neuropathology. 6th ed. London, UK: Arnold Publishers; 1997:375.