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Cerebral hemorrhage produced by ruptured dissecting aneurysm in miliary aneurysm.

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Cerebral Hemorrhage
Produced by Ruptured
Dissecting Aneurysm in
Miliary Aneurysm
William I. Rosenblum, MD
This report describes, for what may be only the second
time, a ruptured miliary aneurysm within a cerebral hemorrhage. The report is unique in that the aneurysm has
arisen at the site of a dissection within the wall of an
arteriole at a site of fibrinoid necrosis. The case not only
is a unique illustration of this pathogenetic pathway to
miliary aneurysm formation, but also reemphasizes the
relationship between fibrinoid and miliary aneurysm formation.
Ann Neurol 2003;54:376 –378
Recently, Fisher1 reported what is apparently the first
demonstration of the remains of a ruptured miliary aneurysm within a cerebral hemorrhage. This demonstration is especially important because the role of miliary
aneurysms and indeed their very existence has been disputed2–5 since their initial description by Charcot and
Bouchard.6 Serial sections may be required to demonstrate miliary aneurysms, and even then their remains
may be “lost” within the hemorrhage.1 Thus, prior to
Fisher’s report1 histological evidence for their importance was indirect, for example, in demonstrations of
unruptured miliary aneurysms4,7 or of fibrosed miliary
aneurysmal sacs in sections taken at random from sites
distant from the hemorrhage itself.4 Such cases4,7 often
also demonstrated fibrinoid necrosis in arteriolar segments, offering support to the hypothesis that such areas might either rupture or might be sites for formation of miliary aneurysms that might rupture.5 In view
of the debate concerning the importance of these aneurysms, it is important to provide additional examples
of ruptured aneurysms within a hemorrhage. This
might best be accomplished by serially sectioning
smaller hemorrhages, thereby reducing the required la-
From the Department of Pathology, Division of Neuropathology,
Virginia Commonwealth University’s Medical College of Virginia,
Richmond, VA.
Received Mar 10, 2003, and in revised form Apr 29. Accepted for
publication Apr 29, 2003.
Address correspondence to Dr Rosenblum, 305 Tarrytown Drive,
Richmond, VA 23229. E-mail
bor and perhaps reducing the chance that large
amounts of rapidly accumulated blood may have displaced the remnants of the aneurysm, making it more
difficult to demonstrate its presence. The following report demonstrates such an aneurysm but does so in a
context never before reported to my knowledge. The
aneurysm has undergone dissection at its point of origin at a site of fibrinoid necrosis, and the outer wall of
the dissection has ruptured, causing the parenchymal
Case Report
A lethargic, 83-year-old African American man was brought
to the hospital in a cachectic (84lb) bedridden state. He was
hypoglycemic without a history of diabetes or insulin therapy. Hypoglycemia responded to glucose. He developed a
right-sided seizure and coma and died 2 days later. Significant general autopsy findings were serous atrophy of fat, hypocellular bone marrow, mild to moderate generalized atherosclerosis, emphysema, mild right ventricular hypertrophy,
and arteriolonephrosclerosis. The heart weighed 275gm with
serous atrophy of adherent epicardial fat.. Although the patient was not hypertensive, the brain displayed lesions commonly associated with hypertension. These are described below. Because of the presence of lesions, it was thought that
the patient had been hypertensive and that his cachectic state
reflected by the serous atrophy was responsible for the absence of a high blood pressure and for the heart falling
within normal weight limits.
The brain showed old and fresh lesions. Old lesions
included thin, bilateral subdural membranes, small bilateral contusions, several lacunar infarcts in the basal
ganglia, and two old hemorrhages in basal ganglia. A
completely fibrosed miliary aneurysm was found adjacent to the old hemorrhages. Recent lesions were bilateral infarctions in frontoparietal lobes and two fresh
hemorrhages. One was 5mm wide, in the left putamen.
The other was 3mm wide in the right basis pontis. A
portion of the former and all of the latter were serially
sectioned. Alternate sections were stained with hematoxylin and eosin, Verhoeff Van Giesen stain for elastic
tissue, and an azocarmine stain. Fibrinoid degeneration
was defined by the presence of amorphous or granular
eosinophilic material within the vessel wall, which
stained red with the azocarmine stain.8 This characteristic red staining parallels the identification of fibrinlike material with other stains such as phosphotungstic
acid–hematoxylin, or the Putz stain, while giving a
clear tinctorial distinction between blue collagen–hyalinized or normal- and red fibrinoid.
A miliary aneurysm was found in the fresh basal
ganglia hemorrhage. A point of rupture was not found,
but a portion of the aneurysm was missing because
only part of the hemorrhage was sampled, and the remaining tissue was discarded after cutting the brain.
© 2003 American Neurological Association
Published by Wiley-Liss, Inc., through Wiley Subscription Services
Fig. (A) Typical double-barreled lumen of a dissecting aneurysm. The outer barrel is 1mm wide. The inner barrel is marked by an
“X.” Panel B shows a different level through the dissection. The inner barrel is marked by an “X.” An arrow in the upper left portion of the outer barrel marks a point of rupture. The area in the white box has been enlarged in panel C to better show the neck
between the inner barrel and the remnant of the parent arteriole. Panel D shows another level stained with hematoxylin and eosin.
The dissecting space between the right side of the inner barrel and the parent vessel is labeled “Y.” The wall of the neck between
inner barrel and parent arteriole is filled with amorphous eosinophilic material as is the outer wall of the parent arteriole (labeled
“F”). This material stained red, like fibrin, with azocarmine stain as shown by the dark amorphous material in the outer wall
(small arrowheads) of the parent arteriole at another level (E) at high magnification. In this panel, the entire image has been rotated 90 degrees so that what was the right edge of the bridge connecting inner barrel to parent arteriole is now its lower edge
(large arrowheads).
Fibrinoid was present at several points at the junction
of the aneurysm with the parent arteriole.
The smaller hemorrhage in the basis pontis was
completely sectioned and revealed the unique findings
shown in the Figure. A blood filled aneurysm approximately 1mm wide was found. Within its lumen, there
was another lumen (see Fig, A). Serial sections showed
a point of rupture (see arrow in Fig, B) in the wall of
the outer lumen. The wall of the inner lumen also
showed evidence of disintegration and a possible point
of rupture (see Fig, D, upper left portion of lumen).
The “double-barreled” configuration is typical of dis-
Rosenblum: Miliary Aneurysm and Hemorrhage
secting aneurysms seen in arteries but never before, to
my knowledge, demonstrated in arterioles. The lumen
of the inner “barrel” was contiguous with a very thin
neck only approximately 40␮m in diameter with its
own narrow lumen connecting the aneurysm to the
parent arteriole (see Fig, B, C). Serial sections showed
that the parent vessel was approximately 100␮m in diameter. The neck that connected the inner “barrel” to
the parent arteriole contained masses of fibrinoid, as
did portions of the wall of the parent arteriole (see F in
Fig, D) also shown at higher magnification (small arrowheads) in panel E.
Because miliary aneurysms have been reported not
only in hypertensives but also in cases of congophilic
(ie, amyloid) angiopathy, note that there was an absence of vascular amyloid as defined by Congo red
staining and green birefringence of vessel walls after
Congo red staining. This absence is consistent with the
central and pontine locations of the hemorrhages, because congophilic angiopathy would be expected to
produce so-called lobar hemorrhages that are in the periphery of the lobes of the hemispheres.
This case strongly supports the assertion that cerebral
hemorrhage may be produced by a ruptured miliary
aneurysm. An unruptured portion of an aneurysm was
found within the partially sectioned fresh hemorrhage.
A ruptured aneurysm was found in the completely sectioned fresh hemorrhage, thus supplying important
confirmation of Fisher’s1 demonstration. However, the
ruptured miliary aneurysm in this case presents a
unique pathogenetic feature. The aneurysm is, in effect, a dissecting aneurysm whose 1mm-wide outer
“barrel” is of microaneurysmal dimensions and whose
inner “barrel” is also “aneurysmal,” being several times
wider than the parent arteriole.
The presence of fibrinoid necrosis presumably weakened the wall of the parent arteriole thereby leading to
both aneurysmal dilation and dissection. The dissection, in turn, may have played a key role in producing
the parenchymal hemorrhage because the thin outer
barrel represents a locus of reduced resistance to rupture. To my knowledge, this is the first demonstration
of either microdissection at a point of fibrinoid degeneration or of miliary aneurysm participating in dissecting aneurysm after arising at the site of the fibrinoid
degeneration. Fisher9 has reported the dissection of a
branch of the basilar artery, producing occlusion of the
lumen and an infarct. There was neither fibrinoid nor
aneurysm formation at the site.
Note that the term fibrinoid degeneration or fibrinoid
necrosis has been used here rather than the term lipohyalinosis. The latter was introduced as a replacement
for the former in the cerebral arterioles and emphasizes
other elements in the degenerated wall of the arteriole.1
Annals of Neurology
Vol 54
No 3
September 2003
However, recent studies2,3 suggest that the fibrinoid
may precede the other changes found in lipohyalinosis
and that the hyalinized collagen represents healed fibrinoid. Whatever the merits of these hypotheses, it
appears probable that it is the fibrinoid that leads to
hemorrhage either directly or via formation of miliary
1. Fisher CM. Hypertensive cerebral hemorrhage. Demonstration
of the source of bleeding. J Neuropath Exp Neurol 2003;62:
104 –107.
2. Kalimo H, Kaste M, Haltia M. Vascular diseases. In: Graham
DI, Lantos PL, eds. Greenfield’s neuropathology. 7th ed. Vol 1.
London: Arnold, 2002:295.
3. Lammie GA. Hypertensive cerebral small vessel disease and
stroke. Brain Pathol 2001;12:358 –370.
4. Rosenblum WI. Miliary aneurysms and “fibrinoid” degeneration
of cerebral blood vessels. Hum Pathol 1977;8:133–139.
5. Rosenblum WI. The importance of fibrinoid necrosis as the
cause of cerebral hemorrhage in hypertension. Commentary.
J Neuropath Exp Neurol 1993;52:11–13.
6. Charcot JM, Bouchard C. Nouvelle recherches sur la pathogenie
de l’hemorrhagie cerebrale. Arch Physiol Norm Pathol 1868;1:
643– 645.
7. Fisher CM. Pathological observations in hypertensive cerebral
hemorrhage. J Neuropath Exp Neurol 1971;30:536 –550.
8. Feigin I, Prose P. Hypertensive fibrinoid arteritis of the brain
and gross cerebral hemorrhage. A form of “hyalinosis.” Arch
Neurol 1959;1:98 –110.
9. Fisher CM. Bilateral occlusion of basilar artery branches. J Neurol Neurosurg Psychiat 1977;40:1182–1189.
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dissection, miliary, rupture, hemorrhagic, producer, aneurysms, cerebral
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