Surgical Neurology 68 (2007) 457 – 460
www.surgicalneurology-online.com

Vascular

A restricted subarachnoid hemorrhage in the cortical sulcus in
cerebral amyloid angiopathy: could it be a warning sign?
Masahito Katoh, MD4, Masami Yoshino, MD, Katsuyuki Asaoka, MD, Takeshi Aoki, MD,
Hiroyuki Imamura, MD, Daina Kashiwazaki, MD, Kazuya Takano, MD, Toshimitsu Aida, MD
Department of Neurosurgery, Hokkaido Neurosurgical Memorial Hospital, Sapporo 060-0022, Japan
Received 14 May 2006; accepted 3 November 2006

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 Ab 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.
D 2007 Elsevier Inc. All rights reserved.

Keywords:

Cerebral amyloid angiopathy; Subarachnoid hemorrhage; Warning sign; Meningeal artery

1. 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.
Abbreviations: Ab, amyloid b protein; CAA, cerebral amyloid
angiopathy; CT, computed tomography; EEG, electroencephalography;
MRA, magnetic resonance angiogram; MRI, magnetic resonance imaging;
SAH, subarachnoid hemorrhage.
4 Corresponding author.
E-mail address: masasama@ceres.ocn.ne.jp (M. Katoh).
0090-3019/$ – see front matter D 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.surneu.2006.11.028

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.

2. Case patient 1
A 74-year-old woman presented herself to the Hokkaido
Neurosurgical Memorial Hospital because of transient left

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M. Katoh et al. / Surgical Neurology 68 (2007) 457 – 460

Fig. 1. Case patient 1: A restricted SAH in the right frontal lobe was
observed on MRI.

Fig. 3. Case patient 1: Amyloid b protein depositions were detected in
vessel walls (direct fast scarlet stain).

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 encephalography, carbamazepine was prescribed.
No abnormal finding was detected on the MRA or in the
cerebrospinal fluid; therefore, we did not know the cause of
the restricted SAH. Because a trauma, brain tumor, or another
unknown origin (eg, mycotic aneurysm, cortical vein
thrombosis, or cavernous angioma) could not be excluded,
epileptic waves were observed on EEG, and seizures could
be controlled with the use of an anticonvulsant drug, we
decided not to perform a biopsy but to conduct a periodic
follow-up by MRI after thorough discussion with the patient.
The patient did not have hypertension, coagulopathy, or a
history of having a malignant neoplasm.

Fourteen days later, left hemiparesis suddenly occurred
in the patient, and she was brought to our hospital by
ambulance. Neurologic examination demonstrated left
hemispatial agnosia, left hemiparesis, and left hemihypesthesia. On CT, a huge subcortical hematoma was observed
in the right frontal lobe (Fig. 2).
Removal of the hematoma was performed, and the
patient was diagnosed with amyloid angiopathy (Fig. 3).
No other lesion that could cause SAH and subcortical
bleeding was found either intraoperatively or pathologically.

Fig. 2. Case patient 1: A huge subcortical hematoma in the right frontal lobe
was observed.

Fig. 4. Case patient 2: A restricted SAH in the right frontal sulcus was
noted.

3. 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).

M. Katoh et al. / Surgical Neurology 68 (2007) 457 – 460

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 attention to his general condition, including his
blood pressure.
The patient did not have hypertension, coagulopathy, or a
history of having a malignant neoplasm.
However, on the day the patient was discharged, he
fainted and was brought back to our hospital by ambulance.
Neurologic examination revealed consciousness disturbance
(E4V4M6 = 14), dysarthria, and left hemiparesis. On CT, a
huge subcortical hematoma was observed in the right
frontoparietal area (Fig. 5).
Hematoma removal was performed, and the patient was
diagnosed with amyloid angiopathy (Fig. 6). No other lesion
that could cause SAH and subcortical bleeding was found
either intraoperatively or pathologically.
4. Discussion
Cerebral amyloid angiopathy is caused by the deposition
of Ab 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 Ab deposits in
vessel walls because of a loss of function in the periarterial
interstitial fluid drainage pathway, which corresponds to the
lymphatics of the brain.
Although vessel ruptures in CAA have been thought to
occur in cortical arteries, Takeda et al [5] examined
6 autopsy cases and 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

459

Fig. 6. Case patient 2: Amyloid b protein depositions were detected in
vessel walls (direct fast scarlet stain).

caused by CAA. Maia et al [1,2] presented a case showing a
restricted SAH on CT and MRI and, although there was no
pathologic evidence, suggested that these findings supported
the theory presented by Takeda et al [5].
In our case patients, a restricted SAH preceded a huge
subcortical hemorrhage and pathologic evidence was
available. This is the first evidence of hemorrhage occurring
in the subarachnoid space in CAA. Takeda et al [4] reported
that they observed many ruptured vessels in subarachnoid
hematomas. Repeated and restricted SAH might result in a
huge subcortical hematoma.
Both our case patients presented with epileptic seizure
without dementia. The case patient reported on by Maia
et al [1,2] also presented with epileptic seizure showing a
restricted SAH.
Could this restricted SAH on CT/MRI be a warning
sign of a huge subcortical hemorrhage in CAA? A
definitive diagnosis of CAA cannot be made from this
finding alone, and there is no indication for biopsy at that
time. However, other etiologies cannot be identified in
elderly patients without a traumatic episode who show a
restricted SAH at a location distant from the common sites
of cerebral aneurysms.
Hemorrhage in CAA, as indicated, results from weakening of the vessel walls. Therefore, the anticipation or
prevention of these hemorrhages is very difficult. However,
attention can be focused on the nature of an attack.
When the precise mechanism of cerebral vessel rupture
in CAA is elucidated, this warning sign will become more
clinically significant.

References

Fig. 5. Case patient 2: A huge subcortical hematoma in the right
frontoparietal area was observed.

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