Neurological Research
A Journal of Progress in Neurosurgery, Neurology and Neurosciences

ISSN: 0161-6412 (Print) 1743-1328 (Online) Journal homepage: http://www.tandfonline.com/loi/yner20

Symptomatic cerebral vasospasm manifested 18
days after aneurysmal subarachnoid haemorrhage
Takakazu Kawamata, Nobuhiko Aoki, Tatsuo Sakai & Koji Arai
To cite this article: Takakazu Kawamata, Nobuhiko Aoki, Tatsuo Sakai & Koji Arai (1993)
Symptomatic cerebral vasospasm manifested 18 days after aneurysmal subarachnoid
haemorrhage, Neurological Research, 15:3, 209-211, DOI: 10.1080/01616412.1993.11740137
To link to this article: https://doi.org/10.1080/01616412.1993.11740137

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Case Report

Symptomatic cerebral vasospasm manifested
18 days after aneurysmal subarachnoid
haemor rhage
Takakazu Kawamata, Nobuhiko Aoki, Tatsuo Sakai and Koji Arai
Department of Neurosurgery, Tokyo Metropolitan Fuchu Hospital, Tokyo, Japan

A patient who suffered rapid deterioration due to cerebral vasospasm 18 days after aneurysmal
subarachnoid haemorrhage is reported. Unusually delayed onset of ischaemic neurological
deficits and its preventative management is discussed. [Neurol Res 1993; 15: 209-211]
Keywords: Subarachnoid haemorrhage; cerebral vasospasm; cerebral aneurysm; delayed
ischaemic neurological deficit
INTRODUCTIO N
Symptomatic cerebral vasospasm is known to occur
commonly in the period between 4 and 14 days after
the onset of aneurysmal subarachnoid haemorrhage
(SAH) 12 • To our knowledge, only a few investigators
have documented the occurrence of delayed ischaemic
neurological deficit (DIND) that developed after 15 days
of aneurysmal SAHH. However, serial cerebral blood
flow (CBF) measurements revealed prolonged reduction
of CBF during the 3rd week after SAW6 • In the practical
setting, unreported cases of DIND with the onset later
than 15 days after the ictus, though rarely, seem to be
experienced at most neurosurgical institutions.
Recently the authors encountered a patient whose
clipping and postoperative course was uneventful until
18 days after SAH, when unexpectedly she was
complicated by severe DIND with an unsatisfactory
response to aggressive treatment. Few publications
have specifically addressed as to how long prophylactic
management for vasospasm be continued. It seems
worthwhile to discuss the value of preventative
management for vasospasm during the 3rd week after
aneurysmal SAH.

Computed tomography (CT) scans revealed thin layers
of SAH, predominantly in the ambient cistern and the
sylvian fissure on the right side (Figure 1). Cerebral
angiography delineated two aneurysms at the junction
of the internal carotid and the posterior communicating
artery, and at the bifurcation of the middle cerebral
artery on the right side (Figure 2),,
Operation
With a preoperative condition of Hunt and Kosnik
grade 2', the patient underwent clipping of both

CASE REPORT
A 57-year-old housewife with a history of mild
hypertension was brought to the emergency room at
our institution for the sudden onset of severe headache
on October 24, 1990.

Examination
Upon arrival the patient was alert and did not show
any neurological abnormalities, including neck stiffness.
Correspondence and .reprint requests to: Dr Takakazu Kawamata,
Department of Neurosurgery, Neurological Institute, Tokyo
Women' s Medical College, 8-1 Kawada-Cho, Shinjuku-Ku Tokyo
162, japan. Accepted for publication November 1992.

© 1993 Forefront Publishing Group
0161-6412/93/030209 -03

Figure 1: A CT scan on admission shows thin layers of SAH, mainly
in the ambient cistern and the sylvian fissure on the right side
(arrows)

Neurological Research, 1993, Volume 15, june

209

Delayed cerebral vasospasm: Takakazu Kawamata et al.

Right carotid angiography on admission discloses two
cerebral aneurysms at the junction of the internal carotid artery
and the posterior communicating artery (arrow), and at the
bifurcation of the middle cerebral artery on the right side
(arrowhead)
Figure 2:

scans taken 14 days after SAH showed a small
low-density lesion in the left thalamus. No other
ischaemic lesions were delineated. The patient w as free
of neurologic deficit until early morning of November
10 (18 days), when she was noted to have mild
hemiparesis on the left side. In addition, she was not
fully alert. Immediately after detection of these
symptoms, hypervolaemic hypertension treatment
with low molecular dextran and urokinase was initiated
without sufficient response. Neurological evaluation the
following day showed complete hemiplegia and severe
dysarthria. Serial CT scans exhibited a small low-density
area in the right prefrontal region on November 10 (18
days), and then diffuse low-density lesions in the
territory of the middle cerebral artery on Noverber 12
(20 day s) (Figure 3).
Post-operative cerebral angiography performed on
November 14 (22 days) disclosed high-grade narrowing
(70-80% reduction in caliber) of the superior and
inferior trunk of the M 2 portion of the right middle
cerebral artery (Figure 4 ). Although the patient showed
resolution of dysarthria, dense hemiparesis remained
despite a 3-month course of rehabilitation.

DISCUSSION
Cerebral vasospasm secondary to ruptured aneurysms
is recognized to have its earliest onset of 4 days after
SAH, and to reduce in severity within 2 weeksv .
Coinciding w ith the narrowing of the vessels,
neurological symptoms such as DIND commonly occur
within 14 days after SAH1.2. In the practical sett ing,
however, though extremely limited, the occurrence of
DIND with its onset 14 days or later after SAH is
documented 3·•. This uncommon phenomenon may
deserve t o be discussed as to how long prophylactic
management for vasospasm should be continued.

Figure 3: A CT scan 20 days after SAH (i.e., 2 days after the onset
of symptomatic vasospasm) reveals large low-density lesions in t he
territory of the right middle cerebral artery (arrowheads)

aneurysms through a right pterional approach on
O ct ober 25. At surgery, rupture of the internal carotid
aneurysm was confirmed to be responsible for the
current SAH.
Post-operative course
The patient awoke from general anaesthesia without
neurological deficits. Her post-operative course w as
uneventful with the management including hypervolaemic haemodilution therapy. Post-operative CT

210

Neuro logical Research, 1993, Volume 15, june

Post-ope rative carotid antiography o n the right side 22
days after SAH demo nstrates severe narrowing (70- 80% red uctio n
in caliber) at the p roximal part of t he M2 po rtion of the right middle
cerebra l artery (a rrows)
Figure 4:

Delayed cerebral vasospasm: Takakazu Kawamata et al.

Although there is a recent report describing
symptomatic arterial luminal narrowing presenting
months after SAH 8 , the mechanism of this pathology
differs from vasospasm exclusively caused by SAH

per se9 •
According to Abiko and his colleagues', very delayed
onset of vasospasm tends to develop in patients with
a large volume of SAH on the initial CT scans. The
outcome of their five patients included 'good' in 2,
'poor' in 2, and 'died' in one, suggesting that
symptomatic vasospasm manifesting 15 days or later
is not necessarily benign in prognosis. The patient
reported here presented with a relatively mild degree
of SAH (Fisher group 2), which resolved early in the
post-operative course. Furthermore, aggressive treatment fo r the prevention of vasospasm was carried out
for 14 days after SAH. Despite these measures,
relentless progression of DIND began 18 days after SAH.
Severe narrowing of the middle cerebral artery was
confirmed on post-operative angiography. Retrospectively, mild dehydration and low blood pressure
seen 15 days after SAH may have contributed to the
occurrence of catastrophe in this patient.
Meyer et a/. studied change in CBF after SAH 6 • They
concluded that CBF fell progressively during the fi rst 2
weeks and remained abnormally low throughout 3
weeks after SAH. Also, Knuckey and his colleagues
revealed that even in good clinical grade patients, with
low CBF on admission, flows may not return to normal
for 3 to 4 weeks after SAH 10 • Thus, serial CBF
measurements indicate that reduction of CBF lasting
more than 2 weeks after SAH is not exceptional.
From a prophylactic standpoint, Ohman et a/.
stressed the effect of their protocol including oral
administration of nimodipine for up to 21 days after
SAH 11 • In the most recent publication, Origitano et a/.
demonstrated the persistent elevation of CBF during
21 days after SAH in patients who were treated with
hypertensive hypervolaemic haemodilution therapy for
10 to 14 days after surgery12 . From these observations,
the possibility of occurrence of symptomatic vasospasm
is thought to be present for more than 2 weeks after
SAH. This may explain the mechanism of very delayed
ischaemic neurological deficits manifesting following
the discontinuation of aggressive prophylactic
management.
To date, reports of patients showing symptomatic
vasospasm 15 days or later after SAH are very few'·' 3;
however, unpublished experience derived from personal
communication s suggests that this phenomenon is not
as rare as it might seem. In an effort to minimize this
complication, there is merit maintaining sufficient
hydration and blood pressure, and continuing the
administration of vasodilating drugs during the 3rd

week after SAH, based on the findings of cerebral
angiography and serial transcranial Doppler evaluation.
Once patients become symptomatic, emergency
treatment with aggressive therapeutic modalities is
mandatory.
In conclusion, cerebral vasospasm may become
symptomatic during the 3rd week after SAH. This is
supported by the results of serial CBF measurements,
indicating reduced CBF lasting more than 2 weeks after
SAH. It is important to continue supportive treatment,
at least including sufficient hydration and avoidance
of low blood pressure, during the 3rd week after SAH.

REFERENCES
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with ruptured saccular aneurysm- The clinical manifestations.
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