New devices

Cerebral hyperperfusion after flow diversion of large
intracranial aneurysms
Albert Ho Yuen Chiu, Jason Wenderoth1,2
1

Interventional Neuroradiology Department, Liverpool Hospital, Liverpool, New South Wales, Australia
Department of Medical Imaging, Prince of Wales Hospital, Sydney, New South Wales, Australia

2

Correspondence to Dr Albert Ho Yuen Chiu, albert.h.chiu@gmail.com

Summary
Cerebral hyperperfusion syndrome has been proposed to be caused by rapidly increased blood flow into chronically hypoperfused
parenchyma with resultant impaired autoregulation, and has been noted after clipping of intracranial aneurysms and carotid stenting. The
occurrence of the syndrome after endovascular flow diversion, however, has not been previously described. A 52-year-old woman was
admitted electively for flow diverter treatment of a recurrent ventral paraclinoid aneurysm arising within a dysplastic segment of the left
internal carotid artery. During the immediate postprocedural period the patient was found to have confusion, right hemiparesis, facial droop
and dysarthria, which resolved with blood pressure control. Subsequent CT perfusion on day 11 demonstrated mildly elevated cerebral
blood flow, cerebral blood volume and permeability values in the left hemisphere.

BACKGROUND

OUTCOME

Cerebral hyperperfusion syndrome has been proposed to
be due to rapidly increased blood flow into chronically
hypoperfused parenchyma with resultant impaired autoregulation,1–3 and has been noted after clipping of intracranial aneurysms4–6 and carotid stenting.1 3 The occurrence
of the syndrome after endovascular flow diversion,
however, has not been previously described. We present a
case of the syndrome after flow diversion of a large
ventral paraclinoid aneurysm.

A CT scan of the brain was performed as an emergency
but no abnormality was demonstrated and abciximab was
given in expectation of embolic disease. However, this
treatment resulted in no improvement. Hyperperfusion
syndrome was then suspected and the patient was placed
on a glyceryl trinitrate infusion with a systolic blood pressure target of 100–120. The target blood pressure was
reached approximately 10.5 h after the procedure, but by

CASE PRESENTATION
A 52-year-old woman was admitted electively for flow
diverter treatment of a recurrent ventral paraclinoid aneurysm arising within a dysplastic segment of the left
internal carotid artery which also demonstrated multiple
smaller unruptured aneurysms. The large paraclinoid
aneurysm had previously been coiled acutely, with the
residual perfusing component measuring 16 mm in diameter with a 10 mm neck. The patient was a heavy smoker
and also had a history of hypertension, which was diagnosed 7 years previously, and appeared medically wellcontrolled with the last reading from the GP measuring
132/89.
Prior to the procedure, the patient was given 100 mg
aspirin and 75 mg clopidogrel daily for 5 days, and an
intraprocedural dose of 5000 U heparin was given to reach
an activated coagulation time of 255. Insertion of a
3.75 mm × 18 mm Pipeline Embolization Device (ev3,
Irvine, California, USA) was performed uneventfully with
a deployment time of approximately 3 min (figure 1).
However, during the immediate postprocedural period,
approximately 1 h after flow diverter deployment, the
patient was found to have confusion, right hemiparesis,
facial droop and dysarthria. Her recorded systolic blood
pressure at this point was 160 mm Hg.
BMJ Case Reports 2012; doi:10.1136/bcr-2012-010479

Figure 1 Immediate post-deployment angiographic image in
oblique projection demonstrating the recurrent aneurysm sac.
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Figure 2 Axial diffusion-weighted imaging performed 7 h after
the procedure showing no evidence of diffusion restriction,
precluding procedural ischemia as a cause for symptomatology.

Figure 4 Axial susceptibility-weighted imaging performed on
day 4 showing no evidence of hypointensity in the left
hemisphere to suggest deposition of blood products.

6 h after the procedure the hemiparesis had already
resolved, at a systolic pressure of 138.
MRI was performed approximately 7 h after the procedure and revealed no evidence of diffusion restriction
(figure 2), with 3D time-of-flight MR angiography demonstrating large vessel patency. Heparin infusion was continued for 24 h, titrated to an activated partial
thromboplastin time of 50–90 as per routine.
Repeat MRI on day 4 demonstrated gyriform left posterior temporal cortical edema (figure 3), but there was no
evidence of regional susceptibility artefact on susceptibilityweighted imaging to suggest hemorrhage (figure 4). The
patient’s blood pressure continued to be controlled with
hydralazine, which resulted in resolution of symptoms over
the next 4 days. Subsequent CT perfusion on day 11 demonstrated mildly elevated cerebral blood flow, cerebral blood
volume and permeability values in the left hemisphere compared with the contralateral hemisphere (figure 5).

FLAIR imaging at a subsequent MRI examination performed 6 months after the procedure (figure 6) demonstrated a normal appearance of the hyperperfused area
with no evidence of gliosis to suggest previous infarct.

Figure 3 Axial FLAIR weighted imaging performed on day 4
showing mild edema of the left insular and opercular cortex.
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DISCUSSION
Cerebral hyperperfusion syndrome has been noted after
carotid stenting1 and clipping of intracranial aneurysms,4–6
but has not been previously described with endovascular
flow diversion. Most studies report an incidence of the syndrome of 0–3% after carotid intervention. A wide range of
symptomatology has been described, ranging from severe
unilateral headache through to seizures, focal neurological
deficits and intracranial hemorrhage.3 As flow-diverting
stents also reduce blood flow into the aneurysmal sac by
directing flow to the distal vessel similar to aneurysm clipping, it is logical to postulate that the syndrome may also
occur with flow diversion and be susceptible to the same
predisposing factors as the more recognized causes of
hyperperfusion. These predisposing factors include hypertension, diabetes, age >75 years, recent carotid procedure
within the past 3 months, high-grade ipsilateral or contralateral stenosis, female sex, vascular malformations and
cerebrovascular reactivity.3
Increased vessel maximum flow rate distal to the aneurysm after clipping has been demonstrated on transcranial
Doppler studies. This has been postulated to be due to
loss of the expansion effect of the aneurysm during
systole, which would otherwise have reduced the available
volume to be expelled into the distal vessel as well as
potentially producing an exaggerated ‘Windkessel effect’.
These changes have been hypothesized to be the cause of
hyperperfusion after clipping1 and have also been suggested as the cause of intraparenchymal hemorrhage after
flow diversion.7 8
Angiography typically shows a reduction or cessation of
the ‘sump’ effect commonly seen with large aneurysms,
with more rapid transit of contrast into the ipsilateral
hemisphere. This angiographic finding is consistent with
BMJ Case Reports 2012; doi:10.1136/bcr-2012-010479

Figure 6 Axial FLAIR imaging performed 6 months after the
procedure showing normal appearances of the left insular and
opercular cortex without evidence of T2 hyperintensity to suggest
gliosis from previous ischemic injury.
We believe, however, that the identification of these
imaging findings will render further weight to hemodynamic changes as a plausible cause for delayed hemorrhage and encourage further research into this new
treatment modality.

Learning points

Figure 5 CT perfusion imaging performed on day 11 showing
mildly elevated cerebral blood volume, cerebral blood flow and
permeability. The differences are subtle, probably due to the delay
to the perfusion study. The permeability map has been included
to demonstrate the region of interest, which has been drawn to
include a large area of each internal carotid territory to attempt to
demonstrate the gross differences between the hemispheres.
previous research involving hyperperfusion after carotid
stenting, where a larger change in cerebral circulation time
after stenting (with a cut-off of 2.7 s) has been correlated
with the development of hemorrhagic hyperperfusion
syndrome.1 Although the change in cerebral circulation
time in our patient was not significant, in view of her
gender and history of hypertension, her suggestive symptomatology and imaging as well as her response to hypotensive therapy, we believe hyperperfusion syndrome
provides an elegant potential unifying diagnosis.
Given the relatively early stage of clinical application of
flow diversion, a number of alternative theories have been
proposed as to the potential etiologies of delayed hemorrhage. Apart from changes in hemodynamic factors, the
possibility of microwire perforations and hemorrhagic
transformation of small infarcts have also been raised
for parenchymal hemorrhage,8 and delayed aneurysmal
rupture has been suggested for subarachnoid hemorrhage.9
BMJ Case Reports 2012; doi:10.1136/bcr-2012-010479

▸ Cerebral hyperperfusion syndrome should be
considered in any case of early neurological
deterioration in patients who have undergone flow
diversion, for which early CT perfusion is suggested to
exclude hyperperfusion.
▸ Awareness of the differences in transit time before and
after flow diversion may be useful in identifying
patients at risk.
▸ Consideration should also be given to cerebral
hyperperfusion syndrome as a potential cause for
hemorrhage after flow diversion, a known complication
of severe cerebral hyperperfusion, especially given the
universal administration of aspirin and clopidogrel prior
to the procedure which may worsen the severity of any
intracranial bleeding.
Acknowledgement Wisdom Tong (CT senior radiographer, Liverpool Hospital)
who provided technical assistance in the manipulation of CT perfusion data.
Contributors Both authors contributed to the interpretation and analysis of
the results and the writing of the paper.
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.

REFERENCES
1. Narita S, Aikawa H, Nagata S, et al. Intraprocedural prediction of
hemorrhagic cerebral hyperperfusion syndrome after carotid artery stenting.
J Stroke Cerebrovasc Dis . Published Online First: 28 Dec 2011.
doi:10.1016/j.jstrokecerebrovasdis.2011.10.015.

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2. Murakami H, Inaba M, Nakamura A, et al. Ipsilateral hyperperfusion after
neck clipping of a giant internal carotid artery aneurysm. J Neurosurg
2002;97:1233–6.
3. Lieb M, Shah U, Hines GL. Cerebral hyperperfusion syndrome after carotid
intervention: a review. Cardiol Rev 2012;20:84–9.
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clipping of a ruptured aneurysm on a dolichoectatic middle cerebral artery.
J Stroke Cerebrovasc Dis 2011;20:260–3.
5. Sugino T, Ohtaki M, Wanibuchi M, et al. Hyperperfusion syndrome after
clipping an unruptured cerebral aneurysm: two case reports. Neurol Med Chir
(Tokyo) 2010;50:306–9.

6. Kuroki K, Taguchi H, Yukawa O. Hyperperfusion syndrome after clipping of an
unruptured aneurysm. Neuro Med Chir (Tokyo) 2006;46:248–50.
7. Velat GJ, Fargen KM, Lawson MF, et al. Delayed intraparenchymal
hemorrhage following pipeline embolization device treatment for a giant
recanalized ophthalmic aneurysm. J Neurointerv Surg 2012;4:e24.
8. Cruz JP, Chow M, O’Kelly C, et al. Delayed ipsilateral parenchymal
hemorrhage following flow diversion for the treatment of anterior circulation
aneurysms. Am J Neuroradiol 2012;33:603–8.
9. Kulcsar Z, Houdart E, Bonafe A, et al. Intra-aneurysmal thrombosis as a
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Am J Neuroradiol 2011;32:20–5.

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Chiu AHY, Wenderoth J. Cerebral hyperperfusion after flow diversion of large intracranial aneurysms. BMJ Case Reports 2012;10.1136/bcr-2012-010479,
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BMJ Case Reports 2012; doi:10.1136/bcr-2012-010479