Hyperperfusion Syndrome After Stenting for Intracranial
Vertebral Stenosis
Marco Túlio Rezende, MD; Laurent Spelle, MD, PhD; Charbel Mounayer, MD; Michel Piotin, MD;
Daniel Giansante Abud, MD; Jacques Moret, MD
Background and Purpose—Hyperperfusion syndrome is a rare but well-described complication after endarterectomy or
stenting in the carotid circulation.
Summary of Case—A 66-year-old man who had vertebrobasilar insufficiency refractory to medical treatment because of
an intracranial right side vertebral stenosis was referred to our institution for endovascular treatment. Stenting was
performed, and after 24 hours, he became extremely agitated, and this was followed by a period of apathy without focal
neurological deficits. MRI showed bilateral thalamic hemorrhage.
Conclusion—To our knowledge, this is the first report of hyperperfusion syndrome with hemorrhagic presentation after
intracranial vertebral artery stenting. (Stroke. 2006;37:e12-e14.)
Key Words: angioplasty 䡲 intracranial atherosclersosis 䡲 intracranial hemorrhage 䡲 reperfusion injury
A
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66-year-old man presented with acute and recurrent
episodes of diploplia and visual field defects associated
with dysarthria and equilibrium disturbances. These episodes
occurred while the patient was undergoing medical treatment
consisting of acetylsalicylic acid (100 mg per day) and
clopidogrel (75 mg per day), suggesting the diagnosis of
vertebrobasilar insufficiency refractory to medical therapy.
The neurological examination during the last ischemic event
revealed mixed dysarthria and a cerebellar static and kinetic
syndrome.
MRI demonstrated left occipital and cerebellar ischemic
lesions of different ages but all were relatively recent. There
were no abnormalities in both thalami (Figure 1). The
cerebral angiogram showed 1 atherosclerotic lesion situated
in the intracranial segment of the right vertebral artery, distal
to the posterior inferior cerebellar artery (PICA) origin with a
length of 7 mm and a stenosis of 98%, causing the reduction
of the flow to the basilar artery (Figure 2A). The left vertebral
artery was extremely thin at its origin and was occluded at
the C2–C3 level. Thus, the left PICA territory was vascularized by the right vertebral artery. The collateral flow
through the carotid system was insufficient to supply the
posterior circulation.
The patient was referred to our institution for assessment
and possible endovascular treatment. We decided to wait 8
weeks after the acute stroke to carry out the procedure. The
patient was premedicated with a loading dose of clopidogrel
(225 mg) on the day before the procedure. The neurological
examination was completely normal. Endovascular stenting
was performed under general anesthesia and full anticoagu-
lation therapy. Through femoral 6F access, a 6F-guiding
catheter was placed inside the right vertebral artery. The
lesion was crossed with a 0.014-inch guide wire and predilatated with a 3.0⫻20 mm VIVA balloon (Boston Scientific).
Then, a 3.5⫻18 mm Cerebrence stent (Medtronic AVE, Inc.)
was deployed at its nominal pressure of 6 atm. The immediate
angiographic control showed restoration of the normal arterial diameter and left-side PICA preservation. No signs of
vessel rupture, dissection, or intraluminal thrombus were
vizualized (Figure 2B). Computed tomography (CT) performed immediately after the procedure did not show hemorrhagic complications. The patient was neurologically intact
after extubation. He was transferred to the intensive care unit
for close monitoring of neurological status and blood pressure
to maintain the patient in a normotensive status.
Twenty-four hours after the procedure, the patient became
extremely agitated and after that, followed an apathetic
period. There was no focal neurological alteration. MRI
showed bilateral thalamic hemorrhages with predominance
on the left side (Figure 3). The diagnosis of hemorrhage
secondary to hyperperfusion was proposed. For this reason, it
was decided to introduce hypotensive therapy to interrupt
heparin therapy while continuing with aspirin and clopidogrel. When patient was discharged after 7 days of hospitalization, he had clinically completely recovered and was
free of the neurological complications noted above.
Discussion
Available retrospective data suggest that there is an annual
stroke incidence of 7% to 8% in patients with symptomatic
Received August 15, 2005; final revision received September 29, 2005; accepted October 12, 2005.
From the Department of Interventional Neuroradiology, Fondation Rothschild, Paris, France.
Reprint requests to Laurent Spelle, MD, PhD, Interventional Neuroradiology Department, Fondation Rothschild Hospital, 25 rue Manin 75940 Paris
Cedex 19 –France. E-mail lspelle@fo-rothschild.fr
© 2005 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org
DOI: 10.1161/01.STR.0000196959.77184.49
e12
Tulio et al
Hyperperfusion Syndrome After Vertebral Stenting
Figure 1. Axial flair MRI shows no lesions in both thalami.
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vertebral artery stenosis.1 The natural history of vertebrobasilar stenosis has been characterized by especially high stroke
rates, and the long-term stroke-free survival in symptomatic
patients is low.2 The most common stroke mechanism is
thrombus formation attributable to the severe stenosis with
subsequent embolism. Although in some instances, hemodynamically significant stenosis without adequate collateral
blood flow can also lead to low-flow ischemia and stroke.
Use of stent as a therapeutic option is supported by its
capacity to act as a support for balloon angioplasty, preventing disruption of the plaque and as a covering for a plaque or
an intimal flap, thus reducing the occurrence of emboli and
flap recurrence. The overall stroke-free survival in the first
year in patients treated with intracranial angioplasty with or
without stent placement has ranged from 88% to 93% in
preliminary studies.3
e13
Figure 3. Axial T2 gradient-echo MRI 24 hours after the procedure shows bilateral thalamic hemorrhage.
Hyperperfusion syndrome is a rare but well-described,
potentially devastating complication after carotid endarterectomy or angioplasty and stenting.4 It designates the development of clinical symptoms as a result of rapidly increased
cerebral blood flow in excess of that required to meet
metabolic demands.5 It is theorized that the capillary bed
beyond the stenosis is prone to perfusion breakthrough
bleeding after increase of the blood flow because of the
presence of impaired autoregulation. Couts et al6 classified
the presentation as (1) an acute focal edema (stroke-like
presentation, attributable to edema immediately after revascularization), (2) acute hemorrhage, or (3) delayed classic
presentation (seizures, focal motor weakness, or late intracerebral hemorrhage ⱖ24 hours after the procedure). In this
series, the incidence of hyperperfusion syndrome was 3.1%
Figure 2. Right vertebral artery angiogram (anteroposterior view) before (A)
and immediately after (B) angioplasty
with stent placement.
e14
Stroke
January 2006
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after carotid endarterectomy and 6.8% after stenting. Kaku et
al,5 using cerebral blood flow studies in patients submitted to
carotid angioplasty with stent placement, concluded that in
older patients, profound cerebral ischemia with impaired
hemodynamic reserve is the highest risk situation for cerebral
hyperperfusion phenomenon.
The first demonstration of hyperfusion syndrome with
intracerebral hemorrhage after intracranial angioplasty was
provided by Liu et al7 in a well-described case report of a
fatal intracerebral hemorrhage after middle cerebral artery
angioplasty. However, hyperperfusion syndrome has never
been reported after intracranial stenting in the posterior
circulation.
In our patient, we do not believe that the parenchymal
hemorrhage was the result of a reperfusion lesion into an area
of tissue infarction. Despite the history of worsening transient
ischemic attacks and 1 cerebellar and occipital stroke, there
were no persistent neurological deficits noted before the
procedure, and CT and MRI did not reveal any ischemic
lesion in the territory involved by the hemorrhagic complication. Moreover, the procedure was performed 8 weeks after
the last clinical ischemic episode, and the patient was clinically intact during the 24 hours after the procedure. Postoperative angiogram did not demonstrate any vessel rupture,
dissection, or intraluminal thrombus. CT scanning performed
immediately after the procedure did not show hemorrhagic
complications. This very early CT scan (just after the intervention) does not rule out an ischemia; but this, associated
with the asymptomatic period between the end of the procedure and the clinical alterations (24 hours), favors the absence
of ischemic complications related to the intervention.
At our institution, we routinely take actions to avoid or
decrease the risk for hyperperfusion lesions and hemorrhagic
complications after intracranial stenting. These include preprocedural MRI searching areas of subtle infarction and very
strict control of blood pressure immediately after stenting.
Anticoagulation was maintained during and after the procedure (partial thromboplastin time was kept at 2.5⫻ the
normal value) to prevent subacute vessel occlusion after stent
placement. Aspirin and clopidogrel were given before the
intervention, and we did not use glycoprotein IIb-IIIa inhibitors. However, there is no consensus in the literature about
the best anticoagulation regimen.
Conclusion
In conclusion, hyperperfusion syndrome with hemorraghic
presentation may occur after intracranial stenting in the
posterior circulation, although arterial pressure is strictly
controlled. This should not discourage to apply this promising
technique in the scenario of recurrent ischemic symptoms
associated with high-grade intracranial vessel stenosis attributable to the lack of effective therapies and poor prognosis
involving this situation. We need to achieve a better understanding of the mechanisms that promote this complication
and determine precise clinical and radiological risk factors to
avoid it.
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