Acta Neurochirurgica
https://doi.org/10.1007/s00701-019-03822-7

CASE REPORT - VASCULAR NEUROSURGERY - ISCHEMIA

Intracranial stenting after tumor exeresis complicated by delayed
kinking of the middle cerebral artery
Davide Simonato 1 & Joseph Domenico Gabrieli 2 & Giacomo Cester 2 & Alessandro Della Puppa 3 & Francesco Causin 2
Received: 15 November 2018 / Accepted: 23 January 2019
# Springer-Verlag GmbH Austria, part of Springer Nature 2019

Abstract
During intracranial tumor resection, the delayed kinking of a major encased vessel has never been described in literature. We
present a case which required urgent endovascular treatment performed through a stent positioning. A patient was hospitalized
with symptomatic sphenoid meningioma in the left middle cranial fossa. Twelve days after surgery, right-sided hemiplegia and
aphasia occurred. Digital subtraction arteriography revealed a kinking of the M1 segment of the left middle cerebral artery and
diffuse vasospasm. At first, intra-arterial nimodipine has been administered, obtaining the remission of the vasospasm. Secondly,
a stent was positioned to treat the kinking, achieving a complete flow restoration.
Keywords Kinking . Vasospasm . Skull-base . Delayed cerebral ischemia

Introduction

Case presentation

Exeresis of skull-base tumors requires precise dissection
in a region characterized by complex anatomical relationships which may be altered by the underlying pathology. As shown by this case, the pathological alteration of these relationships may cause delayed complications even in the setting of a technically uneventful
surgery.
We show a case of sphenoid meningioma resection
complicated by a delayed middle cerebral artery stroke,
related to the kinking of the main arterial trunk that was
previously encased and elongated by the lesion.
Endovascular treatment was performed to reestablish vessel patency.

A 70-year old man presented to our department with a symptomatic meningioma of the left sphenoid wing with worsening
symptoms since 1 year ultimately causing severe hemiparesis
of the right side and mixed aphasia.
Preoperative imaging showed a large extra-axial lesion of
the left sphenoid wing dislocating the supraclinoid internal
carotid artery (ICA) and middle cerebral artery (MCA)
(Fig. 1a) and encasing the M1 segment, which appeared elongated (Fig. 1b).
Surgical exeresis was performed through a left frontopterional craniotomy and allowed complete gross removal of
the lesion with preservation of the MCA branches including
the arachnoid layer between the meningioma and the artery.
Surgery was clinically uneventful and subsequent clinical
course revealed a slow gradual improvement of the symptoms
with partial recovery of the hemiparesis and reduction of the
aphasia; post-operative imaging confirmed complete gross removal of the lesion, absence of ischemic complications, and
mild hemorrhagic staining of the surgical bed; histological analysis confirmed the presence of a meningioma (WHO grade II).
Twelve days after surgery, the patient unexpectedly developed a rapidly progressing right-sided hemiparesis and recurrence of aphasia; following bedside transcranial echo Doppler
examination, which revealed MCA flow acceleration, MRI
was urgently performed and documented the presence of a

This article is part of the Topical Collection on Vascular Neurosurgery Ischemia
* Davide Simonato
david.med4@gmail.com
1

Institute of Radiology, University of Padua, Via Giustiniani 2,
35128 Padua, Italy

2

Neuroradiology Unit, University Hospital of Padova, Padua, Italy

3

Neurosurgery Unit, University Hospital of Padova, Padua, Italy

Acta Neurochir
Fig. 1 Preoperative MRI: axial
enhanced-T1w sequences shows
a large sphenoid wing meningioma (80 × 60 × 50 mm) on the left
(a); in the coronal turbo spin echo
sequences, the lesion seems to
dislocate the supraclinoid ICA
(arrowhead) and MCA (white arrow) (b)

Fig. 2 MRI after surgery: 3D
Time-of-Flight sequences shows
a vasospasm of the proximal
segment of the anterior cerebral
arteries (ACA) and the left middle
cerebral artery (MCA) (a);
apparent diffusion coefficient
maps depict a recent watershed
ischemia between the left ACA
and MCA (b)

Fig. 3 Digital subtraction
angiography (DSA) before (a),
after 24 h–intra-arterial bolus of
nimodipine (b) and following
acute stent release (c). The comparison outlines a gradual improvement of the brain
parenchymography after the procedures as well as a significant
increase of the ACA and the left
MCA calibers

Acta Neurochir
Fig. 4 Unsubtracted (a) and
subtracted (b) digital angiograms
after intra-arterial nimodipine administration show the persistence
of the left M1 stenosis with
kinking-like features

watershed ischemia (Fig. 2b) associated with an irregular stenosis of the M1 segment (Fig. 2a).
The patient was intubated for the worsening of psychomotor agitation and transferred to the angio suite where digital
subtraction angiography (DSA) confirmed the presence of a
moderate vasospasm of the left A1 and M1 segments and a
vascular kink determining a severe focal stenosis of the distal
M1 segment associated with a diffuse delay of the cerebral
parenchymography of the MCA territory (Fig. 3a). Local
intra-arterial treatment was performed via the injection of
1.6 mg/10 min of nimodipine and followed by systemic treatment with 2 mg/h intravenous drip. A second DSA performed
at 24 h documented remission of the vasospasm and partial
recovery of the brain parenchymography (Fig. 3b), however
persistence of the vascular kink (Fig. 4) and residual delayed
cerebral parenchymography in the fronto-opercular and
fronto-parietal regions prompted us for further treatment.
A 6F guide catheter (Envoy, Codman Neurovascular,
Raynham, MA, USA) was positioned in the left ICA and a
coaxial microcatheter (SL10, Stryker Neurovascular,
Fremont, CA, USA) was driven through the stenosis with
the aid of a microguidewire 0.014 in. (Neuroscout standard®,
Codman Neurovascular, Raynham, MA, USA); subsequently,
the microcatheter was exchanged with a larger one
(Headway® 21 MicroVention Inc. CA, USA) in order to deliver the stent (Solitaire™ AB 4–20, ev3 Neurovascular,
Irvine, CA, USA) across the kinking (Fig. 5). Rectification
and complete recanalisation of the artery were obtained as
well as a further improvement of the parenchymography
(Fig. 3c), thus the stent was permanently released (Fig. 6).
Antiplatelet management followed our institutional protocol
for acute stenting (0.4-μg/kg/min loading dose of tirofiban for
30 min, followed by 0.10-μg/kg/min and imbrication with
100 mg aspirin/day and 75 mg clopidogrel/day the following

day); subsequently dual antiplatelet therapy was maintained
for 6 months followed by monoantiaggregation.
Post-operative imaging revealed stability of the known watershed ischemic lesions without appearance of new ischemic
lesions; clinical course revealed persistence of right side
hemiparesis and mild aphasia without new neurological deficits.
The patient was referred for professional rehabilitation; his
modified Rankin Scale score at discharge was evaluated at 3.

Discussion
Kinking of intracranial vessels is a very rare occurrence, mainly reported intraoperatively during neurovascular surgery such
as aneurysm clipping [5].

Fig. 5 Endovascular procedure. Roadmap images of the kink during the
drive of the microwire and the microcatheter beyond the stenosis, in order
to perform the stent-positioning

Acta Neurochir
Fig. 6 Unsubtracted (a) and
subtracted (b) digital angiograms
after the stenting procedure: the
device was properly placed (c)
from the origin of the left M1
segment to the proximal trait of
the superior branch of MCA,
solving the kinking

To our knowledge, this is the first report of a delayed symptomatic intracranial vascular kinking following intracranial
surgery.
Interestingly, the arterial kink corresponded to the left M1
segment, which appeared to be elongated by the mass effect of
the tumor. It is reasonable to hypothesize that chronic elongation
may cause unwanted tortuosity (and eventual kinking) once the
mass is removed and the artery restores to its original location.
A retrospective review of sphenoid wing meningiomas
found the degree of vessel encasement to be predictive of
postoperative ischemic complications and suggested that it
could be related to intraoperative traction injuries induced by
the adherence of the tumor to the arterial wall [4].
Our case suggests that also chronic elongation, which is
likely more frequent in association with large, vesselencasing lesions, may have pathological consequences that
may explain at least some ischemic complications.
Concerning the timing of the occurrence of the ischemic
complication, it should be noted that it appeared concurrently
with vasospasm which is known to occur in approximately
1.9% of cases, following skull-base tumor surgery [3]; nevertheless, progressive healing processes in the surgical bed may
also justify a delayed timing.
It is likely that the etiology of the stroke detailed in our case
was mixed, since both the kinking and the vasospasm have a
potential for flow reduction and since the infusion of
nimodipine had a partial but incomplete effect on the recovery
of cerebral parenchymography.
Treatment of vasospasm following tumor resection may be
similar to that of post-SAH vasospasm; nevertheless, some authors caution that the vasoactive materials from the tumor could
interfere with the drugs’ efficacy [1, 2]. Treatments for intracranial vessel kinking have been proposed in the setting of intraoperatory kinking during neurovascular surgery and include the
placement of space-occupying prosthesis that restores the proper
vessel geometry (5); not unlikely our treatment was aimed to
restore the proper vascular geometry that, in this case, was obtained through the positioning of endovascular prosthesis.

Management of antiplatelet agents remains a concern in the
post-operative period, thus risks should be weighted according to the expected benefits.
This case suggests that large skull-base lesions causing
vessel elongation may cause delayed complications; knowledge of this occurrence among neurovascular specialists may
help in patient care.

Compliance with ethical standards
Conflicts of interest The authors declare that they have no conflict of
interest.
Ethical approval All procedures performed in studies involving human
participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki
declaration and its later amendments or comparable ethical standards.
Informed consent Informed consent was obtained from the individual
participant included in the study.
Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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