Case Report

Endovascular treatment with tirofiban during
the acute stage of cervical spinal cord
infarction due to vertebral artery dissection
Yuanling Wu, Wenxian Li, Xiaomei Xie, Zhen Jing, Weibiao Lu, Li’an Huang
Department of Neurology, First Affiliated Hospital of Jinan University, Guangzhou, Guangdong Province, China
Context: Cervical spinal cord infarction is a rare and severe complication of vertebral artery dissection (VAD). We
report a case of VAD in an acute stage followed by cervical spinal cord infarction that was treated using direct
endovascular tirofiban infusion via digital subtraction angiography (DSA) monitoring.
Findings: A 48-year-old man presented with vertigo, neck pain, numbness and weakness in four limbs with
subsequent cardiac and respiratory arrest. Neurological examination revealed hypoesthesia below the neck
with grade one myodynamia on the right side of the limbs and zero on the left side. The diagnosis of VADrelated cervical spinal infarction was confirmed using DSA imaging and cervical vertebra magnetic
resonance imaging (MRI). The patient received timely treatment with endovascular tirofiban infusion and
achieved good outcome without any sequelae.
Conclusion: Endovascular treatment with tirofiban may be a selective choice for cervical spinal cord infarction
due to VAD in acute stage and warrants further study.
Keywords: Endovascular, Tirofiban, Cervical spinal cord infarction, Vertebral artery dissection

Introduction
The annual incidence of cervical artery dissection (CeAD)
is approximately 2.6-3.0 per 100,000. CeAD is classified
as carotid artery dissection (CAD) or vertebral artery
dissection (VAD).1 Spinal cord stroke accounts for only
0.3-1% of all strokes.2 Therefore, VAD-related cervical
spinal infarction is very rare. The mechanism of dissection
is associated with intimal tear of arteries followed by
hemodynamic-relevant stenosis and secondary thrombosis, which results in acute ischemic stroke and symptom
progression.3 Cervical spinal cord infarction may result
in severe neurological complications, and the prognosis
is closely related to early diagnosis and prompt treatment.4 We describe a case of symptomatic VAD treated
with an endovascular tirofiban infusion during the acute
stage. This treatment ceased progression of the condition,
and the patient exhibited a good outcome.

Case report
A 48-year-old man visited a local clinic with complaints of vertigo, accompanied by neck pain at
Correspondence to: Li’an Huang, Department of Neurology, First Affiliated
Hospital of Jinan University, Guangzhou, 510632, Guangdong Province,
China. Email: huanglian1306@126.com

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© The Academy of Spinal Cord Injury Professionals, Inc. 2018
DOI 10.1080/10790268.2017.1422880

12:00 AM. His blood pressure was 150/120 mmHg.
The physician was able to lower the patient’s blood
pressure, and the patient was sent home. The patient
was admitted to our hospital three hours later due to
the reappearance of vertigo accompanied by numbness
and weakness of the four limbs as well as difficulty
breathing. The patient suddenly developed mental
confusion, and cardiac and respiratory arrest that
required tracheal intubation after 10 minutes. His
heartbeat and breathing resumed after cardiopulmonary resuscitation (CPR). Physical examination
revealed hypoesthesia below the neck with and grade
one myodynamia on the right side of the limbs and
zero on the left side.
Head computed tomography (CT) and computerized
tomography angiography (CTA) scanning were normal
at admission. However, the patient’s condition deteriorated. An immediate DSA was performed approximately 10 hours after onset. Nonselective
arteriography revealed that the blood flow of the right
carotid artery was from an innominate artery, and
blood flow of the left carotid artery was directly from
the aortic arch. Blood flow of the right vertebral
artery (VA) was from the left subclavian artery, which

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was normal but much faster than that of the left VA.
Bilateral internal carotid arteries supplied the middle
cerebral arteries and anterior cerebral arteries, and the
intracranial right VA supplied the basilar artery.
Selective arteriography revealed no visible thrombi but
severe stenosis of the left VA at the V2 segment, which
slowed the blood flow, and disappearance of the
segment of the anterior spinal artery (ASA) that supplied the upper cervical spinal cord had (Fig. 1A). The
left VA was treated using an endovascular 10-ml tirofiban infusion via DSA monitoring. Brain and cervical
vertebrae MRI scanning were performed approximately
48 hours after symptom onset. Brain MRI was normal.
The cervical vertebrae MRI scan revealed high signals
on T2-weighted images, which indicated ischemia
extending from C4 to C1 (Fig. 2A). Axial MRI revealed
the left VA with severe luminal stenosis and hyperintensity of intramural hematoma which indicated dissection
(Fig. 2B). Therefore, the patient was diagnosed with
VAD-related acute cervical spinal cord infarction. An
intravenous drip of tirofiban at 13 ml/h was administered for the first three days. DSA re-examination on
the third day revealed a decreased degree of stenosis at
the left V2 segment, and obvious improvement in
blood flow. The segment of the ASA that supplied the
upper cervical spinal cord and the anterior radiculomedullary arteries reappeared, and blood flow recovered
(Fig. 1B and C). Treatment was adjusted to anticoagulant therapy.
The neurological symptoms of the patient obviously
improved 15 days later. Conventional dual antiplatelet
therapy was recommended instead of anticoagulant
therapy.
At the six-month follow-up, three-dimensional CTA
revealed that the left VA dissection at the V2 segment
had disappeared, and the vasculature was completely
recanalized.

Discussion
Representative cases of spinal cord infarction due to
VAD with manifestations of headache or neck pain,
and neurological deficits of motor weakness and
hypoesthesia have been reported.5 Our patient also suffered cardiac and respiratory arrest because the ischemia
extended from C4 to C1, which is responsible for
respiration.
The segmental spinal arteries supplying the cervical
region vary considerably between individuals because
these arteries generally originate from the vertebral or
subclavian artery.6 ASA is formed by the confluence
of the bilateral vertebral artery branches and descends
to the conus medullaris. ASA is a series of anastomotic

vascular loops, not a single artery, and thus requires a
segmental radiculomedullary arterial supply to provide
adequate blood flow to the anterior two-thirds of the
spinal cord tissue.7 Radiculomedullary arteries at the
cervical segment often originate from a deep cervical
artery or vertebral arteries. The mechanism of dissection
is associated with intimal tears of arteries followed by
hemodynamic-relevant stenosis and secondary thrombosis, which results in acute ischemic stroke and progressive symptoms.3 The dissection in our patient
occurred at the left V2 segment and resulted in stenosis
of the lumen and hemodynamic changes. There was
insufficient time for contralateral vertebral or subclavian
artery compensation; the left radiculomedullary arteries
were suddenly disrupted, and the cervical segment of
ASA was insufficient. The cervical spinal cord infarction
formed over time (Fig. 2A and B). Moreover, the patient
presented with a progressing stroke due to secondary
microemboli induced by dissection, which preceded
the neurological deficit. Timely and effective therapy
was necessary.
VAD-related cervical spinal cord infarction should be
treated on a case-by-case basis, and treatment efficacy is
closely associated with onset time and stroke progression. Several treatment options for VAD are indicated, including thrombolysis, anticoagulation,
antiplatelet, surgical and endovascular repair.1 The
safety and efficacy of thrombolysis are not well established.8 A randomized trial demonstrated no difference
in the efficacy of antiplatelet and anticoagulant drugs
in preventing stroke and death in patients with symptomatic carotid or vertebral artery dissection.9
Endovascular and surgical repair should be considered
when patients are unresponsive to any medical
therapy.1,4 The diagnosis of our patient was not clear
at admission, but his condition deteriorated. We
immediately performed a DSA and found severe stenosis of the left V2 segment. Conservative medication took
effect slowly, and the time window for thrombolysis
passed. No visible thrombus was found to perform
thrombectomy, and stent implantation is not a routine
indication for dissection. Therefore, direct endovascular
tirofiban infusion in the left VA under DSA monitoring
was chosen for the first time because it was the most
direct and effective treatment. American heart association/American stroke association (ASA/AHA) or
Chinese guidelines indicate no definite time window
for tirofiban infusion in the treatment of acute cerebral
or spinal stroke, and more randomized and controlled
trials (RCTs) are required.10,11 Tirofiban is a highly
selective, nonpeptide glycoprotein IIb/IIIa platelet
receptor antagonist that exhibits a short half-life.

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Fig. 1. (A) DSA revealed severe stenosis of the left VA in the V2 segment. The anterior spinal artery and anterior radiculomedullary
arteries had disappeared (thick arrow). (B and C) DSA imaging reexamination revealed that the degree of left VA stenosis in the V2
segment (thick arrow) was approximately 50%, resulting in the reappearance of anterior radiculomedullary arteries (blunt arrows)
and ASA(thin arrow), which supplied the upper cervical spinal cord.

Rapid recovery of prolonged bleeding time is observed
after discontinuation, and its safety was preliminary
demonstrated in the SaTIS trial.12 Intravenous tirofiban
infusion was used previously in coronary and carotid
dissection.13,14 Low-dose intra-arterial tirofiban was
confirmed to improve functional outcome in acute
ischemic stroke with endovascular treatment.15 It may
have directly acted on new microemboli of the ASA
from intimal tears of the left V2 segment in our
patient, and avoided an “artery to artery” embolization

of the basilar occlusion to quickly prevent progression to
stroke.16,17
Spinal cord infarction patients experience more significant improvement and exhibit lower long-term mortality
than do cerebral infarction patients.2 The segment of the
ASA that supplied the upper cervical spinal cord from C4
to C1 reappeared after tirofiban treatment because the
left radiculomedullary arteries from the left VA recovered
their blood flow (Fig. 1B and C). Our patient achieved a
good outcome without any sequelae and exhibited no

Fig. 2. (A) T2-weighted images on sagittal MRI revealed a high signal, which indicated that the ischemia extended from C4 to C1.
These signs were compatible with infarction of the cervical medulla. (B) Axial T2-weighted images revealed severe luminal stenosis
and a hyperintense area of smooth vascular wall thickening, which indicated intramural hematoma of the left VA in the V2 segment.
These signs were compatible with dissection of the left V2 segment.

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recurrence of cervical spinal infarction despite tirofiban
infusion approximately 10 hours after symptom onset.

Conclusion
Spinal cord infarction is a rare complication of VAD
that exhibits atypical manifestations of headache or
neck pain and neurological deficits of motor weakness
and hypoesthesia. Spinal infarction should be considered if these acute symptoms occur, and the cerebral
image is normal. Endovascular tirofiban infusion may
be a good choice for treatment during the acute stage
in select cases of VAD-related infarction, but further
study is warranted.

Disclaimer statements
Contributors None
Funding This work was supported by the Science and
Technology Plan Projects of Guangdong Province
[grant number 2017A020215200].
Conflicts of interest The authors declare that they have
no conflicts of interest to disclose.
Ethics approval None.

References
1 Kim YK, Schulman S. Cervical artery dissection: Pathology, epidemiology and management. Thromb Res 2009;123(6):810–21.
2 Romi F, Naess H. Spinal cord infarction in clinical neurology: A
review of characteristics and long-term prognosis in comparison
to cerebral infarction. Eur Neurol 2016;76(3–4):95–8.
3 Stapf C, Elkind MS, Mohr JP. Carotid artery dissection. Annu Rev
Med 2000;51:329–47.
4 Jennifer J. Robertson, Koyfman A. Cervical artery dissections: A
review. J Emerg Med 2016;51(5):508–18.
5 Hsu CY, Cheng CY, Lee JD, Lee M, Huang YC, Wu CY et al.
Clinical features and outcomes of spinal cord infarction following

vertebral artery dissection: A systematic review of the literature.
Neurol Res 2013;35(7):676–83.
6 Bruce B, Lydia J, Gewertz BL. Blood supply to the spinal cord
anatomic and physiologic correlations. Ann Vasc Surg 1994;8:
394–9.
7 Santillan A, Nacarino V, Greenberg E, Riina HA, Gobin YP,
Patsalides A. Vascular anatomy of the spinal cord. J Neurointerv
Surg 2012;4(1):67–74.
8 Tsivgoulis G, Zand R, Katsanos AH, Sharma VK, Goyal N,
Krogias C et al. Safety and outcomes of intravenous thrombolysis
in dissection-related ischemic stroke: An international multicenter
study and comprehensive meta-analysis of reported case series. J
Neurol 2015;262(9):2135–43.
9 Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J.
Antiplatelet treatment compared with anticoagulation treatment
for cervical artery dissection (CADISS): A randomised trial.
Lancet Neurol 2015;14(4):361–7.
10 Cao YB, Chen YN, Dong Q, Wang D, Fan YM, Gao F et al. 2015
Chinese guidelines for the endovascular treatment of acute
ischemic stroke (in Chinese). Chin J Stroke 2015;10(7):590–606.
11 Powers WJ, Derdeyn CP, Biller J, Coffey CS, Hoh BL, Jauch EC
et al. 2015 American heart association/American stroke association focused update of the 2013 guidelines for the early management of patients with acute ischemic stroke regarding endovascular
treatment: A guideline for healthcare professionals from the
American heart association/American stroke association. Stroke
2015;46(10):3020–35.
12 Siebler M, Hennerici MG, Schneider D, von Reutern GM, Seitz
RJ, Rother J et al. Safety of tirofiban in acute ischemic stroke:
The satis trial. Stroke 2011;42(9):2388–92.
13 Cheung S, Mithani V, Watson RM. Healing of spontaneous coronary dissection in the context of glycoprotein IIb/IIIa inhibitor
therapy: A case report. Catheter Cardiovasc Interv 2000;51:
95–100.
14 Jaipersad AS, Tiivas C, Walton G, Imray CH. A novel treatment
for embolising carotid dissection. Int J Surg Case Rep 2012;3(1):
19–21.
15 Zhao W, Che R, Shang S, Wu C, Li C, Wu L et al. Low-dose tirofiban improves functional outcome in acute ischemic stroke
patients treated with endovascular thrombectomy. Stroke 2017;48
(12):3289–94.
16 Droste DW, Junker K, Stögbauer F, Lowens S, Besselmann M,
Braun B et al. Clinically silent circulating microemboli in 20
patients with carotid or vertebral artery dissection. Cerebrovasc
Dis 2001;12(3):181–5.
17 Junghans U, Siebler M. Cerebral microembolism is blocked by tirofiban, a selective nonpeptide platelet glycoprotein IIb/IIIa receptor antagonist. Circulation 2003;107:2717–21.

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