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Citation: Bencherif L, Neumann L, Tarabay O, Saker L, Nouar R, Manchon E, et al. Non-thrombotic vertebrobasilar stroke in Crohn's disease
patient.Jr.med.res.2020;3(3): 13-14. Bencherif et al © All rights are reserved. https://doi.org/10.32512/jmr.3.3.2020/13.14
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Case report
Bencherif Lamia
1, *
, Neumann Lisa
1
, Tarabay Oriane
1
, Saker Lokbi
1
, Nouar Ryad
1
, Manchon Eric
1
, Varnet Olivier
1
.
Non-thrombotic vertebrobasilar stroke in Crohn's disease patient.
1: Department of Neurology Gonesse
Hospital Center, Gonesse France
* Corresponding author
Correspondence to:
Lamia576@gmail.com
Publication Data:
Submitted: August10,2020
Accepted: October 26,2020
Online: November 30,2020
This article was subject to full peer-review.
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Crohn’s disease is a chronic inflammatory bowel disease (IBD) that could affect any part of
the gastrointestinal tract. The association between posterior circulation stroke and Crohn’s
disease is rarely reported and was controversial for long time. We report herein a case of a
stroke in the right posterior inferior cerebellar artery (PICA) territory in a male patient with
no cardiovascular risk factors who was monitored for ileocolic active Crohn’s Disease.
The aim is to assess the pathophysiological correlation between this inflammatory condition
and the predominance of vertebrobasilar strokes and to highlight appropriate management
characteristics.
Keywords:
Crohn’s Disease; stroke; thrombus; Hypercoagulability.
Introduction
Several concordant studies have ruled out significant increased thromboembolic accidents
risk in Inflammatory bowel disease. However, the mechanisms are still unclear specially
regarding the contribution of the systemic inflammation itself to the coagulability disorders
[1].
Observation
We report a case of 53-year-old Caucasian male smoker with no other cardiovascular risk
factors presenting to the emergency department for rotational vertigo associated with gait
and postural instability that started four days ago. The patient had a 10-year history of
ileocolic Crohn’s disease irregularly followed up. The physical examination revealed discrete
ataxia of the right lower and upper limb, loss of pain and temperature sensation on the left
side of the body sparing the face, abolition of the gag reflex, oropharyngeal muscle paralysis
with uvular deviation to the left, dysphonia, and a right-sided Bernard-Horner syndrome.
The Diagnosis of a complete Wallenberg syndrome retained with NIH stroke scale of 5. Brain
MRI revealed a right paramedian pontine stroke affecting the lower side of the right
cerebellum, consistent with the territory of the right posterior inferior cerebellar artery
(PICA) visible in the FLAIR sequences. No arterial occlusion or thrombus were detected on
the T2-star and 3D-TOF sequences (figure1a, 1b).
The 24-hour Holter monitoring, transthoracic and transesophageal echocardiography, CT
brain angiography and Doppler ultrasound of the neck vessels were normal. Biology revealed
inflammatory syndrome with no hyperleukocytosis or thrombocytosis. CRP was 252 g/L and
fibrinogen 5.58 g. The plasma protein electrophoresis had an inflammatory distribution. Lipid
panel showed high levels of cholesterol. There was no diabetes. Serology for HIV, and
hepatitis B, C were negative. Anti-cardiolipin antibodies and anti-beta2-glycoprotein
antibodies (b2GP1) also revealed negative results. Antiphospholipid syndrome (APS) workup
was negative along with complement levels and ANCA. Vitamin B9, B12 and homocysteine
levels were within normal. The test for arterial thrombophilia turned out to be negative (no
Factor V mutation, no prothrombin gene mutation and no protein S and C deficiency).
However, a high level of Factor VIII (295.9%) and Factor V (210%) were noted. Abdominal
CT scan and colonoscopy confirmed colonic active Crohn’s disease. Antiplatelet aggregation
and corticosteroid therapy were prescribed. The neurological evolution was satisfactory
following functional and motor rehabilitation, reaching an NIHSS score of 1 and a Rankin
score of 1. Only minimal residual ataxia persisted on the right side of the body. Treatment
with ani-TNF alpha was prescribed for the Crohn’s disease.
Abstract
Non-thrombotic vertebrobasilar stroke in Crohn's disease patient.
Citation: Bencherif L, Neumann L, Tarabay O, Saker L, Nouar R, Manchon E, et al. Non-thrombotic vertebrobasilar stroke in Crohn's disease patient.
Jr.med.res.2020;3(3): 13-14. Bencherif et al © All rights are reserved.
Submit your manuscript: www.jmedicalresearch.com
14
Figure 1: a-paramedian pontine stroke affecting the lower side of the right cerebellum
b- No evidence of arterial PICA thrombus on the T2-star and 3D-TOF sequences
Discussion
Several studies in the literature reported significant association between chronic inflammatory bowel disease (IBD) and
thrombo-embolic accidents [2]. Posterior circulation strokes in Crohn disease patients are uncommon. Posterior circulation
strokes could be explained by a slower blood flow creating a high hemodynamic turbulence (hyperviscosity) and the loss
of autoregulation of the smooth muscles of arteries media [3].
Our patient presented a significant increase in Factor VIII, Factor V, CRP and fibrinogen which could generate a different
coagulability status providing favorable field to the stroke development. Several studies noted higher level of coagulation
factors in IBD cases. These patients may be susceptible to experience posterior stroke due to high Factor VIII level. This
factor is an anti-inflammatory marker and prothrombotic protein. Other authors found that Von Willebrand factor drives
the association between elevated factor VIII and poor outcomes in patients with ischemic stroke. However, the exact
physiopathology is still unclear in these cases [4,5]. The contribution of some other blood disorders like thrombocytosis or
hyperhomocysteinemia was reported. IBD integrating bigger inflammatory syndromes including vasculitis and vascular wall
diseases may constitute a bias of the cause-to-effect association of the systemic inflammation and the thromboembolic
disease [6]. Diagnosis of non-thrombotic stroke requires multiple investigations including anti-phospholipid antibodies
(APA), anti-cardiolipin antibodies, anti-beta2-glycoprotein antibodies (b2GP1), ANCA, homocysteine, Antithrombin III,
Protein C, Protein S, Factor V Leiden and Prothrombin II assessment. Small atheromatous plaques must be ruled out on
the imaging as well. The angio-MRI 3D reconstruction of cerebral vessels is the standard diagnostic tool. The management
of non-thrombotic strokes is still non-consensual. In our practice we believe that antiplatelet aggregation agents are
efficient and safe. The control of the systemic inflammation and Crohn disease remission may decrease the risk of stroke
recurrence.
Conflict of Interest: None
References
[1] Card TR, Zittan E, Nguyen GC, Grainge MJ. Disease activity in inflammatory bowel disease is associated with arterial vascular disease. Inflamm Bowel Dis. 2020: izaa156.
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[3] Singh S, Singh H, Loftus EV Jr, Pardi DS. Risk of cerebrovascular accidents and ischemic heart disease in patients with inflammatory bowel disease: a systematic review
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