Case Studies

A Recurrent Case of Ischemic Stroke Caused by Vasospasm
due to Giant Cell Arteritis
Reina Kawamura, MD,* Atsushi Mizuma, MD, PhD,* Maiko Kouchi, MD,*
Eiichiro Nagata, MD, PhD,* Wakoh Takahashi, MD, PhD,† and
Shunya Takizawa, MD, PhD*

A 73-year-old man was admitted with sudden right upper-limb weakness. He had
a temporal headache on the left side and had a 4-month history of fever. Meandering of the left temporal artery (TA) with induration and high inflammatory
responses (white blood cell count 22,500 per microliter, C-reactive protein 35.0 mg/dL,
and elevated sedimentation rate [ESR] 80 mm/h) were observed. Glycometabolism
and lipid metabolism were normal, and autoimmune antibodies were negative.
Cultivation tests revealed no bacteria in either blood culture or cerebrospinal fluid.
Brain magnetic resonance imaging (MRI) showed ischemic lesion in the left frontal
lobe, while magnetic resonance angiography (MRA) and carotid ultrasonography showed unstable plaque lesions in the left extracranial internal carotid artery
(ICA). According to reported criteria (age > 50 years, new onset of headache, abnormality of the TA, and raised ESR), we diagnosed giant cell arteritis (GCA) with
acute ischemic stroke (IS) and gave the patient antithrombotic therapy (aspirin
100 mg, cilostazol 200 mg). After admission, hemiparesis progressed but fluctuated. Subsequent MRI showed new lesions in the left watershed area. MRA also
showed vasospasm in the middle cerebral artery and C5 portion of the ICA. Considering the correlation with GCA pathophysiology, oral prednisolone therapy
was administered. Steroid therapy has prevented stroke recurrence and improved the symptoms and vasospasm. We wish to emphasize that GCA can induce
IS via vasospasm, and steroid therapy is recommended. Key Words: Giant cell
arteritis—unstable carotid plaque—carotid artery stenosis—vasospasm—stroke
recurrence.
© 2017 Published by Elsevier Inc. on behalf of National Stroke Association.

From the *Department of Neurology, Tokai University School of
Medicine, Kanagawa, Japan; and †Department of Neurology, Tokai
University Oiso Hospital, Kanagawa, Japan.
Received June 8, 2017; revision received July 12, 2017; accepted
July 23, 2017.
Address correspondence to Atsushi Mizuma, MD, PhD, Department
of Neurology, Tokai University School of Medicine, 143 Shimokasuya,
Isehara, Kanagawa 259-1193, Japan. E-mail: atushi.mizuma@gmail.com.
1052-3057/$ - see front matter
© 2017 Published by Elsevier Inc. on behalf of National Stroke
Association.
https://doi.org/10.1016/j.jstrokecerebrovasdis.2017.07.023

e216

A 73-year-old man was admitted with sudden onset
of right upper-limb weakness. He reported temporal headache on the left side and had a 4-month history of fever.
Orbital pain and hearing loss were also gradually progressing. Apart from hypertension, he had no noteworthy
medical, family, preference, or drug history. Meandering of the left temporal artery (TA) with induration and
high inflammatory responses (white blood cell count 22,500
per microliter, C-reactive protein 35.0 mg/dL, and elevated sedimentation rate [ESR] 80 mm/h) were observed.
There was no abnormality in glycometabolism/lipid

Journal of Stroke and Cerebrovascular Diseases, Vol. 26, No. 11 (November), 2017: pp e216–e217

STROKE BY GIANT CELL ARTERITIS

e217

Figure 1. (A) Diffusion-weighted image showed high-signal lesion in left frontal lobe (→) (on admission). (B) Magnetic resonance angiography showed
normal findings in intracranial vessels (on admission). (C) Magnetic resonance plaque imaging (by T2 black-blood method) showing unstable plaque lesion
in the left internal carotid artery (â—‹). (D and E) Two days after admission, magnetic resonance imaging and magnetic resonance angiography showed new
ischemic lesions in the left watershed area (→) and vasospasm in the left middle cerebral artery and the C5 portion of the internal carotid artery (→).
(F) Internal carotid artery flow was improved in catheter angiography 2 weeks after starting steroid therapy. (G) Vasospasm in the left middle cerebral
artery and the C5 portion of the internal carotid artery was improved on magnetic resonance angiography performed after 6 months.

metabolism, and autoimmune antibodies (including
antinuclear antibody, anti-SS-A/B antibodies, and
antineutrophil cytoplasmic antibody) were negative. Cerebrospinal fluid showed elevation of protein (97 mg/dL)
and pleocytosis (76 per microliter). Cultivation tests revealed no bacteria. Brain magnetic resonance imaging
showed an ischemic lesion in the left frontal lobe (Fig 1, A).
Magnetic resonance angiography (Fig 1, B,C) and carotid
ultrasonography showed an unstable plaque in the left
extracranial internal carotid artery (ICA). Antithrombotic
therapy (aspirin 100 mg, cilostazol 200 mg) was given for
acute ischemic stroke (IS). Giant cell arteritis (GCA) was
also suspected from the symptoms and examination results.
After admission, hemiparesis progressed but fluctuated,
and subsequent magnetic resonance imaging (Fig 1, D)
showed new lesions in the left watershed area. Magnetic resonance angiography (Fig 1, E) showed vasospasm
in the middle cerebral artery and the C5 portion of the
ICA. Oral prednisolone therapy (from 40 mg to 10 mg as
maintenance therapy) was immediately started after TA
biopsy, considering the correlation with GCA pathophysiology. Fever, headache, orbital pain, hearing loss, TA
abnormality, and inflammatory responses (white blood
cell count 8300 per microliter, C-reactive protein .29 mg/dL,
and ESR 10 mm/h) were improved after 2 weeks. Steroid
therapy has also prevented stroke recurrence and improved vasospasm (Fig 1, F,G). Although inflammatory
infiltration was unclear from the biopsy, the other criteria
for GCA diagnosis (age > 50 years, new onset of headache,

TA abnormality, and raised ESR) were all fulfilled, and
finally he was diagnosed with GCA.1
We considered that IS had been induced by an unstable plaque, but IS recurrence could have occurred through
a hemodynamic mechanism via vasospasm due to GCA.
Improvement of symptoms and vasospasm after steroid
therapy also supported this diagnosis of IS with GCA.
GCA-related vasculitis (vertebral–basilar artery or ICA)
has been reported to induce IS.2-5 However, intracranial
artery vasospasm (especially in the middle cerebral
artery) is rare in IS with GCA.5 We wish to emphasize
that GCA can induce IS via vasospasm, and steroid therapy
is recommended.

References
1. Ness T, Bley TA, Schmidt WA, et al. The diagnosis and
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2. Zarar A, Zafar TT, Khan AA, et al. Internal carotid artery
stenosis associated with giant cell arteritis: case report and
discussion. J Vasc Interv Neurol 2014;7:24-27.
3. Gonzalez-Gay MA, Vazquez-Rodriguez TR, Gomez-Acebo
I, et al. Strokes at time of disease diagnosis in a series of
287 patients with biopsy-proven giant cell arteritis.
Medicine (Baltimore) 2009;88:227-235.
4. Lariviere D, Sacre K, Klein I, et al. Extra- and intacranial
cerebral vasculitis in giant cell arteritis an observational
study. Medicine (Baltimore) 2014;93:1-8.
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involvement of intracranial arteries. Arthritis Rheum
2006;55:985-989.