Successful endovascular therapy for multiple intracranial arterial ...

Journal of the Neurological Sciences 384 (2018) 104–106

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Letter to the Editor Successful endovascular therapy for multiple intracranial arterial stenosis associated with medically intractable giant cell arteritis

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A R T I C L E I N F O Keywords: Giant cell arteritis Endovascular therapy Ischemic stroke Case report

Dear Editor, Giant cell arteritis (GCA) is known to be comorbid with ischemic stroke in 2 to 7% of patients [1,2]. Few cases of GCA in patients who have received endovascular therapy for large artery occlusive disease have been reported [3–5]. We describe a patient with GCA and progressive vertebrobasilar stenosis. Aggressive immunosuppressive therapy and endovascular reperfusion therapy were effective in this patient. An 80-year-old right-handed woman was transferred to our hospital. The patient had a past medical history of coil embolization of dural arteriovenous fistula in cavernous sinus. Two months prior, the magnetic resonance imaging (MRI) scans showed normal findings when she visited at another clinic because of headache. On hospital Day 0, she was admitted to the clinic again after several days of progressing deterioration in consciousness. MRI showed acute cerebellar infarction and stenosis of the right vertebral artery. Antithrombotic therapy with aspirin (100 mg) and clopidogrel (75 mg) was started just after admission. Laboratory test results indicated some inflammation with an erythrocyte sedimentation rate (ESR) of 90 mm/h (cut-off range: 10–15) and C-reactive protein (CRP) level of 7.5 mg/dL (cut-off range: 0.5–1.0). On hospital day 1, intravenous methylprednisolone (1000 mg/day) was started. However, the magnetic resonance angiogram (MRA) revealed newly developed stenosis around the clinoid segment of the right internal carotid artery. On hospital day 6, the patient's headache improved, and she did not have oppressive pain in the temporal arteries. During neurologic examinations, she was alert and conscious, had an abnormal light reflex and abducens palsy due to prior coil embolization treatment of a dural arteriovenous fistula, and had ataxia in the right upper limb. Laboratory tests results showed improvement of inflammation with an ESR of 19 mm/h and CRP level of 0.52 mg/dL. Her blood cell counts, liver and renal functions, and blood glucose levels were normal. Serum levels of proteinase-3specific and myeloperoxidase-specific antineutrophil cytoplasmic antibodies were within normal ranges. Laboratory test results for antiphospholipid antibodies were also negative. Cerebrospinal fluid tests showed normal findings. Fundoscopy showed normal eyeground. The body computed tomography angiogram showed no lesion of the aorta and its branches. The cerebral angiogram on hospital day 12 showed the following: severe stenosis in the transition zone between the extraspinal segment (V3) and intradural segment (V4) of the right vertebral artery, occlusion of V3 in the left vertebral artery with narrowing in the foraminal segment (V2), stenosis in the cavernous segment (C4) of the right internal carotid artery, and normal findings in both superficial temporal arteries. On hospital day 16, we performed a biopsy of the superficial temporal artery. The biopsy results revealed fibrous intimal thickening resulting in stenosis, lymphoplasmacytic infiltration of the media, and fibrosis involving the adventitia and surrounding fatty tissue (Fig. 1A). There was an epithelioid granuloma with giant cells, and infiltrating inflammatory cells were composed of lymphocytes and plasma cells (Fig. 1B). Destruction of the muscular media was also observed in an elastica van Gieson stain (Fig. 1C). Consciousness disturbance deteriorated, and the MRA showed the progression of stenosis in the left vertebral artery. On hospital day 19, intravenous methylprednisolone (1000 mg/day) was started again. On hospital day 25, we administered intravenous cyclophosphamide (670 mg) once. However, consciousness disturbance worsened further (Glasgow coma scale score: eye opening, 2; verbal, 3; motor, 6). On hospital day 28, we performed endovascular therapy with balloon angioplasty after the MRA showed the progression of vertebrobasilar stenosis. The angiogram of the right vertebral artery showed severe stenosis of the V4 segment (Fig. 1E). The Gateway Over-the-Wire 2.0 mm × 12 mm (Stryker, Kalamazoo, MI, USA) was placed in the distal portion of the stenosis. We inflated the balloon four times with a nominal pressure of 6 for 30 s. Balloon inflation was performed with recanalization of the right vertebral artery (Fig. 1F), and the patient recovered from consciousness disturbance (Glasgow coma scale score: eye opening, 4; verbal, 4; motor, 6). After angioplasty, we continued antiplatelet therapy with aspirin (100 mg), clopidogrel (75 mg), and oral prednisolone (45 mg) The MRI scan showed no new ischemic lesion. On hospital day 71, she was discharged with left hemiparesis and a modified Rankin scale score of 3.

Abbreviations: GCA, giant cell arteritis; MRI, magnetic resonance imaging; ESR, erythrocyte sedimentation rate; CRP, C-reactive protein; MRA, magnetic resonance angiogram https://doi.org/10.1016/j.jns.2017.11.027 Received 24 September 2017; Received in revised form 16 November 2017; Accepted 20 November 2017 Available online 22 November 2017 0022-510X/ © 2017 Elsevier B.V. All rights reserved.


Letter to the Editor

Fig. 1. The biopsy specimen of the temporal artery reveals fibrous intimal thickening resulting in stenosis, lymphoplasmacytic infiltration of the media, and fibrosis involving the adventitia and surrounding fatty tissue (A, ×4). Infiltrating inflammatory cells are composed of lymphocytes and plasma cells (B, × 40). Destruction of the muscular media is also observed (C, elastica van Gieson stain, × 10). The angiogram of the right vertebral artery before endovascular therapy with a balloon catheter demonstrates severe stenosis in the transition zone between the extraspinal segment (V3) and intradural segment (V4) of the right vertebral artery (D). Angiogram during inflation of the balloon catheter (E). The final angiogram showing recanalization of the right vertebral artery and improvement of blood flow in the right vertebral artery (F). The absence of contrast filling of the proximal basilar artery was due to the prior coil embolization of dural arteriovenous fistula in the cavernous sinus.

The MRI scan and MRA 27 months after her discharge did not show recurrence of GCA or restenosis. GCA is classified into large vessel vasculitis according to the Chapel Hill Consensus Conference of Nomenclature of Vasculitides [6]. The definition used for the classification of giant cell arteritis consists of five criteria: 1) Age at disease onset more than 50 years, 2) new headache, 3) temporal artery abnormality, 4) increased ESR more than 50 mm/h, 5) abnormal artery biopsy. At least three of five criterions are needed to fulfill for diagnosis of GCA. This case fulfilled four of five criterions except for 3) and was consistent with GCA. The vertebral artery is involved in 40–60% of patients with cerebrovascular ischemic events [7]. The mortality of bilateral vertebral artery occlusion resulting from GCA is 75%, and the prognosis is poor [2,8]. Although corticosteroids are the first-choice treatment for GCA, some refractory patients require adjuvant therapies, such as methotrexate or cyclophosphamide [9,10]. Some studies have shown that methotrexate reduced the proportion of patients who experienced relapse and reduced the duration of prednisone treatment [9]. However, the effectiveness of adjuvant therapy has not been established, and there are medically intractable patients like our particular case. To date, three cases of endovascular treatment in patients with GCA and intracranial stenosis have been reported [3–5]. All patients were refractory to immunosuppression therapy and were treated with angioplasty or stenting. The vertebral artery was involved in only one patient, who was treated with stenting in addition to angioplasty. All three patients had a good clinical course, and the MRI scan in one of the three patients showed no new lesion after 18 months of follow-up [4]. In the present patient, the MRA did not show restenosis, and her neurological findings did not worsen for 27 months. In conclusion, endovascular therapy is an acceptable option for treating intracranial cerebral arterial stenosis with medically intractable GCA. Conflicts of interest None. Funding None. References [1] R.T. Caselli, G. Hunder, J. Whisnant, Neurologic disease in biopsy-proven giant cell (temporal) arteritis, Neurology 38 (1988) 352–359. [2] S. Rüegg, S. Engelter, C. Jeanneret, A. Hetzel, A. Probst, A.J. Steck, P. Lyrer, Bilateral vertebral artery occlusion resulting from giant cell arteritis: report of 3 cases and review of the literature, Medicine (Baltimore) 82 (2003) 1–12. [3] N. Dementovych, R. Mishra, Q.A. Shah, Angioplasty and stent placement for complete occlusion of the vertebral artery secondary to giant cell arteritis, J. Neurointerv. Surg. 4

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Letter to the Editor

(2012) 110–113. [4] A.M. Guerrero, F. Sierra-Hidalgo, P. Calleja, P. Navia, J. Campollo, J. Díaz-Guzmán, Intracranial internal carotid artery angioplasthy and stenting in giant cell arteritis, J. Neuroimaging 25 (2015) 307–309. [5] D. Neutel, L. Biscoito, J. Campos, T.P. e Melo, L. Albuquerque, Giant cell arteritis with symptomatic intracranial stenosis and endovascular treatment, Neurol. Sci. 35 (2014) 609–610. [6] J.C. Jennette, R.J. Falk, P.A. Bacon, N. Basu, M.C. Cid, F. Ferrario, L.F. Flores-Suarez, W.L. Gross, L. Guillevin, E.C. Hagen, G.S. Hoffman, D.R. Jayne, C.G. Kallenberg, P. Lamprecht, C.A. Langford, R.A. Luqmani, A.D. Mahr, E.L. Matteson, P.A. Merkel, S. Ozen, C.D. Pusey, N. Rasmussen, A.J. Rees, D.G. Scott, U. Specks, J.H. Stone, K. Takahashi, R.A. Watts, 2012 revised international Chapel Hill consensus conference nomenclature of vasculitides, Arthritis Rheum. 65 (2013) 1–11. [7] L.R. Solans-Laqué, G.J. Bosch, C.A. Molina, A. Ortega-Aznar, J. Alvarez-Sabin, M. Vilardell-Tarres, Stroke and multi-infarct dementia as presenting symptoms of giant cell arteritis: report of 7 cases and review of the literature, Medicine (Baltimore) 87 (2008) 335–344. [8] R. Andersson, Giant cell arteritis as a cause of death, Clin. Exp. Rheumatol. 18 (2000) S27–S28. [9] A. Mahr, J. Jover, R. Spiera, C. Hernández-García, B. Fernández-Gutiérrez, M.P. Lavalley, P.A. Merkel, Adjunctive methotrexate for treatment of giant cell arteritis: an individual patient data meta-analysis, Arthritis Rheum. 56 (2007) 2789–2797. [10] L. Quartuccio, M. Maset, G. De Maglio, E. Pontarini, M. Fabris, E. Mansutti, L. Mariuzzi, S. Pizzolitto, C.A. Beltrami, S. De Vita, Role of oral cyclophosphamide in the treatment of giant cell arteritis, Rheumatology 51 (2012) 1677–1686. ⁎

Masaya Togoa, , Tomoyuki Konoa, Taku Hoshia, Hirotoshi Imamurab, Kenichi Todoa, Hidemitsu Adachib, Michi Kawamotoa, Yukihiro Imaic, Nobuyuki Sakaib, Nobuo Koharaa a Kobe City Medical Center General Hospital, Department of Neurology, Japan b Kobe City Medical Center General Hospital, Department of Neurosurgery, Japan c Kobe City Medical Center General Hospital, Department of Pathology, Japan E-mail address: [email protected]

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Corresponding author at: Kobe City Medical Center General Hospital, Department of Neurology, 2-1 Minatozima Minami Machi, Chuo-ku, Kobe, Hyogo, Japan.

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