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    Home > Active Ingredient News > Study of Nervous System > Stroke caused by giant cell arteritis - how much do you know about such imaging findings?

    Stroke caused by giant cell arteritis - how much do you know about such imaging findings?

    • Last Update: 2022-03-06
    • Source: Internet
    • Author: User
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    Giant cell arteritis (GCA) is the most common systemic vasculitis in Western countries and the elderly
    .

    It is characterized by granulomatous inflammation of the aortic wall and superior branches of the aorta, including the extracranial carotid and vertebral arteries
    .

    The most common clinical presentation is vasculitis from the branch of the external carotid artery (headache, scalp tenderness, abnormal temporal artery on physical examination, and jaw claudication)
    .

    This article describes a case of mild ischemic stroke with insignificant clinical manifestations of GCA
    .

    Imaging in this case greatly aided early diagnosis
    .

    By understanding the imaging features of this case, it is believed that neurologists will be aware of this diagnosis when evaluating such patients
    .

    Compiled and organized by Yimaitong, please do not reprint without authorization
    .

     A 79-year-old woman with sudden isolated motor aphasia.
    A 79-year-old woman with a history of hypertension, chondrocalcinosis, and giant esophagus with achalasia on low-dose steroids (initially for chondrocalcinosis)1 Years, drug withdrawal 3 weeks before the onset, secondary mild nutritional deficiency, weight loss of 4 kg in the past three months
    .

    She presented with a 5-minute episode of isolated motor aphasia
    .

    Nervous system examination was normal, and bilateral superficial temporal artery pulse perception was good
    .

     Laboratory tests revealed mild anemia with a C-reactive protein of 16 mg/dL and an erythrocyte sedimentation rate of 31 mm/h
    .

    Transthoracic echocardiography revealed bi-atrial dilatation
    .

    Ultrasonography of the neck vessels revealed bilateral internal carotid atherosclerotic plaques
    .

     Head MRI showed a small acute ischemic infarction in the lower left parietal lobe, in the watershed area of ​​the middle and posterior cerebral arteries (Fig.
    1A)
    .

    Similar to TCD, TOF sequences suggested local severe stenosis of the left supraclinoid internal carotid artery (Fig.
    1B)
    .

    Figure 1 Non-enhanced MRI and high-resolution MRIA and DWI demonstrate acute ischemic stroke in the left lower parietal lobe (yellow arrow)
    .

    B, TOF shows focal severe stenosis at the level of the left supraclinoid internal carotid artery (white arrow); suspicious focal stenosis is also seen in the right carotid siphon
    .

    C, T1-enhanced HR-MRI shows mural enhancement at the level of the stenosis (yellow arrow)
    .

     Due to the unexplained elevation of C-reactive protein and the isolated nature of the supraclinoid stenosis, unlike mild atherosclerosis in the neck vessels, to further clarify the cause of the intracranial stenosis, high-resolution vessel wall imaging MRI (HR -MRI) (Fig.
    1C), which suggested vasculitis or active atherosclerotic plaque
    .

    Further refinement of the FDG-PET/CTA scan revealed increased glucose uptake throughout the thoracic aorta, 2 subclavian arteries, common carotid arteries, and internal carotid arteries (Figure 2), consistent with the diagnosis of GCA, which was subsequently confirmed by temporal artery biopsy (Figure 2).
    3)
    .

     Figure 2 Whole body 18FDG-PET/CTAA and B showing increased grade 3 mural uptake at bilateral subclavian (A) and common carotid (B) levels (grade 3 is considered consistent with vasculitis according to a review by Nielsen et al.
    ), indicated in pink
    .

     Figure 3.
    Temporal artery biopsy results A and B showing diffuse arteritis, intimal hyperplasia, and lumen stenosis (A) with infiltration of CD68+ lymphocytes between the intima-media and inner elastic lamina
    .

     Due to severe dysphagia and gastrointestinal stasis, intravenous methylprednisolone (0.
    7 mg/kg) was given
    .

    After esophageal sphincter surgery, long-term oral prednisone was changed to slowly tapering, and there was no recurrence at 3-month follow-up
    .

     Discussion GCA usually occurs after the age of 50, more common in women, and the peak incidence is 70 years old
    .

    GCA may be considered for acute ischemic stroke in older adults with stenosis of large intracranial vessels (even in the absence of headache), especially when the typical clinical manifestations are alleviated by steroid therapy for other reasons
    .

    Both HR-MRI and PET-FDG enhancement and uptake patterns can aid clinicians in diagnosis and treatment
    .

    Yimaitong compiled from: Dimancea A, Guidoux C, Amarenco P.
    Minor Ischemic Stroke and a Smoldering Case of Giant-Cell Arteritis: A Case Report.
    Stroke.
    2021 Nov;52(11):e749-e752.
    doi: 10.
    1161/ STROKEAHA.
    121.
    035432.
    Epub 2021 Oct 8.
    PMID: 34619985.
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