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Internal carotid artery stenosis associated with giant cell arteritis: case report and discussion.
Journal of Vascular and Interventional Neurology 2014 December
BACKGROUND: Cerebrovascular ischemic events associated with giant cell arteritis (GCA) are uncommon and have been reported in 3%-4% of patients. We describe a case report of GCA associated with intracranial stenosis and review various angiographic findings.
CASE PRESENTATION: A 66-year-old man presented with worsening headache and vision loss. A recent magnetic resonance angiogram of the head and neck showed multiple intracranial stenosis. Cerebrospinal fluid (CSF) analysis demonstrated increased protein of 135.6 mg/dL, with two white blood cells/µL. No bacteria were observed in the CSF on gram staining, and cultures were negative for bacterial growth. Erythrocyte sedimentation rate was noted to be 14 mm/h, and C-reactive protein was 1.514 mg/L at admission. Human immunodeficiency virus (HIV) and hepatitis panels were negative. On digital subtraction angiography, patient had predominantly narrowing and irregularities in petrous and cavernous segments of the internal carotid arteries bilaterally. The diagnosis of GCA was confirmed by temporal artery biopsy. He was treated with steroids, and a followup angiogram 6 weeks later showed minimal resolution of the angiographic findings. Patient reported complete resolution of headaches and visual loss.
CONCLUSION: Bilateral internal carotid arteries stenosis may be seen in patients presenting with typical symptoms of GCA and may persist after steroid treatment despite resolution of clinical symptoms.
CASE PRESENTATION: A 66-year-old man presented with worsening headache and vision loss. A recent magnetic resonance angiogram of the head and neck showed multiple intracranial stenosis. Cerebrospinal fluid (CSF) analysis demonstrated increased protein of 135.6 mg/dL, with two white blood cells/µL. No bacteria were observed in the CSF on gram staining, and cultures were negative for bacterial growth. Erythrocyte sedimentation rate was noted to be 14 mm/h, and C-reactive protein was 1.514 mg/L at admission. Human immunodeficiency virus (HIV) and hepatitis panels were negative. On digital subtraction angiography, patient had predominantly narrowing and irregularities in petrous and cavernous segments of the internal carotid arteries bilaterally. The diagnosis of GCA was confirmed by temporal artery biopsy. He was treated with steroids, and a followup angiogram 6 weeks later showed minimal resolution of the angiographic findings. Patient reported complete resolution of headaches and visual loss.
CONCLUSION: Bilateral internal carotid arteries stenosis may be seen in patients presenting with typical symptoms of GCA and may persist after steroid treatment despite resolution of clinical symptoms.
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