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Clinical and pathophysiological features of amaurosis fugax in Japanese stroke patients
1Fourth Department of Internal Medicine, Aichi Medical University, Nagakute.
Insights
Amaurosis fugax (AmF) in Japanese patients is primarily caused by thromboembolism from intracranial carotid artery atheromatous lesions. Less common causes include external carotid artery micro-thromboemboli or hemodynamic insufficiency.
Area of Science:
- Neurology
- Vascular Medicine
- Ophthalmology
Background:
- Amaurosis fugax (AmF) is often attributed to extracranial carotid artery (EC-CA) atherothrombosis in Caucasians.
- Limited research exists on AmF in Japanese populations.
Purpose of the Study:
- To investigate the clinical and pathophysiological features of AmF in Japanese patients.
- To elucidate the pathogenetic mechanisms of AmF in this demographic.
Main Methods:
- Analysis of 43 Japanese AmF patients from a cohort of 2,056 acute ischemic stroke patients.
- Utilized angiography and transcranial Doppler ultrasonography (TCD).
- Examined precipitating factors, treatment, and prognosis.
Main Results:
- Intracranial lesions identified in 51% of patients, extracranial in 37%.
- Thromboembolism originated from the internal carotid artery (ICA) in 25 patients.
- Micro-emboli from the external carotid artery (ECA) or hemodynamic insufficiency were less frequent causes.
Conclusions:
- AmF in this Japanese cohort is predominantly linked to atheromatous disease of the intracranial carotid artery (IC-CA).
- ECA micro-thromboembolism and hemodynamic insufficiency are potential, though less common, etiologies for AmF.
Objective:
It has been emphasized that amaurosis fugax (AmF) is caused by thromboembolism due to atheromatous lesions of the extracranial carotid artery (EC-CA) in Caucasian populations. However, there have been few studies of AmF in Japan. We analyzed the clinical and pathophysiologic features of AmF in 43 Japanese AmF patients.
Subjects And Methods:
Forty-three patients presented with AmF from a group of 2,056 Japanese patients with acute ischemic stroke. We investigated angiographic and transcranial Doppler findings, precipitating factors, medical treatment and prognosis, to elucidate the pathogenetic mechanism of AmF.
Results:
Angiographic findings revealed an intracranial lesion in 22 patients (51%), extracranial lesion in 16 (37%), and no abnormality in 5 (12%). Blood flow in the ophthalmic artery (OA) examined by the transcranial Doppler ultrasonography (TCD) showed normal antegrade flow in 24 patients and reversed flow in 7. Precipitating factors for AmF were seen in 7 out of 43 patients. Regarding the pathogenesis of AmF, the micro-thromboembolism originated from the internal carotid artery (ICA) in 25 patients, the thromboembolism was via the external carotid artery (ECA) in 7, the hemodynamic retinal vascular insufficiency in 6 patients showed various atheromatous changes in the intracranial carotid artery (IC-CA) or EC-CA, and the cause was unknown in 5.
Conclusion:
In this series of patients, AmF was mainly caused by thromboembolism from IC-CA atheromatous lesions. Micro-thromboemboli from the ECA or hemodynamic retinal vascular insufficiency, although less frequent, should also be considered as possible etiologies for AmF.