Keun-Hwa Jung1, Jeong-Min Kim2, Soon-Tae Lee2, Kon Chu2, Jae-Kyu Roh3. 1. Department of Neurology, Biomedical Research Institute, Seoul National University Hospital, Seoul, South Korea; Program in Neuroscience, Neuroscience Research Institute of Seoul National University Medical Research Council, College of Medicine, Seoul National University, Seoul, South Korea. Electronic address: jungkh@gmail.com. 2. Department of Neurology, Biomedical Research Institute, Seoul National University Hospital, Seoul, South Korea; Program in Neuroscience, Neuroscience Research Institute of Seoul National University Medical Research Council, College of Medicine, Seoul National University, Seoul, South Korea. 3. Department of Neurology, Biomedical Research Institute, Seoul National University Hospital, Seoul, South Korea; Program in Neuroscience, Neuroscience Research Institute of Seoul National University Medical Research Council, College of Medicine, Seoul National University, Seoul, South Korea. Electronic address: rohjk777@gmail.com.
Abstract
BACKGROUND: Chronic, repetitive, and sublethal hypoperfusion by intra- or extracranial artery stenosis promotes collateral development and conditions the brain toward preventing subsequent lethal ischemia, although these latent properties have rarely been demonstrated in the clinical setting. This study assessed the previously unexplored role of subclavian steal syndrome (SSS) on inciting and protecting brain damage. METHODS: We enrolled patients diagnosed with SSS associated with subclavian artery stenosis. Subclavian steal was determined by transcranial Doppler and/or digital subtraction angiography. We analyzed the prevalences and predictors of posterior ischemic symptoms and infarcts in SSS patients and also investigated individual cases to demonstrate a clinical evidence of brain conditioning, focusing on cytotoxic and vasogenic edema. RESULTS: Of 54 SSS patients, 36 (66.7%) had been asymptomatic and incidentally diagnosed with SSS, whereas 18 (33.3%) patients had presented with posterior ischemic symptoms. Symptoms and infarcts including old silent lesions occurred more frequently as unstable hemodynamics of the anterior circulation were combined. Of 18 symptomatic patients, 13 patients (72.2%) had transient ischemic attack and 5 (27.8%) patients had an infarct in the posterior circulation territory. Four patients with cytotoxic edema had mild neurologic deficits and rapid and complete recovery, whereas 1 patient had prolonged, severe vasogenic edema after acute hypertension. CONCLUSIONS: Although we noted low rates of disabling or fatal strokes in patients with SSS, a variety of vascular and neural factors beyond severity of subclavian steal could influence the likelihood of brain damage.
BACKGROUND: Chronic, repetitive, and sublethal hypoperfusion by intra- or extracranial artery stenosis promotes collateral development and conditions the brain toward preventing subsequent lethal ischemia, although these latent properties have rarely been demonstrated in the clinical setting. This study assessed the previously unexplored role of subclavian steal syndrome (SSS) on inciting and protecting brain damage. METHODS: We enrolled patients diagnosed with SSS associated with subclavian artery stenosis. Subclavian steal was determined by transcranial Doppler and/or digital subtraction angiography. We analyzed the prevalences and predictors of posterior ischemic symptoms and infarcts in SSS patients and also investigated individual cases to demonstrate a clinical evidence of brain conditioning, focusing on cytotoxic and vasogenic edema. RESULTS: Of 54 SSS patients, 36 (66.7%) had been asymptomatic and incidentally diagnosed with SSS, whereas 18 (33.3%) patients had presented with posterior ischemic symptoms. Symptoms and infarcts including old silent lesions occurred more frequently as unstable hemodynamics of the anterior circulation were combined. Of 18 symptomatic patients, 13 patients (72.2%) had transient ischemic attack and 5 (27.8%) patients had an infarct in the posterior circulation territory. Four patients with cytotoxic edema had mild neurologic deficits and rapid and complete recovery, whereas 1 patient had prolonged, severe vasogenic edema after acute hypertension. CONCLUSIONS: Although we noted low rates of disabling or fatal strokes in patients with SSS, a variety of vascular and neural factors beyond severity of subclavian steal could influence the likelihood of brain damage.