A 66-year-old woman with chronic myeloid leukaemia in nilotinib-induced remission was diagnosed with amaurosis fugax, caused by carotid stenosis. Serum cholesterol was 316 mg/dL (Low-Density Lipoprotein (LDL) cholesterol 213 mg/dL). Nilotinib was discontinued and replaced by interferon. Antiplatelet therapy and atorvastatin 40 mg/day were prescribed. Muscle pain and elevation of serum creatine kinase (CK) occurred; thus, atorvastatin was replaced by ezetimibe. Afterwards, muscle pain subsided and CK reverted to normal, but 2 years later serum cholesterol was still elevated at 218 mg/dL with LDL cholesterol 126 mg/dL. Simvastatin 5 mg/day was then started, but again muscle pain occurred and CK rose to 267 U/L. Simvastatin was stopped and serum cholesterol climbed to 252 mg/dL. Creatine was prescribed and simvastatin was reintroduced. Two months later, cholesterol was 171 mg/dL, CK was 72 U/L and there was no muscle pain. This case supports the view that creatine may prevent statin-induced myopathy.

In its normal anatomy, the extracranial internal carotid artery (ICA) does not have branches. The most common cause of an extracranial ICA branch is the ectopic placement of one of the named external carotid artery branches. Other causes of extracranial ICA branches include persistent fetal carotid-vertebrobasilar anastomoses and recannalized intersegmental arteries. In this case, report we describe a 55-year-old male who was found to have an ascending pharyngeal artery (APA) arising from the ICA during neck dissection. The aberrant APA was not identified on pre-operative imaging. The patient underwent a successful carotid endarterectomy (CEA) with preservation of flow through the ascending pharyngeal. We review the literature on the origin of the APA and discuss the clinical implications of extracranial ICA branches.

Central retinal artery occlusion (CRAO) is a medical emergency that, if not treated, may result in irreversible loss of vision. It continues to be an important cause for acute painless loss of vision. Amaurosis fugax or "transient CRAO" has long been considered an equivalent of transient cerebral ischemic event. Animal models, in addition to data from retrospective and randomized clinical studies, provide valuable insights into the time interval for irreversible retinal ischemia. Subset analyses from 2 large studies of patients with CRAO show benefit from treatment with thrombolysis within 6 hours from symptoms onset. Significant workflow improvements after the intra-arterial therapy trials for acute ischemic stroke have occurred world over in last 5 years. Patients with CRAO are uniquely suited to receive maximum benefits from the changes in workflow for treatment of patient's acute ischemic stroke. Just as in clinical triage of acute ischemic stroke, correct and timely diagnosis of patients with CRAO may help in preventing visual loss. The approach to acute ocular ischemia should mimic that used for acute brain ischemia. Comprehensive stroke centers would be ideal triage centers for these patients in view of availability of multidisciplinary participation from vascular neurology, neuroendovascular surgery, and ophthalmology. Time is Retina!

Ulceration of carotid arterial plaque is associated with cerebral events. Detection of ulcerated plaques will benefit patient from stroke and other ischemic events. The aim of this study was to evaluate morphology of atherosclerotic plaques in the carotid arteries and to assess its clinical impact in predicting cerebral events.A total of 386 patients were examined with 256-multislice spiral computed tomographic angiography (MSCTA).It was found that 356 of the 386 patients had cerebral ischemic symptoms. Specifically, 35 patients had amaurosis fugax (AmF), 178 had transient ischemic attack (TIA), and 143 had ischemic stroke. Abnormal images were found in 658 carotid arteries by MSCTA. Of the 658 abnormal images of carotid arteries, besides the 34 cases of carotid arterial occlusion, 624 cases were atherosclerotic plaques. Of the 624 plaques, 394 (63.2%) were smooth surface plaques, 161 (25.8%) were irregular surface plaques, and 69 (11.1%) were ulcerated plaques. Incidence of ulcerated plaque was higher in the ischemic stroke patients (13.1%) compared with that in the TIA group (10.3%), AmF group (6.6%), or symptom-free group (9.4%) although it was not statistically significant (P = .288). However, there was significant difference in the incidence of ischemic stroke between the ulcerated (20/69, 28.9%) and nonulcerated groups (69/555, 12.4%, P < .05, odds ratio = 2.875).These findings suggested that 256-MSCTA is an advanced imaging tool to determine not only arterial stenosis but also morphologic assessment of atherosclerotic plaques, which will benefit the patients by predicting the cerebral events in advance.

Carotid stump syndrome is defined as the persistence of retinal or cerebral ischaemic events with complete occlusion of the ipsilateral internal carotid artery. The aim of this retrospective cases series was to assess the outcomes for patients with carotid stump syndrome managed with surgical intervention. A series of 11 cases of carotid stump syndrome in nine patients presented to our tertiary vascular centre from October 2004 to February 2016. Indications for intervention were amaurosis fugax, transient ischaemic attacks and stroke. In total, 11 procedures were performed on nine patients including carotid angioplasty and stenting or carotid endarterectomy with patching. The mean follow-up period was 56.6 months. One patient suffered a myocardial infarction 30 days, post-operatively, and one patient was lost to follow-up. In the remaining seven patients, there was a complete resolution of symptoms. There were no incidents of death, stroke, cranial nerve injury, wound haematoma or procedural bleeding. Surgical exclusion of carotid stumps combined with dual antiplatelet agents was found to be a safe and effective treatment method for carotid stump syndrome.

Transient monocular blindness is an acute episode of ischemic origin in which one eye has profound visual loss, followed by full recovery within one hour. Transient monocular blindness most often occurs in the setting of retinal ischemia secondary to carotid embolism, but other mechanisms have been reported, including thrombosis (most often in the setting of giant cell arteritis), hemodynamic disorders (secondary to severe carotid stenosis), or vasospasm. Transient monocular blindness is considered a transient ischemic attack originating in the carotid arteries, and must be managed the same as transient ischemic attack involving the brain, in order to prevent a subsequent stroke.