Symptoms Of Vertebrobasilar Ischemia Research Articles

Bilateral Sudden Hearing Loss Caused by Basilar Artery Dissection: A Case Report

Bilateral sudden sensorineural hearing loss (SNHL) is rare, but a possible symptom of vertebrobasilar ischemia. A 69-year-old female patient with hypertension and atrial fibrillation presented with bilateral sudden hearing loss and vertigo without other neurological symptoms. On examination, she had left-beating horizontal nystagmus with positive head impulse on the left side. Pure tone audiometry revealed severe SNHL on both sides. Brain computed tomography angiography showed a dissection in the proximal portion of the basilar artery (BA) with occlusion of the mid-BA and bilateral anterior inferior cerebellar arteries (AICA), which confirmed on transfemoral cerebral angiography (TFCA). Left common carotid angiography demonstrated retrograde blood flow into the BA and right AICA via the left posterior communicating artery. During TFCA, her right hearing loss dramatically improved. Nine days later, follow-up TFCA showed an improvement of antegrade flow of the BA and AICA. We suggest that vertebrobasilar ischemia can be suspected in patients with bilateral sudden SNHL who present with risk factors for stroke.

Radial Artery Bypass for Intractable Vertebrobasilar Insufficiency: Case Series and Review of the Literature

Vertebrobasilar insufficiency resulting from embolism, atherosclerosis, or arterial dissection has long been a challenge for successful management and outcomes. The main treatment options include medical therapy, angioplasty and stenting, and surgical revascularization. Unlike cardiac or peripheral vascular revascularization, large randomized trials with cerebrorevascularization have not revealed favorable outcomes. In patients who have failed maximal medical therapy, and having persistent debilitating symptomology, cerebral revascularization may still be a viable option. We report 3 patients who presented with symptoms of vertebrobasilar ischemia. The diagnosis was verified by computerized tomographic arteriography and digital subtraction angiography. These patients subsequently underwent revascularization with a radial artery graft. We also present a comprehensive review of the literature of treatment for vertebrobasilar insufficiency. Surgical revascularization should be considered in the posterior circulation in the rare subset of patients with VBI, who remain symptomatic despite having a protracted course of maximal medical therapy with large- and medium-sized vessel occlusions and poor collateral circulation.

Reduced Ischemia in the Medial Vestibular Nucleus after Premedication of Cilostazol and Ginkgo Biloba Extract in Global Hypoperfusion Rat Model

Introduction Approximately 20% of cerebral ischemia is known to develop in the territory of the vertebrobasilar artery and the most common symptoms of vertebrobasilar ischemia (VBI) are dizziness and vertigo [1]. Isolated vertigo without other neurologic symptoms has generally been ascribed to peripheral vestibular diseases [1]. Of the patients with vertigo due to VBI, however, 62% had at least one isolated episode of vertigo, and 19% developed vertigo as the initial symptom [2]. A recent study also found that the patients hospitalized with isolated vertigo have a threefold higher risk for strokes than the general population during the 4year follow-up [3]. Objective: The aim of this study was to determine preventive effects of premedication with combination of cilostazol and ginkgo biloba extract during vertebrobasilar ischemia (VBI) induced by global hypoperfusion in rats. Citation: Lee JO, Kim HJ, Kim JS (2015) Reduced Ischemia in the Vestibular Nucleus after Premedication of Cilostazol and Ginkgo Biloba Extract in Global Hypoperfusion Rat Model. J Neurol Neurol Disord 2(2): 203. doi: 10.15744/2454-4981.2.203

Teaching Neuro Images : Intermittent symptomatic occlusion of the vertebral artery caused by a cervical osteophyte

A 77-year-old man presented with 2 episodes of waking up with symptoms of vertebrobasilar ischemia (figure, A and B) within 6 months. A CT angiogram showed narrowing of the right vertebral artery due to extrinsic compression by an osteophyte of the superior articular process of the fourth cervical vertebra, compromising the foramen transversarium (figure, C and D). Dynamic angiography demonstrated intermittent vascular occlusion associated with head turning (figure, E-G). After recurrence, surgical decompression of the vertebral artery was performed. Extrinsic compressions of the vertebral artery is rare.(1) The most frequent signs are those of vertebrobasilar insufficiency. Surgical treatment has been proposed when conservative management fails.(1).

Vertebrobasilar Occlusion Presenting as Sudden Isolated Bilateral Sensorineural Hearing Loss: Case Report

Isolated bilateral deafness is a rare but possible symptom of vertebrobasilar ischemia, primarily due to occlusion of the anterior inferior cerebellar arteries or their branch, the internal auditory artery. We reported on uncommon case of sudden bilateral sensorineural hearing loss without typical neurological symptoms resulting from vertebrobasilar ischemia. We performed the available examinations, including otoscopy, laboratory tests, and pure tone audiogram, however we were not able to identify the cause of bilateral sensorineural hearing loss. Brain magnetic resonance image showed the cerebellar infarction of the posterior inferior cerebellar artery territory. Brain magnetic resonance angiography showed bilateral vertebral and basilar artery occlusion. We suggest vertebrobasilar ischemia as a cause of sudden isolated deafness.

Atypical suboccipital vertebral artery blood flow in healthy subjects: Case studies using real-time ultrasound

Manual therapists and other professionals are using real-time ultrasound increasingly to visualize vessels and determine their diameter and blood flow. Four case studies are presented to show atypical ultrasound profiles of the suboccipital vertebral artery (VA3) in healthy, young individuals. VA3 diameters and blood flow velocities were measured with the subjects sitting, and the cervical spine in the neutral position then with active, full-range rotation to the left and right. None of the subjects reported any signs or symptoms of vertebrobasilar ischemia (VBI) during the measurement procedure, despite an absence of typical VA3 ultrasound profiles on one side in two of the individuals and a decreased unilateral VA3 blood flow in the other two subjects. Possible reasons for the atypical findings are proposed. Anatomical variations of VA3 and conditions such as obesity may give rise to atypical real-time ultrasound measurements of VA3 blood flow, particularly when associated with cervical spine rotation. The possibility of altered VA3 blood flow because of such factors, which may give rise to false-positive or false-negative findings in the standard VBI test, should be considered by manual therapists in pretreatment assessments and treatment programs in professional practice.

Endovascular Treatment of Supra-Aortic Extracranial Stenoses in Patients with Vertebrobasilar Insufficiency Symptoms

Stenoses and thromboses of vessels feeding the vertebrobasilar territory can evoke serious disturbances including ischemic stroke. We present our experience of endovascular interventions for patients with signs of vertebrobasilar insufficiency (VBI) resulted from subclavian, vertebral and brachiocephalic arterial stenoses. Twenty-one patients (10 men) aged from 35 to 84 years (mean 64.3 years) with symptoms compatible with VBI underwent balloon angioplasty and stenting of subclavian (SA), innominate (IA) and vertebral (VA) arteries. Procedures were done by radiologists experienced in systematic stenting of the lesions. VBI was manifested by persistent signs in 15 patients, and by transitory ischemic attacks in the posterior circulatory territory in 4 (19%). Two patients (10%) experienced ischemic strokes (in the vertebrobasilar circulation in both cases). In 3 patients (14%) VBI was accompanied by upper limb vascular insufficiency symptoms. All cases were resistant to medical treatment. A neurologist assessed complaints, initial VBI signs and their alteration after intervention in all patients. Outcomes were measured with the 5-point scale suggested by Malek et al.: (1) excellent result (asymptomatic, no neurologic deficits and no symptoms of vertebrobasilar ischemia); (2) good (no neurologic deficits, at most one transient episode of vertebrobasilar ischemia over a period of 3 months after treatment); (3) fair (minimal neurologic deficit and at most one transient episode per month of vertebrobasilar ischemia); (4) poor (no improvement compared with neurologic status before treatment and/or persistent symptoms of vertebrobasilar ischemia); (5) death (regardless of cause). Endovascular treatment was performed for SA stenosis in 15 patients, for SA occlusion in 2, for IA stenosis in 2, and for VA stenosis in 2. There were 15 cases of atherosclerosis, 2 of aortoarteritis, 4 of proximal SA kinking. SA and IA stenoses ranged from 60% to 100% (mean 74.5%), VA stenoses were 90% in both cases. Initial technical success was achieved in 96% of cases. There were no postprocedural complications or deaths. During 6-36 months (mean 21.3 months) of follow-up all patients showed improvement in VBI symptoms or upper limb ischemia. Within 36 months after the procedure outcomes were estimated as excellent and good in 13 patients (76%) and poor in 2 (12%), the last being attributed to atherosclerosis progression in other vascular areas. Restenosis in the stented area has developed in 1 patient (6%). Balloon angioplasty and stenting of extracranial vertebrobasilar arterial stenoses appeared to be effective in endovascular treatment of medically resistant VBI. Further investigations are required to clarify the role of subclavian artery kinking in VBI development and indications for various methods of its correction.

Sudden deafness in vertebrobasilar ischemia: clinical features, vascular topographical patterns and long-term outcome

Background and purpose The aim of this study is to document the clinical features and natural history of sudden deafness associated with vertebrobasilar ischemia (VBI) and to describe the vascular topographic patterns of ischemic lesions on brain MRI associated with sudden deafness based on data collected from a prospective acute stroke registry. Methods From 364 consecutive cases of VBI diagnosed by clinical features and brain MRI between January 2000 and September 2003, 29 patients were identified as having sudden deafness as a symptom of VBI. Results In our series, the incidence of sudden deafness following VBI is 8.0% (29/364). Hearing loss occurred unilaterally ( n=27) or bilaterally ( n=2). All but one had vertigo as an associated symptom. Nine patients (31%) presented with an isolated audiovestibular loss initially and subsequently had delayed neurological deficits. Nearly a half of patients (14/29: 48%) showed cochlear features of hearing loss. Seventeen (81%) of 21 patients who were followed for at least 1 year after onset of sudden deafness had a recovery of hearing partially (n=10) or completely (n= 7). The improvement rate of hearing loss in patients with profound hearing loss was significantly lower than that in patients with less than profound hearing loss (40% vs. 89%, P<0.01). In addition to infarction in the territory of anterior inferior cerebellar artery ( n=23), cerebellar infarction in the territory of the medial branch of posterior inferior cerebellar artery ( n=4) or an isolated brainstem infarction ( n=2) was also associated with sudden deafness. Conclusion An isolated sudden deafness with cochlear audiometric features can be the initial presentation of VBI. Sudden deafness due to VBI often has a good outcome. There is topographic heterogeneity of ischemic lesions on brain MRI in patients with sudden deafness due to VBI.

Delayed sequelae of vertebral artery dissection and occult cervical fractures

We report three patients who developed delayed (ie, more than a week after the injury) symptoms of vertebrobasilar ischemia following motor vehicle accidents. The patients all had angiographic evidence of vertebral artery dissection and, upon further evaluation, occult fractures of the second cervical vertebra that were not detected by simple cervical spine radiography and required polytomography or CT for diagnosis. Vertebral artery dissection can result from occult cervical spine fractures and may present with delayed symptoms of brain ischemia.

Vertigo of Vascular Origin

To the Editor. —We were pleasantly surprised to see the article Vertigo of Vascular Origin: Clinical and Electronystagmographic Features in 84 Cases, by Drs Grad and Baloh, 1 in which the authors review the findings of 84 patients who were referred for consultation because of vertigo. A diagnosis of ischemia in the territory of the vertebrobasilar circulation was made. There was a high incidence of isolated episodes of sudden-onset vertigo, and, in some instances, these attacks preceded other symptoms of vertebrobasilar ischemia by months. Vascular insufficiency as the cause of vertigo has not received appropriate emphasis. One author 2 in summarizing peripheral and systemic causes of dizziness does not mention the internal auditory artery and the possible effects of occlusion of that artery or its branches. Little has been written about the interruption of the vascular supply to the inner ear as a potential cause of vertigo, although in a