Hemodynamics of the vertebral artery in subclavian steal syndrome and subclavian steal phenomenon]

To evaluate hemodynamics of the vertebral artery (VA) in subclavian steal syndrome (SSS) and subclavian steal phenomenon (SSP), blood flow velocities of the bilateral VAs were measured by duplex ultrasonography in four patients with SSS and eight patients with SSP. The reversal of flow in the VA was noted in both systolic and diastolic phases in all of the SSS group, and was recorded only in a systolic phase in all but one of the SSP group. The antegrade mean flow velocities in the VA on the unaffected side in the SSS group were significantly higher than those in the SSP group. This indicates that collateral blood flow through the VA in the SSS group is still insufficient to compensate the blood requirement of the upper extremity on the affected side. In conclusion, hemodynamics of the VA in the SSS group could be distinguished from those in the SSP group by duplex ultrasonography.     

Basilar artery blood flow during head rotation in vertebrobasilar ischemia

Patients and methods – Forty-six patients with vertebrobasilar ischemia and 40 control subjects were examined during head rotation using transcranial Doppler ultrasonography. Results – In the control group, no difference in blood flow velocity through the BA was found between the neutral and rotated positions. Based on these data, a blood flow reduction in the BA of more than 20% was considered to be significantly abnormal (p < 0.01). In three of 46 patients no signal was detectable in the BA using TCD. The reduction in blood flow velocity through the BA during head rotation was strongly dependent on the condition of the VA; none of 23 patients without atherosclerotic lesions or hypoplasia of the VA developed a significant reduction in blood flow through the BA. Two of 11 patients with unilateral VA lesions had significantly reduced blood flow in the BA (27% and 31%), although both were asymptomatic. Five of nine patients with bilateral VA lesions showed a significant reduction in blood flow through the BA (mean = 52%, minimum = 30%), and four of these developed clinical symptoms such as vertigo or diplopia during the rotation maneuver. Conclusion – These data suggest that patients with uni- or bilateral lesions of the VA are at risk for developing clinically relevant reductions in blood flow through the BA during head rotation. Because not all patients with VA lesions developed reduced blood flow velocity, we conclude that individual vascular mechanisms must play an important compensatory role.     

转颈对眩晕患者基底动脉流速的影响

目的　采用TCD观测转颈对正常人及眩晕患者基底动脉流速的影响。方法　正常对照组 3 6例 ,眩晕患者 3 1例 ,TCD常规检查椎 -基底动脉及转颈时基底动脉流速的变化。结果　正常人随年龄增大 ,椎 -基底动脉流速下降 ,转颈前后基底动脉流速差异无显著性 ;眩晕患者椎 -基底动脉流速下降 ,转颈后基底动脉流速明显下降 ,较转颈前差异有显著性 (P <0 .0 5 )。结论　转颈后基底动脉流速下降≥ 2 0 % ,即为转颈试验阳性 ,提示患者椎—基底动脉系统代偿能力差 ,存在椎动脉狭窄等病变的可能 ,需进一步检查     

Chronic brainstem ischemia in subclavian steal syndrome

Subclavian steal syndrome is usually an incidental finding and rarely causes vertebrobasilar ischemia. We present a 58-year-old man who, over six months, experienced progressive slowing in both talking and walking. Cervical duplex sonography revealed severe stenosis of the right subclavian artery; fixed retrograde flow was noted in the right vertebral artery on transcranial Doppler. The hyperemia–ischemia cuff test resulted in considerable reduction in flow velocities in both posterior cerebral arteries. We attributed his slowness to chronic vertebrobasilar ischemia and surgical revascularization was performed. His symptoms subsided immediately after surgery. The improved perfusion in the posterior circulation was demonstrated on technetium-99 hexamethylpropyleneamine oxime single photon-emission CT. Early diagnosis and prompt treatment resulted in an improved quality of life.     

Das sog. subclavian steal syndrome

Zusammenfassung Das subclavian steal syndrome ist eine nicht seltene Ursache cerebraler Durchblutungsstörungen, die mit passageren rezidivierenden Seh- und Gleichgewichtsstörungen und mit flüchtigen mitunter nur subjektiv faßbaren Halbseitenerscheinungen einhergehen. Das pathologisch-anatomische Substrat ist eine fast ausschließlich atheromatös-thrombotisch bedingte Stenose oder Occlusion der proximalen Subclaviaanteile vor Abgang der A. vertebralis, das pathophysiologische Kriterium dieser klinischen Symptome eine basiläre Mangeldurchblutung infolge Stromumkehr in der homolateralen A. vertebralis zur kollateralen Armversorgung auf Kosten des Basialis-Kreislaufes (steal). Da — besonders im Alter — die Anpassungsfähigkeit an Sauerstoffmangel bei cerebralen Zentren wesentlich geringer ist als beim Bewegungsapparat, wird bei Belastung des Kollateralsystems die funktionelle Kompensationsfähigkeit dieser Zentren eher verloren gehen, d. h. klinisch steht die Symptomatik der basilären Insuffizienz (claudicatio cerebellaris et vestibularis) gegenüber der der peripheren arteriellen Mangeldurchblutung des Armes (pulseless disease) im Vordergrund. Das diagnostische Verfahren der Wahl ist — nach dynamischer klinischer Diagnostik — die retrograde Aortenbogenangiographie von der A. femoralis nach Seldinger. Therapeutisch stehen operative (Thrombendarteriektomie, Gefäßplastiken) und konservative Maßnahmen zur Verfügung. Besprechung der vielfältigen klinischen Symptomenkonstellationen in Abhängigkeit von anatomischen Varianten des brachiocephalen Gefäßsystems und der häufigen Multiplizität atheromatöser Strömungshindernisse.Als Beitrag zur Kasuistik wird der Befund eines vierjährigen Jungen dargelegt, bei dem hämodynamisch nach dem percutanen Vertebralisangiogramm ein Strömungshindernis im Anfangsteil des Truncus brachiocephalicus mit subclavian steal vorlag. An Hand des Alters, der fehlenden klinischen Symptomatik und des auffällig weitlumigen Vertebralis-Basialis-Systems wird eine aortenbogennahe dysontogenetische Störung (Stenose, Atresie) ursächlich vermutet. Eine autoptische Klärung war nicht möglich.Eingehendes Referat der einschlägigen anglo-amerikanischen und französischen Literatur.

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Summary A subclavian steal syndrome is not infrequently a cause of impaired cerebral circulation. Transitory and recurrent symptoms involve disturbances of equilibrium and vision associated with unilateral neurological signs. A stenosis or occlusion of the proximal part of the subclavian artery, before the origin of the vertebral artery, are the pathological-anatomical substrates. Pathophysiologically, there is a poor basilar circulation due to a reversed collateral blood flow through the homolateral art. vertebralis, in favour of the brachial blood supply (steal). Clinically, symptoms of failing basilar blood flow (claudicatio cerebellaris et vestibularis) are more conspicuous than the signs of circulatory insufficiency of the arm (pulseless disease). This phenomenon is caused by the poor ability of the central nervous system to compensate for functional losses during hypoxemia as compared with the motor system, especially at older ages and during physical strain. In supplementing the clinical diagnosis, retrograde angiography of the aortic arch by way of the femoral artery according to Seldinger is the method of choice.As to the treatment, surgical (thrombarteriectomy, replacement with synthetic material) and conservative measures are employed. Various clinical patterns are discussed and their relationship to anatomical variants of brachiocephalic vessels and atheromatous obstructions, frequently multiple, are considered.A case report of a 4 years old boy is given. Percutaneous vertebral angiography disclosed the hemodynamic equivalent of a circulatory obstruction in the initial part of the brachiocephalic truncus and subclavian steal. A dysontogenetic disorder (stenosis, atresia) near the aortic arch was suspected because of the patient's age, absence of clinical symptoms and strikingly wide lumina of the vertebral and basilar vessels. Verification by autopsy was not possible. The relevant Anglo-American and French literature is reviewed.

     

Basilar artery blood flow velocity changes in patients with panic disorder following 35% carbon dioxide challenge

PURPOSE: We compared the mean basilar artery blood flow velocity (BABFV) between patients with panic disorder and healthy subjects both at rest and immediately following carbon dioxide (CO(2)) challenge, and examined the effects of treatment on BABFV. METHODS: Twenty four patients with panic disorder with or without agoraphobia and 12 healthy comparison subjects were studied. Visual Analog Anxiety Scale was used to evaluate the anxiogenic effect of 35% CO(2) inhalation. Mean BABFV was monitored using transcranial Doppler ultrasonography at rest and 10, 20, 30, 60, 90, 120 s after 35% CO(2) challenge both before and after four weeks treatment with paroxetine. RESULTS: The hemodynamic response pattern of basilar artery to CO(2) inhalation was significantly different between two groups. CO(2) rapidly triggered blood flow velocity in basilar artery amongst panic patients but not in healthy comparisons. The mean time to normalization of BABFV was significantly longer in panic patients. Four weeks of treatment with paroxetine led to a significantly reduced mean BABFV after 35% CO(2) inhalation in comparison with pretreatment. CONCLUSIONS: Patients with panic disorder had impaired cerebral regulatory mechanisms observed as a change in response characteristics in BABFV in response to CO(2) inhalation. Treatment with paroxetine reduced the increase of BABFV seen in patients after the CO(2) challenge.     

Risk of stroke in imaging-proven subclavian steal syndrome

To determine the risk of stroke in patients with subclavian steal syndrome (SSS). We identified 165 patients with imaging-proven SSS from two hospitals. Demographic, clinical and imaging data were retrospectively collected. Patients were followed up for stroke events. Stroke occurred in 43 patients with a median follow-up of 28 months. Seven of these cases were identified prospectively and 36 cases retrospectively. On multivariate analysis, presence of symptoms at presentation (p = 0.029) was a significant predictor of stroke. Presence of symptoms at presentation predicted stroke in imaging-proven SSS.     

Basilar artery occlusion

The clinical presentation of basilar artery occlusion (BAO) ranges from mild transient symptoms to devastating strokes with high fatality and morbidity. Often, non-specific prodromal symptoms such as vertigo or headaches are indicative of BAO, and are followed by the hallmarks of BAO, including decreased consciousness, quadriparesis, pupillary and oculomotor abnormalities, dysarthria, and dysphagia. When clinical findings suggest an acute brainstem disorder, BAO has to be confirmed or ruled out as a matter of urgency. If BAO is recognised early and confirmed with multimodal CT or MRI, intravenous thrombolysis or endovascular treatment can be undertaken. The goal of thrombolysis is to restore blood flow in the occluded artery and salvage brain tissue; however, the best treatment approach to improve clinical outcome still needs to be ascertained.     

Basilar artery occlusion

Basilar artery occlusion is assumed to carry a grave prognosis, with mortality rates of up to 90%. Diagnosis is often delayed, or even missed, as a result of the variety of clinical presentations seen with this condition. The pathogenesis of occlusion can be secondary to both local atherothrombosis or cardioembolism. The use of noninvasive imaging such as magnetic resonance imaging and computed tomography angiography has improved recognition of clinical syndromes associated with occlusion. Although no randomized studies have been performed, recanalization of the vascular occlusion, particularly with thrombolytic agents, appears to result in improved outcomes in selected patients. However, the optimum timing for therapy is unclear, and reperfusion therapy may need to be combined with definitive vascular treatment of underlying vascular stenosis. Increasing awareness of this condition may reveal the natural history to be more diverse than previously recognized.     

Whole body shaking due to intracranial blood flow steal

Unilateral limb shaking has been described as brief, repetitive jerking movements of arm and leg, resembling seizures and attributed to transient cerebral ischemia. We report a patient with numerous episodes of whole body shaking in the setting of bilateral carotid occlusions as well as vertebral stenoocclusive disease. These episodes of whole body shaking occurred in the presence of bilateral intracranial blood flow steal phenomenon. After angioplasty of the vertebral artery and initiation of aggressive medical therapy and non-invasive ventilatory correction, intracranial blood flow improved and whole body shaking episodes were resolved during 6-months follow-up.     

Basilar artery occlusion in rats

The basilar artery is one of the three major sources of blood supply to the circle of Willis. To investigate the effects of basilar artery occlusion, we surgically exposed and coagulated the basilar artery in 25 rats. Basilar artery occlusion at any single point between the foramen magnum and the circle of Willis in 11 rats did not produce histologically detectable infarcts in the brain at 12-24 hours. Two-point occlusions of the basilar artery in 12 rats produced variable infarcts between the occlusion sites but no ischemic lesions elsewhere. After either single- or double-point occlusions, the proximal basilar artery refilled within 2-3 minutes. When the basilar artery was occluded above and below the origins of the anterior inferior cerebellar arteries, the artery segments between the occlusion points initially collapsed but refilled within 2-3 minutes in two rats. Basilar artery occlusions invariably suppressed cortical somatosensory evoked potentials by greater than 50%. Regardless of whether a brain stem infarct developed, somatosensory evoked potential amplitudes recovered to greater than baseline levels by 4 hours in seven of 17 rats and returned to baseline levels by 24 hours in every rat tested. We conclude that the occluded basilar artery receives extensive retrograde collateral blood flow and that somatosensory evoked potentials are exquisitely sensitive to basilar artery occlusion but are insensitive to whether brain stem infarcts develop.     

锁骨下动脉盗血综合征五例临床分析

目的探讨锁骨下动脉盗血综合征(SSS)的临床特点,提高临床医师对本病的认识,降低误诊率。方法分析2008年至2010年9月我科收治的锁骨下动脉盗血综合征患者5例,就其临床表现、经颅多普勒超声(TCD)、彩色多普勒血流显像(CDFI)、数字减影血管造影(DSA)结果以及治疗预后进行分析。结果 TCD为锁骨下动脉盗血的及早诊断和治疗提供了依据,DSA是确诊锁骨下动脉盗血的金标准。结论锁骨下动脉盗血临床表现多样,易误诊漏诊,确诊依靠DSA。DSA结合临床表现,对诊断SSS和选择治疗方案有重要价值。     

Basilar artery stroke in childhood

Aim Little is known about basilar artery stroke (BAS) in children. The objective of this study was to calculate the incidence of BAS in children and to analyse the clinical presentation, risk factors, radiological findings, therapeutic approaches, and outcome of BAS in childhood. Method A prospective, population‐based study including children with arterial ischaemic stroke and a systematic review of the literature was undertaken. Results Seven children with BAS were registered at the Swiss Neuropaediatric Stroke Registry between January 2000 and June 2011 (incidence 0.037 per 100 000 children per year, 95% confidence interval [CI] 0.013–0.080). A further 90 cases were identified through the literature search. The majority of patients were male (73 males, 24 females) and the median age was 9 years (interquartile range [IQR]=6–13y). The median Pediatric National Institutes of Health Stroke Scale (PedNIHSS) score was 15 (IQR=4–27). Presenting signs and symptoms comprised impaired consciousness (n=64), quadri‐ or hemiparesis (n=58), bulbar dysfunction (n=46), vomiting, nausea (n=43), and headache (n=41). Prodromes occurred in 43% of cases. Aetiology was largely vasculopathic (n=38), but often unknown (n=40). Time to diagnosis varied from hours days; six patients received antithrombotic, thrombolytic, or mechanical endovascular treatment 12 hours or less after symptom onset. Outcome was good (modified Rankin Scale 0–2) in 45 patients; eight died. PedNIHSS score of up to 17 was a prognostic factor for good outcome. Interpretation BAS is rare in children. Compared with adults, outcome is more favourable despite a considerable delay in diagnosis and treatment. Outcome was better in children with a PedNIHSS score of 17 or less.