Bilateral Vertebral Artery Occlusion Research Articles

Progressive Growth of a Giant Dolichoectatic Vertebrobasilar Artery Aneurysm after Complete Hunterian Occlusion of the Posterior Circulation: Case Report

Dolichoectatic vertebrobasilar artery aneurysms are often extremely difficult, if not impossible, to treat with microneurosurgical clip reconstruction. As such, a Hunterian strategy via vertebral or basilar artery sacrifice is often used. We have encountered a patient in whom deliberate bilateral vertebral artery sacrifice was insufficient to avoid progressive expansion of a giant dolichoectatic vertebrobasilar artery aneurysm. On the basis of a review of the literature, we are unaware of another reported case. A 60-year-old man presented with signs and symptoms of brainstem compression from a large fusiform aneurysm involving the distal dominant vertebral and proximal basilar arteries. Results of angiographic evaluation were highly characteristic of underlying dolichoectasia. The patient was treated initially with staged bilateral vertebral artery occlusion and adjunctive posterior circulation revascularization. After this therapy failed, he underwent a trapping procedure and aneurysm deflation. Unclippable aneurysms of the vertebrobasilar system are formidable lesions. They are not uniformly treatable by direct surgical reconstruction, and their growth is not consistently stabilized by the implementation of a complete Hunterian strategy. Future developments related to the use of endovascular stent technology may offer a more successful treatment approach for patients with these complex cerebrovascular lesions.

Takayasu arteritis with multiple intracranial aneurysms. A case report.

A rare case of multiple cerebral aneurysms associated with Takayasu aortitis is reported. Only seven cases have been reported so far, all of which are from Japan. This is the first case with this association being reported from India. A 50-year-old hypertensive woman developed sudden onset severe headache and loss of consciousness. CT scan revealed subarachnoid haemorrhage in the suprasellar cisterns and mild hydrocephalus. The patient on admission had a rebleed producing a massive subarachnoid haemorrhage. Angiogram revealed occlusion of bilateral vertebral arteries and right common carotid artery. The left carotid artery was ectatic with saccular aneurysms in the ophthalmic segment and communicating segment. Aortogram showed the radiological picture of Takayasu arteritis Type III. Surgical clipping of the aneurysms was performed. However, the patient developed a massive right cerebral infarct in the postoperative period following which she expired. Abnormal haemodynamics in the overloaded cerebral circulation rather than primary arteritic involvement of intracranial vessels appears to be the cause of aneurysm formation.

Granulocyte-macrophage colony-stimulating factor-induced arteriogenesis reduces energy failure in hemodynamic stroke.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a powerful arteriogenic factor in the hypoperfused rat brain. To test the pathophysiological relevance of this response, the influence of GM-CSF on brain energy state was investigated in a model of hemodynamic stroke. Sprague-Dawley rats were submitted to three-vessel (bilateral vertebral and unilateral common carotid artery) occlusion (3-VO) to induce unilaterally accentuated brain hypoperfusion. One week later, hemodynamic stroke was induced by additional lowering of arterial blood pressure. Experiments were terminated by in situ freezing of the brain. ATP was measured in cryostat sections by using a bioluminescence method. The use of 3-VO, in combination with 15 min of hypotension of 50, 40, or 30 mmHg, did not produce disturbances of energy metabolism, however, focal areas of ATP depletion were unilaterally detected after 3-VO, in combination with 15 min of hypotension of 20 mmHg. Treating such animals with GM-CSF (40 microg.kg(-1).d(-1)) during the 1-week interval between 3-VO and induced hypotension significantly reduced the hemispheric volume of energy depletion from 48.8 +/- 44.2% (untreated group, n = 10) to 15.8 +/- 17.4% (treated group, n = 8, P = 0.033). GM-CSF-induced arteriogenesis is another approach to protect the brain against ischemic injury.

AMPA/kainate-type glutamate receptor antagonist reduces progressive inner hair cell loss after transient cochlear ischemia

We investigated the effect of glutamate receptor antagonists on progressive inner hair cell (IHC) loss following transient cochlear ischemia in gerbils. Transient cochlear ischemia was induced by 15-min bilateral vertebral artery occlusion. An alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kainate-type glutamate receptor antagonist, 6-7-dinitroquinoxaline-2,3-dione (DNQX), or an N-methyl- d-aspartate (NMDA)-type receptor antagonist, MK-801, was administered 10 min before the ischemic insult. Hearing was assessed by sequentially recording compound action potentials (CAPs) before, during, and after the ischemia. The degree of hair cell loss in the organ of Corti was evaluated in specimens stained with rhodamine–phalloidin and Hoechst 33342. On the seventh day after ischemia, the increases in the CAP threshold and the progressive IHC loss were significantly reduced in cochleae treated with DNQX, while MK-801 was ineffective. These results suggest that the AMPA receptor plays a critical role in the development of the progressive IHC loss induced by ischemia/reperfusion injury in the cochlea.

Arteriogenesis in hypoperfused rat brain.

Experimental and clinical studies have provided evidence for spontaneous and therapeutically induced arteriogenesis after occlusion of major peripheral or cardiac vessels. Such evidence is lacking for the cerebrovascular system. In halothane-anesthetized rats, different degrees of brain hypoperfusion were induced by one- to four-vessel occlusion, that is, one or both common carotid arteries in combination with or without bilateral vertebral artery occlusion. The flow decline was monitored by laser Doppler flowmetry, the residual hemodynamic reserve by testing flow reactivity to ventilation with 6% CO(2) and arteriogenesis by intravascular latex infusion and immunohistochemistry of vascular proliferation and monocyte adhesion. The optimum condition for induction of arteriogenesis was three-vessel (one carotid plus both vertebral arteries) occlusion, which led to reduction of blood flow to about 50% and complete suppression of CO(2) reactivity, but no histologic injury. One week after three-vessel occlusion, the ipsilateral posterior cerebral artery significantly enlarged by 39%, and after 3 weeks by 72%, paralleled by the partial return of CO(2) reactivity and the appearance of immunohistochemical markers of arteriogenesis. Three-vessel occlusion is a reliable model for the induction of arteriogenesis in the adult brain and is a new approach for exploring the potentials of arteriogenesis for the prevention of progressing brain ischemia.

Mouse Models of Global Cerebral Ischemia

Use of rodent models of hippocampal neurodegeneration are recommended for use in studies to understand the pathophysiology and molecular mechanisms involved. This unit includes protocols for two-vessel occlusion, three-vessel occlusion, and permanent bilateral vertebral artery occlusion plus methods for histological techniques for preparation of brain tissue and analysis of hippocampal injury.

Ruptured anterior spinal artery aneurysm: a case report

BACKGROUND Spinal artery aneurysms are rare, and are usually found in association with arteriovenous malformations or coarctation of the aorta. CASE REPORT A 42-year-old man with a ruptured anterior spinal artery aneurysm is presented here. He experienced subarachnoid hemorrhage, which was confirmed by computed tomography. Magnetic resonance imaging revealed an aneurysm in front of the upper part of the medulla. Angiography demonstrated bilateral vertebral artery occlusion. Distal vertebral arteries and the basilar artery were perfused via the dilated anterior spinal artery, which originates in the right subclavian artery. The aneurysm was located at the distal part of the anterior spinal artery, and was successfully clipped through a lateral suboccipital craniotomy 2 months after bleeding from the aneurysm. After rehabilitation, the patient was able to walk with no apparent neurologic deficit. CONCLUSIONS This case suggests that the anterior spinal artery as a collateral route after bilateral vertebral arery occlusion is under hemodynamic stress, resulting in aneurysm formation and rupture.

Simulation of therapeutic parent artery occlusion for basilar head aneurysms. Hemodynamic effect of occlusion sites and diameters of collateral arteries

We simulated parent artery occlusion therapy for basilar head aneurysms to elucidate the hemodynamic changes induced by different occlusion sites and diameters of the posterior communicating arteries (PCom) as collateral pathways. A vascular model of the vertebrobasilar system with a basilar head aneurysm was constructed. Four types of occlusion were simulated: Basilar artery occlusion distal to (Type A)I between (Type B) and proximal to (Type C) the superior cerebellar arteriesl and bilateral vertebral artery occlusion (Type D). Glycerol solution was perfused into the modell and the half-life of the dye injected into the aneurysm was calculated and regarded as an index of stagnant flow in the aneurysm. The half-life was increased ~ignificantly and nonlinearly after parent artery occlusionl depending on the occlusion site and the ratio of two PCom diameters (diameter ratio). Intra-aneurysmal stagnation developed markedly in Type A and Type B in the diameter ratio higher than 0.70 and considerably in Type C in the ratio higher than 0.80. Additional P1 occlusion of the posterior cerebral artery enhanced the stagnation in Type A and B. Since the results are consistent with the published clinical datal the simulation study will be useful for speculating the efficacy of the therapeutic occlusion. [Neurol Res 1999; 21: 180-184]

Reperfusion Therapy for Acute Vertebrobasilar Occlusion

We reviewed retrospectively our experience in treating 10 patients with acute vertebrobasilar occlusion. Nine patients were treated with interventional reperfusion therapy and the remaining one patient with top of the basilar embolism was treated conservatively because of deep coma and decerebrate rigidity with severely reduced cerebral blood flow (CBF) in the brain stem. Among 9 patients with reperfusion therapy, 8 patients underwent intra-arterial thrombolytic therapy and the other one patient had direct percutaneous transluminal angioplasty (PTA). Eight patients had basilar artery occlusion, 1 patient treated with direct PTA had bilateral intracranial vertebral artery occlusion and the other patient had left posterior cerebral artery occlusion presumably preceding top of the basilar embolism. In 4 of 10 patients, residual CBF was evaluated by single photon emission computed tomograpy (SPECT). Successful recanalization with clinical improvement was achieved in 6 of 9 patients (66.7%) treated with reperfusion therapy. In patients with progression or fluctuation of incomplete brain stem syndrome, SPECT revealed preserved residual CBF and successful recanalization with clinical improvement was achieved by interventional reperfusion therapy. On the other hand, in patients with persistent deep coma and decerebrate rigidity, SPECT revealed marked reduction of residual CBF in the brain stem and recanalization could not improve clinical outcome. Preoperative SPECT may be useful to make a decision whether rep er fusion therapy should be performed or not in case of vertebrobasilar occlusion.

Bilateral Vertebral Artery Lesion After Dislocating Cervical Spine Trauma

This case report illustrates the problems associated with diagnosis and management of vertebral artery injuries resulting from dislocating cervical spine trauma. Treatment involved the principles of anterior stabilization of dislocating cervical spine fracture as well as the diagnostic procedures and therapeutic modalities appropriate for vertebral artery lesions. Because vertebral artery injuries with cervical spine trauma are rarely symptomatic, they can easily be overlooked. Bilateral or dominant vertebral artery occlusion, however, may cause fatal ischemic damage to the brain stem and cerebellum. Cervical spine dislocation was stabilized immediately after admission using internal fixation by ventral plate and corticocancellous bone graft. Immediate angiography was performed when brain stem neurologic dysfunction manifested 36 hours after surgery. The patient was treated with anticoagulation, osmotherapy, and controlled hypertension. A fatal outcome resulted in this case of dominant left vertebral artery occlusion. Necropsy even revealed bilateral vertebral artery damage at the level of the osseous lesion. The possibility of the complication of a vertebral artery lesion should be kept in mind when examining patients with cervical spine trauma, especially in patients with fracture-dislocation. Immediate identification by vertebral angiography, magnetic resonance imaging, or thin-slice computed tomography scan is necessary for optimal management of this injury.

Simulation study on bypass and therapeutic occlusion in the posterior circulation.

A hydraulic vascular model of the vertebrobasilar artery with an autoregulatory mechanism was constructed. The haemodynamic effect of superficial temporal artery (STA)-posterior cerebral artery (PCA) bypass was investigated in cases of bilateral vertebral artery (VA) occlusion and basilar artery (BA) occlusion. Assuming therapeutic BA occlusion for basilar bifurcation aneurysms, the flow volume through the P1 segment of the PCA was determined in relation to diameters of the posterior communicating artery (PCom). The bypass increases both flow volume and intraluminal pressure in the presence range below 60 mm Hg, while it increases only pressure in the autoregulatory range above 60 mm Hg. Its haemodynamic effect is more marked in BA occlusion than in VA occlusion. The averaged values of the increase in flow volume are 29.0 +/- 4.3% (mean +/- SD) and 16.5 + 1.0%, respectively. The total flow volume increase of the vertebrobasilar system is usually lower than the flow volume measured at the bypassed STA. The difference between the two is equal to the simultaneous decrease in flow volume through the PComs. Flow volume through the P1 segment can be expressed as a function of the PComs diameter ratio squared. A hydraulic simulation study will be useful for speculating on the haemodynamic effects of these operative procedures.

Causes and mechanisms of territorial and nonterritorial cerebellar infarcts in 115 consecutive patients.

Territorial cerebellar infarcts have mainly a thromboembolic mechanism. Cerebellar infarcts less than 2 cm in diameter have recently been reported as nonterritorial infarcts, but it is not clear whether they are low-flow or embolic infarcts. The aim of the present study was to compare the characteristics and causes of territorial and nonterritorial infarcts in a prospective series of 115 patients. We collected data from 115 consecutive patients with cerebellar infarcts (79 territorial and 36 nonterritorial [ie, less than 2 cm]), using magnetic resonance imaging (88 patients) and computed tomography. Patients with territorial infarcts and those with nonterritorial infarcts had similar vascular risk factors and clinical presentations and an equal frequency of cardiac source of embolism (32% versus 42%; P = NS) and of large artery occlusive disease (23% versus 19%; P = NS). Occlusive lesions of large arteries at angiography occurred at the level of one cerebellar artery (5% versus 0%; P = NS) and proximal to the ostia of the cerebellar arteries (18% versus 19%; P = NS). Infarcts distal to occlusive lesions were subdivided into unilateral vertebral artery occlusive disease (presumed artery-to-artery embolic mechanism; 18% versus 5%; P = NS) and low-flow state distal to bilateral vertebral or basilar artery occlusion (presumed hemodynamic mechanism; 0% versus 14%; P = .004). Patients with nonterritorial infarcts had more frequent hypercoagulable state (17% versus 1.25%; odds ratio, 15.6 [95% confidence interval, 1.8 to 135]). For the remaining patients, the mechanism of the infarct was unknown (34% versus 22%; P = NS). Cerebellar infarcts less than 2 cm in diameter (ie, nonterritorial) have the same high rate of embolic mechanism as territorial infarcts (47% versus 49%; P = NS), have more frequent hypercoagulable state, and sometimes have a hemodynamic mechanism.

Transcranial doppler findings during spontaneous recanalization of vertebrobasilar occlusions

Transcranial Doppler sonography (TCD) is of recognized value in the noninvasive detection of intracranial stenosis and occlusion. Serial TCD studies can detect recanalization of middle cerebral artery occlusion. Little information exists on TCD findings during vertebrobasilar recanalization. We report a 25-year-old woman with chronic meningitis who developed severe pontine and cerebellar infarctions due to bilateral distal vertebral and proximal basilar artery occlusion. Initial TCD showed a high-resistance signal from the distal right vertebral artery and no signal from the basilar artery. Evolutionary changes in flow velocities detected by seven TCD studies over a 5-week period suggested spontaneous recanalization of the distal vertebral and proximal basilar artery occlusion. These findings were accompanied by dramatic clinical improvement. Recurrent symptoms and TCD on day 73 suggested reocclusion, confirmed by repeat angiography. TCD may be useful for monitoring posterior circulation hemodynamics during recanalization of vertebrobasilar occlusions in selected patients.

MR-Angiographie des vertebrobasilären Stromgebiets: Einsatzmöglichkeiten der Saturationstechnik zur Bestimmung der Flußrichtung

MR angiography (MRA) combined with selective saturation techniques has proved to be a reliable method for the determination of flow direction and vascular supply at the level of the circle of Willis. We describe its application to the vertebrobasilar system (VBS) in ten volunteers and five patients with abnormal findings. In one patient with postsurgical stenosis of the brachiocephalic artery, reverse flow of the vertebral artery (VA) was demonstrated. Collateral blood flow from the anterior circulation over the posterior communicating arteries was shown in three patients with bilateral vertebral or proximal basilar artery occlusion. Due to increase of pressure during contrast injection into the contralateral VA, DSA showed reverse flow of a dissected VA in one patient. MR flow determination as well as TCD proved antegrade flow. All results correlated with both DSA and transcranial Doppler (TCD). The technique is little time consuming and is a promising add-on examination to conventional and MRA imaging of the VBS.

Hemodynamic Study of Posterior Circulation Using Hydraulic Vascular Model

A hydraulic vascular model with glass and silicone tubes of the intracranial portion of the vertebro-basilar artery was used to determine the critical stenosis causing vertebrobasilar insufficiency, and the minimum diameter of the posterior communicating arteries (PComAs) necessary to tolerate therapeutic vertebrobasilar occlusion for unclippable aneurysms. The critical stenosis of one vertebral artery (VA) or basilar artery (BA) differed greatly depending upon the anatomical variations of the PComA and the posterior cerebral artery (PCA): 1.14 mm diameter when the artery supplies 80 ml/min to the cerebellum and brainstem only, 1.33 mm when 140 ml/min to these structures and one PCA, and 1.56 mm when 200 ml/min to these structures and both PCAs. The minimum PComA diameter to tolerate therapeutic occlusion depended largely upon the occlusion site: one PComA with 1.54 mm diameter for bilateral VA occlusion and 1.25 mm for BA occlusion distal to the branching of the superior cerebellar arteries. The total volume of collateral flow through both PComAs can be estimated by summing the squares of the diameters. These values cannot be applied rigidly to clinical cases, but are useful standards to evaluate the stenotic lesion or tolerance to occlusion.

Hindbrain Ischemia Produced by Bilateral Vertebral Artery Occlusion and Moderate Hypotension in Spontaneously Hypertensive Rats

Hindbrain ischemia was induced by bilateral vertebral artery occlusion and moderate hypotension in spontaneously hypertensive rats (SHRs). Mean arterial blood pressure was lowered to 80 mmHg in SHRs and to 50 mmHg in Wistar-Kyoto rats (WKYs) by a controlled hemorrhage, and then the vertebral artery was bilaterally occluded through alar foramina of the first cervical vertebra. Following vertebral occlusion, blood flow of the cerebellum was significantly decreased to 9.4 +/- 2.0 mL/100g/min (+/- SEM) while flow of the cerebrum remained at 32.1 +/- 5.4 in SHRs. In contrast, cerebellar blood flow in WKYs was preserved at 24.2 +/- 2.9 mL/100g/min. Brain lactate, pyruvate, and adenosine triphosphate (ATP) were determined in SHRs after sixty minutes of hypotension with or without vertebral occlusion. Although infratentorial metabolites were actually unaltered in rats with hypotension alone, infratentorial lactate and lactate/pyruvate ratio significantly increased to 14.38 +/- 3.61 mmol/kg and 67.7 +/- 12.1, respectively, with a concomitant decrease in ATP in SHRs with hypotension and vertebral occlusion. Bilateral vertebral artery occlusion, together with moderate hypotension, was shown to produce a marked reduction of cerebellar blood flow and to induce ischemic metabolic changes in the infratentorial brain in SHRs.

Arterial pathology in cerebellar infarction.

We reviewed 88 pathologically proven cerebellar infarcts, examining the entire thoracocervical arterial system (including the spinal part of the vertebral artery, the intracranial arteries, and the heart) in all cases. For 50 infarcts, we found an arterial occlusion. The intracranial part of the vertebral artery was involved in 38 infarcts (76%), the basilar artery in 20 infarcts (40%), and a cerebellar artery in 12 infarcts (24%). Eight infarcts were due to bilateral distal vertebral artery occlusions. For the 50 infarcts, the cause of the occlusion was atherosclerosis in 28 (56%) and a cardiac embolism in 12 (24%). For the remaining 38 infarcts, we found no arterial occlusions on postmortem examination. Of these 38 infarcts, 26 (68%) were associated with a cardiac source of emboli. For the entire group of 88 infarcts, atherosclerosis was the cause in 31 (35%), while a cardiac embolism was proven or presumed in 38 (43%). Dissecting aneurysms, atherosclerotic artery-to-artery embolism, or hemodynamic mechanisms could have been responsible for a few infarcts. We conclude that cerebellar infarcts often arise from cardiogenic embolism.

Clinical features of proven basilar artery occlusion.

Our study describes the early symptoms and signs of 85 patients with either basilar artery occlusion or bilateral distal vertebral artery occlusion documented by selective angiography. The most common prodromal symptoms were vertigo, nausea, and headache, which occurred during the 2 weeks before the stroke. Angiographic findings of 49 patients were classified into proximal, middle, and distal basilar artery occlusions. Twenty-two of these patients had additional vertebral artery lesions. A fourth group was composed of 36 patients with bilateral distal vertebral artery occlusion without opacification of the basilar artery through a vertebral artery injection. Onset was sudden in 20 patients; sudden, but preceded by prodromal symptoms in 11 patients; and progressive in 54 patients. Patients with progressive strokes often had bilateral vertebral artery occlusions. Most patients with acute onset had occlusion of the middle and distal basilar artery. An embolic origin of basilar artery occlusion from an arteriosclerotic vertebral artery lesion was assumed to be an important mechanism. An embolus reaching the basilar artery may not necessarily reach the top of the artery, but may also become lodged more proximally.

Giant cell (temporal) arteritis

Dementia occurs infrequently in patients with giant cell (temporal) arteritis (GCA). Three elderly women with biopsy-proven GCA showed abrupt cognitive decline during periods of clinically active GCA, 1 to 6 months after diagnostic temporal artery biopsy, during periods of corticosteroid taper. One patient had additional clinical signs of cerebral infarction and other ischemic phenomena. Reinstitution of higher oral doses of corticosteroids successfully prevented further cognitive losses and permitted gradual but incomplete improvement of cognitive function in 1 patient. Neuropsychologic data from 2 patients 7 to 10 months after temporal artery biopsy suggested multifocal cognitive impairment, and the 3rd patient appeared clinically to be globally, severely demented. Neuroimaging studies revealed multiple areas of infarction, predominantly in the posterior circulation territory. One patient had bilateral vertebral artery occlusions (digital subtraction angiography) and bilaterally reduced carotid system perfusion pressures (oculoplethysmography). There were no associated cardiovascular risk factors or family history of dementia in these patients.

Superficial temporal and occipital artery bypass pedicles to superior, anterior inferior, and posterior inferior cerebellar arteries for vertebrobasilar insufficiency

Eighty-three patients underwent 85 intracranial to extracranial pedicle bypass anastomosis procedures to the posterior circulation. There were 15 patients with occipital artery (OA) to posterior inferior cerebellar artery (PICA) anastomosis, 20 patients with OA to anterior inferior cerebellar artery (AICA) anastomosis, and 50 patients with superficial temporal artery (STA) to superior cerebellar artery (SCA) anastomosis. All patients had transient ischemic attacks (TIA's) suggestive of vertebrobasilar ischemia. Twenty-seven patients had crescendo TIA's or stroke in evolution and were considered to be clinically unstable. All patients had severe bilateral distal vertebral artery or basilar artery disease. Twenty-two patients had bilateral vertebral artery occlusion and three had basilar artery occlusion. In this series, 69% had complete resolution of symptoms; the mortality rate was 8.4% and the morbidity rate 13.3%. Clinically stable patients did better than unstable patients. The STA-SCA anastomosis was well tolerated and technically less demanding than the OA-PICA or OA-AICA anastomosis procedures. Patients with symptomatic severe bilateral vertebral or basilar artery disease have a grave prognosis and the option of a surgical arterial pedicle revascularization procedure should be offered to them.