Bilateral Vertebral Artery Occlusion Research Articles

Reversible middle cerebral artery occlusion without craniectomy in rats.

To develop a simple, relatively noninvasive small-animal model of reversible regional cerebral ischemia, we tested various methods of inducing infarction in the territory of the right middle cerebral artery (MCA) by extracranial vascular occlusion in rats. In preliminary studies, 60 rats were anesthetized with ketamine and different combinations of vessels were occluded; blood pressure and arterial blood gases were monitored. Neurologic deficit, mortality rate, gross pathology, and in some instances, electroencephalogram and histochemical staining results were evaluated in all surviving rats. The principal procedure consisted of introducing a 4-0 nylon intraluminal suture into the cervical internal carotid artery (ICA) and advancing it intracranially to block blood flow into the MCA; collateral blood flow was reduced by interrupting all branches of the external carotid artery (ECA) and all extracranial branches of the ICA. In some groups of rats, bilateral vertebral or contralateral carotid artery occlusion was also performed. India ink perfusion studies in 20 rats documented blockage of MCA blood flow in 14 rats subjected to permanent occlusion and the restoration of blood flow to the MCA territory in six rats after withdrawal of the suture from the ICA. The best method of MCA occlusion was then selected for further confirmatory studies, including histologic examination, in five additional groups of rats anesthetized with halothane. Seven of eight rats that underwent permanent occlusion of the MCA had resolving moderately severe neurologic deficits (Grade 2 of 4) and unilateral infarcts averaging 37.6 +/- 5.5% of the coronal sectional area at 72 hours after the onset of occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Vertebral artery doppler sonography

We have examined the vertebral and subclavian arteries in 1,205 patients using directional continuous-wave (c-w) Doppler sonography, and compared the sonographic findings with the results of unilateral or bilateral retrograde brachial arteriographies in the same patients. Doppler sonography revealed 33 false positives among 909 cases with normal angiographic findings. Some types of vertebral artery (VA) lesions allowed an excellent, others a fairly good differentiation by Doppler sonography: the complete subclavian steal syndrome with constant reversal of VA flow was reliably detected (16 cases). In the incomplete steal syndrome (5 cases) sonography was superior to angiography. Two bilateral distal VA occlusions and seven basilar artery occlusions - six in the proximal third and one in the rostral third - were detected sonographically; four basilar occlusions sparing the caudal third and one case exhibiting rete mirabile anastomoses were not identified by Doppler sonography. Our acoustically defined sonographic criteria did not permit an unequivocal assignment to an anatomical variant or a vascular lesion. The sensitivity in the detection of a severe stenosis at the VA origin amounted to 16 out of 31, and to 12 of 25 in cases with a proximal VA occlusion and reconstitution of the distal VA through cervical collaterals. Our results confirm that the conventional hand-held c-w Doppler sonography cannot replace angiography in the evaluation of vertebro-basilar insufficiency. It rather serves as an aid to the decision for or against angiography, and in the follow-up of angiographically proven lesions. However, several therapeutically important lesions are readily diagnosed by sonography.

Sequential in vivo measurement of cerebral intracellular metabolites with phosphorus-31 magnetic resonance spectroscopy during global cerebral ischemia and reperfusion in rats

Phosphorus-31 magnetic resonance (31P MR) spectroscopy was used to obtain serial in vivo measurements of cerebral adenosine triphosphate (ATP), phosphocreatine (PCr), inorganic phosphate (Pi), and intracellular pH levels in rats during temporary global cerebral ischemia and reperfusion. Three groups of 4 rats each that recovered from permanent bilateral vertebral artery occlusion were placed in a MR spectrometer and subjected to remotely controlled bilateral carotid artery occlusion lasting 6, 15, or 30 minutes followed by 1 hour of reperfusion. Four additional rats that developed systemic hypotension (2 during a 6-minute occlusion and 2 during a 15-minute occlusion) were also studied. 31P MR spectra were obtained in each rat before, during, and after ischemia. Rats in which MR spectra showed metabolic recovery underwent a second occlusion followed by reperfusion and sacrifice. In the 12 normotensive rats, metabolic alterations began within 3 minutes after the onset of global ischemia. By the end of the occlusion period, cerebral ATP had decreased by 20 to 100% in 10 rats and PCr had decreased by 15 to 75% in all 12; Pi increased by 25 to 240%. The mean intracellular pH decreased from 7.33 to 6.9 ± 0.6. The degree of metabolic deterioration during ischemia was not related to the duration of occlusion. During reperfusion, ATP, PCr, Pi, and intracellular pH returned to normal in 4 rats; 5 rats had partial metabolic recovery, and 3 had minimal or transient metabolic recovery followed by progressive deterioration. All rats that developed systemic hypotension had a decrease in ATP, PCr, and intracellular pH and an increase in Pi during the initial occlusion. Each had transient partial recovery in ATP during reperfusion, and 2 had slight recovery of PCr. The onset of hypotension was followed by depletion of these metabolites, progressive increase in Pi, and progressive intracellular acidosis. All rats that deteriorated metabolically after reversal of carotid occlusion died by the end of the reperfusion period or soon after. The 8 rats that recovered from the first occlusion were subjected to a second period of ischemia, during which each rat showed severe depletion of metabolites. During the second reperfusion, only 1 rat showed significant metabolic recovery, which lasted only 30 minutes and was followed by progressive deterioration. Severe global cerebral ischemia was associated with a progressive decline in both ATP and PCr, whereas less complete ischemia seemed to be characterized by stabilization or recovery of ATP and continued depression of PCr. In the animal model studied, the variability in the degree of metabolic derangement during global ischemia and in the degree and rate of metabolic recovery during reperfusion was detected by MR spectroscopy. This study demonstrates that 31P MR spectroscopy can provide noninvasive, serial, in vivo measurements of critical high energy phosphate metabolites and intracellular pH during global cerebral ischemia and reperfusion in rats. (Neurosurgery 21:699-708, 1987)

Sequential in vivo measurement of cerebral intracellular metabolites with phosphorus-31 magnetic resonance spectroscopy during global cerebral ischemia and reperfusion in rats.

Phosphorus-31 magnetic resonance (31P MR) spectroscopy was used to obtain serial in vivo measurements of cerebral adenosine triphosphate (ATP), phosphocreatine (PCr), inorganic phosphate (Pi), and intracellular pH levels in rats during temporary global cerebral ischemia and reperfusion. Three groups of 4 rats each that recovered from permanent bilateral vertebral artery occlusion were placed in a MR spectrometer and subjected to remotely controlled bilateral carotid artery occlusion lasting 6, 15, or 30 minutes followed by 1 hour of reperfusion. Four additional rats that developed systemic hypotension (2 during a 6-minute occlusion and 2 during a 15-minute occlusion) were also studied. 31P MR spectra were obtained in each rat before, during, and after ischemia. Rats in which MR spectra showed metabolic recovery underwent a second occlusion followed by reperfusion and sacrifice. In the 12 normotensive rats, metabolic alterations began within 3 minutes after the onset of global ischemia. By the end of the occlusion period, cerebral ATP had decreased by 20 to 100% in 10 rats and PCr had decreased by 15 to 75% in all 12; Pi increased by 25 to 240%. The mean intracellular pH decreased from 7.33 to 6.9 +/- 0.6. The degree of metabolic deterioration during ischemia was not related to the duration of occlusion. During reperfusion, ATP, PCr, Pi, and intracellular pH returned to normal in 4 rats; 5 rats had partial metabolic recovery, and 3 had minimal or transient metabolic recovery followed by progressive deterioration. All rats that developed systemic hypotension had a decrease in ATP, PCr, and intracellular pH and an increase in Pi during the initial occlusion. Each had transient partial recovery in ATP during reperfusion, and 2 had slight recovery of PCr. The onset of hypotension was followed by depletion of these metabolites, progressive increase in Pi, and progressive intracellular acidosis. All rats that deteriorated metabolically after reversal of carotid occlusion died by the end of the reperfusion period or soon after. The 8 rats that recovered from the first occlusion were subjected to a second period of ischemia, during which each rat showed severe depletion of metabolites. During the second reperfusion, only 1 rat showed significant metabolic recovery, which lasted only 30 minutes and was followed by progressive deterioration. Severe global cerebral ischemia was associated with a progressive decline in both ATP and PCr, whereas less complete ischemia seemed to be characterized by stabilization or recovery of ATP and continued depression of PCr.(ABSTRACT TRUNCATED AT 400 WORDS)

O-18 - Neuropharmacological study of the cereurai ischemic rats produced by bilateral vertebral and carotid artery occlusion

O-18 - Neuropharmacological study of the cereurai ischemic rats produced by bilateral vertebral and carotid artery occlusion

Bilateral occlusion of vertebral artery: clinical patterns and long-term prognosis.

We studied 17 patients with atherosclerotic bilateral occlusion of vertebral arteries (VA) identified by angiography. Seven had vertebrobasilar TIAs, eight a brainstem stroke (severe in two), and two had only carotid symptoms. Brainstem strokes were more frequent with bilateral intracranial occlusion (60%) than with at least one extracranial occlusion (28.6%), but long-term prognosis did not differ in these two groups. In follow-up, the mortality rate was 4.5% per year, and the stroke rate was 1.8% per year. Major functional disability was seen in 16.7% of the survivors. Bilateral distal VA occlusion may sometimes have a better prognosis than previously assumed. These findings raise doubts about the value of extra-intracranial surgical bypass procedures in patients with these lesions.

Surgical correction of lesions affecting the second portion of the vertebral artery.

Substantial controversy has surrounded the diagnosis and management of vertebrobasilar ischemic events, with no consensus on the value of medical or surgical treatment of patients symptomatic with brain stem ischemia who have angiographically proven vertebral artery lesions. This report presents our experience with the surgical treatment of 12 of 88 patients with angiographically verified lesions in the vertebral artery who were symptomatic for 1 to 12 months before their evaluation. None experienced symptomatic relief with antiplatelet agents, nor did the administration of anticoagulants in 4 of the patients provide any benefit. The lesions included bilateral vertebral artery occlusion with distal reconstitution through muscular collaterals in 6 patients, unilateral vertebral artery hypoplasia with contralateral long-tailed lesions from the vertebral artery origin to C-5 in 3 patients, and severe bilateral vertebral artery origin lesions extending beyond the C-5 level in 3 patients. A vertebral endarterectomy and vertebral-carotid transposition in the second portion of the artery were successfully used to reestablish flow and obtain symptomatic relief in 10 of the 12 cases; 1 of these procedures had to be redone because of a persistent stenosis at C-4. Another patient had a saphenous vein graft from the common carotid to the vertebral artery at C-5. The remaining patient had an anastomosis of the distal external carotid to the vertebral artery at C-3, but this failed and an anastomosis of the occipital artery to the anterior inferior cerebellar artery had to be completed to reestablish flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Recovery from locked-in syndrome after posttraumatic bilateral distal vertebral artery occlusion

A 55-year-old man developed a delayed locked-in syndrome after a mild head injury. Angiography showed bilateral distal vertebral artery occlusion. Anticoagulant therapy and energetic medical management to promote collateral circulation to the structures in the posterior fossa led to a functional recovery. A review of the reported cases of posttraumatic locked-in syndrome has allowed the authors to differentiate between two types: the first is due to primary brainstem injury and the second is due to secondary brainstem ischemia. Both types have different modes of onset, mechanisms of production, angiographic findings, and prognosis. It is concluded that, with early diagnosis and vigorous medical management, expectations for a useful recovery are high, especially in those cases of posttraumatic locked-in syndrome due to secondary brainstem ischemia.

Surgical reconstruction of the proximal vertebral artery

The authors have reviewed their experience in the management of 55 patients admitted to Henry Ford Hospital with symptoms of vertebrobasilar insufficiency and associated proximal vertebral artery stenosis or occlusion. In 48 patients, the symptoms occurred as multiple repeated events, five of which resulted in permanent deficits. The remaining seven patients had single events, four of which caused permanent deficit. These patients had been treated unsuccessfully with antiplatelet agents (37 cases) and with anticoagulant drugs (15 cases) before surgery. Most patients had multiple angiographic abnormalities, including bilateral vertebral stenosis in 19 cases, unilateral vertebral stenosis and contralateral occlusion in 18, unilateral vertebral hypoplasia and contralateral stenosis in 10, subclavian artery stenosis with steal in seven, and bilateral vertebral artery occlusion in one case. Posterior communicating arteries could not be demonstrated angiographically in 18 patients. Thirty-four patients had associated stenotic or occlusive lesions of the internal carotid artery. Forty-eight underwent a vertebral-to-carotid artery transposition. Of these, 18 had an associated carotid endarterectomy and seven had a vertebral artery endarterectomy immediately before the transposition. Two patients had saphenous vein grafts, one from the subclavian and one from the common carotid artery to the vertebral artery. Other surgical procedures included vertebral artery ligation in one case, transposition of the vertebral artery to the thyrocervical trunk in two cases and to the subclavian artery in one case, and endarterectomy of the origin of the vertebral artery in one case. All but two patients had complete resolution of their symptoms: one had persistent dizziness and the other had syncopal episodes. Complications included transient Horner's syndrome (30 cases) which became permanent in four cases, vocal cord paralysis (three cases), elevated hemidiaphragm without respiratory difficulty (two cases), and superficial would infection (one case). There were no deaths. Although the presentation of patients with vertebrobasilar insufficiency is generally characteristic, we believe that a specific diagnosis can be established only by angiographic means. Anticoagulants have been used to alleviate symptoms in some cases but are ineffective in solving the primary hemodynamic problem. Surgical reconstruction of the affected area deserves further evaluation in the management of these patients.

Basilar artery occlusion: clinical and radiological correlation.

Twenty patients with basilar artery occlusion and three patients with bilateral vertebral artery occlusions have been studied. The clinical data at the time of the ictus and the long-term follow-up data have been correlated with the site and extent of the basilar artery occlusion and the type of collateral flow. Patients with hypertension and with coma at the outset have a grave prognosis. The presence of surface collateral flow may not indicate adequate perfusion of the paramedian penetrating branches of the basilar artery or the thalamoperforating branches of the posterior communicating or posterior cerebral arteries. It is these vessels which supply the territory regulating the level of consciousness and containing some of the control mechanisms for respiratory function.

Nonpenetrating injuries of the neck and cerebrovascular accident.

A patient with traumatic quadriplegia had arteriographic evidence of bilateral vertebral artery occlusions. The mechanism for such trauma is explained on the basis of the anatomic relation of the arteries to the cervical vertebrae. Unaccountable death in high spinal cord injuries may be related to this phenomenon.

Critical stenosis of the carotid artery in the dog.

Critical stenosis was determined for the canine carotid artery. With all four cephalic vessels patent, the critical stenosis was demonstrated to be 81%, at which level a 15% reduction in flow occurred. The superimposition of bilateral vertebral artery and contralateral carotid artery occlusion lowered the level of critical stenosis to 72% luminal constriction. When both exter nal carotid arteries were ligated and common carotid artery flow represented internal carotid flow, critical stenosis was determined to be 90%, and this did not change with superimposed bilateral vertebral arterial and con tralateral carotid arterial occlusion.

Pressor effect of increased cerebrospinal fluid pressure and vertebral artery occlusion with and without anesthesia.

The intracranial pressures of conscious, lightly anesthetized and fully anesthetized dogs were altered by means of previously implanted intraventricular cannulas, while systemic arterial pressures were simultaneously measured. One vertebral artery was occluded in all these experiments by the catheter used to record aortic pressure. Increased intracranial pressure, which probably acts by reducing cerebral blood flow, caused a rise in systemic arterial pressure whose magnitude depended on the presence and depth of anesthesia. When anesthesia was not used, but when the animals were resting quietly, a significant pressor response occurred within the physiological range of CSF pressure. The response was typically of slow onset, developing over a period of one half to two minutes. It was reproducible, but tended to diminish gradually in the course of several hours if the experiment was continued, although it could be restored if CSF pressure was further increased. The pulse rate tended to increase slightly, or remain the same, providing CSF pressure was not increased too greatly or too rapidly. Respiratory effects were variable, but most commonly a slightly increased rate and depth of respiration occurred at first, with a return towards normal as the systemic arterial pressure rose. Similar responses were seen during bilateral artery occlusion, by means of previously implanted inflatable cuffs, in dogs whose carotid sinuses had been excised. These effects were also slow in onset, and were accompanied by comparable respiratory changes. In anesthetized animals with intact carotid arteries, bilateral vertebral artery occlusion produced negligible pressor effects, but was found to augment the response to increased intracranial pressure. Observations in four dogs with chronic experimental renal hypertension did not reveal notable differences, except that these animals may be less sensitive than normal to increases in intracranial pressure. The results of these experiments are compatible with the hypothesis that basal systemic arterial pressure during sleep in some degree depends on the cerebrovascular resistance, although it will be important to determine the nature of the slow adaptation seen in these experiments. If this adaptation is brought about by compensatory cerebral vasodilation, this investigation is in accord with the concept of Dickinson and Thomson that some forms of chronic high blood pressure in man might be initiated by cerebral artery occlusion or narrowing of sufficient severity and extent to prevent adequate compensatory vasodilation.