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Endovascular treatment of a fusiform basilar artery aneurysm using multiple “in-stent stents”

Technical note

R. Webster Crowley, Avery J. Evans, Neal F. Kassell, Mary E. Jensen, and Aaron S. Dumont

Fusiform aneurysms of the basilar artery present difficult challenges for the treating physician. On one hand, these aneurysms are difficult and dangerous to treat. On the other, the relatively high rupture rate, risk of thromboemboli, and the frequent presence of mass effect on the brainstem often demand treatment rather than observation. While conservative treatment may be reasonable in an elderly patient, the relative resiliency and the larger lifetime cumulative risks of pediatric patients are compelling arguments for treatment. With the advancement of endovascular techniques some of these lesions have become treatable without the high morbidity and mortality rates associated with open surgical treatment, albeit with risks of their own. The authors present the case of a fusiform aneurysm arising from a severely tortuous basilar artery in a 22-month-old boy. The aneurysm was successfully treated using flow diversion by placing multiple intracranial stents without coil embolization. This allowed for thrombosis of the aneurysm and resolution of the mass effect on the brainstem without compromising blood flow to the brainstem.

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Combined surgical/endovascular treatment of a complex dural arteriovenous fistula in 21-month-old

Technical note

R. Webster Crowley, Avery J. Evans, Mary E. Jensen, Neal F. Kassell, and Aaron S. Dumont

The treatment of intracranial dural arteriovenous fistulas (AVF) has progressed considerably over the past few decades. With the introduction of new embolic materials and refinement of endovascular techniques, lesions that in the past may have required extensive surgery, or were considered untreatable, have increasingly become curable. Despite improvements in technology, not every condition is amenable to an endovascular treatment, including those patients with preexisting vascular abnormalities that preclude an endovascular approach. In these cases, the patient may be left with suboptimal treatment options with higher associated risks. The authors here report on the treatment of a dural AVF in a pediatric patient in whom prior procedures rendered his cerebrovascular anatomy unnavigable using traditional endovascular techniques. To circumvent these vascular abnormalities the patient underwent combined surgical/endovascular treatment that included surgical exposure and cannulation of the cervical carotid artery, as well as simultaneous femoral artery access, with subsequent successful transarterial embolization of the dural AVF.

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Barrier disruption in the major cerebral arteries following experimental subarachnoid hemorrhage

Tomio Sasaki, Neal F. Kassell, Masanori Yamashita, Shigeru Fujiwara, and Mario Zuccarello

✓ The effects of experimental subarachnoid hemorrhage (SAH) on the blood-arterial wall barrier in the major cerebral arteries were studied in 20 normotensive dogs. Horseradish peroxidase (HRP) was given intravenously before the animals were sacrificed to assess the integrity of the barrier. Transient elevation of intracranial pressure (ICP) produced by cisternal injection of saline solution resulted in HRP leakage at the branching points of the major cerebral arteries. Extensive disturbance of the blood-arterial wall barrier was consistently observed in the major cerebral arteries after SAH, with or without elevation of ICP. These results suggest that both subarachnoid clot and a sudden rise in the ICP are important factors causing the breakdown of the blood-arterial wall barrier, but that the effect of the clot is the most profound. Electron microscopy revealed that opening of the interendothelial junctions is one of the important mechanisms responsible for the HRP leakage in the major cerebral arteries following SAH. Disturbance of arterial permeability in the major cerebral arteries following SAH probably accounts for the abnormal post-contrast enhancement that occurs in patients who are prone to develop vasospasm following aneurysm rupture, and is probably involved in the pathogenesis of vasospasm.

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Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension

David J. Boarini, Neal F. Kassell, James A. Sprowell, Julie J. Olin, and Hans C. Coester

✓ Profound arterial hypotension is à commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole.

In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

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Selective hemoglobin inhibition of endothelium-dependent vasodilation of rabbit basilar artery

Shigeru Fujiwara, Neal F. Kassell, Tomio Sasaki, Tadayoshi Nakagomi, and Richard M. Lehman

✓ The effect of hemoglobin on endothelium-dependent vasodilation of the isolated rabbit basilar artery was examined using an isometric tension recording method. Acetylcholine (ACh) (10−7−10−4 M) evoked a dose-dependent vasodilation of isolated rabbit basilar artery previously contracted by 10−6 M serotonin. This vasodilating action disappeared after removal of the endothelium. The ACh-induced vasodilation of rabbit basilar artery is thought to be strictly endothelium-dependent. Hemoglobin (10−7-10−5 M) inhibited this ACh-induced endothelium-dependent vasodilation conditional upon the dose. Adenosine triphosphate (ATP, 10−7-10−4 M) also relaxed isolated rabbit basilar artery already contracted by 10−6 M serotonin. This vasodilating action was slightly inhibited by adenosine antagonist, 8-phenyltheophylline (8-PT), and markedly attenuated by removal of the endothelium. This ATP-induced vasodilation is thought to be composed of ATP itself (endothelium-dependent) and ATP degradation products (endothelium-independent) such as adenosine monophosphate or adenosine. Hemoglobin markedly inhibited ATP-induced vasodilation, but there still remained a small vasodilation, which was blocked by 8-PT. Papaverine-induced vasodilation was not affected by removal of the endothelium, and hemoglobin did not inhibit the papaverine-induced vasodilation. These results suggest that rabbit basilar artery has endothelium-dependent vasodilating mechanisms induced by ACh and ATP, and that hemoglobin selectively blocks the endothelium-dependent vasodilation. This finding may relate to the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage: there is a possibility that the presence of hemoglobin released from lysed erythrocytes inhibits the endothelium-dependent vasodilation of cerebral arteries; furthermore, the endothelial degeneration following subarachnoid hemorrhage may impair the vasodilating mechanisms of cerebral artery smooth-muscle cells.

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Cerebral and systemic circulatory effects of arterial hypotension induced by adenosine

Neal F. Kassell, David J. Boarini, Julie J. Olin, and James A. Sprowell

✓ In six dogs anesthetized with halothane and nitrous oxide, mean arterial pressure (MAP) was lowered to 40 mm Hg for an average of 90 minutes by intravenous infusion of adenosine. The hypotensive effect of the adenosine was potentiated by administering dipyridamole to block its intravascular inactivation. Blood flow to the brain, spinal cord, heart, kidneys, and skeletal muscle was measured six times in each animal using the radioactive microsphere technique. Determinations were made before, during, and 30 minutes after the hypotensive period.

During the hypotensive period, MAP was decreased 61% and was related to a proportional decrease in peripheral vascular resistance. Cardiac index decreased 14%. Total cerebral blood flow (CBF) decreased an average of 28% and cerebral vascular resistance decreased 53%. The reduction in CBF was heterogeneous; the cerebral cortex and corpus callosum were most affected and the brain stem least affected. No change occurred in the cerebral metabolic rate of oxygen usage (CMRO2). Left ventricle flow increased 147% and right ventricle flow increased 271%. Blood flow to the kidneys decreased 70%, and to the liver decreased to 6% of control. Jejunum blood flow increased 138% during recovery, while stomach flow varied but showed no statistical change. There was no tachyphylaxis, rebound hypertension, or toxicity associated with the adenosine-induced hypotension. These properties suggest that adenosine may be a useful agent for inducing arterial hypotension in neurosurgical patients.

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Pharmacologically induced profound arterial hypotension in the anesthetized dog

Neal F. Kassell, David J. Boarini, James A. Sprowell, and Julie J. Olin

✓ The purpose of this study was to compare the behavioral, hematological, and biochemical effects of profound arterial hypotension induced by adenosine potentiated with dipyridamole with those of hypotension induced by trimethaphan camsylate or sodium nitroprusside. Twenty dogs were anesthetized with halothane and nitrous oxide, paralyzed with pancuronium, and ventilated to an arterial pCO2 of 40 torr. Arterial pressure and heart rate were monitored continuously. The animals were divided into four groups of five dogs each. The first group served as controls, while in the remaining groups the mean arterial pressure (MAP) was lowered to 40 mm Hg with adenosine/dipyridamole, trimethaphan, or nitroprusside for 1 hour, following which the animals were allowed to recover from the anesthetic and observed for 48 hours. Determinations of arterial blood gases and hematological and biochemical parameters were made immediately prior to and at the completion of the 1-hour hypotensive period and 48 hours later.

Reduction of MAP to 40 mm Hg was readily achieved with adenosine/dipyridamole. There was no tachyphylaxis to this drug, and arterial pressure promptly returned toward control levels without overshoot after the infusion was discontinued. In contrast, hypotension of this degree could be produced only with toxic doses of nitroprusside. Trimethaphan was more effective in producing hypotension than nitroprusside, but the dose required was extremely variable, and prolonged intervals were required for pressure to return toward normal after the agent was stopped. The control animals and those that received adenosine/dipyridamole recovered promptly from the anesthetic and were neurologically intact. The animals that received trimethaphan recovered more slowly but were neurologically normal within 12 hours. All of the animals that received nitroprusside died without recovering from the anesthesia. Aside from a mild transient metabolic acidosis and transient elevation of blood urea nitrogen and creatinine in the dogs that received adenosine/dipyridamole or trimethaphan, no specific cardiovascular, hematological, hepatic, or renal toxic effects were noted. Evidence of fatal cyanide toxicity was present in the nitroprusside group.

These data suggest that hypotension using adenosine/dipyridamole is readily induced, maintained, and reversed, and is not associated with any apparent hematological, or biochemical evidence of toxicity. Further studies leading to a clinical trial of adenosine-induced hypotension appear to be indicated.

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Systemic and cerebral effects of prostacyclin-induced arterial hypotension in the dog

David J. Boarini, Neal F. Kassell, Julie J. Olin, and James A. Sprowell

✓ Prostacyclin has strong vasodilating and antiplatelet properties. This study was performed to investigate its potential for producing profound intraoperative hypotension. Five dogs were anesthetized with morphine, nitrous oxide, and oxygen, paralyzed with pancuronium, and ventilated to a PaCO2 of 40 torr. Mean arterial blood pressure (MABP) was lowered to 40 mm Hg with an intravenous infusion of prostacyclin in 0.05 M Tris buffer (average rate of infusion 3 ± 1 µg/kg/min). Blood flow was determined using the radioactive microsphere technique. Measurements were made before and after 20, 40, and 60 minutes of hypotension; and after a 40-minute recovery period. Infusion of prostacyclin reduced MABP 63% while increasing heart rate 51%. Tachyarrhythmias occurred in all dogs, and cardiac index decreased 18%. Myocardial blood flow decreased an average of 29%, cerebral blood flow decreased 30%, cerebellar blood flow decreased 18%, and blood flow in the brain stem and spinal cord was unchanged. Cerebral metabolic rate of oxygen, determined by measuring the oxygen content of the sagittal sinus, was unchanged. Hypotension was easily induced and maintained using prostacyclin, without apparent tachyphylaxis. However, the cardiac changes caused by this drug are more severe than those accompanying hypotension induced by most other agents, and may represent a serious contraindication to its clinical use.

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Phenoxybenzamine in the treatment of causalgia

Report of 40 cases

Salim Y. Ghostine, Youssef G. Comair, Donn M. Turner, Neal F. Kassell, and Camille G. Azar

✓ Forty consecutive cases of causalgia treated during a 7-year period are presented. The patients ranged in age between 17 and 55 years, and all patients were males who received their nerve injuries from missile or shrapnel wounds. The greater occipital nerve was involved in two cases, median nerve in 10, sciatic nerve in 12, brachial plexus in seven, cauda equina in five, and multiple nerves in four cases. Each patient was treated with phenoxybenzamine, a postsynaptic α 1-blocker and presynaptic α 2-blocking agent. The drug was given orally in gradually increasing increments until a maximum daily dose of 40 to 120 mg was reached. Duration of treatment was usually 6 to 8 weeks. Total resolution of pain was achieved in all cases. The follow-up period ranged between 6 months and 6 years. Side effects of phenoxybenzamine were minimal and transient, consisting primarily of mild orthostatic hypotension and ejaculatory problems. We conclude that oral phenoxybenzamine is a simple, safe, and effective treatment of causalgia.

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Endothelium and Cerebral Vasospasm