Delayed cerebrovascular complications of intrathecal colloidal gold.

OBJECTIVE: Therapy with intrathecal colloidal gold has been used in the past as an adjunct in the treatment of childhood neoplasms, including medulloblastoma and leukemia. We describe the long-term follow-up period of a series of patients treated with intrathecal colloidal gold and emphasize the high incidence of delayed cerebrovascular complications and their management. METHODS: Between 1967 and 1970, 14 children with posterior fossa medulloblastoma underwent treatment at the University of Minnesota. Treatment consisted of surgical resection, external beam radiotherapy, and intrathecal colloidal gold. All patients underwent long-term follow-up periods. RESULTS: Of the 14 original patients, 6 died within 2 years of treatment; all experienced persistent or recurrent disease. The eight surviving patients developed significant neurovascular complications 5 to 20 years after treatment. Three patients died as a result of aneurysmal subarachnoid hemorrhage, and five developed ischemic symptoms from severe vasculopathy that resembled moyamoya disease. CONCLUSION: Although therapy with colloidal gold resulted in long-term survival in a number of cases of childhood medulloblastoma, our experience suggests that the severe cerebrovascular side effects fail to justify its use. The unique complications associated with colloidal gold therapy, as well as the management of these complications, are presented. We recommend routine screening of any long-term survivors to exclude the presence of an intracranial aneurysm and to document the possibility of moyamoya syndrome.

Transient cardiac standstill induced by adenosine in the management of intraoperative aneurysmal rupture: technical case report.

OBJECTIVE AND IMPORTANCE: Intraoperative aneurysmal rupture represents a potentially catastrophic event. We describe the use of an intravenous adenosine bolus to induce transient cardiac asystole to control a severe intraoperative aneurysmal rupture. This treatment resulted in a brief period of severe hypotension, which enabled successful clipping of the aneurysm. CLINICAL PRESENTATION: A 55-year-old man was referred to our institution 7 days after experiencing a mild subarachnoid hemorrhage from a fusiform, multilobulated aneurysm of the anterior communicating artery. The patient was found to have multiple additional fusiform aneurysms as well as a large parietal arteriovenous malformation. INTERVENTION: A craniotomy was performed to clip the aneurysm, but surgical dissection was complicated by premature rebleeding that could not be controlled satisfactorily with tamponade or temporary arterial occlusion. Infusion of adenosine resulted in the rapid onset of profound hypotension, allowing for safe completion of the dissection and clipping of the aneurysm with a good outcome. There were no complications identified in relation to the use of adenosine. CONCLUSION: In the setting of severe intraoperative aneurysmal rupture, intravenous adenosine represents a potential means of achieving a near-immediate profound decrease in the blood pressure that may allow for safe completion of the dissection and aneurysm clipping.

Use of gadolinium as an intraarterial contrast agent in digital subtraction angiography of the cervical carotid arteries and intracranial circulation. Technical note.

Patients with renal insufficiency or other contraindications to iodine-based contrast agents present a significant management dilemma when conventional arteriography is required. The authors describe the use of gadolinium as an alternative contrast agent for arterial digital subtraction (DS) angiography of the cervical carotid arteries (CAs) and intracranial circulation. Three patients with renal insufficiency presented with symptoms of ischemic cerebrovascular disease and inconclusive noninvasive imaging studies, which necessitated conventional angiography. Traditional transfemoral catheterization of the cervical CAs was performed and DS angiographic studies were obtained using gadolinium as an intraarterial contrast agent. In one case, selective arteriographic examination of the internal carotid arteries and vertebrobasilar system was performed as well. High-quality, diagnostic images essentially indistinguishable from routine angiographic studies were obtained in all cases. No patient suffered a complication related to the use of gadolinium, and no patient demonstrated worsened renal function after the procedure. In the setting of a contraindication to iodine-based contrast agents, gadolinium represents an important alternative contrast material that allows for excellent visualization of the cervical CAs and intracranial circulation.

Intra-aortic balloon counterpulsation augments cerebral blood flow in the patient with cerebral vasospasm: a xenon-enhanced computed tomography study.

OBJECTIVE: We previously established the ability of intra-aortic balloon counterpulsation (IABC) to improve cerebral blood flow (CBF) significantly in a canine model of cerebral vasospasm. This study was performed to assess the efficacy of IABC in a patient with cardiac dysfunction and severe cerebral vasospasm that was refractory to traditional treatment measures. METHODS: We report our experience with the clinical use of IABC to treat cerebral vasospasm in a patient who suffered subarachnoid hemorrhage and concomitant myocardial infarction. Hypertensive, hypervolemic, hemodilution therapy was ineffective, and IABC was instituted. Xenon-enhanced computed tomography (Xe-CT) was utilized to obtain serial measurements of CBF with and without IABC over a 4-day period. RESULTS: IABC dramatically improved cardiac function in this patient, and Xe-CT demonstrated significant improvement in CBF with IABC. The average global CBF was 20.5 +/- 4.4 ml/100g/min before versus 34.7 +/- 3.8 ml/100g/min after IABC (p < 0.0001, paired student's t-test). The lower the CBF before IABC, the greater the improvement with IABC (correlation coefficient r = 0.83, p = 0.0007). CBF improvement ranged from 33% to 161% above baseline, average 69.3%. No complications of IABC were observed. CONCLUSIONS: This is the first report demonstrating the ability of IABC to improve CBF in a patient with vasospasm. We suggest that IABC is a rational treatment option in select patients with refractory cerebral vasospasm who do not respond to traditional treatment measures.

Intracranial aneurysm rupture presenting as delayed stroke secondary to cerebral vasospasm.

BACKGROUND: Days after aneurysmal subarachnoid hemorrhage (SAH), cerebral vasospasm can result in the delayed appearance of ischemic neurological deficit identical to that produced by other causes of stroke. Despite the well-described, "classic" presentation of SAH, up to 25% of patients are initially misdiagnosed, and the initial hemorrhage from a ruptured aneurysm will not always bring the patient to medical attention. CASE DESCRIPTIONS: We report our experience with two patients who presented with signs and symptoms of ischemic stroke resulting from cerebral vasospasm that followed unrecognized rupture of a brain aneurysm. In one case, it was the recent complaint of significant headache and a prior history of SAH that led to the correct diagnosis. In the other case, a major rebleed occurred before the accurate diagnosis was recognized. CONCLUSIONS: It is critical to make the correct diagnosis of stroke due to vasospasm so that appropriate treatment can be instituted, thrombolytic and anticoagulant therapy can be avoided, and the unsecured aneurysm can be obliterated to prevent potentially catastrophic rebleeding.

Intra-aortic balloon counterpulsation augments cerebral blood flow in a canine model of subarachnoid hemorrhage-induced cerebral vasospasm.

We tested the effect of intra-aortic balloon counterpulsation (IABC) on cerebral blood flow (CBF) in a canine model of cerebral vasospasm. Cerebral vasospasm was induced in ten adult mongrel dogs using a "two-hemorrhage" model. CBF was then measured using radiolabeled microspheres, before and after activation of an intra-aortic balloon pump. Physiologic parameters including pCO2 and cardiac filling pressures were maintained constant during the experiment. Cardiac output was monitored in each animal. CBF increased with IABC in all ten animals. The mean CBF was 78.5 milliliters per 100 grams per minute (ml/100g/min) before versus 93.3ml/100g/min after IABC (P = 0.0001). Increases in CBF were associated in most, but not all, cases with increases in cardiac output. This study supports the ability of IABC to raise CBF in the setting of cerebral vasospasm. IABC may represent an important clinical option in cases of refractory vasospasm following aneurysmal subarachnoid hemorrhage.

Myelographic and enhanced computed tomographic appearance of acute traumatic spinal cord avulsion.

The neuroradiological findings that revealed spinal cord transection/laceration in 6 patients with acute, blunt spinal trauma are described. Four patients suffered cervical spine injuries, and two had thoracic injuries. Initially, all patients had complete neurological deficit at the level of injury. The deficit improved in only 1 patient. On the basis of clinical history and spinal radiographs, spinal hyperflexion with distraction was the predominant mechanism of injury in our patients. Computed tomography with intrathecal contrast was performed on all patients and was always diagnostic. Visualization of intrathecal contrast material accumulating within the cord or the absence of cord shadow within the contrast column established the diagnosis in all cases. A dural tear was noted in 3 patients. Thoracic myelography was performed in 2 patients and, in both, demonstrated contrast pooling within the spinal cord at the level of the laceration. Magnetic resonance imaging was obtained in 1 patient and revealed an irregular, low-signal-intensity, intramedullary region extending to the cord surface on T1-weighted axial images. The myelographic and enhanced computed tomographic appearances of acute, traumatic spinal cord avulsion/laceration, which have been infrequently reported in the literature, are described.

Low affinity binding of taurine to phospholiposomes and cardiac sarcolemma.

A sarcolemma-enriched membrane fraction was prepared from the hearts of Sprague-Dawley rats and its ability to bind taurine (0.5-150 mM) was measured. In the absence of cations, the sarcolemma bound a maximum of 661 nmol taurine/mg protein, with a dissociation constant of 19.2 mM and a Hill coefficient of 1.9, indicating positive cooperativity. Scatchard analysis of taurine binding to sarcolemma gave a bell-shaped curve. Neither beta-alanine nor guanidinoethane sulfonate, inhibitors of taurine transport, affected the degree of taurine binding to sarcolemma. However, hypotaurine was an effective antagonist. Equimolar concentrations of Ca2+, Na+ or K+ also reduced taurine binding. Heterogeneous phospholipid vesicles of phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol, and phosphatidylserine (18:19:2:1) also bound taurine with positive cooperativity, yielding a bell-shaped Scatchard curve. The affinity of taurine for these mixed phospholipid vesicles was enhanced by the inclusion of cholesterol (50%). Taurine associated in a maximum ratio of 1:1 with homogeneous vesicles of phosphatidylcholine or phosphatidylserine. Vesicles of phosphatidylethanolamine bound taurine in a maximum ratio of 2:1, whereas those of phosphatidylinositol bound insignificant amounts of taurine. These studies demonstrate a low affinity binding to sarcolemma of taurine at concentrations normally present in rat heart. Similar levels of binding were observed in phospholipid vesicles, suggesting that the interaction of taurine with biological membranes involves phospholipids.

Taurine modulation of calcium binding to cardiac sarcolemma.

A sarcolemma-enriched membrane fraction (SL) was prepared from the hearts of Sprague-Dawley rats and its ability to bind Ca++ was measured by equilibrium dialysis. We found that the effect of taurine on SL Ca++ binding varied with the buffer and with Na+ concentration. In Tris, in the presence of Na+ (140 mM), taurine (10 mM) increased the affinity but decreased the maximal binding of Ca++ (0.5-7 mM). In the absence of Na+, taurine decreased the affinity without altering the maximal binding. These effects on Ca++ binding were absent in bicarbonate or Krebs-Henseleit buffers. However, incubations with A23187, a Ca++ ionophore, and lanthanum, a Ca++ antagonist, indicated that SL membranes incubated in Tris, but not in buffers containing bicarbonate, were sealed vesicles with internal environments low in Ca++. High-affinity binding of Ca++ (10(-6)-10(-4) M) was measured in modified Krebs-Henseleit buffers. Taurine decreased Ca++ binding in a high-Na+ (145 mM), low-K+ (4.7 mM) buffer. Taurine increased Ca++ binding in both 4.7 mM Na+-145 mM K+ and 25 mM Na+-4.7 mM K+ buffers. Taurine also increased Ca++ binding in the presence of ATP. Thus, taurine increased high-affinity Ca++ binding in "intracellular" buffers, but it did not affect low-affinity Ca++ binding in "extracellular" buffers. These results suggest taurine may exert its cardiotonic actions through modulation of the high-affinity Ca++ binding sites on the internal aspect of the SL.