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C J Prestigiacomo

Publications and source records attributed to C J Prestigiacomo.

16 recordsLinked to original sources
PubMed2001

Anti-Ri-associated paraneoplastic opsoclonus-ataxia syndrome in a man with transitional cell carcinoma.

BACKGROUND: There are several case reports describing paraneoplastic syndromes in patients with various forms of bladder carcinoma. Current immunologic analyses have enabled the identification of the antineuronal autoantibodies associated with specific syndromes. METHODS: A patient with a history of bladder carcinoma presented with opsoclonus and myoclonus. RESULTS: Workup confirmed the presence of anti-Ri antibodies in the patient's serum and cerebrospinal fluid. The target Ri antigen was found to be expressed by the tumor. CONCLUSIONS: To the authors' knowledge, there are few reports in the literature describing the long-term clinical follow-up and postmortem evaluation in a patient with this form of paraneoplastic syndrome. More important, the authors believe the current study represents the first time that the presence of anti-Ri antibodies has been noted in a paraneoplastic syndrome associated with transitional cell carcinoma of the bladder.

Antibodies↗
PubMed2000

Management of residual dysplastic vessels after cerebral arteriovenous malformation resection: implications for postoperative angiography.

OBJECTIVE: The verification of surgical resection of cerebral arteriovenous malformations (AVMs) relies on angiography. Abnormal vasculature often is identified after removal of the AVM. Differentiation of dysplastic feeding vessels that resemble the neovascularity of moyamoya disease, as distinct from residual AVM, is crucial for preserving critical brain areas. We review a large experience with immediate postoperative angiography after AVM resection and discuss the implications for management of abnormal dysplastic vessels discovered after AVM resection. METHODS: Beginning in 1992, 86 consecutive patients with AVMs underwent operations by standard protocol for immediate postoperative angiography under the same general anesthetic. Angiographic interpretation dictated admission to the intensive care unit or return to the operating room for further resection. RESULTS: In 78 patients, the angiogram revealed complete resection. Two patients were returned to the operating room, one for residual malformation with an early draining vein, and one for resection of residual dysplastic vessels. There was one postoperative hemorrhage in a patient whose postoperative angiogram was falsely negative for AVM. Six patients with residual dysplastic vessels mimicking residual AVM, but without an early draining vein, were managed conservatively. Delayed follow-up angiography demonstrated spontaneous involution of these abnormal vessels in all of these patients. CONCLUSION: Residual dysplastic feeding vessels resembling the neovascularity of moyamoya disease but not associated with an early draining vein do not necessarily represent residual malformation after AVM resection. The abnormal vessels will proceed to complete spontaneous resolution. Given the difficulty of interpreting intraoperative angiography, immediate postoperative angiography may be a viable alternative after AVM resection.

Adult↗
PubMed1999

Dysarthria during basilar artery balloon occlusion.

A 49-year-old woman presenting with recurrent, reversible brainstem symptoms and a distal basilar artery aneurysm underwent balloon test occlusion. Five minutes after balloon inflation she developed a reversible isolated dysarthria. Despite failing the test occlusion (and after an additional brainstem event), the patient underwent surgery with placement of a clip across the basilar artery. The operation was tolerated without complication. The authors conclude that 1) pure dysarthria may be a symptom of temporary basilar artery occlusion and 2) balloon testing may overestimate the risk of basilar artery clipping.

Angioplasty, Balloon↗
PubMed1999

Targeted inhibition of intrinsic coagulation limits cerebral injury in stroke without increasing intracerebral hemorrhage.

Agents that restore vascular patency in stroke also increase the risk of intracerebral hemorrhage (ICH). As Factor IXa is a key intermediary in the intrinsic pathway of coagulation, targeted inhibition of Factor IXa-dependent coagulation might inhibit microvascular thrombosis in stroke without impairing extrinsic hemostatic mechanisms that limit ICH. A competitive inhibitor of native Factor IXa for assembly into the intrinsic Factor X activation complex, Factor IXai, was prepared by covalent modification of the Factor IXa active site. In a modified cephalin clotting time assay, in vivo administration of Factor IXai caused a dose-dependent increase in time to clot formation (3.6-fold increase at the 300 micrograms/kg dose compared with vehicle-treated control animals, P < 0.05). Mice given Factor IXai and subjected to middle cerebral artery occlusion and reperfusion demonstrated reduced microvascular fibrin accumulation by immunoblotting and immunostaining, reduced 111In-labeled platelet deposition (42% decrease, P < 0.05), increased cerebral perfusion (2.6-fold increase in ipsilateral blood flow by laser doppler, P < 0.05), and smaller cerebral infarcts than vehicle-treated controls (70% reduction, P < 0.05) based on triphenyl tetrazolium chloride staining of serial cerebral sections. At therapeutically effective doses, Factor IXai was not associated with increased ICH, as opposed to tissue plasminogen activator (tPA) or heparin, both of which significantly increased ICH. Factor IXai was cerebroprotective even when given after the onset of stroke, indicating that microvascular thrombosis continues to evolve (and may be inhibited) even after primary occlusion of a major cerebrovascular tributary.

Animals↗
PubMed1999

Adenosine-induced cardiac pause for endovascular embolization of cerebral arteriovenous malformations: technical case report.

OBJECTIVE: Extremely high flow through arteriovenous malformations (AVMs) may limit the safety and effectiveness of endovascular glue therapy. To achieve a more controlled deposition of glue, we used transient but profound systemic hypotension afforded by an intravenously administered bolus of adenosine to induce rapidly reversible high-degree atrioventricular block. METHODS AND CASE REPORT: A patient with a large high-flow occipital AVM fed primarily by the posterior cerebral artery underwent n-butyl cyanoacrylate glue embolization. Nitroprusside-induced systemic hypotension did not adequately reduce flow through the nidus, as determined by contrast injection in the feeding artery. In a dose-escalation fashion, boluses of adenosine were administered to optimize the dose and verify that there was no flow reversal in the AVM and no other unexpected hemodynamic abnormalities by arterial pressure measurements and transcranial Doppler monitoring of the posterior cerebral artery feeding the AVM. Thereafter, 64 mg of adenosine was rapidly injected as a bolus to provide 10 to 15 seconds of systemic hypotension (approximately 20 mm Hg). Although there were conducted beats and some residual forward flow through the AVM during this time, the mean systemic and feeding artery pressures were roughly similar and remained relatively constant. A slow controlled injection of n-butyl cyanoacrylate glue was then performed, with excellent filling of the nidus. CONCLUSION: Adenosine-induced cardiac pause may be a viable method of partial flow arrest in the treatment of cerebral AVMs. Safe, deep, and complete embolization with a permanent agent may increase the likelihood of endovascular therapy's being curative or may further improve the safety of microsurgical resection.

Adenosine↗
PubMed1999

CD18-mediated neutrophil recruitment contributes to the pathogenesis of reperfused but not nonreperfused stroke.

BACKGROUND AND PURPOSE: Neutrophil (PMN) recruitment mediated by increased expression of intercellular adhesion molecule-1 expression (ICAM-1, CD54) in the cerebral microvasculature contributes to the pathogenesis of tissue injury in stroke. However, studies using blocking antibodies against the common beta2-integrin subunit on the PMN, the counterligand for ICAM-1 (CD18), have demonstrated equivocal efficacy. The current study tested the hypothesis that mice deficient in CD18 would be protected in the setting of reperfused but not nonreperfused stroke. METHODS: Two groups of mice were studied, those whose PMNs could express CD18 (CD18 +/+) and those mice hypomorphic for the CD-18 gene (CD18 -/-). PMNs obtained from CD18 -/- or CD18 +/+ mice were fluorescently labeled and tested for binding to murine brain endothelial monolayers. Using a murine model of focal cerebral ischemia in which an occluding suture placed in the middle cerebral artery (MCA) is removed after 45 minutes (transient ischemia, reperfused stroke) or left in place (permanent ischemia, nonreperfused stroke), cerebral infarct volumes (% ipsilateral hemisphere by TTC staining), cerebral blood flow (CBF, % contralateral hemisphere by laser-Doppler flowmetry), and survival (%) were examined 24 hours after the initial ischemic event. Adoptive transfer studies used 111In-labeled PMNs (from either CD18 +/+ or CD18 -/- mice) to examine the relative accumulation of PMNs in the ischemic region. RESULTS: PMNs obtained from CD18 -/- mice exhibit reduced adhesivity (compared with CD18 +/+ PMNs) for both quiescent and cytokine-activated endothelial monolayers. CD18 -/- mice (n=14) subjected to transient focal cerebral ischemia demonstrated a 53% decrease in infarct volumes versus CD18 +/+ mice (n=26, P<0.05), improved penumbral CBF at 24 hours (1.8-fold, P=0.02), and a 3.7-fold decrease in mortality (P=0.02). However, when CD18 -/- mice (n=12) were subjected to permanent focal cerebral ischemia, no differences were noted in infarct volume, mortality, or CBF versus similarly treated CD18 +/+ mice (n=10). There was a greater accumulation of CD18 +/+ PMNs in the ischemic zone of CD18 +/+ animals than CD18 -/- animals subjected to reperfused stroke (82% increase, P=0.02), although there was no difference between groups when subjected to permanent MCA occlusion. CONCLUSIONS: Deficiency for the CD18 gene confers cerebral protection in a murine model of reperfused stroke, but this benefit does not extend to CD18-deficient animals subjected to permanent MCA occlusion. These data suggest that anti-PMN strategies should be targeted to reperfused stroke and may perhaps be used in conjunction with thrombolytic therapy that establishes reperfusion.

Animals↗
PubMed1999

Ventricular volume following third ventriculostomy.

OBJECT: Ventricular size often shows no obvious change following third ventriculostomy, particularly in the early postoperative period, making postoperative evaluation difficult without expensive and often invasive testing in patients with equivocal clinical responses. The authors hypothesized that performing careful volumetric measurements would show decreases in size within the first 3 weeks after surgery. METHODS: Volumetric measurements were calculated from standard 3 x 3-mm axial computerized tomography (CT) scans obtained immediately before and 3 and 21 days after surgery. Two independent investigators measured third ventricular volume in a series of 16 patients and lateral ventricular volume in 10 of the patients undergoing stereotactically guided endoscopic third ventriculostomy for noncommunicating hydrocephalus. Fifteen patients were symptomatically improved at the time the follow-up scan was obtained. Third ventricular volume decreased in all patients by a mean of 35% (range 7.8-95.1%) and lateral ventricular volume decreased in all patients by a mean of 33% (range 4.5-80.3%). The degree of change correlated with the length of preoperative symptoms (p < 0.005). The one patient who experienced no improvement showed no decrease in third ventricular volume. In seven of 10 patients, the decrease in third ventricular volume exceeded the decrease in lateral ventricular volume. Repeated measurements indicated that the 95% confidence interval for the authors' calculations varied around the mean by 2.5% for third ventricular volume and 1.2% for lateral ventricular volume. Long-term outcome was excellent, with only one case of delayed failure. The mean follow-up duration was 12 months. CONCLUSIONS: Volumetric measurements calculated from standard CT scans will show a demonstrable decrease in ventricular volume soon after successful third ventriculostomy and can be helpful in assessing patients postoperatively. Although the third ventricle may exhibit a greater decrease, the lateral ventricular measurements are more accurate. Patients with more indolent symptoms show the smallest change.

Adolescent↗
PubMed1998

Reduced microvascular thrombosis and improved outcome in acute murine stroke by inhibiting GP IIb/IIIa receptor-mediated platelet aggregation.

Treatment options in acute stroke are limited by a dearth of safe and effective regimens for recanalization of an occluded cerebrovascular tributary, as well as by the fact that patients present only after the occlusive event is established. We hypothesized that even if the site of major arterial occlusion is recanalized after stroke, microvascular thrombosis continues to occur at distal sites, reducing postischemic flow and contributing to ongoing neuronal death. To test this hypothesis, and to show that microvascular thrombosis occurs as an ongoing, dynamic process after the onset of stroke, we tested the effects of a potent antiplatelet agent given both before and after the onset of middle cerebral arterial (MCA) occlusion in a murine model of stroke. After 45 min of MCA occlusion and 23 h of reperfusion, fibrin accumulates in the ipsilateral cerebral hemisphere, based upon immunoblotting, and localizes to microvascular lumena, based upon immunostaining. In concordance with these data, there is a nearly threefold increase in the ipsilateral accumulation of 111In-labeled platelets in mice subjected to stroke compared with mice not subjected to stroke. When a novel inhibitor of the glycoprotein IIb/IIIa receptor (SDZ GPI 562) was administered immediately before MCA occlusion, platelet accumulation was reduced 48%, and fibrin accumulation was reduced by 47% by immunoblot densitometry. GPI 562 exhibited a dose-dependent reduction of cerebral infarct volumes measured by triphenyltetrazolium chloride staining, as well as improvement in postischemic cerebral blood flow, measured by laser doppler. GPI 562 caused a dose-dependent increase in tail vein bleeding time, but intracerebral hemorrhage (ICH) was not significantly increased at therapeutic doses; however, there was an increase in ICH at the highest doses tested. When given immediately after withdrawal of the MCA occluding suture, GPI 562 was shown to reduce cerebral infarct volumes by 70%. These data support the hypothesis that in ischemic regions of brain, microvascular thrombi continue to accumulate even after recanalization of the MCA, contributing to postischemic hypoperfusion and ongoing neuronal damage.

Animals↗
PubMed1998

Diagnosis and monitoring of cerebral hyperfusion after carotid endarterectomy with single photon emission computed tomography: case report.

OBJECTIVE AND IMPORTANCE: Focal neurological deficits after carotid endarterectomy may result from ischemia or hyperperfusion. The usefulness of single photon emission computed tomography (SPECT) for differentiating between these two mechanisms has not been previously emphasized. CLINICAL PRESENTATION: An 83-year-old man experienced dysarthria and left-sided weakness immediately after undergoing endarterectomy of the right internal carotid artery. The results of computed tomography of the head were normal, and transcranial Doppler sonography showed symmetrically elevated velocities in both middle cerebral arteries. On the 1st postoperative day, the patient's deficits worsened in parallel with spontaneous increases in blood pressure, and blood pressure reduction with labetalol resulted in clinical improvement. INTERVENTION: On the 2nd postoperative day, technetium-99-hexametazime SPECT demonstrated markedly increased flow in the right basal ganglia and inferior frontal cortex, confirming the diagnosis of cerebral hyperperfusion. The patient's deficits continued to improve with antihypertensive therapy, and SPECT performed 7 and 48 days after surgery showed gradual normalization of the focal hyperemia. CONCLUSION: SPECT can be used to diagnose and monitor cerebral hyperperfusion after carotid endarterectomy and may be of particular value for differentiating hyperperfusion from ischemia when characteristic computed tomographic and transcranial Doppler sonographic findings are absent.

Aged↗
PubMed1997

Matrix metalloproteinase-9 in cerebral aneurysms.

OBJECTIVE: Generalized disruption of arterial wall morphological changes in patients harboring cerebral aneurysms has been documented; however, little is known regarding the pathogenesis of these changes. To explore the role of the elastolytic gelatinase, matrix metalloproteinase-9 (MMP-9), levels of this enzyme in the wall of intracranial aneurysms were compared with those in both intracranial and extracranial arteries. The tissue levels of its major inhibitor, tissue inhibitor of metalloproteinase (TIMP), were measured in these tissues as well. The activity of MMP-9 in plasma was also evaluated. METHODS: The aneurysm wall was excised from three of six patients undergoing craniotomies for aneurysm clipping. A 1-cm segment of superficial temporal artery (STA) was obtained from each of six patients. Additional STAs were obtained from six patients in the control group who were undergoing craniotomies for nonvascular disease. An intracranial artery was also obtained from the anterior temporal neocortical resection of a patient undergoing a craniotomy for mesial temporal sclerosis. MMP-9 and TIMP levels were determined via Western blot analysis. Using substrate gel Zymography, MMP-9 plasma activity was determined for a separate cohort of patients with aneurysms (n = 6) and patients in the control group (n = 6). RESULTS: MMP-9 and TIMP levels in the aneurysm wall were markedly increased beyond levels in both extracranial arteries (STAs from patients with aneurysms and patients in the control group) and the intracranial artery. There were no differences in the levels of MMP-9 in the STAs of patients harboring aneurysms when compared with patients in the control group. Also, no differences were noted in plasma MMP-9 activity. CONCLUSION: Local rather than systemic perturbations in MMP-9 levels may contribute to the matrix disruption associated with cerebral aneurysms. This local up-regulation is not the result of TIMP down-regulation. The lack of increased systemic metalloproteinase activity precludes the use of plasma MMP-9 activity as a screening tool for presymptomatic aneurysms. However, local therapeutic modulation of MMP-9 activity may help arrest aneurysm progression.

Aneurysm, Ruptured↗
PubMed1997

Exacerbation of cerebral injury in mice that express the P-selectin gene: identification of P-selectin blockade as a new target for the treatment of stroke.

There is currently a stark therapeutic void in the treatment of evolving stroke. Although P-selectin is rapidly expressed by hypoxic endothelial cells in vitro, the functional significance of P-selectin expression in stroke remains unexplored. In order to identify the pathophysiological consequences of P-selectin expression and to identify P-selectin blockade as a potential new approach for the treatment of stroke, experiments were performed using a murine model of focal cerebral ischemia and reperfusion. Early P-selectin expression in the postischemic cerebral cortex was demonstrated by the specific accumulation of radiolabeled anti-murine P-selectin IgG, with the increased P-selectin expression localized to the ipsilateral cerebral microvascular endothelial cells by immunohistochemistry. In experiments designed to test the functional significance of increased P-selectin expression in stroke, neutrophil accumulation in the ischemic cortex of mice expressing the P-selectin gene (PS +/+) was demonstrated to be significantly greater than that in homozygous P-selectin-null mice (PS -/-). Reduced neutrophil influx was accompanied by greater postischemic cerebral reflow (measured by laser Doppler) in the PS -/- mice. In addition, PS -/- mice demonstrated smaller infarct volumes (5-fold reduction, P<.05) and improved survival compared with PS +/+ mice (88% versus 44%, P<.05). Functional blockade of P-selectin in PS +/+ mice using a monoclonal antibody directed against murine P-selectin also improved early reflow and stroke outcome compared with control mice, with reduced cerebral infarction volumes noted even when the blocking antibody was administered after occlusion of the middle cerebral artery. These data are the first to demonstrate a pathophysiological role for P-selectin in stroke and suggest that P-selectin blockade may represent a new therapeutic target in the treatment of stroke.

Animals↗
PubMed1996

Use of carotid ultrasound as a preoperative assessment of extracranial carotid artery blood flow and vascular anatomy.

Carotid ultrasound evaluation as a preoperative assessment of internal carotid artery blood flow and anatomic stenosis is efficacious and safe. The technique, although operator dependent, is both inexpensive and easily repeated with essentially no risk to the patient. Furthermore, when combined with MR angiography, it usually can obviate the need for angiography in most endarterectomy candidates.

Blood Flow Velocity↗
PubMed1995

Short-term perioperative anticonvulsant prophylaxis for the surgical treatment of low-risk patients with intracranial aneurysms.

The long-term use of anticonvulsant medication to prevent postoperative seizures in patients with aneurysms has been accepted medical practice for many years. The low incidence of seizures in more recent aneurysm series makes it appropriate to re-evaluate the use of prophylactic anticonvulsants to prevent postoperative epilepsy, especially in patients at low risk of seizure disorders. On the basis of preoperative presentation, we categorized 387 of the 420 craniotomies for aneurysms over a 4-year period to be at low risk of seizure. Postoperative anticonvulsant medication in this group was restricted to an average of 3 days. A retrospective analysis of the incidence of early postoperative seizures and late postoperative seizure disorders was performed in the populations of patients with ruptured aneurysms and with unruptured aneurysms with an average follow-up of 2.4 years. The overall seizure rate in the study group was 5.4%. Patients with ruptured aneurysms had an early postoperative seizure rate of 1.5% and a long-term seizure disorder rate of 3.0%. Early and long-term seizure rates for unruptured aneurysms were 2.6 and 4.4%, respectively. No patients who had early seizures went on to develop epilepsy, and all seizure disorders were well controlled once anticonvulsants were begun. These data support the idea that anticonvulsant medication may be safely restricted to the immediate perioperative period for most patients with aneurysms.

Adult↗
PubMed1994

Mild hypothermia and MK-801 have similar but not additive degrees of cerebroprotection in the rat permanent focal ischemia model.

Although not the sole factor, glutamate-mediated excitotoxicity is accepted as a major mechanism of ischemic neuronal damage. MK-801 and mild hypothermia, two cerebroprotective modalities, which have been documented to alter glutamatergic action, were tested in the rat middle cerebral artery occlusion (MCAO) model simulating permanent focal ischemia. We administered normothermic (37 degrees C) animals with either MK-801 (1.0 mg/kg 30 min before MCAO or 2.5 mg/kg 30 min before, immediately after, 4 hours, and 8 hours after MCAO) or saline vehicle (30 min before MCAO). Mildly hypothermic (33 degrees C) animals were administered either MK-801 (1.0 mg/kg) or saline vehicle 30 minutes before MCAO. Mild hypothermia was induced over a 20-minute period before MCAO in hypothermic animals. All animals were killed 24 hours after MCAO; their brains were sectioned and stained with 2,3,5-triphenyltetrazolium chloride and their infarct volumes were calculated. In normothermica animals given 1.0 mg/kg and multidose 2.5-mg/kg intraperitoneal injections of MK-801, the infarct volumes (as a percentage of right hemispheric volume) were 16.8 +/- 3.5% and 16.3 +/- 3.0%, respectively. These infarct volumes were significantly different (P < 0.05; single-variable analysis of variance) from the normothermic, drug-free control (26.8 +/- 1.9%), but not significantly different from each other. Analysis of the data using a nonparametric test (Kruskal-Wallis; P = 0.02) confirmed the same significant differences in infarct size. The infarct volumes from the mildly hypothermic groups were not different (1 mg/kg of MK-801, 15.5 +/- 2.3% and saline control, 15.4 +/- 1.1%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Hypothermic protection following middle cerebral artery occlusion in the rat.

The effects of deep hypothermia on ischemic neuronal injury were examined using a permanent middle cerebral artery occlusion model in the rat. Animals were maintained at temporalis temperatures of either 24 degrees C or 36 degrees C and killed 6 hours after arterial occlusion. Normothermic rats displayed an average infarct volume of 25.1% +/- 1.6% of the right hemisphere, whereas hypothermic rats had an average infarct volume of 4.1% +/- 1.3% (p less than 0.001). The right/left hemispheric ratio was 1.05 +/- 0.02 in the normothermic group and 1.00 +/- 0.02 in the hypothermic group (p less than 0.05). These results suggest that hypothermia to 24 degrees C may reduce cerebral infarction and edema formation following middle cerebral artery occlusion in the rat.

Animals↗