PubMed Health⌕ Search

Biomedical subjects

Rafael J Tamargo

Publications and source records attributed to Rafael J Tamargo.

At least 19 recordsLinked to original sources
PubMed2007

Delayed cerebral vasospasm secondary to bacterial meningitis after lumbosacral spinal surgery: case report.

OBJECTIVE: Delayed cerebral vasospasm is an under-recognized complication of meningitis. This case report is important because it is the first to definitively associate vasospasm with meningitis using catheter angiography. Furthermore, it is the first to correlate the time course of delayed cerebral vasospasm with meningitis. CLINICAL PRESENTATION: We present a patient who developed a partial expressive aphasia 9 days after developing meningitis, consistent with cerebral vasospasm, after lumbosacral spinal surgery. INTERVENTION: Vasospasm was confirmed by angiography and transcranial Doppler sonography, and symptoms responded to hypervolemia, hypertension, and hemodilution therapy. CONCLUSION: If a patient develops neurological symptoms consistent with a timeline of delayed cerebral vasospasm in the setting of meningitis, angiographic evaluation and appropriate therapy should be pursued.

Aphasia↗
PubMed2006

Safety of cerebral digital subtraction angiography in children: complication rate analysis in 241 consecutive diagnostic angiograms.

BACKGROUND AND PURPOSE: Catheter-based cerebral angiography remains an important diagnostic tool in the pediatric population, particularly considering the currently growing interest in diagnosing and treating cerebrovascular disorders in children. There are no recent estimates of the complication rate associated with modern diagnostic digital subtraction angiography (DSA) in the pediatric population. The purpose of this study was to estimate the rate of complications occurring during cerebral angiography in children. METHODS: Data from 241 consecutive pediatric cerebral angiograms performed at a single institution were entered into an institutional review board-approved database. Information on patient demographics, DSA indication, neurovascular diagnosis, and intra procedural and postprocedural complications was collected. RESULTS: Our population included 115 boys and 90 girls, with age ranging from 1 week to 18 years (mean+/-SD, 12+/-5 years). All angiograms were technically successful. No intraprocedural complication was noted; in particular, there was no occurrence of iatrogenic vessel injury (dissection) and no transient or permanent neurological deficit secondary to a thromboembolic event. One child with a complex dural arteriovenous fistula experienced a fatal intracranial rehemorrhage secondary to a posterior fossa varix rupture 3 hours after completion of an uneventful diagnostic angiogram. The rates of intraprocedural and postprocedural complications were therefore 0.0% (95% CI, 0.0% to 1.4%) and 0.4% (95% CI, 0.012% to 2.29%), respectively. CONCLUSIONS: The rate of immediate complications occurring during diagnostic cerebral angiography in children is very low. No intraprocedural complication was documented in the reported series. DSA performed by experienced angiographers is a safe procedure that can provide critical diagnostic information.

Adolescent↗
PubMed2006

Inflammation in stroke and focal cerebral ischemia.

BACKGROUND: A growing number of recent investigations have established a critical role for leukocytes in propagating tissue damage after ischemia and reperfusion in stroke. Experimental data obtained from animal models of middle cerebral artery occlusion implicate inflammatory cell adhesion molecules, chemokines, and cytokines in the pathogenesis of this ischemic damage. METHODS: Data from recent animal and human studies were reviewed to demonstrate that inflammatory events occurring at the blood-endothelium interface of the cerebral capillaries underlie the resultant ischemic tissue damage. RESULTS: After arterial occlusion, the up-regulated expression of cytokines including IL-1, and IL-6 act upon the vascular endothelium to increase the expression of intercellular adhesion molecule-1, P-selectin, and E-selectin, which promote leukocyte adherence and accumulation. Integrins then serve to structurally modify the basal lamina and extracellular matrix. These inflammatory signals then promote leukocyte transmigration across the endothelium and mediate inflammatory cascades leading to further cerebral infarction. CONCLUSIONS: Inflammatory interactions that occur at the blood-endothelium interface, involving cytokines, adhesion molecules, chemokines and leukocytes, are critical to the pathogenesis of tissue damage in cerebral infarction. Exploring these pathophysiological mechanisms underlying ischemic tissue damage may direct rational drug design in the therapeutic treatment of stroke.

Animals↗
PubMed2006

Controlled release of lipopolysaccharide in the subarachnoid space of rabbits induces chronic vasospasm in the absence of blood.

OBJECTIVE: Leukocyte-endothelial cell interactions appear to play a role in the development of vasospasm after SAH. Using a purely inflammatory protein, LPS, we evaluated the effect of inflammation on the development of chronic vasospasm in the absence of blood and compared it to SAH-induced vasospasm in rabbits. METHODS: Lipopolysaccharide was incorporated into EVAc polymers to produce 20% LPS/EVAc polymers (wt/wt). Rabbits (n = 23) were randomized to 4 experimental groups: (1) empty polymer (n = 6), (2) SAH (n = 5), (3) 0.7 mg/kg polymeric LPS dose (n = 6), and (4) 1.4 mg/kg polymeric LPS dose (n = 6). Blood and polymers were inserted into the cisterna magna. The rabbits were killed 3 days postoperatively, and the basilar arteries were harvested for morphometric analysis. Clinical response and lumen patencies were analyzed using ANOVA and a post hoc Newman-Keuls Multiple Comparisons test. RESULTS: Significant narrowing of the basilar artery was observed by insertion of 20% LPS/EVAc polymers into the subarachnoid space at a polymeric dose of 1.4 mg/kg (actual dose, 66 microg kg(-1) d(-1)) (75.4% +/- 4.2%; P < .01) and by SAH (80.3% +/- 8.1%; P < .01) as compared with the empty polymer group. A trend toward narrowing was observed in the 0.7 mg/kg polymeric LPS dose group (actual dose, 33 microg kg(-1) d(-1)) (85.2% +/- 2.6%; P > .05). Symptoms associated with SAH were noted in 50% of the rabbits in the 0.7 mg/kg LPS group and in 100% of rabbits in the 1.4 mg/kg LPS group. CONCLUSION: Controlled release of LPS into the subarachnoid space of rabbits produced chronic vasospasm in a dose-dependent manner. At a polymeric dose of 1.4 mg/kg, LPS-induced vasospasm was equivalent to that induced by SAH. This suggests that LPS and SAH may induce vasospasm through similar mechanisms and provides further evidence that inflammation plays a central role in the etiology of chronic vasospasm.

Animals↗
PubMed2006

Leukocyte-endothelial cell interactions in chronic vasospasm after subarachnoid hemorrhage.

Leukocyte-endothelial cell interactions appear to be the root cause of chronic vasospasm after aneurysmal subarachnoid hemorrhage (aSAH). Early clinical observations and indirect experimental evidence suggested an association between inflammation and chronic vasospasm. Early clinical observations in patients with post-hemorrhagic vasospasm included pyrexia, leukocytosis and the presence of circulating immune complexes. Inflammatory infiltrates and increased levels of immunoglobulins and complement fractions within spastic cerebral arteries also provided early evidence for an inflammatory mechanism underlying chronic vasospasm. Early indirect experimental evidence included the ability to reproduce chronic vasospasm with the introduction of inflammatory agents into the subarachnoid space and the inhibition of vasospasm with anti-inflammatory agents. Currently, however, there is an increasing body of direct molecular evidence that demonstrates the pivotal role of leukocyte-endothelial cell interactions in the development of chronic vasospasm. Cell adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1), lymphocyte function-associated antigen-1 (LFA-1), macrophage antigen-1 (Mac-1) and endothelial (E)-selectin mediate interactions between circulating leukocytes and cerebral endothelium. Following aSAH, ICAM-1 is up-regulated in cerebral endothelial cells and along with other cell adhesion molecules, can be detected in the serum and cerebrospinal fluid (CSF) of patients with post-hemorrhagic vasospasm. Monoclonal antibody blocking experiments have demonstrated that the prevention of leukocyte extravasation into the subarachnoid space prevents chronic vasospasm. Similarly, drugs like ibuprofen, which prevent ICAM-1 up-regulation and transendothelial cell migration of leukocytes, prevent vasospasm. In this review, we highlight early observations that suggested an association between inflammation and post-hemorrhagic vasospasm, detail the role of leukocyte-endothelial cell interactions in the development of chronic vasospasm and discuss therapeutic implications of an inflammatory etiology of post-hemorrhagic cerebral vasospasm.

Animals↗
PubMed2006

Intracranial delivery of the nitric oxide donor diethylenetriamine/nitric oxide from a controlled-release polymer: toxicity in cynomolgus monkeys.

OBJECTIVE: Diethylenetriamine/nitric oxide (DETA/NO) has been shown to be an effective treatment for delayed posthemorrhagic vasospasm when released abluminally from ethylene-vinyl acetate copolymer (EVAc). However, the observed mortality associated with this drug warrants further investigation. To establish a maximum tolerable dose, this study evaluated the toxicity of DETA/NO released from EVAc in a dose-escalation series in cynomolgus monkeys (Macaca fascicularis). METHODS: DETA/NO was incorporated into EVAc at a 20:80 dry weight ratio (DETA/NO:EVAc). A total of 13 animals underwent a right frontotemporal craniotomy for placement of a single polymer delivering no drug (n = 3), 0.5 +/- 0.1 mg/kg (n = 3), 0.9 +/- 0.1 mg/kg (n = 3), 1.9 +/- 0.2 mg/kg (n = 3), or a 3.2 mg/kg dose (n = 1) into the subarachnoid space. RESULTS: The animal receiving the highest dose of DETA/NO (3.2 mg/kg) died 46 hours after surgery. The remaining animals survived for the planned duration of the study. One animal in the group receiving the 1.9 mg/kg dose experienced a seizure 25 hours after surgery and remained lethargic for 2 days before making a complete recovery. The remaining animals exhibited no adverse behavioral effects. Histopathological examination of brain tissue revealed hemorrhagic and ischemic changes at doses above 0.9 mg/kg. No evidence of vascular wall pathology or infection was observed in any animal. CONCLUSION: The greatest amount of DETA/NO safely delivered from EVAc copolymer to the subarachnoid space of the cynomolgus monkey is approximately 1.0 mg/kg. These findings show that continuous intracisternal delivery of DETA/NO is a safe and potentially effective strategy for prophylactic treatment of delayed cerebral vasospasm.

Animals↗
PubMed2006

Systemic administration of simvastatin after the onset of experimental subarachnoid hemorrhage attenuates cerebral vasospasm.

OBJECTIVE: Experimental evidence suggests that intercellular adhesion molecule-1 mediated leukocyte extravasation contributes to the pathogenesis of cerebral vasospasm. Simvastatin, an HMG-CoA reductase inhibitor, decreases intercellular adhesion molecule-1 expression and competitively inhibits leukocyte intercellular adhesion molecule-1 binding. We hypothesized that administration of simvastatin after the onset of subarachnoid hemorrhage (SAH) would attenuate perivascular granulocyte migration and ameliorate cerebral vasospasm in a rabbit model of SAH. METHODS: New Zealand white rabbits (n = 15) underwent injection of autologous blood into the cisterna magna or sham surgery followed by subcutaneous injection of simvastatin (40 mg/kg) or vehicle 30 minutes, 24 hours, and 48 hours after SAH or sham surgery. Seventy-two hours later, basilar artery lumen diameter was measured by in situ perfusion/fixation and image analysis. CD-18 monoclonal antibody stained perivascular granulocytes and macrophages were counted under light microscopy. RESULTS: In vehicle treated rabbits, mean +/- standard deviation basilar artery diameter was reduced 3 days after SAH (n = 5) versus sham (n = 5) rabbits (0.49 +/- 0.08 mm versus 0.75 +/- 0.03 mm, P < 0.01). After SAH, mean +/- standard deviation basilar artery diameter was greater in simvastatin (n = 5) treated rabbits versus vehicle (n = 5) (0.63 +/- 0.04 mm versus 0.49 +/- 0.08 mm, P < 0.01). In vehicle treated rabbits, SAH resulted in an increase in the mean +/- standard deviation perivascular CD18 cell count (sham-vehicle, 2.8 +/- 2; SAH-vehicle 90 +/- 27; P < 0.01). Subcutaneous administration of simvastatin attenuated this increase in perivascular CD18-positive cells after SAH (SAH statin, 41.6 +/- 13; SAH vehicle, 90 +/- 27; P < 0.001). CONCLUSION: Subcutaneous administration of simvastatin after the onset of SAH attenuates perivascular granulocyte migration and ameliorates basilar artery vasospasm after experimental SAH in rabbits. 5-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, such as simvastatin, may potentially serve as agents in the prevention of cerebral vasospasm after SAH.

Animals↗
PubMed2006

Hyperglycemia independently increases the risk of perioperative stroke, myocardial infarction, and death after carotid endarterectomy.

OBJECTIVE: Clinical and experimental evidence suggests that hyperglycemia lowers the neuronal ischemic threshold, potentiates stroke volume in focal ischemia, and is associated with morbidity and mortality in the surgical critical care setting. It remains unknown whether hyperglycemia during carotid endarterectomy (CEA) predisposes patients to perioperative stroke and operative related morbidity and mortality. METHODS: The clinical and radiological records of all patients undergoing CEA and operative day glucose measurement from 1994 to 2004 at an academic institution were reviewed and 30-day outcomes were assessed. The independent association of operative day glucose before CEA and perioperative morbidity and mortality were assessed via multivariate logistic regression analysis. RESULTS: One thousand two hundred and one patients with a mean age of 72 +/- 10 years (748 men, 453 women) underwent CEA (676 asymptomatic, 525 symptomatic). Overall, stroke occurred in 46 (3.8%) patients, transient ischemic attack occurred in 19 (1.6%), myocardial infarction occurred in 19 (1.6%), and death occurred in 17 (1.4%). Increasing operative day glucose was independently associated with perioperative stroke or transient ischemic attack (Odds ratio [OR], 1.005; 95% confidence interval [CI], 1.00-1.01; P = 0.03), myocardial infarction (OR, 1.01; 95% CI, 1.004-1.016; P = 0.017), and death (OR, 1.007; 95% CI, 1.00-1.015; P = 0.04). Patients with operative day glucose greater than 200 mg/dl were 2.8-fold, 4.3-fold, and 3.3-fold more likely to experience perioperative stroke or transient ischemic attack (OR, 2.78; 95% CI, 1.37-5.67; P = 0.005), myocardial infarction (OR, 4.29; 95% CI, 1.28-14.4; P = 0.018), or death (OR, 3.29; 95% CI, 1.07-10.1; P = 0.037), respectively. Median and interquartile range length of hospitalization was greater for patients with operative day glucose greater than 200 mg/dl (4 d [interquartile range, 2-15 d] versus 3 d [interquartile range, 2-7 d]; P < 0.05). CONCLUSION: Independent of previous cardiac disease, diabetes, or other comorbidities, hyperglycemia at the time of CEA was associated with an increased risk of perioperative stroke or transient ischemic attack, myocardial infarction, and death. Strict glucose control should be attempted before surgery to minimize the risk of morbidity and mortality after CEA.

Aged↗
PubMed2006

Orthogonal interlocking tandem clipping technique for the reconstruction of complex middle cerebral artery aneurysms.

OBJECTIVE: Complex aneurysms arising at the middle cerebral artery (MCA) bifurcation frequently present a microsurgical challenge to effectively obliterate while maintaining patency of the distal MCA branches. These aneurysms are often multilobed, with their long axis aligned with the long axis of the M1 trunk, placing the dome of the aneurysm in the surgeons' line of sight, preventing an unobstructed view of the entire bifurcation and proximal M1 segment. MCA aneurysms often have a broad neck, splaying the bifurcation. An orthogonal interlocking tandem clipping technique, maximizing the use of fenestrated aneurysm clips, is presented as a means to completely obliterate the aneurysm and simultaneously "reconstruct" the MCA bifurcation. CLINICAL PRESENTATIONS AND INTERVENTION: Fifteen complex MCA aneurysms were treated using an interlocking tandem clipping technique. In its simplest application, the blades of the initial aneurysm clip are incorporated into the fenestration of the second clip. Obliteration of the residual aneurysm is achieved with the blades of the second, fenestrated clip. RESULTS: Satisfactory aneurysm obliteration and reconstruction of the MCA bifurcation was achieved in all cases using this technique, with excellent neurological outcomes. CONCLUSION: Morphologically complex multilobed MCA aneurysms can be effectively clipped with "reconstruction" of the normal vascular anatomy using a tandem interlocking clipping technique. A fenestrated clip is used to incorporate the blades of the initial clip, while obliterating the remainder of the aneurysm.

Adult↗
PubMed2006

Acute subdural hematoma caused by an unruptured, thrombosed giant intracavernous aneurysm.

INTRODUCTION: Acute subdural hematoma (SDH) is an infrequent complication after aneurysmal subarachnoid hemorrhage. SDH associated with unruputed intracavernous aneurysm has never been reported. METHODS: Single patient case report and review of relevent literature. RESULTS: A 65-year-old woman with an unruptured, thrombosed giant intracavernous aneurysm developed an acute SDH 2 days after admission for cavernous sinus syndrome. Despite emergent evacuation of the SDH, the patient never regained consciousness because of brain herniation. CONCLUSION: Acute SDH is a rare complication of ruptured, giant intracavernous aneurysms. Erosion of the cavernous sinus wall by acute enlargement of the aneurysm after thrombosis is the proposed mechanism for development of the SDH.

Aged↗
PubMed2006

Lysis of intracerebral hematoma with stereotactically implanted tissue plasminogen activator polymers in a rabbit model.

OBJECT: Currently no adequate surgical treatment exists for spontaneous intracerebral hemorrhage (ICH). Implantable polymers can be used effectively to deliver therapeutic agents to the local site of the pathological process, thus reducing adverse systemic effects. The authors report the use of stereotactically implanted polymers loaded with tissue plasminogen activator (tPA) to induce lysis of ICH in a rabbit model. METHODS: Ethylene vinyl acetate (EVAc) polymers were loaded with bovine serum albumin (BSA) only or with BSA plus tPA. In vitro pharmacokinetic (three polymers) and thrombolysis (12 polymers) studies were performed. For the in vivo study, 12 rabbits were fixed in a stereotactic frame, and 0.2 ml of clotted autologous blood was injected into the right frontal lobe parenchyma. After 20 minutes, control BSA polymers were stereotactically implanted at the hemorrhage site in six rabbits, and experimental BSA plus tPA polymers were implanted in six rabbits. Animals were killed at 3 days, and blood clot volume was assessed. The pharmacokinetic study showed release of 146 ng of tPA over 3 days. The tPA activity correlated with in vitro thrombolysis. In the in vivo study, the six animals treated with tPA polymers had a mean (+/- standard error of the mean [SEM]) thrombus volume of 1.43 +/- 0.29 mm3 at 3 days, whereas the six animals treated with blank (BSA-only) polymers had a mean (+/- SEM) thrombus volume of 19.99 +/- 3.74 mm3 (p < 0.001). CONCLUSIONS: Ethylene vinyl acetate polymers release tPA over the course of 3 days. Stereotactic implantation of tPA-loaded EVAc polymers significantly reduced ICH volume. Polymers loaded with tPA may be useful clinically for lysis of ICH without the side effects of systemic administration of tPA.

Animals↗
PubMed2006

Personal recollections of Walter E. Dandy and his brain team.

Walter Edward Dandy (1886-1946) began his surgical training at the Johns Hopkins Hospital in 1910 and joined the faculty in 1918. During the next 28 years at Johns Hopkins, Dandy established a neurosurgery residency training program that was initially part of the revolutionary surgical training system established by William S. Halsted but eventually became a separate entity. Dandy's residents were part of his "Brain Team," a highly efficient organization that allowed Dandy to perform over 1000 operations per year, not counting ventriculograms. This team also provided rigorous training in the Halsted mold for the neurosurgical residents. Although exacting and demanding, Dandy was universally admired by his residents and staff. This article describes Dandy's neurosurgical residency program at Johns Hopkins, and provides personal recollections of training under Walter Dandy.

Baltimore↗
PubMed2005

3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors reduce the risk of perioperative stroke and mortality after carotid endarterectomy.

OBJECTIVE: There is increasing evidence that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) reduce cardiovascular and cerebrovascular events through anti-inflammatory, plaque stabilization, and neuroprotective effects independent of lipid lowering. This study was designed to investigate whether statin use reduces the incidence of perioperative stroke and mortality among patients undergoing carotid endarterectomy (CEA). METHODS: All patients undergoing CEA from 1994 to 2004 at a large academic medical center were retrospectively reviewed. The independent association of statin use and perioperative morbidity was assessed via multivariate logistic regression analysis. RESULTS: CEA was performed by 13 surgeons on 1566 patients (987 men and 579 women; mean age, 72 +/- 10 years), including 1440 (92%) isolated and 126 (8%) combined CEA/coronary artery bypass grafting procedures. The indication for CEA was symptomatic disease in 660 (42%) cases. Six hundred fifty-seven (42%) patients received a statin medication for at least 1 week before surgery. Statin use was associated with a reduction in perioperative strokes (1.2% vs 4.5%; P < .01), transient ischemic attacks (1.5% vs 3.6%; P < .01), all-cause mortality (0.3% vs 2.1%; P < .01), and median (interquartile range) length of hospitalization (2 days [2-5 days] vs 3 days [2-7 days]; P < .05). Adjusting for all demographics and comorbidities in multivariate analysis, statin use independently reduced the odds of stroke threefold (odds ratio [95% confidence interval], 0.35 [0.15-0.85]; P < .05) and death fivefold (odds ratio [95% confidence interval], 0.20 [0.04-0.99]; P < .05). CONCLUSIONS: These data suggest that perioperative statin use may reduce the incidence of cerebrovascular events and mortality among patients undergoing CEA.

Aged↗
PubMed2005

Intracranial aneurysms in the pediatric population: case series and literature review.

BACKGROUND: Intracranial aneurysms in children (< or =18 years old) are rare, and their epidemiology is poorly understood. We present a prospective 14-year experience at our institution and review the literature to clarify the characteristics and outcomes of pediatric patients with intracranial aneurysms. METHODS: Review of medical records in the Johns Hopkins aneurysm prospective database and review of the literature since 1939 were performed. RESULTS: Of 1377 intracranial aneurysm cases at our institution from 1991 to 2004, 19 (1.4%) pediatric patients were treated using microsurgical or endovascular techniques. Male/female ratio was 2.2:1. Eleven percent occurred at the internal carotid artery (ICA) bifurcation, and 42% were located in the posterior circulation. Seven (37%) were giant lesions; 58% presented with subarachnoid hemorrhage. Patients in good Hunt and Hess grade (I-III) comprised 42%, and poor-grade (IV-V) patients comprised 16%. At a mean follow-up duration of 3.0 +/- 3 years, 95% of patients demonstrated favorable outcomes with Glasgow Outcome Scale score of 4 or 5. In the literature, a total of 706 pediatric intracranial aneurysm cases have been described since 1939. The male/female ratio is 1.8:1. The ICA bifurcation was the location in 26%, and only 17% were in the posterior circulation. Twenty percent were giant lesions, and 80% presented with subarachnoid hemorrhage. Good- and poor-grade patients comprise 49% and 36% of the total cases, respectively. Favorable outcome was reported in 60%. CONCLUSIONS: During recent decades, good outcomes after the treatment of ruptured and unruptured pediatric aneurysms have increased, reaching 95% in the current series. Pediatric intracranial aneurysms occur more commonly in male patients and have a predilection for the terminal ICA bifurcation.

Adolescent↗
PubMed2005

Diagnosis and management of vein of galen aneurysmal malformations.

Vein of Galen aneurysmal malformations (VGAM) are rare intracranial vascular anomalies typically found in children. The anatomic landmark of a VGAM is the presence of multiple arteriovenous shunts draining into a dilated median prosencephalic vein, an embryonic vessel normally absent at the adult stage. This article reviews the developmental anatomy, the clinical presentation, and the current management of VGAM.

Bioethical Issues↗
PubMed2005

Contralateral approaches to multiple cerebral aneurysms.

Not infrequently, patients with bilateral cerebral aneurysms are encountered. In such patients, the ability to treat bilateral aneurysms through a unilateral approach spares the patient the risk and inconvenience associated with a separate craniotomy. The contralateral approach for aneurysm repair is technically feasible and safe in appropriately selected patients. Herein, we review our technique for maximizing contralateral exposure and clipping contralateral aneurysms through the four anatomic triangles that serve as corridors in this approach.

Humans↗