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Search Results: 1 - 10 of 297455 matches for " J Mocco "
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Normal Perfusion Pressure Breakthrough Following AVM Resection: A Case Report and Review of the Literature  [PDF]
T. E. O’Connor, K. M. Fargen, J. Mocco
Open Journal of Modern Neurosurgery (OJMN) , 2013, DOI: 10.4236/ojmn.2013.34015
Abstract: Objective: To report a patient’s clinical course illustrative of the NPPB mechanism for hyperperfusion-induced injury. Methods: A 65-year-old female presented with a severe headache and was found to have a 6-cm right parietal AVM on imaging. The patient underwent staged, pre-operative embolization and the AVM was surgically resected without intra-operative complication. After the patient emerged from anesthesia she exhibited left hemiplegia and hemispatial neglect. Her systolic blood pressure (SBP) at that time was between 110-120 mmHg. SBP was reduced to 90-100 mmHg and the patient’s symptoms resolved shortly thereafter. The patient’s strict blood pressure goal was relaxed the next morning. However, with her SBP 110-120 mmHg in the ensuing hours, the patient’s left-sided neglect and hemiparesis returned. Her SBP was reduced again to 90-100 mmHg, leading to resolution of her symptoms. Results: This patient’s clinical course supports the NPPB theory of hyperperfusion-induced injury. Despite CT imaging demonstrating no residual AVM following resection, the patient developed neurological deficits in the immediate postoperative period. Aggressive systemic hypotension improved clinical symptoms repeatedly, whereas a brief period of normotension triggered a return of neurological deficits. As a result, there was a direct correlation between fluctuations of neurological status and SBP. This case suggests that the intrinsic autoregulatory capacity was altered in our patient, and that aggressive hypotension was necessary to compensate for diminished autonomic reactivity. Conclusions: This case provides further evidence that NPPB plays a role in hyperperfusion-induced injury following AVM excision and that blood pressure control is vital in managing hyperemic complications following complete resection of cerebral AVMs.
Nitric Oxide in Cerebral Vasospasm: Theories, Measurement, and Treatment
Michael Siuta,Scott L. Zuckerman,J. Mocco
Neurology Research International , 2013, DOI: 10.1155/2013/972417
Abstract: In recent decades, a large body of research has focused on the role of nitric oxide (NO) in the development of cerebral vasospasm (CV) following subarachnoid hemorrhage (SAH). Literature searches were therefore conducted regarding the role of NO in cerebral vasospasm, specifically focusing on NO donors, reactive nitrogen species, and peroxynitrite in manifestation of vasospasm. Based off the assessment of available evidence, two competing theories are reviewed regarding the role of NO in vasospasm. One school of thought describes a deficiency in NO due to scavenging by hemoglobin in the cisternal space, leading to an NO signaling deficit and vasospastic collapse. A second hypothesis focuses on the dysfunction of nitric oxide synthase, an enzyme that synthesizes NO, and subsequent generation of reactive nitrogen species. Both theories have strong experimental evidence behind them and hold promise for translation into clinical practice. Furthermore, NO donors show definitive promise for preventing vasospasm at the angiographic and clinical level. However, NO augmentation may also cause systemic hypotension and worsen vasospasm due to oxidative distress. Recent evidence indicates that targeting NOS dysfunction, for example, through erythropoietin or statin administration, also shows promise at preventing vasospasm and neurotoxicity. Ultimately, the role of NO in neurovascular disease is complex. Neither of these theories is mutually exclusive, and both should be considered for future research directions and treatment strategies. 1. Introduction Subarachnoid hemorrhage (SAH) is a form of stroke that affects 28,000 individuals in North America each year [1]. A frequent cause of SAH is the rupture of an intracranial aneurysm, leading to extravasation of blood into the subarachnoid space. While aneurysmal SAH accounts for only 7% of all cerebrovascular accidents (CVAs), those that suffer SAH have an average age of 51 years, significantly younger than those with a thromboembolic or hemorrhagic stroke [1]. Due to the young age of these patients, they have great potential to return to their premorbid state and level of productivity, with successful intervention. However, even with endovascular or surgical repair of the offending aneurysm, those that survive the initial insult can still accumulate additional neurologic defects in the days and weeks post-hemorrhage. Enormous efforts to understand and prevent additional mortality following SAH led to the discovery of the phenomenon known as cerebral vasospasm (CV) [1]. CV refers to the constriction of smooth muscle
Evidence-Based Cerebral Vasospasm Surveillance
Heather Kistka,Michael C. Dewan,J. Mocco
Neurology Research International , 2013, DOI: 10.1155/2013/256713
Abstract: Subarachnoid hemorrhage related to aneurysmal rupture (aSAH) carries significant morbidity and mortality, and its treatment is focused on preventing secondary injury. The most common—and devastating—complication is delayed cerebral ischemia resulting from vasospasm. In this paper, the authors review the various surveillance technologies available to detect cerebral vasospasm in the days following aSAH. First, evidence related to the most common modalities, including transcranial doppler ultrasonography and computed tomography, are reviewed. Continuous electroencephalography and older instruments such as positron emission tomography, xenon-enhanced CT, and single-photon emission computed tomography are also discussed. Invasive strategies including brain tissue oxygen monitoring, microdialysis, thermal diffusion, and jugular bulb oximetry are examined. Lastly, near-infrared spectroscopy, a recent addition to the field, is briefly reviewed. Each surveillance tool carries its own set of advantages and limitations, and the concomitant use of multiple modalities serves to improve diagnostic sensitivity and specificity. 1. Introduction Subarachnoid hemorrhage (SAH) resulting from a ruptured intracranial aneurysm affects approximately 30,000 individuals in USA each year [1]. While many of these patients die before reaching a hospital, the majority are admitted to an intensive care unit where their clinical status can be closely monitored. The damage created by the initial insult of an SAH is irreversible. Therefore, treatment of SAH patients is focused on preventing secondary injury in an effort to minimize morbidity and mortality. The most devastating injury is also among the most common: delayed cerebral ischemia (DCI). Delayed cerebral ischemia affects approximately 30% of all SAH patients and is correlated with a poor outcome as measured by long-term disability and mortality [2, 3]. There have been inconsistencies in the literature regarding the definition of DCI and its frequent precursor, vasospasm. As not all DCI is preceded by vasospasm, this has led to recent efforts to standardize terminology. In general, vasospasm is the result of vasoconstriction or vascular endothelial swelling resulting in a narrowing of the intracranial arteries [4]. On the other hand, DCI is characterized by a new focal neurological deficit, a decrease in the level of consciousness, or radiographic evidence of new infarct [5]. Vasospasm is a radiographic diagnosis that does not necessarily correlate with functional outcome whereas DCI is directly related to morbidity and
Current Controversies in the Prediction, Diagnosis, and Management of Cerebral Vasospasm: Where Do We Stand?
Young Lee,Scott L. Zuckerman,J. Mocco
Neurology Research International , 2013, DOI: 10.1155/2013/373458
Abstract: Aneurysmal subarachnoid hemorrhage occurs in approximately 30,000 persons in the United States each year. Around 30 percent of patients with aneurysmal subarachnoid hemorrhage suffer from cerebral ischemia and infarction due to cerebral vasospasm, a leading cause of treatable death and disability following aneurysmal subarachnoid hemorrhage. Methods used to predict, diagnose, and manage vasospasm are the topic of recent active research. This paper utilizes a comprehensive review of the recent literature to address controversies surrounding these topics. Evidence regarding the effect of age, smoking, and cocaine use on the incidence and outcome of vasospasm is reviewed. The abilities of different computed tomography grading schemes to predict vasospasm in the aftermath of subarachnoid hemorrhage are presented. Additionally, the utility of different diagnostic methods for the detection and visualization of vasospasm, including transcranial Doppler ultrasonography, CT angiography, digital subtraction angiography, and CT perfusion imaging is discussed. Finally, the recent literature regarding interventions for the prophylaxis and treatment of vasospasm, including hyperdynamic therapy, albumin, calcium channel agonists, statins, magnesium sulfate, and endothelin antagonists is summarized. Recent studies regarding each topic were reviewed for consensus recommendations from the literature, which were then presented. 1. Introduction Aneurysmal subarachnoid hemorrhage (aSAH) is a relatively rare cause of stroke, occurring in approximately 30,000 persons in the United States each year. However, its impact equals that of cerebral ischemia, the most common cause of stroke, due to its higher morbidity, higher mortality, and occurrence in younger individuals. Approximately 20 to 30 percent of patients with aSAH suffer from cerebral ischemia and infarction due to cerebral vasospasm, which is the number one cause of treatable death and disability following aSAH. Vasospasm occurs most frequently at 7 to 8 days after aSAH and can last for a prolonged period. Clinical vasospasm is defined as a decline in neurologic status due to vasospasm and can result in severe morbidity and mortality. However, clinical vasospasm has also been observed after other invasive and traumatic processes such as craniotomy and traumatic brain injury. The pathogenesis and etiology of this vasospasm are very poorly understood, and treatments to prevent post-SAH vasospasm are widely varied and have greatly different magnitudes of effectiveness. New methods to predict, diagnosis, and manage
The Role of Magnesium in the Management of Cerebral Vasospasm
Mitchell J. Odom,Scott L. Zuckerman,J Mocco
Neurology Research International , 2013, DOI: 10.1155/2013/943914
Abstract: Subarachnoid hemorrhage (SAH) is characterized by bleeding into the subarachnoid space, often caused by ruptured aneurysm. Aneurysmal rupture occurs in 700,000 individuals per year worldwide, with 40,000 cases taking place in the United States. Beyond the high mortality associated with SAH alone, morbidity and mortality are further increased with the occurrence of cerebral vasospasm, a pathologic constriction of blood vessels that can lead to delayed ischemic neurologic deficits (DIND). Treatment of cerebral vasospasm is a source of contention. One extensively studied therapy is Magnesium (Mg) as both a competitive antagonist of calcium at the N-methyl D-aspartate (NMDA) receptor, and a noncompetitive antagonist of both IP3 and voltage-gated calcium channels, leading to smooth muscle relaxation. In our literature review, several animal and human studies are summarized in addition to two Phase III trials assessing the use of intravenous Mg in the treatment of SAH (IMASH and MASH-2). Though many studies have shown promise for the use of Mg in SAH, there has been inconsistency in study design and outcomes. Furthermore, the results of the recently completed clinical trials have shown no significant benefit from using intravenous Mg as adjuvant therapy in the treatment of cerebral vasospasm. 1. Introduction Subarachnoid hemorrhage (SAH) due to ruptured aneurysm occurs in 700,000 individuals a year [1], with nearly 40,000 of those cases occurring in the United States [2]. The mortality rate associated with the occurrence of SAH appears to have improved over the last 50 years [3], though it still remains that nearly half of all patients with a SAH will die within one month of the initial bleed [1]. Treatment of SAH is challenged by a number of complications. Cerebral vasospasm can occur in a majority of patients [4, 5] and is associated with poor outcome [5–8]. Despite having been recorded in patients treated for aneurysmal subarachnoid hemorrhage in 1951 [9], cerebral vasospasm (CVS) still remains a prevalent and morbid complication of SAH [10]. The occurrence of secondary ischemia and delayed ischemic neurologic deficits (DIND) is common sequelae in vasospasm and often leads to poor long-term outcomes. The diagnosis and treatment of CVS are made complicated by the heterogeneity of presentation and ambiguous etiology. Cerebral vasospasm is defined both clinically and angiographically, though these definitions are not mutually inclusive [11]. The occurrence of vasospasm is biphasic [1] with an acute phase that has been reported to begin 10 minutes [12] to 3-4
Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia
Kevin R. Carr,Scott L. Zuckerman,J Mocco
Neurology Research International , 2013, DOI: 10.1155/2013/506584
Abstract: Cerebral vasospasm (CVS) is a potentially lethal complication of aneurysmal subarachnoid hemorrhage (aSAH). Recently, the symptomatic presentation of CVS has been termed delayed cerebral ischemia (DCI), occurring as early as 3-4 days after the sentinel bleed. For the past 5-6 decades, scientific research has promulgated the theory that cerebral vasospasm plays a primary role in the pathology of DCI and subsequently delayed ischemic neurological decline (DIND). Approximately 70% of patients develop CVS after aSAH with 50% long-term morbidity rates. The exact etiology of CVS is unknown; however, a well-described theory involves an antecedent inflammatory cascade with alterations of intracellular calcium dynamics and nitric oxide fluxes, though the intricacies of this inflammatory theory are currently unknown. Consequently, there have been few advances in the clinical treatment of this patient cohort, and morbidity remains high. Identification of intermediaries in the inflammatory cascade can provide insight into newer clinical interventions in the prevention and management of cerebral vasospasm and will hopefully prevent neurological decline. In this review, we discuss current theories implicating the inflammatory cascade in the development of CVS and potential treatment targets. 1. Introduction Subarachnoid hemorrhage (SAH) is a devastating neurological insult that causes significant morbidity and mortality [1]. One of the greatest sources of this morbidity and mortality is cerebral vasospasm (CVS), leading to delayed cerebral ischemia (DCI) [2]. While angiographic vasospasm is thought to occur in approximately 70% of patients after aSAH, only 25% develop symptomatic CVS [3, 4]. Morbidity remains high despite years of clinical and basic science research done on the topic, with approximately 50% infarction rates in affected patients [5, 6]. An antecedent inflammatory cascade is one of the many etiologies thought to be responsible for the development of CVS. Experimental studies have shown involvement of cytokines, cell adhesion molecules, and leukocytes, and early clinical studies have attempted to inhibit components of the inflammatory cascade to mitigate CVS [7–19]. Additionally, endothelin receptor activation, nitric oxide inhibition, thromboxane receptor modification, and many cell signaling cascades are thought to play an integral role in the development of this pathology [20–27]. Currently, the primary treatment for this patient population involves hemodynamic augmentation and medically or surgically mediated intra-arterial vasodilation. These
Genetics of Cerebral Vasospasm
Travis R. Ladner,Scott L. Zuckerman,J Mocco
Neurology Research International , 2013, DOI: 10.1155/2013/291895
Abstract: Cerebral vasospasm (CV) is a major source of morbidity and mortality in aneurysmal subarachnoid hemorrhage (aSAH). It is thought that an inflammatory cascade initiated by extravasated blood products precipitates CV, disrupting vascular smooth muscle cell function of major cerebral arteries, leading to vasoconstriction. Mechanisms of CV and modes of therapy are an active area of research. Understanding the genetic basis of CV holds promise for the recognition and treatment for this devastating neurovascular event. In our review, we summarize the most recent research involving key areas within the genetics and vasospasm discussion: (1) Prognostic role of genetics—risk stratification based on gene sequencing, biomarkers, and polymorphisms; (2) Signaling pathways—pinpointing key inflammatory molecules responsible for downstream cellular signaling and altering these mediators to provide therapeutic benefit; and (3) Gene therapy and gene delivery—using viral vectors or novel protein delivery methods to overexpress protective genes in the vasospasm cascade. 1. Introduction Cerebral vasospasm (CV) is the narrowing of the major cerebral arteries following aneurysmal subarachnoid hemorrhage (aSAH) and is a leading contributor to the morbidity and mortality associated with aSAH. The annual incidence of aSAH in the United States is between 21,000 and 33,000 people [1]. Of these, approximately 67% will develop vasospasm [2, 3]. In the setting of aSAH, CV has a biphasic course, with an acute and chronic phase. The acute phase typically begins 3 to 4 hours after hemorrhage, with rapid, spontaneous resolution. In contrast, the chronic phase begins 3 to 5 days later, with maximum narrowing between days 6 and 8, resolving after about 14 days [4]. CV can be diagnosed angiographically or clinically. Angiographic vasospasm refers to the observed narrowing of contrast medium in the major cerebral arteries. Radiologic modalities used to diagnose CV include computed tomography angiography (CTA), magnetic resonance angiography (MRA), and catheter angiography. Clinical vasospasm is the sequelae of neurocognitive deficits presumably as a result of a prolonged ischemic state. Both angiographic and clinical vasospasms can lead to cerebral infarction. Angiographic and clinical vasospasms appear to be distinct phenomena, with aSAH patients presenting with angiographic CV only (43% of patients), both angiographic and clinical CV (33% of patients), or none of them (24% of patients) [5]. Although there are many hypotheses on the pathogenesis of CV, it still remains a poorly understood
SDF1-A Facilitates Lin?/Sca1+ Cell Homing following Murine Experimental Cerebral Ischemia
J. Mocco, Aqeela Afzal, Saeed Ansari, Annemarie Wolfe, Kenneth Caldwell, E S. Connolly, Edward W. Scott
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0085615
Abstract: Background Hematopoietic stem cells mobilize to the peripheral circulation in response to stroke. However, the mechanism by which the brain initiates this mobilization is uncharacterized. Methods Animals underwent a murine intraluminal filament model of focal cerebral ischemia and the SDF1-A pathway was evaluated in a blinded manner via serum and brain SDF1-A level assessment, Lin?/Sca1+ cell mobilization quantification, and exogenous cell migration confirmation; all with or without SDF1-A blockade. Results Bone marrow demonstrated a significant increase in Lin?/Sca1+ cell counts at 24 hrs (272±60%; P<0.05 vs sham). Mobilization of Lin?/Sca1+ cells to blood was significantly elevated at 24 hrs (607±159%; P<0.05). Serum SDF1-A levels were significant at 24 hrs (Sham (103±14), 4 hrs (94±20%, p = NS) and 24 hrs (130±17; p<0.05)). Brain SDF1-A levels were significantly elevated at both 4 hrs and 24 hrs (113±7 pg/ml and 112±10 pg/ml, respectively; p<0.05 versus sham 76±11 pg/ml). Following administration of an SDF1-A antibody, Lin?/Sca1+ cells failed to mobilize to peripheral blood following stroke, despite continued up regulation in bone marrow (stroke bone marrow cell count: 536±65, blood cell count: 127±24; p<0.05 versus placebo). Exogenously administered Lin?/Sca1+ cells resulted in a significant reduction in infarct volume: 42±5% (stroke alone), versus 21±15% (Stroke+Lin?/Sca1+ cells), and administration of an SDF1-A antibody concomitant to exogenous administration of the Lin?/Sca1+ cells prevented this reduction. Following stroke, exogenously administered Lin?/Sca1+ FISH positive cells were significantly reduced when administered concomitant to an SDF1-A antibody as compared to without SDF1-A antibody (10±4 vs 0.7±1, p<0.05). Conclusions SDF1-A appears to play a critical role in modulating Lin?/Sca1+ cell migration to ischemic brain.
The baboon (Papio anubis) extracranial carotid artery: An anatomical guide for endovascular experimentation
J Mocco, Daniel J Hoh, M Nathan Nair, Tanvir F Choudhri, William J Mack, Ilya Laufer, E Sander Connolly
BMC Cardiovascular Disorders , 2001, DOI: 10.1186/1471-2261-1-4
Abstract: We characterized the extracranial carotid system often male baboons (Papio anubis, range 15.1–28.4 kg) by early post-mortem dissection. Photographic documentation of vessel lengths, lumen diameters, and angles of origin were measured for each segment of the carotid bilaterally.The common carotid arteries averaged 94.7 ± 1.7 mm (left) and 87.1 ± 1.6 mm (right) in length. The average minimal common carotid lumen diameters were 3.0 ± 0.3 mm (left) and 2.9 ± 0.2 mm (right). Each animal had a common brachiocephalic artery arising from the aorta which bifurcated into the left common carotid artery and right braciocephalic artery after 21.5 ± 1.6 mm. The vascular anatomy was found to be consistent among animals despite a wide range of animal weights.The consistency in the Papio anubis extracranial carotid system may promote the use of this species in the preclinical investigation of neuro-interventional therapies.There has been a recent interest in developing aggressive interventional strategies for the treatment of a variety of neurological diseases including stroke, subarachnoid hemorrhage, and head trauma [1-4]. Successful translation of these therapies to the clinical arena, however, is critically dependent on the use of appropriate experimental models [5]. Non-human primate models of neurological diseases currently exist and have the advantage of most closely mimicking human physiology [6]. These models are particularly relevant to neuro-interventional research in that anatomical similarities permit routine vascular access and evaluation of devices designed on a clinically relevant scale.Conducting experimental primate endovascular studies, however, requires a comprehensive understanding of the carotid vascular system. Previous investigations of non-human primate vascular anatomy have focused primarily on the general morphology of the vessels and not on vessel angles, lengths, or lumen diameters which are necessary for guiding endovascular technology [7,8]. To answer
New components of the mercury’s perihelion precession  [PDF]
J. J. Smulsky
Natural Science (NS) , 2011, DOI: 10.4236/ns.2011.34034
Abstract: The velocity of perihelion rotation of Mercury's orbit relatively motionless space is computed. It is prove that it coincides with that calculated by the Newtonian interaction of the planets and of the compound model of the Sun’s rotation.
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