Establishment of primary stroke centers: a survey of physician attitudes and hospital resources.

OBJECTIVES: To survey US physicians involved in acute stroke care to determine the proportion of hospitals that currently meet the recommended Brain Attack Coalition (BAC) criteria for Primary Stroke Centers (PSC) and obtain opinions regarding the value of stroke centers. METHODS: A survey regarding the BAC guidelines for the establishment of stroke centers was mailed to 3,245 US neurologists, neurosurgeons, and emergency physicians. RESULTS: A total of 1,032 responses were received. Seventy-nine percent (range by specialty 58 to 98%) of respondents believed there was a need for stroke centers. If formal stroke center designation were established, 81% (range 72 to 90%) would like their hospital to become a PSC. Although 77% of respondents believed that their hospital currently met recommended criteria for a PSC, only 7% actually meet all recommended elements. However, 44% of hospitals already provide most acute stroke services. The BAC criteria most frequently lacking were continuing medical education for professional stroke center staff, stroke training for emergency department staff, formal establishment of a stroke unit, and designation of a stroke center director. CONCLUSIONS: The majority of emergency medicine and neuroscience physician respondents involved in acute stroke care support the designation of primary stroke centers. Although respondents globally overestimated the extent to which their facilities currently meet BAC recommended criteria for PSC, detailed responses suggested that over 40% of hospitals possess substantial existing acute stroke care resources and are poised to function as PSC with modest additional administrative and financial commitment.

Advances in the genetics of cerebrovascular disease and stroke.

MEDLINE searches identified epidemiologic, experimental, and clinical studies on the genetics of cerebrovascular disease and stroke, including the following topics: genetic epidemiology of stroke; genetics of systemic disorders that cause ischemic stroke, including coagulation disorders, connective tissue disorders, vasculopathies, metabolic disorders, and disorders of unknown etiology; and genetics of systemic disorders that cause hemorrhagic stroke. Recent discoveries in stroke genetics involve the genetic basis of monogenic disorders such as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy and sickle cell disease. Reproducing similar advances in other forms of cerebrovascular disease and stroke will be more difficult because their inheritance is complex, multigenic, and heterogeneous. However, the future is promising with the application of molecular genetic approaches such as linkage analysis, allele-sharing methods, association studies, and polygenic analysis of experimental crosses as well as the transmission/disequilibrium test--a statistical method for detection of linkage between a marker and a disease-susceptibility locus.

Experimental radiosurgery simulations using a theoretical model of cerebral arteriovenous malformations.

BACKGROUND AND PURPOSE: A novel biomathematical arteriovenous malformation (AVM) model based on electric network analysis was used to investigate theoretically the potential role of intranidal hemodynamic perturbations in elevating the risk of rupture after simulated brain AVM radiosurgery. METHODS: The effects of radiation on 28 interconnected plexiform and fistulous AVM nidus vessels were simulated by predefined random or stepwise occlusion. Electric circuit analysis revealed the changes in intranidal flow, pressure, and risk of rupture at intervals of 3 months during a 3-year latency period after simulated partial/complete irradiation of the nidus using doses <25 and >/=25 Gy. An expression for risk of rupture was derived on the basis of the functional distribution of the critical radii of component vessels. The theoretical effects of radiation were also tested on AVM nidus vessels with progressively increasing elastic modulus (E:) and wall thickness during the latency period, simulating their eventual fibrosis. RESULTS: In an AVM with E=5. 0x10(4) dyne/cm(2), 4 (14.3%) of a total 28 sets of AVM radiosurgery simulations revealed theoretical nidus rupture (risk of rupture >/=100%). Three of these were associated with partial nidus coverage and 1 with complete treatment. All ruptures occurred after random occlusion of nidus vessels in AVMs receiving low-dose radiosurgery. Intranidal hemodynamic perturbations were observed in all cases of AVM rupture; the occlusion of a fistulous component resulted in intranidal rerouting of flow and escalation of the intravascular pressure in adjacent plexiform components. Risk of rupture was found to correlate with nidus vessel wall strength: a low E: of 1.9x10(4) dyne/cm(2) resulted in a 92.8% incidence of AVM rupture, whereas a higher E: of 7.0x10(4) dyne/cm(2) resulted in only a 3.6% incidence of AVM rupture. A dramatic reduction in rupture incidence was observed when increasing fibrosis of the nidus was modeled during the latency period. CONCLUSIONS: It was found that the theoretical occurrence of AVM hemorrhage after radiosurgery was low, particularly when radiation-induced fibrosis of nidus vessels was considered. When rupture does occur, it would appear from a theoretical standpoint that the occlusion of intranidal fistulas or larger-caliber plexiform vessels could be a significant culprit in the generation of critical intranidal hemodynamic surges resulting in nidus rupture. The described AVM model should serve as a useful research tool for further theoretical investigations of cerebral AVM radiosurgery and its hemodynamic sequelae.

Can induction of systemic hypotension help prevent nidus rupture complicating arteriovenous malformation embolization?: analysis of underlying mechanism achieved using a theoretical model.

BACKGROUND AND PURPOSE: Nidus rupture is a serious complication of intracranial arteriovenous malformation (AVM) embolotherapy, but its pathogenetic mechanisms are not well described. An AVM model based on electrical network analysis was used to investigate theoretically the potential role of hemodynamic perturbations for elevating the risk of nidus vessel rupture (Rrupt) after simulated AVM embolotherapy, and to assess the potential benefit of systemic hypotension for preventing rupture. METHODS: Five separate hypothetical mechanisms for nidus hemorrhage were studied: 1) intranidal rerouting of blood pressure; 2) extranidal rerouting of blood pressure; 3) occlusion of draining veins with glue; 4) delayed thrombosis of draining veins; and 5) excessively high injection pressures proximal to the nidus. Simulated occlusion of vessels or elevated injection pressures were implemented into the AVM model, and electrical circuit analysis revealed the consequent changes in intranidal flow, pressure, and Rrupt for the nidus vessels. An expression for Rrupt was derived based on the functional distribution of the critical radii of component vessels. If AVM rupture was observed (Rrupt > or = 100%) at systemic normotension (mean pressure [P] = 74 mm Hg), the theoretical embolization was repeated under systemic hypotension (minor P = 70 mm Hg, moderate P = 50 mm Hg, or profound P = 25 mm Hg) to assess the potential benefit of this maneuver in reducing hemorrhage rates. RESULTS: All five pathogenetic mechanisms under investigation were able to produce rupture of AVMs during or after embolotherapy. These different mechanisms had in common the capability of generating surges in intranidal hemodynamic parameters resulting in nidus vessel rupture. The theoretical induction of systemic hypotension during and after treatment was shown to be of significant benefit in attenuating these surges and reducing Rrupt to safer levels below 100%. CONCLUSION: The induction of systemic hypotension during and after AVM embolization would appear theoretically to be of potential use in preventing iatrogenic nidus hemorrhage. The described AVM model should serve as a useful research tool for further theoretical investigations of AVM embolotherapy and its hemodynamic sequelae.

Transvenous retrograde nidus sclerotherapy under controlled hypotension (TRENSH): a newly proposed treatment for brain arteriovenous malformations--concepts and rationale.

PURPOSE: An alternative endovascular treatment to conventional transarterial embolization of cerebral arteriovenous malformations (AVMs) is proposed. CONCEPT: According to this proposed treatment, selected AVMs could undergo transvenous retrograde nidus sclerotherapy under controlled hypotensive anesthesia (TRENSH). RATIONALE: It is hypothesized that TRENSH may provide the means of avoiding delivery of embolic agents via arterial feeders (thus preventing ischemic complications), in addition to a possible more complete permeation of an AVM nidus with a sclerosant than can otherwise be obtained with current agents via arterial feeders. DISCUSSION: Instead of relying on access to an AVM nidus from the arterial side (with its usual complexity), TRENSH would require retrograde access to the lesion via much larger and anatomically simpler draining veins. Retrograde permeation of the AVM nidus may then be possible with a liquid sclerosant (to effect a "chemical embolization") provided that the arterial inflow is reduced sufficiently by temporary controlled systemic hypotension, with or without the aid of temporary balloon occlusion of the main arterial feeder(s). Retrograde spread of sclerosant within the nidus that falls short of filling arterial feeders and their branches to normal brain tissue may then be possible. Angioarchitectural and hemodynamic considerations are addressed, as are the potential role and limitations of TRENSH in the management of cerebral pial AVMs. Future implementation of this new technique in some specific selected cases in which the anatomic configuration of the AVM and its draining veins might be favorable could prove to be a potentially useful addition to the armamentarium of AVM therapies, which currently includes microsurgery, radiosurgery, and transarterial embolotherapy. Experimental studies directed at assessing the feasibility of TRENSH before potential future clinical application seem justified.

Theoretical modelling of arteriovenous malformation rupture risk: a feasibility and validation study.

PURPOSE: To explore the feasibility of using a theoretical computational model to simulate the risk of spontaneous arteriovenous malformation (AVM) haemorrhage. METHODS: Data from 12 patients were collected from a prospective databank which documented the angioarchitecture and morphological characteristics of the AVM and the feeding mean arterial pressure (FMAP) measured during initial superselective angiography prior to any treatment. Using the data, a computational model of the cerebral circulation and the AVM was constructed for each patient (patient-specific model). Two model risk (Risk(model)) calculations (haemodynamic- and structural-weighted estimates) were performed by using the patient-specific models. In our previously developed method of haemodynamic-weighted estimate, Risk(model) was calculated with the simulated intranidal pressures related to its maximal and minimal values. In the method of structural-weighted estimate developed and described in this paper, the vessel mechanical properties and probability calculation were considered in more detail than in the haemodynamic-weighted estimate. Risk(model) was then compared to experimentally determined risk which was calculated using a statistical method for determining the relative risk of having initially presented with AVM haemorrhage, termed Risk(exp). RESULTS: The Risk(model) calculated by both haemodynamic- and structural-weighted estimates correlated with experimental risks with chi2 = 6.0 and 0.64, respectively. The risks of the structural-weighted estimate were more correlated to experimental risks. CONCLUSIONS: Using two different approaches to the calculation of AVM haemorrhage risk, we found a general agreement with independent statistical estimates of haemorrhagic risk based on patient data. Computational approaches are feasible; future work can focus on specific pathomechanistic questions. Detailed patient-specific computational models can also be developed as an adjunct to individual patient risk assessment for risk-stratification purposes.

Anatomical and morphological factors correlating with rupture of intracranial aneurysms in patients referred for endovascular treatment.

The size of intracranial aneurysms is the only characteristic shown to correlate with their rupture. However, the critical size for rupture has varied considerably among previous accounts and remains a point of controversy. Our goal was to identify statistically significant clinical and morphological factors predictive of the occurrence of rupture and aneurysm size in patients referred for endovascular treatment. We retrospectively recorded the following factors from 74 patients who presented with ruptured (40) or unruptured (34) aneurysms: aneurysm morphology (uni/multilobulated), location (anterior/posterior), maximum diameter, diameter of the neck, and the patient's age and sex. We performed stepwise discriminant, and stepwise and logistic regression analysis to identify factors predicting rupture and the size of the aneurysm at rupture. The mean diameter of the ruptured aneurysms was 11.9+/-6.3 mm, range 3.0-33.0 mm, and that of the unruptured aneurysm 13.5+/-5.8 mm, range 5.0-30 mm. Stepwise discriminant analysis identified aneurysm morphology (P < 0.001) and location in the intracranial circulation (P < 0.001) as statistically significant factors in predicting rupture. Stepwise regression analysis revealed that aneurysm morphology and the size of the neck were predictors of aneurysm size at rupture.

Principles and philosophy of modeling in biomedical research.

Despite widespread applications in biomedical research, the role of models and modeling is often controversial and ill understood. It is usual to find that fundamental definitions, axioms, and postulates used in the modeling process have become tacit assumptions. What is essential, however, is a clear vision of the fundamental principles of modeling. This is even more compelling for new and emerging interdisciplinary fields that use techniques from previously separate scientific disciplines. This article outlines and reviews the central nature and philosophy of modeling, the rules that govern it, and its underlying key integral relationship to the 'scientific method'. A comprehensive understanding of these issues is indispensable to successful research and meaningful progress in all facets of biomedicine.

Biophysical mechanisms of stroke.

BACKGROUND: Stroke is the third leading cause of death and the leading cause of long-term disability in the United States. Although a host of genetic, biochemical, physiological, anatomic, and histological factors have been implicated, to varying degrees, in the pathogenesis of stroke, biophysical factors are believed to play a significant role in the development, diagnosis, and therapy of stroke. The purpose of this review article is to identify, describe, and illustrate these causes and biophysical and hemodynamic mechanisms predisposing a person to stroke, which often form the basis for novel methods of diagnosis and therapy. SUMMARY OF REVIEW: This mini-review begins by describing the physical principles that govern the flow of blood through normal and stenosed carotid artery bifurcations. In addition to the tortuosity, curvature, and tensile forces of the carotid artery bifurcation, the effects of biophysical phenomena from flowing blood such as viscous forces, pressure forces, velocity, kinetic energy, momentum, impulse, shear stress, and vibrational displacements exerted by the flowing blood on the vessel wall are conducive to abnormal flow behavior and patterns, degrading the vessel wall and creating the potential for stroke. CONCLUSIONS: Recent advances in the treatment of stroke are based on increasing knowledge of its underlying biophysical mechanisms, as well as on better-publicized advances in imaging instrumentation and procedures for the management and treatment of patients.

Assessment of intraaxial and extraaxial brain lesions with digitized computed tomographic images versus film: ROC analysis.

RATIONALE AND OBJECTIVES: The authors evaluated the diagnostic accuracy of viewing computed tomographic (CT) scans as film versus soft-copy images at a workstation. METHODS: Receiver operating characteristic analysis of the interpretation of 202 CT scans (103 were normal, 99 were abnormal) by five neuroradiologists was performed. Abnormal images contained high- or low-attenuation intraaxial lesions or extraaxial fluid (subdural, subarachnoid, or epidural hemorrhage). Hard copies were read on a standard light box, and digital images were examined at a 1,024 x 1,250 workstation. Lesion location and type and confidence ratings were recorded on a worksheet. RESULTS: There were no statistically significant differences in diagnostic accuracy between the two display modes. Reader performance was slightly better with the workstation in the assessment of low-attenuation lesions. CONCLUSION: Diagnostic accuracy is similar for CT scans displayed at a workstation and those displayed as hard copy in the assessment of subtle intra- and extraaxial brain lesions.

An electrical network model of intracranial arteriovenous malformations: analysis of variations in hemodynamic and biophysical parameters.

The propensity of intracranial arteriovenous malformations (AVMs) to hemorrhage is correlated significantly with their hemodynamic features. Biomathematical models offer a theoretical approach to analyse complex AVM hemodynamics, which otherwise are difficult to quantify, particularly within or in close proximity to the nidus. Our purpose was to investigate a newly developed biomathematical AVM model based on electrical network analysis in which morphological, biophysical, and hemodynamic characteristics of intracranial AVMs were replicated accurately. Several factors implemented into the model were altered systematically to study the effects of a possible wide range of normal variations in AVM hemodynamic and biophysical parameters on the behavior of this model and its fidelity to physiological reality. The model represented a complex, noncompartmentalized AVM with four arterial feeders, two draining veins, and a nidus consisting of 28 interconnected plexiform and fistulous components. Various clinically-determined experimentally-observed, or hypothetically-assumed values for the nidus vessel radii (plexiform: 0.01 cm-0.1 cm; fistulous: 0.1 cm-0.2 cm), mean systemic arterial pressure (71 mm Hg-125 mm Hg), mean arterial feeder pressures (21 mm Hg-80 mm Hg), mean draining vein pressures (5 mm Hg-23 mm Hg), wall thickness of nidus vessels (20 microns-70 microns), and elastic modulus of nidus vessels (1 x 10(4) dyn/cm2 to 1 x 10(5) dyn/cm2) were used as normal or realistic ranges of parameters implemented in the model. Using an electrical analogy of Ohm's law, flow was determined based on Poiseuille's law given the aforementioned pressures and resistance of each nidus vessel. Circuit analysis of the AVM vasculature based on the conservation of flow and voltage revealed the flow rate through each vessel in the AVM network. An expression for the risk of AVM nidus rupture was derived based on the functional distribution of the critical radii of component vessels. The two characteristics which were used to judge the fidelity of the theoretical performance of the AVM model against the physiological one of human AVMs were total volumetric flow through the AVM (< or = 900 ml/min), and its risk of rupture (< 100%). Applying these criteria, a series of 216 (out of 260) AVM models using different combinations of these hemodynamic and biophysical parameters resulted in a physiologically-realistic conduct of the model (yielding a total flow through the AVM model varying from 449.9 ml/min to 888.6 ml/min, and a maximum risk of rupture varying from 26.4 to 99.9%). The described novel biomathematical model characterizes the transnidal and intranidal hemodynamics of an intracranial AVM more accurately than previously possible. A wide range of hemodynamic and biophysical parameters can be implemented in this AVM model to result in simulation of human AVMs with differing characteristics (e.g. low-flow and high-flow AVMs). This experimental model should serve as a useful research tool for further theoretical investigations of a variety of intracranial AVMs and their hemodynamic sequelae.

Risk of intracranial arteriovenous malformation rupture due to venous drainage impairment. A theoretical analysis.

BACKGROUND AND PURPOSE: Increased resistance in the venous drainage of intracranial arteriovenous malformations (AVMs) may contribute to their increased risk of hemorrhage. Venous drainage impairment may result from naturally occurring stenoses/occlusions, or if draining veins (DVs) undergo occlusion before feeding arteries during surgical removal, or after surgery in the presence of "occlusive hyperemia." We employed a detailed biomathematical AVM model using electrical network analysis to investigate theoretically the hemodynamic consequences and the risk of AVM rupture due to venous drainage impairment. METHODS: The AVM model consisted of a noncompartmentalized nidus with 28 vessels (24 plexiform components and 4 fistulous components), 4 arterial feeders, and 2 DVs. An expression for the risk of AVM nidus rupture was derived on the basis of functional distribution of the critical radii of component vessels. Risk was calculated from biomathematical simulations of volumetric flow rate with both DVs patent and for four stages of venous drainage obstruction: (1) 25%, (2) 50%, (3) 75%, and (4) 100%. Each stage of occlusion was applied to each DV while the other DV was patent and then to the patent DV while the other DV was totally occluded. RESULTS: For flow through the AVM when both DVs were unobstructed, the baseline risk of AVM nidus rupture ranged from 4.4% to 91.2%. Theoretical rupture occurred in nidus components proximal to the DVs when the risk exceeded 100%, as was observed with the obstruction of DV1 and a patent DV2. The ranges for risk of rupture across the nidus for the four stages were (1) 4.7% to 90.5%, (2) 5.9% to 86.9%, (3) 0% to 98.4%, and (4) 0% to 106.3%, respectively. Rupture was observed for an 86% occlusion of DV1 (ie, the DV fed by the intranidal fistula) and DV2 patent, primarily because of the dramatic shift in the hemodynamic burden toward the weaker plexiform nidus vessels. CONCLUSIONS: On theoretical grounds, venous drainage impairment was predictive of AVM nidus rupture and was strongly dependent on AVM morphology (presence of intranidal fistulas and their spatial relation to DVs) and hemodynamics. Specifically, stenosis/occlusion of a high-flow DV induces a rapid redistribution of blood into the weak plexiform vessels of the opposing region of the nidus, causing a hemodynamic overload and an increased risk of rupture. These findings should be carefully considered among all factors affecting the natural history of intracranial AVMs and the mechanisms implicated in their spontaneous rupture. They may also provide a theoretical rationale for some of the hemorrhagic complications that occur during and after surgical treatment.

A biomathematical model of intracranial arteriovenous malformations based on electrical network analysis: theory and hemodynamics.

Hemodynamics play a significant role in the propensity of intracranial arteriovenous malformations (AVMs) to hemorrhage and in influencing both therapeutic strategies and their complications. AVM hemodynamics are difficult to quantitate, particularly within or in close proximity to the nidus. Biomathematical models represent a theoretical method of investigating AVM hemodynamics but currently provide limited information because of the simplicity of simulated anatomic and physiological characteristics in available models. Our purpose was to develop a new detailed biomathematical model in which the morphological, biophysical, and hemodynamic characteristics of an intracranial AVM are replicated more faithfully. The technique of electrical network analysis was used to construct the biomathematical AVM model to provide an accurate rendering of transnidal and intranidal hemodynamics. The model represented a complex, noncompartmentalized AVM with 4 arterial feeders (with simulated pial and transdural supply), 2 draining veins, and a nidus consisting of 28 interconnecting plexiform and fistulous components. Simulated vessel radii were defined as observed in human AVMs. Common values were assigned for normal systemic arterial pressure, arterial feeder pressures, draining vein pressures, and central venous pressure. Using an electrical analogy of Ohm's law, flow was determined based on Poiseuille's law given the aforementioned pressures and resistances of each nidus vessel. Circuit analysis of the AVM vasculature based on the conservation of flow and voltage revealed the flow rate through each vessel in the AVM network. Once the flow rate was established, the velocity, the intravascular pressure gradient, and the wall shear stress were determined. Total volumetric flow through the AVM was 814 ml/min. Hemodynamic analysis of the AVM showed increased flow rate, flow velocity, and wall shear stress through the fistulous component. The intranidal flow rate varied from 5.5 to 57.0 ml/min with and average of 31.3 ml/min for the plexiform vessels and from 595.1 to 640.1 ml/min with an average of 617.6 ml/min for the fistulous component. The blood flow velocity through the AVM nidus ranged from 11.7 to 121.1 cm/s with an average of 66.4 cm/s for the plexiform vessels and from 446.9 to 480 dyne/cm2 with an average of 463.5 dyne/cm2 for the fistulous component. The wall shear stress ranged in magnitude from 33.2 to 342.1 dyne/cm2 with an average of 187.7 dyne/cm2 for the plexiform vessels and from 315.9 to 339.7 cm/s with an average of 327.8 cm/s for the fistulous component. The described novel biomathematical model characterizes the transnidal and intranidal hemodynamics of an intracranial AVM more accurately than was possible previously. This model should serve as a useful research tool for further theoretical investigations of intracranial AVMs and their hemodynamic sequelae.

Quantitation of intracranial aneurysm neck size from diagnostic angiograms based on a biomathematical model.

Accurate measurement of the aneurysm neck size from diagnostic angiograms is crucial in the consideration and implementation of interventional embolotherapeutic procedures. Due to inherent problems in angiography, aneurysm morphology and location, and obstruction by overlying structures, accurate measurement of the aneurysm neck size is difficult. We are proposing a method for the angiographic measurement of aneurysm neck size based on a biomathematical model of an aneurysm. A biomathematical model of an intracranial saccular aneurysm was developed based on Laplace's law for a spherical elastic object, given by: Stress = Pressure x Radius/2 x Wall thickness. In addition, another biomechanical parameter used to describe an elastic sphere is the strain: Strain = delta R/Ri = (R-Ri)/Ri where R is the current aneurysm radius and Ri is the initial radius prior to aneurysm development. The stress and strain of an elastic structure are used to describe the elastic modulus, E: E = stress/strain = [PR/2h]/[(R-Ri)/Ri] = [PRRi]/[2hR-2hri]. It is assumed at this point that no additional tissue growth occurs through the developmental course of the aneurysm. The expression for E is now solved for Ri which, in essence, represents the radius of the aneurysm neck: Ri = [2hER]/[PR + 2hE]. Thus, the diameter of the neck, Dn, is given by Dn = 2 + i = 2 ([2hER]/[PR + 2hE]). During diagnostic angiography, the radius, R, and pressure, P, are easily obtained during the examination procedure. However, it is not possible to angiographically determine the elastic modulus, E, and the wall thickness, h. In this case, the following average values are used: E = 1.0 MPa and h = 50 microns. From the diagnostic angiograms and hospital records of 23 patients, the aneurysm neck size was determined using the biomathematical model and compared to the results obtained from the correlative relationship between the measured and accepted ratios of neck size to diameter of parent artery. The neck diameter as measured from the accepted ratios of neck size to parent artery diameter for the 23 patients ranged from 1.5 mm to 8.7 mm. The angiographically measured neck sizes were in excellent agreement with those obtained from the biomathematical model, particularly for the wide-necked aneurysms, as evidenced by the fact that all but two chi 2 values were < 1.0. We have described a simple yet accurate method for obtaining aneurysm neck size measurements from diagnostic angiograms using a biomathematical model. The model requires knowledge of only the aneurysm radius and blood pressure and becomes particularly important in characterizing wide-necked aneurysms.

Simultaneous dual-isotope technetium-99m/thallium-201 cardiac SPET imaging using a projection-dependent spilldown correction factor.

A spilldown correction method is proposed for the thallium-201 window image in simultaneous dual-isotope technetium-99m/thallium-201 single-photon emission tomographic (SPET) imaging based on a single acquisition into three energy windows. In this method, images are simultaneously acquired in two standard energy windows over the 99mTc and 201Tl photopeak regions and a third spilldown window adjacent to the 201Tl window. Using a Monte Carlo simulation of SPET, the fractional amount of 99mTc and 201Tl spilldown in the 201Tl window with respect to the total counts from the spilldown window, k12, was calculated for simulated images of point sources at varying depths within a water-filled elliptical tub phantom. When applied to experimental acquisitions, k12, multiplied by the total counts from the spilldown window, is then subtracted from the 201Tl window image to produce the corrected image. However, for successful applications in SPET, k12 must be determined on a projection-by-projection basis since k12 is depth dependent. Thus, a regression relation was obtained between k12 and the total count ratio of the spilldown to 99mTc windows, k23. The spilldown correction method was applied to 201Tl photopeak images of an extended source distribution in uniform and nonuniform attenuating media with dual-isotope 99mTc/201Tl and single-isotope 201Tl. A marked improvement in image contrast was observed between the corrected and uncorrected 201Tl window images. The average count ratio of uncorrected dual-isotope 201Tl/single-isotope 201Tl was 3.08 for uniform and 2.99 for non-uniform attenuating media.(ABSTRACT TRUNCATED AT 250 WORDS)

Neuroangiographic assessment of aneurysm stability and impending rupture based on a non-linear biomathematical model.

The probability or risk of aneurysm rupture is assessed using conventional angiography by applying the aneurysm radius and systolic blood pressure obtained at examination to a non-linear biomathematical model of an aneurysm. A non-linear biomathematical model was developed based on Laplace's law to represent the viscoelastic relation between the wall tension and the radius. A differential expression of this relation was used to derive the critical radius: Rc = [2Et/P]2At/P where E is the elastic modulus of the aneurysm, t is the wall thickness, P is the pressure, and A is the elastic modulus of collagen. Using average values of E, A, and t, the risk of aneurysm rupture is defined as the area of integration under the curve defined by the minimum value of pressure (50 mmHg) and the patient pressure recorded at examination. This area was normalized by the area of integration defined by the pressure limits: 50 to 300 mmHg. This method of risk assessment was applied to four previously published case studies of patients with documented aneurysm rupture in which both the aneurysm size at rupture and the patient systolic blood pressure were reported. Two additional parameters were calculated to further evaluate aneurysm stability: (1) a ratio given as (Rexp/Rth) where Rexp is the radius of aneurysm rupture measured from angiography and Rth is the critical radius based on the model; and (2) chi 2 analysis defined by chi 2 = (O - E)2/E where O and E are the observed (Rexp) and expected (Rth) variables, respectively. The average systolic blood pressure and radius of aneurysm rupture was 147.2 mmHg and 3.95 mm, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

A nonlinear mathematical model for the development and rupture of intracranial fusiform aneurysms.

Laplace's law, which describes a linear relation between the tension and the radius, is often used to characterize the mechanical response of the aneurysm wall to distending pressures. However, histopathological studies have confirmed that the wall of the fully developed aneurysm consists primarily of collagen and is subject to large increases in tension for small increases in the radius, i.e., a nonlinear relationship exists between the tension within the aneurysm wall and the radius. Thus, a nonlinear version of Laplace's law is proposed to accurately describe the development and rupture of a fusiform saccular aneurysm. The fusiform aneurysm was modelled as a thin-walled ellipsoidal shell with a major axis radius, Ra, minor axis radius, Rb, circumferential tension, S0, and meridional tension, S phi, with phi defining the angle from the surface normal. Using both linear and nonlinear models, differential expressions of the volume distensibility evaluated at 90 degrees were used to determine the critical radius of the aneurysm along the minor axis from S0 and S phi in terms of the following geometric and biophysical variables; A, elastic modulus of collagen; E, elastic modulus of the aneurysm (elastin and collagen); t, wall thickness; P, systolic pressure; and Ra. For typical physiological values of A = 2.8 MPa, E = 1.0 MPa, T = 40 microns, P = 150 mmHg, and Ra = 4Rb, the linear model yielded critical radii of 4.0 mm from S phi and 2.2 mm from S0. The resultant critical radius was 4.56 mm. Using the same values, the critical radii from the tension components of the nonlinear model were 3.5 mm from S phi and 1.9 mm from S0.(ABSTRACT TRUNCATED AT 250 WORDS)

A nonlinear mathematical model for the development and rupture of intracranial saccular aneurysms.

Mathematical models of aneurysms are typically based on Laplace's law which defines a linear relation between the circumferential tension and the radius. However, since the aneurysm wall is viscoelastic, a nonlinear model was developed to characterize the development and rupture of intracranial spherical aneurysms within an arterial bifurcation and describes the aneurysm in terms of biophysical and geometric variables at static equilibrium. A comparison is made between mathematical models of a spherical aneurysm based on linear and nonlinear forms of Laplace's law. The first form is the standard Laplace's law which states that a linear relation exists between the circumferential tension, T, and the radius, R, of the aneurysm given by T = PR/2t where P is the systolic pressure. The second is a 'modified' Laplace's law which describes a nonlinear power relation between the tension and the radius defined by T = ARP/2At where A is the elastic modulus for collagen and t is the wall thickness. Differential expressions of these two relations were used to describe the critical radius or the radius prior to aneurysm rupture. Using the standard Laplace's law, the critical radius was derived to be Rc = 2Et/P where E is the elastic modulus of the aneurysm. The critical radius from the modified Laplace's law was R = [2Et/P]2At/P. Substituting typical values of E = 1.0 MPa, t = 40 microns, P = 150 mmHg, and A = 2.8 MPa, the critical radius is 4.0 mm using the standard Laplace's law and 4.8 mm for the modified Laplace's law.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of four scatter correction methods using Monte Carlo simulated source distributions.

UNLABELLED: Scatter correction in SPECT is important for improving image quality, boundary detection and the quantification of activity in different regions. This paper presents a comparison of four scatter correction methods, three using more than one energy window and one convolution-subtraction correction method using spatial variant scatter line-spread functions. METHODS: The comparison is based on Monte Carlo simulated data for point sources on- and off-axis, hot and cold spheres of different diameters, and a clinically realistic source distribution simulating brain imaging. All studies were made for a uniform cylindrical water phantom. Since the nature of the detected photon is known with Monte Carlo simulation, separate images of primary and scattered photons can be recorded. These can then be compared with estimated scatter and primary images obtained from the different scatter correction methods. The criteria for comparison were the normalized mean square error, scatter fraction, % recovery and image contrast. RESULTS: All correction methods significantly improved image quality and quantification compared to those obtained with no correction. Quantitatively, no single method was observed to be the best by all criteria for all the source distributions. Three of the methods were observed to perform the best by at least one of the criteria for one of the source distributions. For brain imaging, the differences between all the methods were much less than the difference between them and no correction at all. CONCLUSION: It is concluded that performing scatter correction is essential for accurate quantification, and that all four methods yield a good, but not perfect, scatter correction. Since it is hard to distinguish the methods consistently in terms of their performance, it may be that the choice should be made on the basis of ease of implementation.

A dual-photopeak window method for scatter correction.

The imaging of scattered photons degrades contrast and is a major source of error in the quantitation of activity. It was hypothesized that, if the photopeak was divided into two nonoverlapping energy windows, a regression relation could be obtained between the ratio of counts within these windows and the scatter fraction for counts within the total region. This idea was tested by acquiring dual photopeak window acquisitions of a 99mTc point source in an elliptical attenuator, and at the same locations in air. From these, a regression between the scatter fraction and window ratio was determined. When this regression was applied to estimate the scatter distribution for acquisitions in both uniform and nonuniform elliptical attenuators, the residual scatter fraction was reduced approximately ten-fold and the estimated scatter line spread functions matched very closely the tails of the total line spread functions. In SPECT acquisitions, dual-photopeak window scatter correction was observed to significantly increase the contrast of "cold" spheres, improve the accuracy of estimating activity at the center of "hot" spheres, and return the three-dimensional modulation transfer function for point sources in an elliptical attenuator to near their in-air shape.