PubMed Health⌕ Search

Biomedical subjects

J Pile-Spellman

Publications and source records attributed to J Pile-Spellman.

At least 37 records · Page 2Linked to original sources
PubMed2000

Adenosine-induced ventricular asystole to induce transient profound systemic hypotension in patients undergoing endovascular therapy. Dose-response characteristics.

BACKGROUND: Adenosine-induced asystole has been used to induce transient systemic hypotension for various vascular procedures. Dose-response characteristics of adenosine-induced ventricular asystole have not been determined. METHODS: During endovascular embolization of cerebral arteriovenous malformations, the authors performed a series of adenosine test injections to establish a dose-response relation in each patient. After an interval of 3-10 min, the dose was escalated by 10-20 mg for each injection to achieve an end point of 20-30 s of stable mean arterial pressure (MAP) reduction to 25-30 mmHg. All patients received constant infusion of nitroprusside (approximately 1 microgram. kg-1. min-1) throughout the procedure. RESULTS: The authors studied four adult patients (age, 22-44 yr; two patients had two separate procedures) and one pediatric patient (age, 4 yr). Twenty-three adenosine injections resulted in measurable asystole. The adenosine dose was 0. 98 +/- 0.40 mg/kg (mean +/- SD), and the dose range was 0.24-1.76 mg/kg (6-90 mg). The duration of asystole, MAP < 30 mmHg, and MAP < 50 mmHg, were 8 +/- 3 s, 18 +/- 12 s, and 50 +/- 29 s, respectively. The minimum MAP and the MAP for the first 20 s were 16 +/- 3 mmHg and 30 +/- 9 mmHg, respectively. There was a linear relation between adenosine dose and the duration of hypotension with MAP < 30 mmHg and MAP < 50 mmHg. CONCLUSIONS: In the dose range studied, a series of adenosine test injections can be used to determine optimal adenosine dose for induction of transient profound hypotension.

Adenosine↗
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↗
PubMed2000

The epidemiology of brain arteriovenous malformations.

OBJECTIVE: Common estimates of the prevalence rate for pial arteriovenous malformations (AVMs) of the brain vary widely, and their accuracy is questionable. Our objective was to critically review the original sources from which these rates were derived and to establish best estimates for both the incidence and prevalence of the disease. METHODS: We reviewed all of the relevant original literature: autopsy series, the Cooperative Study of Intracranial Aneurysms and Subarachnoid Hemorrhage and related analyses, and other population-based studies. We also modeled the confidence intervals of estimates for a process of low prevalence such as AVMs. RESULTS: Many of the prevalence estimates (500-600/100,000 population) were based on autopsy data, a source that is inherently biased. Other estimates (140/100,000 population) originated from an inappropriate analysis of data from the Cooperative Study. The most reliable information comes from a population-based study of Olmsted County, MN, but prevalence data specific to AVMs was not found in that study. CONCLUSION: The estimates for AVM prevalence that are published in the medical literature are unfounded. Because of the rarity of the disease and the existence of asymptomatic patients, establishing a true prevalence rate is not feasible. Owing to variation in the detection rate of asymptomatic AVMs, the most reliable estimate for the occurrence of the disease is the detection rate for symptomatic lesions: 0.94 per 100,000 person-years (95% confidence interval, 0.57-1.30/100,000 person-years). This figure is derived from a single population-based study, but it is supported by a reanalysis of other data sources. The prevalence of detected, active (at risk) AVM disease is unknown, but it can be inferred from incidence data to be lower than 10.3 per 100,000 population.

Autopsy↗
PubMed2000

Incident hemorrhage risk of brain arteriovenous malformations located in the arterial borderzones.

BACKGROUND AND PURPOSE: We sought to assess the relative risk of hemorrhagic presentation of brain arteriovenous malformations (AVMs) located in the arterial borderzone territories. METHODS: The 464 consecutive, prospectively enrolled patients from the New York AVM Databank were analyzed. AVM borderzone location was coded positive when the malformation was supplied by branches of at least 2 of the major circle of Willis arteries (anterior, middle, and/or posterior cerebral arteries). AVMs fed by branches of only 1 major pial or any other single artery served as a comparison group. Clinical presentation (diagnostic event) was categorized as (1) intracranial hemorrhage, proven by brain imaging, or (2) seizure, focal neurological deficit, headache, or other event with no signs of AVM hemorrhage on brain imaging. RESULTS: In 48% (n=222) of the patients, AVMs were located in the arterial borderzone territories; in 52% (n=242) a non-borderzone location was found. Hemorrhage was the presenting symptom in 44% (n=205); 28% (n=132) presented with seizures, 11% (n=52) with headaches, 7% (n=34) with a neurological deficit, and 9% (n=41) with other or no AVM-related symptoms. The frequency of incident AVM hemorrhage was significantly lower in borderzone AVMs (27%, n=61) than in non-borderzone malformations (60%, n=144; P:<0.001). This difference remained significant in a multivariate model controlling for age, sex, AVM size, deep venous drainage, and presence of aneurysms (odds ratio, 0.4; 95% CI, 0.25 to 0.66). CONCLUSIONS: Our findings suggest that borderzone location is an independent determinant for a lower risk of AVM hemorrhage at initial presentation.

Adult↗
PubMed2000

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.

Blood Pressure↗
PubMed1999

Developmental deficits in adult patients with arteriovenous malformations.

BACKGROUND: Cerebral arteriovenous malformations (AVMs) are congenital masses of arteries and veins that appear to undergo an unclear "maturation" for many years. Using structured interviews, we compared developmental history of adult patients with AVM with a comparison group of patients with cerebral tumor or aneurysm. OBJECTIVE: To determine whether a remote history of developmental abnormality in adult patients with AVM might be an early marker of cerebral status. DESIGN: Adult patients with AVM and a comparison group of patients with cerebral aneurysm or low-grade tumor participated in a survey. SETTING: Urban medical school-based tertiary care center. PATIENTS: Forty-four randomly selected patients with AVM from the Columbia-Presbyterian AVM Database. There were 32 comparison patients:15 randomly chosen patients from the institution's Cerebral Aneurysm Database and all 17 patients who underwent a biopsy from 1990 to 1995 with a diagnosis of low-grade tumor and who could be contacted. MAIN OUTCOME MEASURES: A brief, structured interview adapted from the Centers for Disease Control and Prevention for its 1994 study of the prevalence of learning disabilities in American children. We defined the positive occurrence of a condition as an affirmative answer to the question, " Did have (condition) during his/her school-age years?" Each patient was also asked if there had been any problems in the following skill areas: reading, writing, listening, speaking, attention, impulsivity, organization, mathematics, or drawing. The AVM size was calculated on the angiographic film by measuring its longest diameter in any dimension. RESULTS: Patients with AVM were significantly more likely to report a positive occurrence to any survey question (P<.05). Two thirds of all patients with AVM (66%) reported at least 1 skill difficulty during their school years, significantly more than the comparison group (P<.001). Neither the maximum AVM diameter nor the occurrence of hemorrhage as an adult differed between patients with AVM with and without early skill difficulty. CONCLUSIONS: Patients with AVM are more likely to report a developmental learning disorder than patients with tumor or aneurysm despite the absence of other neurologic symptoms of diseases not diagnosed for another 20 years. These data support the notion that disorders of behavioral and intellectual function are sensitive markers of early cerebral status.

Adult↗
PubMed1999

Recurrent abrupt occlusion after transluminal angioplasty for basilar artery stenosis: case report.

OBJECTIVE AND IMPORTANCE: Angioplasty for basilar artery stenosis is often complicated by recurrent abrupt vessel closure. The clinical results can be catastrophic. In this case report, we assess the effects of intra-arterial papaverine (American Regent Laboratories Inc., Shirley, NJ) on rebound occlusion. CLINICAL PRESENTATION: The patient presented with crescendo transient ischemic attacks from atherosclerotic narrowing of the midbasilar artery despite maximal medical treatment. INTERVENTION: Angioplasty of the midbasilar artery was performed with serial balloon inflations. The patient was treated successfully with intra-arterial papaverine and achieved a nearly full recovery, with only mild dysarthria, by the time of the 7-month follow-up examination. CONCLUSION: Using intra-arterial papaverine, we were able to reverse the effects of this potentially life-threatening complication of basilar artery angioplasty.

Angioplasty, Balloon↗
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

Higher cerebral function and hemispheric blood flow during awake carotid artery balloon test occlusions.

OBJECTIVES: Measures capable of detecting early alterations of brain function during acute cerebral ischaemia have not been adequately defined. Internal carotid artery (ICA) test occlusions provide a well controlled environment to investigate the effects of reversible acute hemispheric hypoperfusion on brain function. A continuous time estimation task was developed that reliably demonstrated alterations in higher cerebral function before development of any deficits in elementary neurological function during ICA balloon catheter test occlusions. In the present study, we hypothesised that alterations in our behavioural task would correlate significantly with absolute level of ipsilateral CBF. METHODS: Twenty five patients underwent awake ICA test occlusions during which sustained attention and ipsilateral CBF were measured simultaneously using our time estimation task and the intracarotid 133Xe washout method. Alteration in sustained attention was correlated with CBF after occlusion using Fisher's exact test. RESULTS: Deterioration in sustained attention was significantly associated with ipsilateral CBF below 30 ml/g/min (Fisher's exact test, p=0.047). Changes in individual patients' performance on the behavioural task correlated in real time with changes occurring either at the point of occlusion or at a specific threshold of induced hypotension. Sensitivity for our behavioural test in predicting CBF was 75%; specificity 70%. CONCLUSIONS: Monitoring sustained attention during carotid balloon test occlusions seems to be a sensitive means to detect decreases in CBF as measured by 133Xe washout. Correlation between higher cerebral function and CBF can allow more detailed investigations of physiological relations between cerebral haemodynamics and brain function in human conditions of cerebral ischaemia.

Adult↗
PubMed1999

Human endothelium: endovascular biopsy and molecular analysis.

PURPOSE: To develop a safe and reproducible method for harvesting viable vascular endothelium to analyze gene expression at sites of vascular lesions. MATERIALS AND METHODS: Coaxial curved stainless-steel guide wires were used to obtain samples of endothelial cells from large arteries and veins in 29 patients undergoing routine endovascular procedures. Three immunocytochemical markers were used to identify cells as endothelial. Cellular viability was evaluated in terms of cell membrane integrity, energy-dependent uptake of acetylated low-density lipoprotein, and cellular response to lipopolysaccharide. Single-cell reverse transcription polymerase chain reaction (PCR) and immunocytochemistry were used to study endothelial gene expression. RESULTS: Cells with endothelial morphology and immunoreactivity for von Willebrand factor, thrombomodulin, and angiotensin-converting enzyme were consistently obtained from iliac and carotid arteries and large veins (average yield [+/- standard error] from 26 iliac arteries, 262 endothelial cells +/- 45, 20%-30% of which were viable). These cells displayed induction of E-selection messenger RNA at PCR after exposure to lipopolysaccharide. Expression of vascular cell adhesion molecule 1 transcripts in endothelial cells increased with patient age (P < .01), whereas expression of intercellular adhesion molecule 1 did not. CONCLUSION: Viable endothelium can be obtained during routine angiography. Immunocytochemical and reverse transcription PCR analyses of these cells allowed determination of transcripts and proteins expressed by endothelium at sites of vascular lesions. Such information could aid in understanding mechanisms of vascular diseases and in clinical decision making.

Adolescent↗
PubMed1998

[Therapy of cerebral arteriovenous malformations].

The rapid development of modern endovascular, microsurgical, and radiation therapies has considerably expanded the treatment options for encephalic arteriovenous malformations (AVMs). Surgery has the longest history. Single or staged intravascular procedures (embolizations) using fast-acting glues, sclerotic agents, and thrombogenic coils serve to reduce the size of AVM to that suitable for extirpation and may reduce the risk of surgery. Radiation ("gamma-knife") therapy, most frequently used in small, non-operable AVMs, is also viewed by some authors as an alternative or even superior tool in small, operable malformations. Partial embolization to reduce the mass-effect of space-occupying AVMs, to reverse diaschisis, and to treat AVM-related seizure disorders is being discussed and practiced. Given the in part competing or even controversial options, the selection of optimal treatment for AVM patients is becoming increasingly difficult. Current management is impeded by the paucity of information on the exact risks of invasive therapies and by insufficient criteria for identifying patients at risk of spontaneous bleeding during the natural course, including the seriousness of such hemorrhage.

Cerebral Angiography↗
PubMed1998

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.

Cerebral Hemorrhage↗
PubMed1998

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.

Communication↗
PubMed1998

The feasibility of intracarotid adenosine for the manipulation of human cerebrovascular resistance.

UNLABELLED: To assess the feasibility of manipulating human cerebrovascular resistance with adenosine, we measured cerebral blood flow (CBF) by determining the initial slope (IS) of tracer washout 20-80 s after intracarotid 133Xe injection (standard IS) during sequential 3-min intracarotid infusions of (a) saline; (b) adenosine 1.2-mg bolus followed by an infusion of 1 mg/min (bolus + infusion); (c) saline; and (d) nicardipine (0.1 mg/min). During 133Xe washout, adenosine caused a rapidly clearing compartment. Therefore, tracer washout was also analyzed 5-25 s after injection (early IS). Nicardipine (n = 8) increased both standard IS (from 39+/-12 to 53+/-16 mL 100g.min(-1); P < 0.005) and early IS (from 40+/-9 to 55+/-20 arbitrary units; P < 0.02) to a similar degree. Adenosine bolus + infusion increased early IS (from 33+/-6 to 82+/-43 arbitrary units; P < 0.02) but did not increase standard IS (from 41+/-12 to 43 +/-16 mL 100g(-1) min(-1)). Standard and early IS values were then determined before and after adenosine delivered either by infusion alone (2 mg/min for 3 min, n = 5) or bolus alone (2 mg in 1 s, n = 3). Neither standard nor early IS changed after adenosine infusion alone. Early IS increased after adenosine bolus alone. Increase in early IS, but not standard IS, suggests a transient (<30 s) increase in CBF. IMPLICATIONS: Intracarotid adenosine, in the 1- to 2-mg dose range, may cause a transient, but not a sustained, increase in cerebral blood flow. Intracarotid adenosine in such a dose range does not seem to be an appropriate drug for sustained manipulation of cerebrovascular resistance.

Adenosine↗
PubMed1998

Complex intracranial aneurysms: combined operative and endovascular approaches.

OBJECTIVE: Endovascular management of complex intracranial aneurysms is increasingly being considered as an alternative to standard surgical clipping. However, little attention has been paid to the complementary nature of surgery and endovascular therapy. METHODS: Between September 1992 and May 1997, 12 patients with complex intracranial aneurysms were treated with combined operative and endovascular methods. Seven patients demonstrated subarachnoid hemorrhage (two of Grade II, two of Grade III, and three of Grade IV). Five patients demonstrated unruptured aneurysms, i.e., three giant aneurysms (one vertebrobasilar junction aneurysm, one middle cerebral artery bifurcation aneurysm, and one internal carotid artery-ophthalmic artery aneurysm), one large internal carotid artery-ophthalmic artery aneurysm, and one middle cerebral artery serpentine aneurysm. Management strategies involved either surgery followed by endovascular therapy (S-E; n = 5) or endovascular therapy followed by surgery (E-S; n = 7). S-E paradigms included aneurysm exploration followed by endovascular treatment (S-E1; n = 3), partial aneurysm clipping followed by endovascular aneurysm packing (S-E2; n = 1), and extracranial-to-intracranial bypass followed by endovascular parent vessel occlusion (S-E3; n = 1). E-S paradigms included superselective angiography followed by surgical clipping (E-S1; n = 2), Guglielmi detachable coil partial dome packing followed by delayed surgical clipping (E-S2; n = 2), proximal temporary vessel balloon occlusion followed by aneurysm clipping (E-S3; n = 2), and proximal permanent vessel occlusion followed by surgical aneurysm decompression for mass effect treatment (E-S4; n = 1). RESULTS: Eleven aneurysms (92%) were completely eliminated. The remaining aneurysm was 90% obliterated and remained quiescent at the 34-month follow-up examination, despite presenting with subarachnoid hemorrhage. No patient experienced repeat bleeding (follow-up period, 23+/-28 mo). There were no deaths. One patient achieved a fair outcome (Glasgow Outcome Scale score of III); all other patients experienced excellent outcomes (Glasgow Outcome Scale score of I). In all cases, the aneurysm management paradigm chosen had a positive effect on definitive therapy. CONCLUSION: Several factors can contribute to the complexity of intracranial aneurysms. Management strategies that combine operative and endovascular techniques in a complementary way, for the best possible outcomes for these patients, can be designed accordingly.

Adult↗
PubMed1998

Mathematical considerations for modeling cerebral blood flow autoregulation to systemic arterial pressure.

The shape of the autoregulation curve for cerebral blood flow (CBF) vs. pressure is depicted in a variety of ways to fit experimentally derived data. However, there is no general empirical description to reproduce CBF changes resulting from systemic arterial pressure variations that is consistent with the reported data. We analyzed previously reported experimental data used to construct autoregulation curves. To improve on existing portrayals of the fitting of the observed data, a compartmental model was developed for synthesis of the autoregulation curve. The resistive arterial and arteriolar network was simplified as an autoregulation device (ARD), which consists of four compartments in series controlling CBF. Each compartment consists of a group of identical vessels in parallel. The response of each vessel category to changes in perfusion pressure was simulated using reported experimental data. The CBF-pressure curve was calculated from the resistance of the ARD. The predicted autoregulation curve was consistent with reported experimental data. The lower and upper limits of autoregulation (LLA and ULA) were predicted as 69 and 153 mmHg, respectively. The average value of the slope of the CBF-pressure curve below LLA and beyond ULA was predicted as 1.3 and 3.3% change in CBF per mmHg, respectively. Our four-compartment ARD model, which simulated small arteries and arterioles, predicted an autoregulation function similar to experimental data with respect to the LLA, ULA, and average slopes of the autoregulation curve below LLA and above ULA.

Animals↗
PubMed1998

Morbidity of intracranial hemorrhage in patients with cerebral arteriovenous malformation.

BACKGROUND AND PURPOSE: Decisions on invasive arteriovenous malformation (AVM) treatment are currently based on natural-course risk estimates of AVM bleeding and assumptions on morbidity from cerebral hemorrhage in general. However, morbidity of AVM hemorrhage has rarely been reported. We sought to assess the morbidity of intracranial hemorrhage in patients with cerebral AVMs. METHODS: From a prospective AVM database, 119 patients were analyzed: 115 had a hemorrhage as the diagnostic event, and 27 of them suffered a second hemorrhage during follow-up; an additional 4 patients had other diagnostic symptoms but bled during follow-up. The type (parenchymal, subarachnoid, intraventricular) and location of AVM hemorrhage were determined by CT/MR brain imaging. Disability and neurological impairment were assessed with the Barthel Index, the Rankin Scale, and the National Institutes of Health Stroke Scale, with a mean follow-up time of 16.2 months. RESULTS: Of the 115 incident hemorrhages, 34 (30%) were subarachnoid, 27 (23%) parenchymal, 18 (16%) intraventricular, and 36 (31%) in combined locations. In 54 patients (47%; 95% confidence interval [CI], 38% to 56%) the incident hemorrhage resulted in no neurological deficit, and an additional 43 patients (37%; 95% CI, 28% to 46%) were independent in their daily activities (Rankin 1). Fifteen patients (13%; 95% CI, 7% to 19%) were moderately disabled (Rankin 2 or 3), and 3 (3%; 95% CI, 0% to 6%) were severely disabled (Rankin > or =4). Parenchymal hemorrhages were most likely to result in a neurological deficit (52%). Type and morbidity of hemorrhage during follow-up were similar to incident events. Twenty (74%) of 27 patients with both incident and follow-up hemorrhages were normal or independent (Rankin 0 or 1). None of the patients with a hemorrhage during follow-up died during the observation period. CONCLUSIONS: Hemorrhage from cerebral AVMs appears to have a lower morbidity than currently assumed. This finding encourages a reevaluation of the risks and benefits of invasive AVM treatment.

Activities of Daily Living↗