David W Newell

University of Washington Seattle, Seattle, Washington, United States

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Publications (193)680.96 Total impact

  • Mark R. Harrigan · David W. Newell · Andrei V. Alexandrov
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    ABSTRACT: This chapter contains sections titled: IntroductionBiologic and physiological aspects of vasospasmClinical and diagnostic features of DIND and vasospasmUse of transcranial Doppler and cerebral blood flow studies for vasospasmOptions for treatment of vasospasmConclusions References
    Cerebrovascular Ultrasound in Stroke Prevention and Treatment, 03/2011: pages 207-213; , ISBN: 9781405195768
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    ABSTRACT: The online version of this article, along with updated information and services, is located on the World Wide Web at:
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    ABSTRACT: The aim of the present study was to evaluate the time course for cerebral autoregulation (AR) recovery following severe traumatic brain injury (TBI). Thirty-six patients (27 males and 9 females, mean +/- SEM age 33 +/- 15.1 years) with severe TBI underwent serial dynamic AR studies with leg cuff deflation as a stimulus, until recovery of the AR responses was measured. The AR was impaired (AR index < 2.8) in 30 (83%) of 36 patients on Days 3-5 after injury, and in 19 individuals (53%) impairments were found on Days 9-11 after the injury. Nine (25%) of 36 patients exhibited a poor AR response (AR index < 1) on postinjury Days 12-14, which eventually recovered on Days 15-23. Fifty-eight percent of the patients with a Glasgow Coma Scale score of 3-5, 50% of those with diffuse brain injury, 54% of those with elevated intracranial pressure, and 40% of those with poor outcome had no AR recovery in the first 11 days after injury. Autoregulation recovery after severe TBI can be delayed, and failure to recover during the 2nd week after injury occurs mainly in patients with a lower Glasgow Coma Scale score, diffuse brain injury, elevated ICP, or unfavorable outcome. The finding suggests that perfusion pressure management should be considered in some of the patients for a period of at least 2 weeks.
    Journal of Neurosurgery 05/2009; 111(4):695-700. DOI:10.3171/2008.10.17686 · 3.15 Impact Factor
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    ABSTRACT: Cerebral vasospasm continues to be a major cause of poor outcome in patients with ruptured aneurysms. Prophylactic Transluminal Balloon Angioplasty (pTBA) appeared to prevent delayed ischemic neurological deficit in a pilot study. A phase II multicenter randomized clinical trial was subsequently designed. One hundred and seventy patients with Fisher Grade III subarachnoid hemorrhage were enrolled in the study. Of these, 85 patients were randomized to the treatment group and underwent pTBA within 96 hours after subarachnoid hemorrhage. Main end points of the study included the 3-month dichotomized Glasgow Outcome Score (GOS), development of delayed ischemic neurological deficit (DIND), occurrence of Transcranial Doppler (TCD) vasospasm, and length of stay in the ICU and hospital. The incidence of DIND was lower in the pTBA group (P=0.30) and fewer patients required therapeutic angioplasty to treat DIND (P=0.03). Overall pTBA resulted in an absolute risk reduction of 5.9% and a relative risk reduction of 10.4% unfavorable outcome (P=0.54). Good grade patients had absolute and relative risk reductions of respectively 9.5 and 29.4% (P=0.73). Length of stay in ICU and hospital was similar in both groups. Four patients had a procedure-related vessel perforation, of which three patients died. While the trial is unsuccessful as defined by the primary end point (GOS), proof of concept is confirmed by these results. Fewer patients tend to develop vasospasm after treatment with pTBA and there is a statistically significantly decreased need for therapeutic angioplasty. pTBA does not improve the poor outcome of patients with Fisher grade III subarachnoid hemorrhage.
    Stroke 07/2008; 39(6):1759-65. DOI:10.1161/STROKEAHA.107.502666 · 6.02 Impact Factor
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    ABSTRACT: Nurses' ability to rapidly detect decreases in cerebral perfusion pressure (CPP), which may contribute to secondary brain injury, may be limited by poor visibility of CPP displays. To evaluate the impact of a highly visible CPP display on the functional outcome in individuals with cerebral aneurysms. Patients with cerebral aneurysms (n = 100) who underwent continuous CPP monitoring were enrolled and randomized to beds with or without the additional CPP display. Six-month outcome was assessed. Functional outcome was not significantly different between control and intervention groups after controlling for initial neurologic condition (odds ratio .904, 95% confidence interval 0.317 to 2.573). However, greater time below CPP thresholds (55 to 70 mm Hg) was significantly associated with poorer outcome (P = .005 to .010). Although the enhanced CPP display was not associated with significantly better outcome, longer periods of CPP below set levels were associated with poorer outcome.
    Heart & lung: the journal of critical care 05/2008; 37(3):227-37. DOI:10.1016/j.hrtlng.2007.05.015 · 1.32 Impact Factor
  • Journal of Neurosurgery 04/2008; 108(3):607. DOI:10.3171/JNS/2008/108/3/0607 · 3.23 Impact Factor
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    ABSTRACT: The authors report the long-term results of a series of direct superficial temporal artery-middle cerebral artery (STA-MCA) bypass procedures in patients with moyamoya disease from the western US. All patients with moyamoya disease treated at the University of Washington from 1990 through 2004 (39 patients) were included in this study. Patients underwent pre- and postoperative evaluation of cerebral perfusion dynamics. Surgical revascularization procedures were performed in all patients with impaired cerebral blood flow (CBF) findings. The mean age of patients at diagnosis was 34 years (range 10-55 years). All 39 patients had impaired CBF and/or vasomotor reserve and underwent revascularization procedures: 26 patients underwent bilateral operations, 13 unilateral (65 total procedures). An STA-MCA bypass was technically possible in 56 procedures (86.2%); saphenous vein interposition grafts were required in 3 procedures (4.6%); encephaloduroarteriosynangiosis was performed in 6 procedures (9.2%). Three patients died due to postoperative complications, yielding a procedure-related mortality rate of 4.61%, and 8 experienced non-life threatening complications (for a procedure-related rate of 12.3%). Long-term follow-up appeared to indicate a reduction in further ischemic events in surviving patients compared with the natural history. Cerebral perfusion dynamics improved postoperatively in all 36 surviving patients. Moyamoya disease may differ in the US and Asia, and STA-MCA bypass procedures may prevent future ischemic events in patients with this condition.
    Neurosurgical FOCUS 02/2008; 24(2):E15. DOI:10.3171/FOC/2008/24/2/E15 · 2.14 Impact Factor
  • David W Newell · Gavin W Britz · Jonathan Brisman
    Neurosurgical FOCUS 02/2008; 24(2):E1. DOI:10.3171/FOC/2008/24/2/E1 · 2.14 Impact Factor
  • Marcelo D Vilela · David W Newell
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    ABSTRACT: The aim of this study was to review the historical developments and current status of superficial temporal artery (STA) to middle cerebral artery (MCA) bypass. A literature review was performed to review the origins and current uses of the STA bypass procedure in neurosurgery. The idea of providing additional blood supply to the brain to prevent stroke and maintain neurological function has been present in the mind of neurosurgeons for many decades. In 1967 the first STA-MCA bypass was done by M. G. Yaşargil, and an enormous step was made into the field of microneurosurgery and cerebral revascularization. During the decades that followed, this technique was used as an adjuvant or a definitive surgical treatment for occlusive disease of the extracranial and intracranial cerebral vessels, skull base tumors, aneurysms, carotid-cavernous fistulas, cerebral vasospasm, acute cerebral ischemia, and moyamoya disease. With the results of the first randomized extracranial-intracranial (EC-IC) bypass trial and the development of endovascular techniques such as angioplasty for intracranial atherosclerotic disease and cerebral vasospasm, the indications for STA-MCA bypass became limited. Neurosurgeons continued to perform EC-IC bypasses as an adjuvant to clipping of aneurysms and in the treatment of skull base tumors and moyamoya disease; the procedure is less commonly used for atherosclerotic carotid artery occlusion (CAO) with definite evidence of hemodynamic insufficiency. The evidence that patients with symptomatic CAO and "misery perfusion" have an increased stroke risk has prompted a second trial for evaluating EC-IC bypass for stroke prevention. The Carotid Occlusion Surgery Study is a new trial designed to determine whether STA-MCA bypass can reduce the incidence of stroke in these patients. New trials will also reveal the role of the STA-MCA bypass in the prevention of hemorrhages in moyamoya disease. The role of STA-MCA bypass in the management of cerebrovascular disease continues to be refined and evaluated using advanced imaging techniques and by performing randomized trials for specific purposes, including symptomatic CAO.
    Neurosurgical FOCUS 02/2008; 24(2):E2. DOI:10.3171/FOC/2008/24/2/E2 · 2.14 Impact Factor
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    ABSTRACT: The aim of the present study was to define the influence of basilar artery (BA) vasospasm on the outcome of patients with delayed ischemic deterioration after aneurysmal subarachnoid hemorrhage (aSAH). Sixty-five patients with clinically suspected severe cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH) were included in the study. All patients had angiographies done within 48 h from the initial bleeding and on the day when clinical significant vasospasm was suspected. Basilar arteries with ≥25% narrowing was found in 23 of 65 patients. Stepwise logistic regression after adjusting for age with Hunt and Hess grade, Fisher’s grade, hydrocephalus and aneurysmal location as covariables revealed basilar artery narrowing ≥25% to be significantly and independently associated with unfavorable 3-month outcome (p=0.0001, OR: 10.1, 95% CI: 2.5–40.8). Basilar artery vasospasm after aSAH is an independent and significant prognostic factor associated with poor outcome in patients with clinically suspected severe cerebral vasospasm endovascular therapy.
    12/2007: pages 387-389;
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    ABSTRACT: The aim of the study is to better define transcranial Doppler (TCD) criteria for posterior circulation vasospasm. Basilar artery (BA) diameters were measured and compared with diameters obtained from baseline arteriograms in 144 artheriographies done in patients with aneurysmal subarachnoid haemorrhage (SAH). Both BA and extracranial vertebral artery (ECVA) flow velocities (FV) were measured by TCD in order to obtain an intracranial/extracranial flow velocities ratio. The velocity ratio between the basilar artery and the extracranial vertebral arteries (BA/VA) strongly correlated with the degree of BA narrowing (p<0.0001). A ratio higher than 2.0 was associated with 73% sensitivity and 80% specificity for BA vasospasm. A ratio higher than 2.5 with BA velocity greater than 85 cm/sec was associated with 86% sensitivity and 97% specificity for BA narrowing of more than 25%. A BA/VA ratio higher than 3.0 with BA velocities higher than 85 cm/sec was associated with 92% sensitivity and 97% specificity for BA narrowing of more than 50%. Our data show that the BA/VA ratio improves the sensitivity and specificity of TCD detection of BA vasospasm.
    12/2007: pages 255-257;
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    ABSTRACT: Dynamic cerebral autoregulation has been shown to be fast and effective, but it is not well known if the mechanism is symmetric, that is to say, it acts with equal compensatory action to upward as compared with downward abrupt changes in arterial blood pressure (ABP). Fourteen patients with head injuries and 10 normal subjects had bilateral transcranial Doppler and continuous ABP recording. Cyclic ABP stimuli were generated by large thigh cuffs, which were rapidly inflated above systolic pressure for 15 seconds alternating with 15 seconds of deflation. At least 8 such cycles were ensemble-averaged and the dynamic autoregulatory gain (AG(up) and AG(dn)) was estimated separately for upward and downward changes in ABP. The results were compared with the autoregulation index using conventional leg cuff releases. In normal subjects, AG(dn) was 0.74+/-0.18 and AG(up) was 0.77+/-0.17 (mean+/-SD); the difference was insignificant. The correlation between AG(dn) and AG(up), however, was weak (r=0.24). In the patients with head injury, AG(dn) was 0.30+/-0.21 and AG(up) was 1.27+/-0.76, the difference being highly significant (P<0.001). There was a negative relationship between AG(dn) and AG(up) (r=-0.33). Autoregulation index correlated well with AG(dn) (r=0.79) and weakly negatively with AG(up) (r=-0.47). A strongly asymmetric dynamic response of the cerebral autoregulation was seen the majority of patients with head injury. It might also have been present, albeit to a lesser degree, in the normal subjects. The findings suggest that nonlinear effects may be present in the operation of the cerebral autoregulation mechanism.
    Stroke 05/2007; 38(5):1465-9. DOI:10.1161/STROKEAHA.106.473462 · 6.02 Impact Factor
  • Journal of Neurotrauma 05/2007; 24(supplement 1-supplement 1):S-45-S-54. DOI:10.1089/neu.2007.9989 · 3.97 Impact Factor
  • Journal of Neurotrauma 05/2007; 24(supplement 1-supplement 1):S-65-S-70. DOI:10.1089/neu.2007.9986 · 3.97 Impact Factor
  • Journal of Neurotrauma 05/2007; 24(supplement 1-supplement 1):S-37-S-44. DOI:10.1089/neu.2007.9990 · 3.97 Impact Factor
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    ABSTRACT: Reduction of cerebral blood flow by caffeine has been shown in multiple studies. However, the effect of this substance on pathologically dilated cerebral vessels is not clearly defined. The aim of this study was to investigate the effect of caffeine on an already dilated cerebral circulation and specify if these vessels are still able to constrict as a consequence of caffeine stimulation. A second aim of this study was to compare results of cerebral vasomotor CO(2) reactivity testing with and without caffeine ingestion. Seventeen healthy adult volunteers had vasomotor reactivity tested before and thirty minutes after ingestion of 300 mg of caffeine. Each vasomotor reactivity test consisted of velocity measurements from both middle cerebral arteries using transcranial Doppler ultrasound during normocapnia, hypercapnia, and hypocapnia. Hemodynamic data and end-tidal CO(2) (etCO(2)) concentration were also recorded. The vasomotor reactivity (VMR) and CO(2) reactivity were calculated from a measured data pool. At a level of etCO(2)=40 mmHg the resting velocity in the middle cerebral artery (V(MCA)) dropped from 70.7+/-22.8 cm/sec to 60.7 +/- 15.4 cm/sec 30 minutes after caffeine stimulation (14.1% decrease, p<0.001). During hypercapnia of etCO(2)=50 mmHg there was also a significant decline of V(MCA) from 103.1+/-25.4 to 91.4+/-21.8 cm/sec (11.3%, p<0.001). There was not a statistically significant reduction of V(MCA) during hypocapnia. Calculated VMR and CO(2) reactivity before and after caffeine intake were not statistically significant. The presented data demonstrate a significant decrease in cerebral blood flow velocities after caffeine ingestion both in a normal cerebrovascular bed and under conditions of peripheral cerebrovascular vasodilatation. These findings support the important role of caffeine in regulation of CBF under different pathological conditions. Despite significant reactive vasodilatation in the brain microcirculation, caffeine is still able to act as a competitive antagonist of CO(2) on cerebral microvessels. The fact that caffeine may decrease CBF despite significant pathological vasodilatation offers the possibility of therapeutic manipulation in patients with traumatic vasoparalysis. For routine clinical testing of CO(2) reactivity it is not necessary to insist on pre-test dietary restrictions.
    Journal of Clinical Neuroscience 05/2007; 14(5):464-7. DOI:10.1016/j.jocn.2006.03.019 · 1.32 Impact Factor
  • Journal of Neurotrauma 05/2007; 24(supplement 1):S-59-S-64. DOI:10.1089/neu.2007.9987 · 3.97 Impact Factor
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    Journal of Neurotrauma 02/2007; 24 Suppl 1:S21-5. DOI:10.1089/neu.2007.9993 · 3.97 Impact Factor
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    ABSTRACT: Mannitol is effective for control of raised intracranial pressure (ICP) at doses of 0.25 gm/kg to 1 g/kg body weight. Arterial hypotension (systolic blood pressure 90 mm Hg) should be avoided. C. Level III Restrict mannitol use prior to ICP monitoring to pa-tients with signs of transtentorial herniation or progres-sive neurological deterioration not attributable to ex-tracranial causes. II. OVERVIEW Hyperosmolar agents currently in clinical use for trau-matic brain injury (TBI) are mannitol and hypertonic saline (HS) (Table 1). Mannitol Mannitol is widely used in the control of raised ICP following TBI. Its use is advocated in two circumstances. First, a single administration can have short term bene-ficial effects, during which further diagnostic procedures (e.g., CT scan) and interventions (e.g., evacuation of in-tracranial mass lesions) can be accomplished. Second, mannitol has been used as a prolonged therapy for raised ICP. There is, however, a lack of evidence to recommend repeated, regular administration of mannitol over several days. Although there are data regarding its basic mecha-nism of action, there are few human studies that validate different regimens of mannitol administration.
    Journal of Neurotrauma 02/2007; 24 Suppl 1:S14-20. DOI:10.1089/neu.2007.9994 · 3.97 Impact Factor

Publication Stats

7k Citations
680.96 Total Impact Points

Institutions

  • 1989–2011
    • University of Washington Seattle
      • • Department of Biobehavioral Nursing and Health Systems
      • • Department of Neurological Surgery
      Seattle, Washington, United States
  • 2009
    • Technion - Israel Institute of Technology
      • Rambam Medical Center
      Haifa, Haifa District, Israel
  • 1993–2008
    • Swedish Medical Center Seattle
      Seattle, Washington, United States
  • 2007
    • The Washington Institute
      Washington, Washington, D.C., United States
  • 2006
    • JFK Medical Center
      Edison, New Jersey, United States
    • Virginia Commonwealth University
      Richmond, Virginia, United States
  • 1998
    • University of New Mexico
      • Department of Neurosurgery
      Albuquerque, NM, United States