The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Elizabeth C. Lovett - One of the best experts on this subject based on the ideXlab platform.
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The venous manifestations of pulse wave encephalopathy: Windkessel dysfunction in normal aging and senile dementia
Neuroradiology, 2008Co-Authors: Grant A. Bateman, Christopher R. Levi, Yang Wang, Peter Schofield, Elizabeth C. LovettAbstract:Introduction Cerebral arterial, venous and cerebrospinal fluid (CSF) pulsations are closely coupled and this produces pulsation dampening or the Windkessel Effect. Normal pressure hydrocephalus is a manifestation of the breakdown of this Windkessel Effect with altered CSF and venous pulsations being noted. The aim of this study was to show that dysfunction of the Windkessel mechanism is also a component of normal aging and senile dementia. Methods The study group comprised 24 patients classified as either early senile dementia of Alzheimer’s type (SDAT) or vascular dementia (VaD). The patients with dementia were compared with 12 age-matched non-cognitively impaired subjects, and 12 normal young individuals were compared with the normal aging group. MRI flow quantification was used to measure the nonpulsatile and pulsatile components of blood flow as well as the pulsation at the tentorial incisura. Results With normal aging blood flow decreased but arterial pulsations increased in volume by 49% ( P = 0.003). The CSF vented via the tentorial incisura does not change significantly with age and therefore increased venous pulsation is necessary. In patients with VaD the arterial pulse volume was higher by 24% and the straight sinus pulsation was higher by 57% than in normal aging subjects ( P = 0.05 and P = 0.03, respectively). In patients with SDAT the total venous pulsation volumes were similar to those in normal aging subjects but there was less basal sinus pulsation. Conclusion Normal aging, SDAT and VaD are associated with alterations in venous pulsation due to a breakdown of the Windkessel Effect.
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The venous manifestations of pulse wave encephalopathy: Windkessel dysfunction in normal aging and senile dementia
Neuroradiology, 2008Co-Authors: Grant A. Bateman, Christopher R. Levi, Peter R. Schofield, Yang Wang, Elizabeth C. LovettAbstract:Introduction Cerebral arterial, venous and cerebrospinal fluid (CSF) pulsations are closely coupled and this produces pulsation dampening or the Windkessel Effect. Normal pressure hydrocephalus is a manifestation of the breakdown of this Windkessel Effect with altered CSF and venous pulsations being noted. The aim of this study was to show that dysfunction of the Windkessel mechanism is also a component of normal aging and senile dementia.
Wojciech Guminski - One of the best experts on this subject based on the ideXlab platform.
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influence of acute jugular vein compression on the cerebral blood flow velocity pial artery pulsation and width of subarachnoid space in humans
PLOS ONE, 2012Co-Authors: Andrzej F Frydrychowski, Pawel J Winklewski, Wojciech GuminskiAbstract:Purpose The aim of this study was to assess the Effect of acute bilateral jugular vein compression on: (1) pial artery pulsation (cc-TQ); (2) cerebral blood flow velocity (CBFV); (3) peripheral blood pressure; and (4) possible relations between mentioned parameters. Methods Experiments were performed on a group of 32 healthy 19–30 years old male subjects. cc-TQ and the subarachnoid width (sas-TQ) were measured using near-infrared transillumination/backscattering sounding (NIR-T/BSS), CBFV in the left anterior cerebral artery using transcranial Doppler, blood pressure was measured using Finapres, while end-tidal CO2 was measured using medical gas analyser. Bilateral jugular vein compression was achieved with the use of a sphygmomanometer held on the neck of the participant and pumped at the pressure of 40 mmHg, and was performed in the bend-over (BOPT) and swayed to the back (initial) position. Results In the first group (n = 10) during BOPT, sas-TQ and pulse pressure (PP) decreased (−17.6% and −17.9%, respectively) and CBFV increased (+35.0%), while cc-TQ did not change (+1.91%). In the second group, in the initial position (n = 22) cc-TQ and CBFV increased (106.6% and 20.1%, respectively), while sas-TQ and PP decreases were not statistically significant (−15.5% and −9.0%, respectively). End-tidal CO2 remained stable during BOPT and venous compression in both groups. Significant interdependence between changes in cc-TQ and PP after bilateral jugular vein compression in the initial position was found (r = −0.74). Conclusions Acute bilateral jugular venous insufficiency leads to hyperkinetic cerebral circulation characterised by augmented pial artery pulsation and CBFV and direct transmission of PP into the brain microcirculation. The Windkessel Effect with impaired jugular outflow and more likely increased intracranial pressure is described. This study clarifies the potential mechanism linking jugular outflow insufficiency with arterial small vessel cerebral disease.
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Influence of acute jugular vein compression on the cerebral blood flow velocity, pial artery pulsation and width of subarachnoid space in humans.
PloS one, 2012Co-Authors: Andrzej F Frydrychowski, Pawel J Winklewski, Wojciech GuminskiAbstract:Purpose The aim of this study was to assess the Effect of acute bilateral jugular vein compression on: (1) pial artery pulsation (cc-TQ); (2) cerebral blood flow velocity (CBFV); (3) peripheral blood pressure; and (4) possible relations between mentioned parameters. Methods Experiments were performed on a group of 32 healthy 19–30 years old male subjects. cc-TQ and the subarachnoid width (sas-TQ) were measured using near-infrared transillumination/backscattering sounding (NIR-T/BSS), CBFV in the left anterior cerebral artery using transcranial Doppler, blood pressure was measured using Finapres, while end-tidal CO2 was measured using medical gas analyser. Bilateral jugular vein compression was achieved with the use of a sphygmomanometer held on the neck of the participant and pumped at the pressure of 40 mmHg, and was performed in the bend-over (BOPT) and swayed to the back (initial) position. Results In the first group (n = 10) during BOPT, sas-TQ and pulse pressure (PP) decreased (−17.6% and −17.9%, respectively) and CBFV increased (+35.0%), while cc-TQ did not change (+1.91%). In the second group, in the initial position (n = 22) cc-TQ and CBFV increased (106.6% and 20.1%, respectively), while sas-TQ and PP decreases were not statistically significant (−15.5% and −9.0%, respectively). End-tidal CO2 remained stable during BOPT and venous compression in both groups. Significant interdependence between changes in cc-TQ and PP after bilateral jugular vein compression in the initial position was found (r = −0.74). Conclusions Acute bilateral jugular venous insufficiency leads to hyperkinetic cerebral circulation characterised by augmented pial artery pulsation and CBFV and direct transmission of PP into the brain microcirculation. The Windkessel Effect with impaired jugular outflow and more likely increased intracranial pressure is described. This study clarifies the potential mechanism linking jugular outflow insufficiency with arterial small vessel cerebral disease.
Grant A. Bateman - One of the best experts on this subject based on the ideXlab platform.
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the incidence of transverse sinus stenosis in multiple sclerosis further evidence of pulse wave encephalopathy
Multiple sclerosis and related disorders, 2020Co-Authors: Grant A. Bateman, Jeannette Lechnerscott, Alexander Robert Bateman, John Attia, Rodney Arthur LeaAbstract:Abstract Background Multiple sclerosis (MS) is associated with a breakdown in the intracranial pulse wave dampening or Windkessel Effect. This is manifest by an increase in the arterial stroke volume and a decrease in the dampening afforded by both the CSF displaced into the spinal canal and the blood displaced by the venous sinus pulsation. There is evidence that the reduction in compliance of the sagittal and straight sinuses in MS is caused by an increase in venous pressure despite the jugular bulb pressures being normal. This implies MS patients have a venous outflow stenosis somewhere between the torcular and jugular bulbs. The purpose of the current study is to define the site, significance and cause of these stenoses. Methods 50 patients with MS were prospectively recruited from an MS clinic and compared to 50 matched control patients. Using 3DT1 post contrast images, a survey of the venous sinuses was performed looking for the narrowest portion of the sinuses in each of 4 segments from the sagittal sinus to jugular bulbs. The cross sectional areas and wetted circumferences of the venous sinuses were measured at each site to calculate the minimum hydraulic and Effective diameters. The BMI, optic nerve sheath diameters and pituitary heights were measured. Statistical analysis was performed using non-parametric methods and was assessed using α≤0.05. Results Compared to controls, the MS patients’ sagittal sinuses were 24% larger in cross-section (p=0.0001) with an 18% larger wetted circumference (p=0.0001). The MS patients’ transverse sinuses had an average Effective stenosis of 38% by area (p 65% by area and 16/50 a low grade stenosis of between 40-65% by area compared to 1/50 low grade stenoses in this segment in the controls. The commonest cause of the stenosis was a giant arachnoid granulation. The optic nerve sheaths were larger in MS than controls (p=0.0006). Comparing MS patients with transverse sinus stenosis to those without, the pituitary height was 16% smaller and BMI 25% larger (p=0.02 and 0.003 respectively) Conclusion In patients with MS, the reduction in venous sinus compliance is associated with venous outflow stenoses in the transverse sinuses which increases the upstream venous pressure and dilates the sagittal sinuses. This finding suggests a continuum exists between MS and idiopathic intracranial hypertension.
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The venous manifestations of pulse wave encephalopathy: Windkessel dysfunction in normal aging and senile dementia
Neuroradiology, 2008Co-Authors: Grant A. Bateman, Christopher R. Levi, Yang Wang, Peter Schofield, Elizabeth C. LovettAbstract:Introduction Cerebral arterial, venous and cerebrospinal fluid (CSF) pulsations are closely coupled and this produces pulsation dampening or the Windkessel Effect. Normal pressure hydrocephalus is a manifestation of the breakdown of this Windkessel Effect with altered CSF and venous pulsations being noted. The aim of this study was to show that dysfunction of the Windkessel mechanism is also a component of normal aging and senile dementia. Methods The study group comprised 24 patients classified as either early senile dementia of Alzheimer’s type (SDAT) or vascular dementia (VaD). The patients with dementia were compared with 12 age-matched non-cognitively impaired subjects, and 12 normal young individuals were compared with the normal aging group. MRI flow quantification was used to measure the nonpulsatile and pulsatile components of blood flow as well as the pulsation at the tentorial incisura. Results With normal aging blood flow decreased but arterial pulsations increased in volume by 49% ( P = 0.003). The CSF vented via the tentorial incisura does not change significantly with age and therefore increased venous pulsation is necessary. In patients with VaD the arterial pulse volume was higher by 24% and the straight sinus pulsation was higher by 57% than in normal aging subjects ( P = 0.05 and P = 0.03, respectively). In patients with SDAT the total venous pulsation volumes were similar to those in normal aging subjects but there was less basal sinus pulsation. Conclusion Normal aging, SDAT and VaD are associated with alterations in venous pulsation due to a breakdown of the Windkessel Effect.
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The venous manifestations of pulse wave encephalopathy: Windkessel dysfunction in normal aging and senile dementia
Neuroradiology, 2008Co-Authors: Grant A. Bateman, Christopher R. Levi, Peter R. Schofield, Yang Wang, Elizabeth C. LovettAbstract:Introduction Cerebral arterial, venous and cerebrospinal fluid (CSF) pulsations are closely coupled and this produces pulsation dampening or the Windkessel Effect. Normal pressure hydrocephalus is a manifestation of the breakdown of this Windkessel Effect with altered CSF and venous pulsations being noted. The aim of this study was to show that dysfunction of the Windkessel mechanism is also a component of normal aging and senile dementia.
Yang Wang - One of the best experts on this subject based on the ideXlab platform.
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The venous manifestations of pulse wave encephalopathy: Windkessel dysfunction in normal aging and senile dementia
Neuroradiology, 2008Co-Authors: Grant A. Bateman, Christopher R. Levi, Yang Wang, Peter Schofield, Elizabeth C. LovettAbstract:Introduction Cerebral arterial, venous and cerebrospinal fluid (CSF) pulsations are closely coupled and this produces pulsation dampening or the Windkessel Effect. Normal pressure hydrocephalus is a manifestation of the breakdown of this Windkessel Effect with altered CSF and venous pulsations being noted. The aim of this study was to show that dysfunction of the Windkessel mechanism is also a component of normal aging and senile dementia. Methods The study group comprised 24 patients classified as either early senile dementia of Alzheimer’s type (SDAT) or vascular dementia (VaD). The patients with dementia were compared with 12 age-matched non-cognitively impaired subjects, and 12 normal young individuals were compared with the normal aging group. MRI flow quantification was used to measure the nonpulsatile and pulsatile components of blood flow as well as the pulsation at the tentorial incisura. Results With normal aging blood flow decreased but arterial pulsations increased in volume by 49% ( P = 0.003). The CSF vented via the tentorial incisura does not change significantly with age and therefore increased venous pulsation is necessary. In patients with VaD the arterial pulse volume was higher by 24% and the straight sinus pulsation was higher by 57% than in normal aging subjects ( P = 0.05 and P = 0.03, respectively). In patients with SDAT the total venous pulsation volumes were similar to those in normal aging subjects but there was less basal sinus pulsation. Conclusion Normal aging, SDAT and VaD are associated with alterations in venous pulsation due to a breakdown of the Windkessel Effect.
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The venous manifestations of pulse wave encephalopathy: Windkessel dysfunction in normal aging and senile dementia
Neuroradiology, 2008Co-Authors: Grant A. Bateman, Christopher R. Levi, Peter R. Schofield, Yang Wang, Elizabeth C. LovettAbstract:Introduction Cerebral arterial, venous and cerebrospinal fluid (CSF) pulsations are closely coupled and this produces pulsation dampening or the Windkessel Effect. Normal pressure hydrocephalus is a manifestation of the breakdown of this Windkessel Effect with altered CSF and venous pulsations being noted. The aim of this study was to show that dysfunction of the Windkessel mechanism is also a component of normal aging and senile dementia.
Christopher R. Levi - One of the best experts on this subject based on the ideXlab platform.
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The venous manifestations of pulse wave encephalopathy: Windkessel dysfunction in normal aging and senile dementia
Neuroradiology, 2008Co-Authors: Grant A. Bateman, Christopher R. Levi, Yang Wang, Peter Schofield, Elizabeth C. LovettAbstract:Introduction Cerebral arterial, venous and cerebrospinal fluid (CSF) pulsations are closely coupled and this produces pulsation dampening or the Windkessel Effect. Normal pressure hydrocephalus is a manifestation of the breakdown of this Windkessel Effect with altered CSF and venous pulsations being noted. The aim of this study was to show that dysfunction of the Windkessel mechanism is also a component of normal aging and senile dementia. Methods The study group comprised 24 patients classified as either early senile dementia of Alzheimer’s type (SDAT) or vascular dementia (VaD). The patients with dementia were compared with 12 age-matched non-cognitively impaired subjects, and 12 normal young individuals were compared with the normal aging group. MRI flow quantification was used to measure the nonpulsatile and pulsatile components of blood flow as well as the pulsation at the tentorial incisura. Results With normal aging blood flow decreased but arterial pulsations increased in volume by 49% ( P = 0.003). The CSF vented via the tentorial incisura does not change significantly with age and therefore increased venous pulsation is necessary. In patients with VaD the arterial pulse volume was higher by 24% and the straight sinus pulsation was higher by 57% than in normal aging subjects ( P = 0.05 and P = 0.03, respectively). In patients with SDAT the total venous pulsation volumes were similar to those in normal aging subjects but there was less basal sinus pulsation. Conclusion Normal aging, SDAT and VaD are associated with alterations in venous pulsation due to a breakdown of the Windkessel Effect.
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The venous manifestations of pulse wave encephalopathy: Windkessel dysfunction in normal aging and senile dementia
Neuroradiology, 2008Co-Authors: Grant A. Bateman, Christopher R. Levi, Peter R. Schofield, Yang Wang, Elizabeth C. LovettAbstract:Introduction Cerebral arterial, venous and cerebrospinal fluid (CSF) pulsations are closely coupled and this produces pulsation dampening or the Windkessel Effect. Normal pressure hydrocephalus is a manifestation of the breakdown of this Windkessel Effect with altered CSF and venous pulsations being noted. The aim of this study was to show that dysfunction of the Windkessel mechanism is also a component of normal aging and senile dementia.
