scholarly journals Transcranial Doppler: The Fifth Decade

2020 ◽  
pp. 154431672097621
Author(s):  
Thomas H. Alexander ◽  
Allison Hennigan ◽  
Preston Harrison ◽  
George Plotkin
Keyword(s):  
Blood Flow ◽  
Human Brain ◽  
Flow Velocity ◽  
Transcranial Doppler ◽  
Blood Flow Velocity ◽  
Single Element ◽  
Simple Test ◽  
Large Arteries ◽  
Single Discipline ◽  
Practicable Method

In 1981, the Norwegian physiologist, Rune Aaslid, developed a device that made it possible to apply the transcranial Doppler (TCD) sonographic technique to the human brain. In 1983, Albrecht Harders, a German neurosurgeon, worked out a clinically practicable method that would allow for bedside, atraumatic measurements to be made of the blood flow velocity in the large arteries in the Circle of Willis. This simple test is based on a single-element transducer technology but requires a knowledge of anatomy, physiology, and pathology that transcends any single discipline.

scholarly journals Association of transcranial Doppler blood flow velocity slow waves with delayed cerebral ischemia in patients suffering from subarachnoid hemorrhage: a retrospective study

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Vasilios E. Papaioannou ◽  
Karol P. Budohoski ◽  
Michal M. Placek ◽  
Zofia Czosnyka ◽  
Peter Smielewski ◽  
...  
Keyword(s):  
Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Flow Velocity ◽  
Transcranial Doppler ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Delayed Cerebral Ischemia ◽  
Area Under The Curve ◽  
Slow Waves

Abstract Background Cerebral vasospasm (VS) and delayed cerebral ischemia (DCI) constitute major complications following subarachnoid hemorrhage (SAH). A few studies have examined the relationship between different indices of cerebrovascular dynamics with the occurrence of VS. However, their potential association with the development of DCI remains elusive. In this study, we investigated the pattern of changes of different transcranial Doppler (TCD)-derived indices of cerebrovascular dynamics during vasospasm in patients suffering from subarachnoid hemorrhage, dichotomized by the presence of delayed cerebral ischemia. Methods A retrospective analysis was performed using recordings from 32 SAH patients, diagnosed with VS. Patients were divided in two groups, depending on development of DCI. Magnitude of slow waves (SWs) of cerebral blood flow velocity (CBFV) was measured. Cerebral autoregulation was estimated using the moving correlation coefficient Mxa. Cerebral arterial time constant (tau) was expressed as the product of resistance and compliance. Complexity of CBFV was estimated through measurement of sample entropy (SampEn). Results In the whole population (N = 32), magnitude of SWs of ipsilateral to VS side CBFV was higher during vasospasm (4.15 ± 1.55 vs before: 2.86 ± 1.21 cm/s, p < 0.001). Ipsilateral SWs of CBFV before VS had higher magnitude in DCI group (N = 19, p < 0.001) and were strongly predictive of DCI, with area under the curve (AUC) = 0.745 (p = 0.02). Vasospasm caused a non-significant shortening of ipsilateral values of tau and increase in SampEn in all patients related to pre-VS measurements, as well as an insignificant increase of Mxa in DCI related to non-DCI group (N = 13). Conclusions In patients suffering from subarachnoid hemorrhage, TCD-detected VS was associated with higher ipsilateral CBFV SWs, related to pre-VS measurements. Higher CBFV SWs before VS were significantly predictive of delayed cerebral ischemia.

scholarly journals Dexmedetomidine Decreases Cerebral Blood Flow Velocity in Humans

1993 ◽  
Vol 13 (2) ◽  
pp. 350-353 ◽  
Author(s):  
Mark H. Zornow ◽  
Mervyn Maze ◽  
J. Barry Dyck ◽  
Steven L. Shafer
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Flow Velocity ◽  
Transcranial Doppler ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Infusion Pump ◽  
Plasma Concentrations ◽  
Transcranial Doppler Sonography ◽  
Drug Infusion

This study was designed to determine the effects of dexmedetomidine on CBF velocity as measured by transcranial Doppler sonography in human volunteers. Dexmedetomidine, a potent α-2 adrenergic agonist, was administered by computer-driven infusion pump to six male volunteers. Serial measurements of middle cerebral artery blood flow velocity at four steady-state plasma concentrations of dexmedetomidine were made with a 2-MHz transcranial Doppler transducer via the temporal window. The targeted plasma concentrations were 0.49, 0.65, 0.81, and 0.97 ng/ml. These represent 60, 80, 100, and 120%, respectively, of the mean peak concentration following the intramuscular administration of 2 μg/kg of dexmedetomidine. Subjects experienced a significant degree of sedation at the highest infusion rates. Mean CBF velocity decreased with each increase in plasma concentration of dexmedetomidine and then began to return to basal levels after termination of the infusion. A trend toward an increase in the pulsatility index at the higher levels of dexmedetomidine suggests that the observed decrement in CBF velocity was due to an increase in cerebral vascular resistance. Upon initiation of the drug infusion, mean arterial pressure decreased from ∼95 mm Hg to 78 mm Hg. There were no further decreases in arterial pressure with subsequent increases in plasma concentrations of dexmedetomidine. Arterial carbon dioxide tension increased to a maximum of 45 mm Hg during the drug infusion, but this increase from baseline was not statistically significant. These studies are in agreement with previous animal studies which demonstrate a decrease in CBF after administration of dexmedetomidine.

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