Translational Neurosonology
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Translational Neurosonology

A. Alonso, M. G. Hennerici, S. Meairs

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eBook - ePub

Translational Neurosonology

A. Alonso, M. G. Hennerici, S. Meairs

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About This Book

Diagnostic ultrasound has become an elementary tool for evaluating cerebrovascular diseases and plays a prominent role in routine clinical practice. Many publications attempt to cover the continuous progress of its diagnostic and even therapeutic applications. However, the impact ultrasound has made in recent years in the fields of animal studies and human research is less well known. This publication provides an overview on exciting current attempts in neurological diseases, ranging from experimental approaches to established imaging modes ready to be incorporated into the routine of daily practice. The first part of the book concentrates on basic principles of neurosonology and focuses on contrast imaging, specific ultrasound contrast agents and safety aspects. The following chapters deal with different vascular ultrasound applications, allowing an optimized characterization of atherosclerotic disease and monitoring of cerebral autoregulation. In addition, the role of parenchymal ultrasound imaging in cerebrovascular diseases and movement disorders is illustrated. The final chapters look at promising new therapeutic approaches implementing ultrasound although they are still no more than experimental. The book can be highly recommended to clinical neurologists with good knowledge in clinical ultrasound who wish to gain a compact and updated insight into the plethora of capabilities of neurosonology in the future.

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Information

Publisher
S. Karger
Year
2014
ISBN
9783318027914
Alonso A, Hennerici MG, Meairs S (eds): Translational Neurosonology.
Front Neurol Neurosci. Basel, Karger, 2015, vol 36, pp 40-56 (DOI: 10.1159/000366236)
______________________

Functional TCD: Regulation of Cerebral Hemodynamics - Cerebral Autoregulation, Vasomotor Reactivity, and Neurovascular Coupling

Marc E. Wolf
Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, Mannheim, Germany
______________________

Abstract

Three main mechanisms influence cerebral hemodynamics, with the aim of adapting the cerebral blood flow to the metabolic demand of the brain. Cerebral autoregulation ensures stable perfusion of the brain, independent of the systemic blood pressure. Vasomotor reactivity reflects the hemodynamic responses to modifications of the arterial pCO2/pH of the brain tissue. Neurovascular coupling adapts the perfusion to increased metabolic demand as a consequence of enhanced brain activity to permit reasonable functioning of cells. Different methods using transcranial Doppler sonography have been developed to characterize these mechanisms in healthy subjects and under pathologic conditions. The most established applications in clinical settings are described, and the results of specific research studies are briefly reported.
© 2015 S. Karger AG, Basel

Introduction

Three main mechanisms influence cerebral hemodynamics, with the aim of adapting the cerebral blood flow (CBF) to the metabolic demand of the brain. The goal of all of these mechanisms is to provide the necessary amount of oxygen to the brain tissue in situations of systemically decreased blood flow or increased demand during enhanced brain activity. This chapter will focus on hemodynamic mechanisms, as illustrated in figure 1:
(1) Cerebral autoregulation ensures stable perfusion of the brain, independent of the systemic blood pressure (within a certain range).
(2) Vasomotor reactivity adapts hemodynamics to the arterial pCO2/pH of the tissue, which reflects its need for oxygen.
Img
Fig. 1. Illustration of hemodynamic mechanisms influencing cerebral blood flow: cerebral autoregulation, vasomotor reactivity, and neurovascular coupling.
(3) Neurovascular coupling (NVC) adapts the perfusion to increased metabolic demand as a consequence of enhanced brain activity.
The changes in CBF underlying these mechanisms can be recorded and analyzed with functional transcranial Doppler sonography (fTCD), which not only assesses the blood flow velocities of the cerebral vessels but also considers the changes in and reaction of the vasculature induced by external or internal stimuli under normal or pathologic conditions, with a high temporal resolution.
As physiologic background, the diameter of the intracranial vessels is assumed to be stable under different conditions. Therefore, an increase in the CBF velocity (CBFV) reflects an elevation of CBF, the parameter of interest.
First, some general comments about fTCD: Major strengths are its high temporal resolution, the non-invasiveness of the technique, the possibility of using it even at beside (e.g. in intensive care units (ICUs) or actually during surgery), and its relatively easy handling. This entails the possibility of performing follow-up investigations. For the patient, the test procedure is not very stressful compared with competing techniques such as fMRI. In general, the costs are affordable. However, one should be aware of some weaknesses. The technique has a low spatial resolution, and no direct anatomical image is procured. The measurements reflect relative differences (interhemispheric comparisons or maximum vs. minimum) rather than absolute values, and the recording and interpretation are somehow operator dependent. Some patients are not assessable due to an insufficient bone window, and some might have pathologies (e.g. intracranial vascular stenosis or systemic disorders such as anemia or cardiac pathologies) affecting the results of the TCD.
The aim of this book is to focus on the translational aspects of ultrasound. Therefore, an effort was made to include the results of animal studies, when possible. However, since fTCD may be applied in humans without affecting their health, experimental studies are scarce, and studies in humans are more appropriate to characterize the respective mechanisms.
Given the large number of different methods, evaluation systems, and clinical studies in this field, the discussion of some aspects needed to be shortened or omitted. This is not always mentioned explicitly. However, an effort was made to provide additional references to give the reader the opportunity to further deepen his knowledge of issues in which he is specifically interested.

Cerebral Autoregulation

Definition

Cerebral autoregulation (CA) accounts for the stabilization of cerebral perfusion in the presence of systemic hypo- or hypertension. For mean systemic arterial blood pressures (ABPs) between 50-60 and 150-170 mm Hg (and the respective cerebral perfusion pressures, or CPPs), the CBF is kept constant. Above and below these limits, the mechanism does not evolve reasonably, entailing potentially harmful hypo- or hyperperfusion of the brain tissue.
The regulation is based on cerebrovascular resistance (CVR) and is mainly adjusted in the small arterioles and precapillary sphincters. Three mechanisms play a role: metabolic regulation, mediated by the release of vasoactive substances, when oxygen is needed; myogenic regulation, mediated by adapting the vascular tone to the transmural blood pressure (BP); and neurogenic regulation, mediated by sympathetic innervation of the vascular smooth cells.
One can distinguish between two types of CA. Static CA adapts the CBF to slow/ gradual changes in ABP within minutes or hours. This dates back to the pre-fTCD era since available methods needed to average several minutes of recording. With the high temporal resolution of fTCD, dynamic cerebral autoregulation (dCA), responding to immediate ABP changes within seconds, can be analyzed by considering the beat-to-beat dynamics.
CA and CBF show some variations related to daytime, exercise, forced respiration (with changes in the arterial pCO2), body position, and functional activation. Food intake, caffeine intake, and hormonal changes like the menstrual cycle also play a role. These fluctuations have to be kept in mind for standardization when performing CA tests either in a cohort (to evaluate each patient under the same conditions) or in intra-individual longitudinal studies. One should also consider the influence of anesthetics [1].

Animal Studies

Animal studies have been published since the 1960s. Most of them have used different techniques, such as electromagnetic flowmetry (see review by Panerai) [2]. Precursor studies of the carotid compression test have been performed in monkeys. CA studies with concomitant intracerebral pressure (ICP) measurements have been performed in piglet brains. Impaired CA in hypertensive rats has been associated with larger ischemic lesions in experimental stroke models.
With the development of fTCD, direct non-invasive investigation of human subjects was possible. Autoregulation seems to be more important in humans, who are subjected to severe orthostatic stresses more than quadrupeds are. Therefore, the mechanisms might differ.

Methods in Humans

Stimulation Techniques

Evaluation of static CA has mostly been performed using pharmacological interventions to achieve gradual changes in ABP.
Several techniques using a stimulus-response method have been established to assess and quantify dCA. The dynamics of the CBFV after a rapid ABP drop (and the time until the CBFV reaches steady state again) are considered. Simple or oscillatory stimuli are used. For further details, see the review by Panerai [2].
The leg-cuff method (Aaslid et al. [3]) involves the perfusion of both proximal lower extremities being blocked for 2-3 min with a BP cuff (> the systemic pressure), followed by rapid deflation. This entails a rapid step-wise systemic decrease in the ABP (by about 20 mm Hg) and should activate an increase in the CBFV of 20%/s under normal conditions.
Contraindications are a vascular disease or fracture of the leg and, in general, an unstable ICP [4]. The stimulus might not represent the typical physiologic situation in daily life (e.g. changes in posture or pharmacological stimuli due to medication). However, the test is performed in a supine position, and therefore, bedfast patients can be investigated.
The carotid artery compression test/transient hyperemic response [5] involves the common carotid artery being compressed within the neck as low as possible. With a CBFV decrease of 30-50%, compression is considered as sufficient, and after 3 s, the compression is released in the diastole. This manipulation induces a ‘transient hyperemic response’ (THR) with a compensatory vasodilatation of the arterioles. The response can be quantified according to the ‘transient hyperemic response ratio’ (THRR):
Img
(vhyperemic = the systolic CBFV 2 cycles after compression release; vbasic = the systolic CBFV 5 cycles before compression).
Normal values vary between 1.105 and 1.29. There is a risk of generating emboli, and t...

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