Slow Rhythmic Oscillations in Intracranial CSF and Blood Flow: Registered by MRI

Strik, C.; Klose, Uwe; Kiefer, C.; Grodd, Wolfgang

doi:10.1007/978-3-7091-6738-0_36

Cited by 16 publications

(18 citation statements)

References 4 publications

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“…Because the BOLD signal is derived from the hemodynamic response, one source of BOLD signal oscillation that may not be neurally driven is that associated with the mechanical fluctuations of the cerebral vasculature. Studies have indeed found that BOLD signal oscillations may contain properties of vascular oscillation (Strik et al, 2002; Wise et al, 2004; Frederick et al, 2012). At the same time however, these studies do not demonstrate that BOLD signal fluctuations are purely driven by the physical properties of the vasculature.…”

Section: Discussionmentioning

confidence: 99%

L-DOPA changes spontaneous low-frequency BOLD signal oscillations in Parkinson's disease: a resting state fMRI study

Kwak¹,

Peltier²,

Bohnen³

et al. 2012

Front. Syst. Neurosci.

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Analysis of the amplitude of low frequency BOLD signal fluctuations (ALFF) in the resting state has recently been used to study the dynamics of intrinsic neural activity. Several studies have also suggested its potential as a biomarker for neuropsychiatric disease. In the current study, we quantified ALFF to determine changes in intrinsic neural oscillations in patients with Parkinson's disease (PD) on and off L-DOPA. Twenty-four PD patients and 24 healthy age-matched controls participated in the study. PD patients underwent two resting state fMRI sessions, either ON a controlled dose of L-DOPA or following a placebo pill (OFF). Control participants underwent one test session. We found that there was increased amplitude of low frequency BOLD signal oscillations for PD patients OFF L-DOPA in the primary and secondary motor areas, and in the middle and medial prefrontal cortices. L-DOPA significantly reduced the amplitude of low frequency oscillations within these regions. The degree of ALFF in the premotor cortex predicted patients' motor performance as measured by the Grooved Pegboard task, such that greater ALFF was associated with poorer performance. These results are in line with the pathophysiology of PD, which shows changes in neural oscillations. Thus, frequency domain analyses of resting state BOLD fMRI signals may provide a useful means to study the pathophysiology of PD and the physiology of the brain's dopaminergic pathways.

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Section: Discussionmentioning

confidence: 99%

L-DOPA changes spontaneous low-frequency BOLD signal oscillations in Parkinson's disease: a resting state fMRI study

Kwak¹,

Peltier²,

Bohnen³

et al. 2012

Front. Syst. Neurosci.

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“…Oscillations in concentrations of oxyhemoglobin in the prefrontal cortex, with a frequency of approximately 0.07-0.13 Hz, correlate with respiration in response to specific breathing patterns [37]. Finally, oscillations in the flow of cerebrospinal fluid (frequencies between 0.15 and 0.6 Hz) overlap with those in cerebral blood flow [38]. Respiratory rhythms also directly influence neuronal membrane potentials in the olfactory bulb and the RTN.…”

Section: Influence Of Respiratory Rhythm On Blood Pressure and Periphmentioning

confidence: 99%

Widespread depolarization during expiration: A source of respiratory drive?

Jerath¹,

Crawford²,

Barnes

et al. 2015

Medical Hypotheses

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a b s t r a c tRespiration influences various pacemakers and rhythms of the body during inspiration and expiration but the underlying mechanisms are relatively unknown. Understanding this phenomenon is important, as breathing disorders, breath holding, and hyperventilation can lead to significant medical conditions. We discuss the physiological modulation of heart rhythm, blood pressure, sympathetic nerve activity, EEG, and other changes observed during inspiration and expiration. We also correlate the intracellular mitochondrial respiratory metabolic processes with real-time breathing and correlate membrane potential changes with inspiration and expiration. We propose that widespread minor hyperpolarization occurs during inspiration and widespread minor depolarization occurs during expiration. This depolarization is likely a source of respiratory drive. Further knowledge of intracellular and extracellular ionic changes associated with respiration will enhance our understanding of respiration and its role as a modulator of cellular membrane potential. This could expand treatment options for a wide range of health conditions, such as breathing disorders, stress-related disorders, and further our understanding of the Hering-Breuer reflex and respiratory sinus arrhythmia.Ó 2014 Elsevier Ltd. All rights reserved. IntroductionIn addition to gas exchange and oxygenation of the blood, respiration in the lungs can regulate multiple physiological processes throughout the body. Studies of the cardiovascular system, the peripheral nervous system, and the central nervous system provide evidence that respiratory patterns can exert a significant and immediate influence on a wide range of bodily functions, including changes in blood pressure and sympathovagal balance. Patterned respiration can regulate blood pressure and heart rate [1], as well as regulate rhythmic centers of the brain that control cardiovascular output [2,3]. While the majority of these findings have demonstrated the impact of respiration on cardiac output and other processes in isolated preparations, little work has focused on respiration's direct influence on membrane potential.This article reviews the current understanding of respiration as a regulator of cardiovascular physiology and nervous system function. More specifically, we discuss the role of respiratory rhythm and rate on both systemic and local control of these systems. We describe the role of pulmonary stretch receptors (with a focus on slowly adapting receptors) in converting breathing patterns into a functional, multi-faceted, mechanism that allows respiration to communicate with, and direct various aspects of cardiovascular and nervous system physiology. We propose a hypothesis in which inspiration and expiration are associated with transient increases and decreases in membrane potential that may underlie these widespread changes and how these membrane potential changes may underlie the chaotic dynamics of rhythmic breathing.Many studies focus on the brainstem as the primary modulator of resp...

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“…Consequently, cholinergic monoaminergic blockade can partially reverse EEG slowing and (Dringenberg, 2000). Varying with changes in metabolism and blood flow consequent upon the insult (Meinzer et al, 2004;Strik et al, 2002;Vieth et al, 2001), abnormal slow wave activity has been attributed to a 'dysfunctional state' of the neuronal tissue (Lewine and Orrison, 1995). We may assume that 'de-afferented' neural networks cut off from major input sources produce focally generated slow waves.…”

Section: E-mail Addressmentioning

confidence: 99%

Abnormal slow wave mapping (ASWAM)—A tool for the investigation of abnormal slow wave activity in the human brain

Wienbruch¹

2007

Journal of Neuroscience Methods

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Slow waves in the delta and theta frequency range, normal signs of deactivated networks in sleep stages, are considered 'abnormal' when prominent in the waking state and when generated in circumscribed brain areas. Structural cortical lesions, e.g. related to stroke, tumors, or scars, generate focal electric and magnetic slow wave activity in the penumbra. Focal concentrations of slow wave activity exceeding those of healthy subjects have also been found in individuals suffering from psychiatric disorders without obvious structural brain damage. Hence, identification and mapping of abnormal slow wave activity might contribute to the investigation of cortical indications of psychopathology.Here I propose a method for abnormal slow wave mapping (ASWAM), based on a 5 min resting magnetoencephalogramm (MEG) and equivalent current dipole fitting to sources in the 1-4 Hz frequency band (delta) in anatomically defined cortical regions. The method was tested in a sample of 116 healthy subjects (59 males), with the aim to provide a basis for later comparison with patient samples. As to be expected, delta dipole density was low in healthy subjects. However, its distribution differed between genders with fronto-central > posterior dipole density in male and posterior dominance in female participants, which was not significantly related to either age or headsize. Results suggest that this method allows the identification of ASWA, so that comparison against Z-scores from a larger normal control group might assist diagnostic purposes in patient groups. As specific distributions seem to reflect differences between genders, this should be considered also in the analysis of patient samples.

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Slow Rhythmic Oscillations in Intracranial CSF and Blood Flow: Registered by MRI

Cited by 16 publications

References 4 publications

L-DOPA changes spontaneous low-frequency BOLD signal oscillations in Parkinson's disease: a resting state fMRI study

L-DOPA changes spontaneous low-frequency BOLD signal oscillations in Parkinson's disease: a resting state fMRI study

Widespread depolarization during expiration: A source of respiratory drive?

Abnormal slow wave mapping (ASWAM)—A tool for the investigation of abnormal slow wave activity in the human brain

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