Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, November 24, 2022

Assessment of dynamic cerebral autoregulation in near-infrared spectroscopy using short channels: A feasibility study in acute ischemic stroke patients

So you assessed that there is a problem, offered NO solution. What the hell are you doing in stroke anyway? Isn't it to solve stroke problems?

Assessment of dynamic cerebral autoregulation in near-infrared spectroscopy using short channels: A feasibility study in acute ischemic stroke patients

Sabeth Becker1*, Franziska Klein2, Katja König1,3, Christian Mathys4,5, Thomas Liman1,3 and Karsten Witt1,3,4
  • 1Department of Neurology, School of Medicine and Health Sciences, Carl von Ossietzky University of Oldenburg, Oldenburg, Germany
  • 2Neurocognition and Functional Neurorehabilitation Group, Neuropsychology Lab, Department of Psychology, Faculty of Medicine and Health Sciences, University of Oldenburg, Oldenburg, Germany
  • 3University Clinic for Neurology, Evangelical Hospital, Oldenburg, Germany
  • 4Institute of Radiology and Neuroradiology, Evangelical Hospital, Oldenburg, Germany
  • 5Research Centre Neurosensory Science, Department of Human Medicine, Faculty of Medicine and Health Sciences, University of Oldenburg, Oldenburg, Germany

Introduction: In acute ischemic stroke, progressive impairment of cerebral autoregulation (CA) is frequent and associated with unfavorable outcomes. Easy assessment of cerebral blood flow and CA in stroke units bedside tools like near-infrared spectroscopy (NIRS) might improve early detection of CA deterioration. This study aimed to assess dynamic CA with multichannel CW-NIRS in acute ischemic stroke (AIS) patients compared to agematched healthy controls.

Methods: CA reaction was amplified by changes in head of bed position. Long- and short channels were used to monitor systemic artery pressure- and intracranial oscillations simultaneously. Gain and phase shift in spontaneous low- and very low-frequency oscillations (LFO, VLFO) of blood pressure were assessed.

Results: A total of 54 participants, 27 with AIS and 27 age-matched controls were included. Gain was significantly lower in the AIS group in the LFO range (i) when the upper body was steadily elevated to 30. and (ii) after its abrupt elevation to 30°. No other differences were found between groups.

Discussion: This study demonstrates the feasibility of NIRS short channels to measure CA in AIS patients in one single instrument. A lower gain in AIS might indicate decreased CA activity in this pilot study, but further studies investigating the role of NIRS short channels in AIS are needed.

Introduction

Cerebral blood flow is substantially regulated by the mechanism of cerebral autoregulation (CA). CA continuously adjusts vascular resistance and diameter to intercept systemic blood pressure (BP) changes. For that, it uses myogenic mechanisms (14), the autonomic nervous system (27), and CO2 partial pressure changes (8). CA protects brain tissue from reduced perfusion and hence brain ischemia and remains unaltered with aging and hypertension (9, 10). However, major impairment of CA is frequent in AIS (1113). The effect of postural changes on cerebral blood flow (1416), e.g., seen in controlled changes in an orthostatic maneuver [changes in upper body position, head of bed (HOB)] serves as an indicator for severity of CA impairment. This orthostatic maneuver could be analyzed with spontaneous blood pressure oscillations that provide comprehensive information on CA (17).

Near-infrared spectroscopy (NIRS) measures hemodynamic changes. By using optodes (i.e., light sources and light detectors) near-infrared light is transmitted through the head surface into the tissue. Hence, hemoglobin absorption can be quantified as concentration changes in oxygenated and deoxygenated hemoglobin in vivo (18). NIRS provides information on both scalp perfusion, which represents regulation of the extracerebral vessels, and cerebral perfusion, which is constantly modified by CA. Hence, NIRS is an excellent tool to assess the differences between extra- and intracerebral vascular autoregulation. It is a useful, non-invasive and investigator-independent bedside measurement for CA (19). Global blood flow regulation processes are the main source of physiological signals measured superficially by NIRS in the scalp (20, 21), and is often considered as disturbing factor. In the past years, extracerebral NIRS signals have been eliminated using short distance correction as a filter to obtain only the adjusted intracerebral signals (2224).

NIRS records cerebral changes in the local oxygenated and deoxygenated hemoglobin concentrations on the cerebral cortex. In this signal, systemic arterial BP oscillations can indirectly be displayed (2527), and subdivided into frequency ranges. Each range provides information about different aspects of CA: Low-frequency oscillations (LFO or Mayer waves, ~0.1 Hz) reflect the local myogenic activity in the terminal arterioles and are further influenced by sympathetic tone and control mechanisms (28, 29). Very low-frequency oscillations (VLFO or B-Waves) range in the minute range (30). Upper VLFO (~0.05 Hz) stem from large arterioles under neurogenic innervation (3133) and are modulated by arterial CO2 partial pressure (34, 35). Lower VLFO (~0.01 Hz) are endothelial dependent and thus connected to metabolic changes in the microvessels (36). Intact CA constantly modifies spontaneous dynamic oscillations resulting in higher desynchronization of intra- and extracranial BP oscillations. However, an impaired CA (as in AIS) is unable to modulate BP, and therefore intracranial oscillations passively and synchronously follow those of systemic BP (37).

So far, in NIRS studies on (dynamic) CA, the use of an external tool that measures systematic blood pressure variations were necessary: While intracranial BP changes have been assessed by NIRS or transcranial doppler, systemic BP changes were recorded using a finger plethysmograph (26, 3841) or an arterial or aortic catheter (32, 42, 43). Afterwards, these independent datasets needed to be synchronized to detect modulation by CA. However, this synchronization, accurate to milliseconds, is complex and error-prone. Therefore, one main aim of the present study was to address this using the short channel signal instead.

To assess the synchronicity of extra- and intracerebral oscillations and, therefore, the extent of modification by CA, fourier analyses such as discrete fourier transform (DFT) are commonly used (17). By DFT, measuring points are periodically continued into sinus curves. Input-sinusoids (=systemic BP-signal) are transformed into sinusoids of the same frequency at the output (=intracranial BP-signal) but with a different amplitude (gain) and shifted in time (the phase shift of the response). In this study, the synchronicity of two signals will be assessed: The oscillation in the short channels (input signal), which detect the systemic oscillations of the ABP via the scalp, and the oscillation modified by CA, which is measured via long channels (output signal).

The feasibility of NIRS has rarely been tested in AIS patients. The aims of this study are (i) to detect CA changes in AIS patients in comparison to matched-healthy controls and (ii) to test if these changes can be assessed using a single NIRS system, including short- and long channels, in an acute stroke unit setting.

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