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Jarvela, M.

Publications and source records attributed to Jarvela, M..

4 recordsLinked to original sources

Reduced harmonic complexity of brain parenchymal cardiovascular pulse waveforms in Alzheimer's disease

Alzheimers disease (AD) is characterized by specific neuropathologies, and is associated with arterial wall {beta}-amyloid accumulations, which lead to radiologically detectable amplitude increases and variable propagation speed of cardiovascular impulses in brain. In this study, we developed a fast frequency domain imaging method know as relative harmonic power of magnetic resonance encephalography (MREGRHP), aiming to investigate the configuration of the cardiovascular impulses independently of the mean magnetic resonance signal intensity and physiological impulse amplitude. In the initial analyses in healthy controls, we found that a wide 0.8 - 5Hz bandpass produced the most physiologically realistic cardiovascular waveforms. Whereas the data recorded in cerebrospinal fluid (CSF) from flip angle (FA) of 25{degrees} yielded up to 7-fold higher cardiac signal intensity as compared to FA of 5{degrees}, within the brain tissue recordings with FA of 5{degrees} were markedly more sensitive to cardiac waveform. We detected arterial impulses originating from major arteries and extending into the surrounding brain parenchyma, with simultaneous dampening of amplitude as a function of distance from source. Finally, we compared MREGRHP results in 34 AD patients (mean age: 60.7{+/-}4.7 years; 53% female) against 29 controls (mean age: 56.9{+/-}7.9 years; 66% female). We show that the harmonic power of cardiovascular brain pulses is significantly reduced in cortical frontoparietal areas of AD patients, indicating monotonous impulse patterns colocalizing with the previously reported areas of increased impulse propagation speed. In conclusion, the MREGRHP offers a fast Fourier transform (FFT)-based method to non-invasively quantify and locate human arterial blood vessel wall pathology.

neuroscience↗

Sleep increases propagation speed of physiological brain pulsations

During sleep, there is an increase in the brain cerebrospinal fluid (CSF) solute convection driven by physiological pulsations. Although the main drivers of CSF flow, namely cardiac, respiratory, and vasomotor pulsations, become more powerful during sleep, there is relatively little information regarding their effects on CSF flow velocity across human brain during sleep. Here, we used functional magnetic resonance encephalography (MREG) to measure non-invasively changes in brain water flow during to sleep by tracking the propagating ultrafast signal changes induced by physiological brain pulsations. We first undertook a phantom study confirming that dense optical flow analysis of MREG data accurately detects water flow velocity, and reflects the power of the physiological pulsations. We then applied the method to quantify CSF water flow velocity in brain of healthy volunteers during EEG-verified awake and sleep recordings of ultrafast MREG data. Sleep induced an increase in CSF flow speed, as demonstrated by elevated vasomotor and respiratory pulsation speeds, while the speed of cardiovascular impulse propagation remained unchanged. The speed increases match previous findings of respective pulsation power changes, and correlated with slow delta EEG power. The sleep-induced CSF flow speed increases occurred dynamically over both pulsation cycles, without the large effects on flow directions reported previously in several neurological conditions. In conclusion, sleep increases 3D water flow speed dynamically in human brain regions showing concomitant pulse power increases, supporting a porous media model of hydrodynamics in brain cortex.

neuroscience↗

Cardiovascular and vasomotor pulsations in the brain and periphery during awake and NREM sleep in a multimodal fMRI study

The glymphatic brain clearance mechanism convects brain cerebrospinal fluid driven by physiological pulsations such as cardiovascular and very low-frequency (VLF < 0.1 Hz) vasomotor waves. Presently, ultrafast functional magnetic resonance imaging (fMRI) facilitates the measurement of these signals from both venous and arterial compartments. In this study, we compared the interaction of these two pulsations in awake and sleep using fMRI and peripheral fingertip photoplethysmography in both arterial and venous signals in ten subjects (5 female). Sleep increased the power of brain cardiovascular pulsations, decreased peripheral pulsation and desynchronized them. Vasomotor waves, however, increase in both power and synchronicity in brain and peripheral signals during sleep. Peculiarly, vasomotor lag reversed in sleep within the default mode network vs. peripheral signal. Finally, sleep synchronized cerebral arterial vasomotion measured with cardiovascular hemodynamic envelope (CHe) vs. venous blood oxygenation level dependent (BOLD) signals in parasagittal brain tissue. These changes in power and pulsation synchrony may reflect differential changes in vascular control between the periphery and brain vasculature, while the increased synchrony of arterial and venous compartments may reflect increased convection of neurofluids in parasagittal areas in sleep. Statement of SignificanceThis study shows that while sleep attenuated the cardiovascular synchrony and powers of pulsatility between the periphery and brain, it also increased brain tissue synchrony of venous and arterial vasomotor waves, specifically in the parasagittal regions. The study also shows that vasomotor waves increased in the human brain and the periphery during NREM sleep. Thus, sleep induces a whole-body vasomotor synchronization where the initiation of peripheral vasomotor waves is preceded within the default mode network area. Based on these results, we suggest that the synchronization of vasomotor waves may be a significant contributor to the enhancement of glymphatic fluid exchange in the human brain during sleep.

neuroscience↗

Sleep-specific changes in physiological brain pulsations

Sleep is known to increase the convection of interstitial brain metabolites along with cerebrospinal fluid (CSF). We used ultrafast magnetic resonance encephalography (MREGBOLD) to quantify the effect of sleep on physiological (vasomotor, respiratory and cardiac) brain pulsations driving the CSF convection in humans. Transition to electroencephalography verified sleep occurred in conjunction with power increase and reduced spectral entropy (SE) of physiological brain pulsations. During sleep, the greatest increase in spectral power was in very-low frequency (VLF < 0.1 Hz) waves, followed by respiratory and cardiac brain pulsations. SE reduction coincided with decreased vigilance in awake state and could robustly (ROC 0.88, p < 0.001) differentiate between sleep vs. awake states, indicating the sensitivity of SE of the MREGBOLD signal as a marker for sleep level. In conclusion, the three physiological brain pulsation contribute to the sleep-associated increase in glymphatic CSF convective flow in an inverse frequency order. HighlightsO_LIBrain tissue contains almost no connective tissue, this enabling pressure waves to initiate long-distance brain pulsations C_LIO_LIBrain pulsations are induced by vasomotion, respiration, and the cardiac cycle C_LIO_LISleep strikingly increases spectral power and decreases spectral entropy of brain pulsations, especially for the very low frequency vasomotor waves C_LIO_LISpectral entropy of brain pulsations detected by MREG is a sensitive measure of vigilance, resembling the corresponding entropy changes detected by scalp EEG C_LI

neuroscience↗