Regression analysis for peak designation in pulsatile pressure signals

Following recent studies, the automatic analysis of intracranial pressure (ICP) pulses appears to be a promising tool for forecasting critical intracranial and cerebrovascular pathophysiological variations during the management of many disorders. A pulse analysis framework has been recently developed to automatically extract morphological features of ICP pulses. The algorithm is able to enhance the quality of ICP signals, to segment ICP pulses, and to designate the locations of the three ICP sub-peaks in a pulse. This paper extends this algorithm by utilizing machine learning techniques to replace Gaussian priors used in the peak designation process with more versatile regression models. The experimental evaluations are conducted on a database of ICP signals built from 700 h of recordings from 64 neurosurgical patients. A comparative analysis of different state-of-the-art regression analysis methods is conducted and the best approach is then compared to the original pulse analysis algorithm. The results demonstrate a significant improvement in terms of accuracy in favor of our regression-based recognition framework. It reaches an average peak designation accuracy of 99% using a kernel spectral regression against 93% for the original algorithm

Robust Peak Recognition in Intracranial Pressure Signals

<p>Abstract</p> <p>Background</p> <p>The waveform morphology of intracranial pressure pulses (ICP) is an essential indicator for monitoring, and forecasting critical intracranial and cerebrovascular pathophysiological variations. While current ICP pulse analysis frameworks offer satisfying results on most of the pulses, we observed that the performance of several of them deteriorates significantly on abnormal, or simply more challenging pulses.</p> <p>Methods</p> <p>This paper provides two contributions to this problem. First, it introduces MOCAIP++, a generic ICP pulse processing framework that generalizes MOCAIP (Morphological Clustering and Analysis of ICP Pulse). Its strength is to integrate several peak recognition methods to describe ICP morphology, and to exploit different ICP features to improve peak recognition. Second, it investigates the effect of incorporating, automatically identified, challenging pulses into the training set of peak recognition models.</p> <p>Results</p> <p>Experiments on a large dataset of ICP signals, as well as on a representative collection of sampled challenging ICP pulses, demonstrate that both contributions are complementary and significantly improve peak recognition performance in clinical conditions.</p> <p>Conclusion</p> <p>The proposed framework allows to extract more reliable statistics about the ICP waveform morphology on challenging pulses to investigate the predictive power of these pulses on the condition of the patient.</p

The pulsating brain: A review of experimental and clinical studies of intracranial pulsatility

The maintenance of adequate blood flow to the brain is critical for normal brain function; cerebral blood flow, its regulation and the effect of alteration in this flow with disease have been studied extensively and are very well understood. This flow is not steady, however; the systolic increase in blood pressure over the cardiac cycle causes regular variations in blood flow into and throughout the brain that are synchronous with the heart beat. Because the brain is contained within the fixed skull, these pulsations in flow and pressure are in turn transferred into brain tissue and all of the fluids contained therein including cerebrospinal fluid. While intracranial pulsatility has not been a primary focus of the clinical community, considerable data have accrued over the last sixty years and new applications are emerging to this day. Investigators have found it a useful marker in certain diseases, particularly in hydrocephalus and traumatic brain injury where large changes in intracranial pressure and in the biomechanical properties of the brain can lead to significant changes in pressure and flow pulsatility. In this work, we review the history of intracranial pulsatility beginning with its discovery and early characterization, consider the specific technologies such as transcranial Doppler and phase contrast MRI used to assess various aspects of brain pulsations, and examine the experimental and clinical studies which have used pulsatility to better understand brain function in health and with disease

PHOTOPLETHYSMOGRAPHIC WAVEFORM ANALYSIS DURING LOWER BODY NEGATIVE PRESSURE SIMULATED HYPOVOLEMIA AS A TOOL TO DISTINGUISH REGIONAL DIFFERENCES IN MICROVASCULAR BLOOD FLOW REGULATION.

The purpose of this investigation was to explore modulation of the photoplethsymographic (PPG) waveform in the setting of simulated hypovolemia as a tool to distinguish regional differences in regulation of the microvasculature. The primary goal was to glean useful physiological and clinical information as it pertains to these regional differences in regulation of microvascular blood flow. This entailed examining the cardiovascular, autonomic nervous, and respiratory systems interplay in the functional hemodynamics of regulation of microvascular blood flow to both central (ear, forehead) and peripheral (finger) sites. We monitored ten healthy volunteers (both men and women age 24-37 ) non-invasively with central and peripheral photoplethysmographs and laser Doppler flowmeters during Lower Body Negative Pressure (LBNP). Waveform amplitude, width, and oscillatory changes were characterized using waveform analysis software (Chart, ADInstruments). Data were analyzed with the Wilcoxon Signed Ranks Test, paired t-tests, and linear regression. Finger PPG amplitude decreased by 34.6 ± 17.6% (p = 0.009) between baseline and the highest tolerated LBNP. In contrast, forehead amplitude changed by only 2.4 ± 16.0% (p=NS). Forehead and finger PPG width decreased by 48.4% and 32.7%, respectively. Linear regression analysis of the forehead and finger PPG waveform widths as functions of time generated slopes of -1.113 (R = -0.727) and -0.591 (R = -0.666), respectively. A 150% increase in amplitude density of the ear PPG waveform was noted within the range encompassing the respiratory frequency (0.19-0.3Hz) (p=0.021) attributable to changes in stroke volume. We also noted autonomic modulation of the ear PPG signal in a different frequency band (0.12 0.18 Hz). The data indicate that during a hypovolemic challenge, healthy volunteers had a relative sparing of central cutaneous blood flow when compared to a peripheral site as indicated by observable and quantifiable changes in the PPG waveform. These results are the first documentation of a local vasodilatation at the level of the terminal arterioles of the forehead that may be attributable to recently documented cholinergic mechanisms on the microvasculature

Short-term vascular hemodynamic responses to isometric exercise in young adults and in the elderly

Background: Vascular aging is known to induce progressive stiffening of the large elastic arteries, altering vascular hemodynamics under both rest and stress conditions. In this study, we aimed to investigate changes in vascular hemodynamics in response to isometric handgrip exercise across ages. Participants and methods: We included 62 participants, who were divided into three age categories: 20-40 (n=22), 41-60 (n=20), and 61-80 (n=20) years. Vascular hemodynamics were measured using the Mobil-o-Graph® based on the pulsatile pressure changes in the brachial artery. One-way ANOVA test was performed to analyze the changes induced by isometric handgrip exercise. Results: After isometric handgrip exercise, aortic pulse wave velocity (PWV) increased by 0.10 m/s in the youngest, 0.06 m/s in the middle-age, and 0.02 m/s in the oldest age category. Changes in PWV strongly correlated with those in central systolic blood pressure (cSBP) (r=0.878, P<0.01). After isometric exercise, the mean change of systolic blood pressure (SBP) was −1.9% in the youngest, 0.6% in the middle-aged, and 8.2% in the oldest subjects. Increasing handgrip strength was associated with an increase in SBP and cSBP (1.08 and 1.37 mmHg per 1 kg increase in handgrip strength, res

Computer analysis of physiologic signals in a cardiovascular research laboratory

A comprehensive computer program which provides immediate computation and feedback has been developed for data acquisition and analysis of signals in a cardiovascular animal laboratory. The system is based on a microcomputer equipped with analog-to-digital converter and supports function modules which digitize, filter, and differentiate up to 8 simultaneously sampled cardiovascular signals. The program detects, analyses, and plots incoming and averaged beats. Beat-by-beat signal averaging for each channel is performed and cardiac cycles are partitioned automatically. For each cardiac and average cycle the amplitude at 6 physiologic fiducial markers are measured and derived calculations are made. Channel vs channel plots and loop area measurements are also computed and displayed. The computer algorithms have been shown to give accurate, precise, and reproducible results when tested on canine cardiovascular data. Also, it has been demonstrated that signal averaging is an appropriate analysis technique for cardiovascular signals.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/29539/1/0000627.pd

Effects of Adaptation in a Somatosensory Thalamocortical Circuit

In the mammalian brain, thalamocortical circuits perform the initial stage of processing before information is sent to higher levels of the cerebral cortex. Substantial changes in receptive field properties are produced in the thalamocortical response transformation. In the whisker-to-barrel thalamocortical pathway, the response magnitude of barrel excitatory cells is sensitive to the velocity of whisker deflections, whereas in the thalamus, velocity is only encoded by firing synchrony. The behavior of this circuit can be captured in a model which contains a window of opportunity for thalamic firing synchrony to engage intra-barrel recurrent excitation before being 'damped' by slightly delayed, but strong, local feedforward inhibition. Some remaining aspects of the model that require investigation are: (1) how does adaptation with ongoing and repetitive sensory stimulation affect processing in this circuit and (2) what are the rules governing intra-barrel interactions. By examining sensory processing in thalamic barreloids and cortical barrels, before and after adaptation with repetitive high-frequency whisker stimulation, I have determined that adaptation modifies the operations of the thalamocortical circuit without fundamentally changing it. In the non-adapted state, higher velocities produce larger responses in barrel cells than lower velocities. Similarly, in the adapted barrel, putative excitatory and inhibitory neurons can respond with temporal fidelity to high-frequency whisker deflections if they are of sufficient velocity. Additionally, before and after adaptation, relative to putative excitatory cells, inhibitory cells produce larger responses and are more broadly-tuned for stimulus parameters (e.g., the angle of whisker deflection). In barrel excitatory cells, adaptation is angularly-nonspecific; that is, response suppression is not specific to the angle of the adapting stimulus. The angular tuning of barrel excitatory cells is sharpened and the original angular preference is maintained. This is consistent with intra-barrel interactions being angularly-nonspecific. The maintenance of the original angular preference also suggests that the same thalamocortical inputs determine angular tuning before and after adaptation. In summary, the present findings suggest that adaptation narrows the window of opportunity for synchronous thalamic inputs to engage recurrent excitation so that it can withstand strong, local inhibition. These results from the whisker-to-barrel thalamocortical response transformation are likely to have parallels in other systems

Monitoring of Intracranial Pressure in Patients with Traumatic Brain Injury

Since Monro published his observations on the nature of the contents of the intracranial space in 1783 there has been investigation of the unique relationship between the contents of the skull and the intracranial pressure (ICP). This is particularly true following traumatic brain injury (TBI), where it is clear that elevated ICP due to the underlying pathological processes is associated with a poorer clinical outcome. Consequently, there is considerable interest in monitoring and manipulating ICP In patients with TBI.The two techniques most commonly used in clinical practice to monitor ICP are via an intraventricular or intraparenchymal catheter with a microtransducer system. Both of these techniques are invasive and are thus associated with complications such as haemorrhage and infection. For this reason, significant research effort has been directed towards development of a non-invasive method to measure ICP. These include imaging based studies using computed tomography (CT) and magnetic resonance imaging (MRI), transcranial Doppler sonography (TCD), near-infrared spectroscopy (NIRS), tympanic membrane displacement (TMD), visual-evoked potentials (VEPs), measurements of optic nerve sheath diameter (ONSD) and other measurements of the optic nerve, retina, pupil and ophthalmic artery.The principle aims of ICP monitoring in TBI are to allow early detection of secondary haemorrhage or ischaemic processes and to guide therapies that limit intracranial hypertension and optimise cerebral perfusion. However, information from the ICP value and the ICP waveform can also be used to estimate intracranial compliance, assess cerebrovascular pressure reactivity and attempt to forecast future episodes of intracranial hypertension

Coronary Arterial Dynamics and Atherogenesis

While documented risk factors (e.g., hypertension, diabetes, etc.) for atherosclerosis are systemic in nature, atherosclerotic plaques appear in a heterogeneous distribution in the vasculature. This heterogeneity is thought to be related in part to the fact that the plaques tend to develop in areas of disturbed blood flow such as bifurcations and curvatures. Moreover, the coronary arteries, which also experience the added mechanical deformations of cyclic flexing, stretching, and twisting due to their tethering to a beating heart, are particularly susceptible to atherogenesis. This suggests that both fluid-induced (shear) and deformation-induced (mural) stress contribute to location specific susceptibility or protection from disease. We hypothesized that local variations in shear and mural stress associated with dynamic motion of arterial segments influence the distribution of early markers of atherogenesis. To test this hypothesis, we utilized our unique, well-established, and validated ex vivo vascular perfusion system in a combined experimental / computational study. Pairs of freshly-harvested porcine arterial segments were perfused ex vivo under normal hemodynamic conditions. One of the paired segments was exposed to coronary levels of either cyclic axial stretching, flexure, or twist. Post-perfusion tissue processing provided the extent and spatial distribution of early markers of atherogenesis, including endothelial permeability, apoptosis, and proliferation. Finite element analysis and computational fluid dynamics techniques were used to estimate the mural and shear stress distributions, respectively, for reconstructed models of each experimentally perfused segment. Quantitative correlations between biological marker and mechanical stress distributions were determined using multiple linear regression analysis. Vessel segments exposed to cyclic axial stretch and flexure showed significant increases in both permeability and apoptosis. In addition, we demonstrated that all three deformations generated complex, non-uniform distributions of both biologic endpoints and mechanical stresses. These distributions displayed a high degree of specimen-to-specimen variability which was attributed to the highly variable vessel geometries. Several specific mechanical stress measures, both mural and shear, were shown to be associated with cellular atherogenic marker distribution. Future work should be aimed at more fully elucidating the molecular mechanism linking mechanical stress in the tissue to these cellular based responses