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The effect of untreated Obstructive Sleep Apnoea (OSA) on cerebral haemodynamics and CA impairment is an active field of research interest. A breath-hold challenge is usually used in clinical and research settings to simulate cardiovascular and cerebrovascular changes that mimic OSA events. This work utilises temporal arterial oxygen saturation (SpO 2 ) and photoplethysmography (PPG) signals to estimate the temporal cerebral blood flow velocity (CBFv) waveform. Measurements of CBFv, SpO 2 , and PPG, were acquired concurrently from volunteers performing two different protocols of breath-hold challenge in the supine position. Past values of the SpO 2 and PPG signals were used to estimate the current values of CBFv using different permutations and topologies of supervised learning with shallow artificial neural networks (ANNs). The measurements from one protocol were used to train the ANNs and find the optimum topologies, which in turn were tested using the other protocol. Data collected from 10 normotensive, healthy subjects (four females, age 28.5 ± 6.1 years, Body Mass Index (BMI) 24.0 ± 4.7 kg/m 2 ) were used in this study. The results show that different subjects have different optimum topologies for ANNs, thus indicating the effects of inter-subject variability on ANNs. Successfully reconstructed blind waveforms for the same subject group in the second protocol showed a reasonable accuracy of 60-80% estimation compared to the measured waveforms., Hypothesis: Temporal waveforms for SpO 2 and PPG contain adequate information to estimate the temporal CBFv waveform using ANNs., Methodology: Concurrent measurements of SpO 2 and PPG using pulse oximetry from the forehead and CBFv from the middle cerebral artery (MCA) using transcranial Doppler (TCD) were recorded from healthy, normotensive subjects performing a breath-hold challenge. The breath-hold challenge mimicked the cerebrovascular response to apnoea, and was recorded by measuring CBFv in MCA. Two protocols were used, each consisting of five breath-holding manoeuvres and differing in terms of the time between the five successive breath-holds. Using data from one protocol, several permutations of the temporal values of SpO 2 and PPG signals were used as inputs to different ANN topologies, in order to train and find the optimum model. The optimum model was evaluated using the data from the other protocol as a blind dataset., Results: Using the first protocol for training, optimum ANN configurations were found to be different for each subject, and accuracy of 75-87% was achieved. When these optimum ANN models were tested using the second protocol as a blind dataset, the accuracy achieved was around 60-80%., Conclusions: A novel approach employing temporal records of SpO 2 and PPG can be used to estimate the CBFv waveform using ANNs with acceptable accuracy. Increases in the size and diversity of the population dataset and the use of features extracted from SpO 2 and PPG signals are needed for generalisation of the method and potential future clinical applications., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Monitoring apnea-induced cerebral blood flow oscillations is of importance for assessing apnea patient brain health. Using an autoregressive moving average model, peak and trough values of cerebral blood flow were estimated from a concurrently recorded forehead photoplethysmography signal. Preliminary testing of the method in 7 subjects (4 F, 32±4 yrs., BMI 24.57±3.87 kg/m 2 ) using a breath hold paradigm for simulating apnea shows that maximum mean and standard deviation of the prediction error is -1.10±8.49 cm/s and the maximum root mean squared of the error is 8.92 cm/s.

Monitoring apnea-induced cerebral blood flow (CBF) oscillations is of importance for assessing apnea patient brain health. Blood pressure (BP) oscillations during apnea can induce oscillations in CBF. Preliminary results of testing an Auto Regressive Moving Average model relating nocturnal CBP oscillations to nocturnal BP variations in 8 obstructive sleep apnea subjects (3 F, 55±8 yrs., BMI 34.2±7.85 kg/m 2 ) showed that largest mean and standard deviation of the CBF estimation errors was 4.49±7.57 cm/s and maximum root mean squared of the errors was 8.80 cm/s. Hence, reasonable accuracy in estimating CBF from BP during sleep apnea events was observed.

Sleep apnea is identified by repetitive reduction or complete cessation of breathing during sleep. Sleep apnea affects cerebral hemodynamics and it is important to study this effect. Measuring cerebral blood flow during sleep is challenging due to the need to maintain a contact between the flow probe and the skull. It is hypothesized that there exists a relationship between the variations in the exhaled CO2 and Cerebral Blood Flow during sleep apnea. To test this hypothesis, the present study was conducted in two parts: simulated and nocturnal sleep study. 9 volunteer subjects (6 Male and 3 Female Age: 23.11±1.59 years BMI: 21.9±2.409kg/m2) participated in the simulated study and 10 volunteer subjects (9 Male and 1 Female Age: 50.2±7.48 years BMI: 31.541±4.56 kg/m2 AHI: 62.84±20.44) participated in a nocturnal sleep study. Analyzing full waveforms of cerebral blood flow velocity (CBFV) and exhaled CO2, the relationship between 4 metrics from CBFV and 2 metrics from exhaled CO2 were investigated. Although one metric pair showed statistically significant and relatively high correlation (ρ= 0.68 p=7.96×10-7) during the simulated study, the same was not observed during the nocturnal study. Therefore, the proposed hypothesis could not be proven.

Obstructive Sleep Apnea (OSA) is characterized by partial (hypopnea) or complete cessation (apnea) of airflow to the lungs during sleep. It has been previously reported that apnea episodes lead to significant rise in instantaneous blood pressure concomitant with a rise in cerebral blood flow velocity, indicating loss of cerebral autoregulation during the episodes. In this study, we have used Auto Regressive Moving Average model (ARMA (n a , n b , n k )) to quantify OSA induced dynamic changes in cerebral blood flow velocity (CBFV) with beat to beat blood pressure (BP) as an input. BP and CBFV were recorded from 11 positively diagnosed sleep apnea subjects (6 Males, 5 Females; Age: 54.27±6.23 years, BMI:34.95±7.06kg/m 2 , AHI: 57.39±28.43). The results suggest that two separate models, ARMA (5, 9, 1) and ARMA (5, 10, 0) can be used to quantify dynamic CBFV variations during apneas with a duration of less than and greater than 30s respectively with reasonable accuracy (<;6% error).

Obstructive Sleep Apnea (OSA), defined by shallow breaths or complete cessation of breathing for more than 10s, is a significant contributing factor for the developments of hypertension, myocardial infarction, stroke and neuropsychological impairments. In this study, we have investigated the relation between apnea duration and apnea induced variations in cerebral blood flow velocity (CBFV) concomitant with blood pressure changes in 9 sleep apnea subjects (8 male and 1 female; Age: 46.0±11.6 years; BMI: 34.5±7.8 kg/m(2); AHI: 81.6±41). As apnea duration increased from 10s to greater than 30s, the mean percentage rise in CBFV increased from 22% to 42% for amplitude and 22% to 33% for area respectively. For blood pressure, the values increased from 14% to 26% for amplitude and 14% to 23% for area respectively. The results suggest that the apnea duration has a measurable effect on the degree of rise in both cerebral blood flow velocity and arterial blood pressure during apnea episodes (p=0.0002).

Obstructive Sleep Apnea (OSA) is one of the most common breathing disorder, affecting approximately 27% of U.S. adults. Limited data have suggested that OSA causes cerebral autoregulation impairment, thus being an important risk factor to stroke. The objective of this paper is to investigate and measure the relation between arterial blood pressure (BP) and cerebral blood flow velocity (CBFV) in simulated apnea. Sixteen healthy subjects (9 male, 7 female) of 29±4.89 yrs age and body mass index of 24.07±4.84 kg/m(2) participated in the study. Four protocols were used; sitting 30 seconds, 90 s, and supine 30 s and 90 s. Our results showed that systolic BP and peak CBFV were correlated with average r=0.672 +0.265. Also, CBFV exhibited a significantly higher percent rise than BP. Thus, our findings suggest that cerebral autoregulation may be impaired during apnea episodes.

Obstructive Sleep Apnea (OSA) is a major sleep disorder with a prevalence of about 15 % among US adult population and can lead to cardiovascular diseases and stroke. In this study, we have investigated the OSA-induced concurrent rise in cerebral blood flow velocity and blood pressure in 5 positively diagnosed sleep apnea subjects. The subject population had a mean AHI of 57.94±25.73 and BMI of 33.66±7.27 kg/m(2). The results of this preliminary study yielded a relatively high correlation between rise in blood pressure and rise in cerebral blood flow velocity during apnea episodes (r=0.61±0.16) compared to normal breathing (r=0.28±0.26). These findings suggest that cerebral autoregulation may be less effective during apnea episodes.

Obstructive Sleep Apnea (OSA) is one of the most common sleep disordered breathing which affects about 15 % of US adult population. OSA is considered to be an important risk factor for the development of cardiac dysfunction and stroke. In this paper, we present the initial results of our investigation of the relationship between arterial blood pressure and cerebral blood flow velocity in simulated apnea. Sixteen healthy subjects (9 male, 7 female) of 29 ± 4.89 yrs age and body mass index of 24.07 ± 4.84 kg/m(2) participated in the study. Our findings indicate that cerebral blood flow velocity variations has a relatively high correlation to changes in blood pressure during simulated apnea (r = 0.74 ± 0.06), suggesting that cerebral autoregulation may not compensate for the pressure changes during apnea.

The physiological mechanism(s) for the regulation of the dynamic pressure-flow relationship of the cerebral circulation are not well understood. We studied the effects of acute cerebral vasoconstriction on the transfer function between spontaneous changes in blood pressure (BP) and cerebral blood flow velocity (CBFV) in 13 healthy subjects (30 +/- 7 years). CBFV was measured in the middle cerebral artery using transcranial Doppler. BP was increased stepwise with phenylephrine infusion at 0.5, 1.0 and 2.0 microg kg(-1) min(-1). Phenylephrine increased BP by 11, 23 and 37% from baseline, while CBFV increased (11%) only with the highest increase in BP. Cerebrovascular resistance index (BP/CBFV) increased progressively by 6, 17 and 23%, demonstrating effective steady-state autoregulation. Transfer function gain at the low frequencies (LF, 0.07-0.20 Hz) was reduced by 15, 14 and 14%, while the phase was reduced by 10, 17 and 31%. A similar trend of changes was observed at the high frequencies (HF, 0.20-0.35 Hz), but gain and phase remained unchanged at the very low frequencies (VLF, 0.02-0.07 Hz). Windkessel model simulation suggests that increases in steady-state cerebrovascular resistance and/or decreases in vascular compliance during cerebral vasoconstriction contribute to the changes in gain and phase. These findings suggest that changes in steady-state cerebrovascular resistance and/or vascular compliance modulate the dynamic pressure-flow relationship at the low and high frequencies, while dynamic autoregulation is likely to be dominant at the very low frequencies. Thus, oscillations in CBFV are modulated not only by dynamic autoregulation, but also by changes in steady-state cerebrovascular resistance and/or vascular compliance.