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Alice 5

Manufactured by Philips
Sourced in United States, Australia, Germany, Switzerland

Alice 5 is a comprehensive sleep diagnostic device designed for the assessment of sleep disorders. It provides comprehensive data collection and analysis capabilities to support the diagnosis and management of sleep-related conditions.

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46 protocols using alice 5

1

Diagnostic Polysomnography and Multiple Sleep Latency Test Protocol

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Diagnostic nocturnal video-PSGs were performed using a standard system (Alice 5; Philips Respironics) including six channels of scalp electroencephalographic (EEG) data (F3/A2, F4/A1, C3/A2, C4/A1, O1/A2, O2/A1), two electrooculographs, submental electromyography (EMG), electrocardiography, nasal/oral airflow data, a percutaneous oximetry sensor for recording oxygen saturation data, a microphone for detecting snoring sounds, chest/abdominal respiratory effort data, and bilateral anterior tibialis EMG. Sleep stages and EEG arousal, PLMS, respiratory events and RWA were scored according to the criteria set by American Academy of Sleep Medicine (AASM)[29 ]. REM sleep periods observed within 15 min from sleep onset on n-PSG were defined as SOREMPs.
The MSLT consist of five naps was performed according to the standard protocol using a standard system (Alice 5; Philips Respironics) including six channels of scalp electroencephalographic (EEG) data (C3/A2, C4/A1, O1/A2, O2/A1), two electrooculographs, submental electromyography (EMG) and electrocardiography[30 (link), 31 (link)]. A sleep onset REM sleep period (SOREMP) was defined as the appearance of an epoch of REM sleep during the first 15 min of naps on the MSLT.
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2

High-Density EEG Analysis of REM Sleep

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Sleep recordings were made at the Wisconsin Institute for Sleep and Consciousness (University of Wisconsin–Madison) sleep laboratory. hd-EEG recordings were collected using a 256-channel dense array geodesic sensor net (GSN; Electrical Geodesics, Inc.) with a sampling rate of 500 Hz and online referencing to the vertex (CZ). Simultaneous PSG [anterior tibialis, chin electromyogram (EMG), electrocardiogram (EKG), pulse oximetry, pulse oximetry, and respiratory inductance] was recorded in parallel by Respironics Alice5 software (Philips Respironics). Sleep staging was performed offline using standard criteria of the American Academy of Sleep Medicine (AASM; Iber et al., 2007 ). From the all-night hd-EEG recordings, data segments corresponding to the complete first and last cycle of REM sleep for each participant were selected for further analysis. REM sleep epochs were further divided in tonic and phasic epochs, with phasic REM sleep visually classified by a trained technician as any epochs that contained REMs and/or myoclonic twitches.
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3

Polysomnographic Assessment of Obstructive Sleep Apnea

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Individuals underwent PSG (Alice 5 software, Philips- Respironics, Suresnes, France or Micromed Système Plus Evolution, Italy) for one or more nights. The recorded parameters, according included electroencephalogram (EEG) with six channels (F3A2, F4A1, C3A2, C4A1, O1A2, O2A1), electro-oculogram (EOG) on the right and left, chin electromyogram (EMG), anterior tibial electromyogram and an electrocardiogram (ECG). Respiratory recording included nasobuccal flow recording by nasal cannula and oral thermistor, thoracic and abdominal movements by inductance plethysmography and oxygen saturation by finger pulse oximetry. Sleep stages were manually scored according to the AASM 2012 criteria [36 ].
The primary outcome was the presence of OSA syndrome, defined as an AHI ≥15/hour.
Secondary outcome criteria included polysomnographic data, clinical characteristics and results of questionnaires as described below.
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4

Polysomnographic Sleep Assessment

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Sleep related events were investigated via standard polysomnography (PSG) Alice 5, Koninklijke Philips N.V. Philips Respironics, Murrysville, USA. The following parameters were recorded: F3; F4; C3; C4; O1; O2, M1, and M2. We used the standard referential montage of scalp electrodes against the contra-lateral mastoid electrode (e.g., C3/M2). Further parameters consisted of submental electrodes, strain gauges to record respiratory movements, EMG at both legs according to standard PSG procedures. Peripheral oxygen saturation was analyzed by pulse oximetry. The scoring of sleep and sleep-related events was based on the recommendation of the American Academy of Sleep Medicine published in 2007 [12 ].
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5

Diagnosis and Classification of Obstructive Sleep Apnea

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An overnight PSG (Alice 5; Philips Respironics, Amsterdam, Netherlands) was performed to record the respiratory events and determine the presence of OSA. According to recent criteria in the American Academy of Sleep Medicine manual, the apnea–hypopnea index (AHI) was manually scored by a trained sleep technician5 (link). Apnea in adults was defined as a drop in the peak signal excursion of ≥90% from that of pre-event baseline using an oronasal thermal sensor for ≥10 seconds. Hypopnea in adults was defined as a peak signal excursion drop of ≥30% from that of pre-event baseline using nasal pressure for ≥10 seconds in association with either ≥3% arterial oxygen desaturation or an arousal. OSA was diagnosed with an AHI ≥ 5 and OSA severity was classified into three groups; mild OSA (5 ≤ AHI < 15), moderate OSA (15 ≤ AHI < 30), and severe OSA (AHI ≥ 30).
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6

Polysomnography-Based Obstructive Sleep Apnea Diagnosis

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All patients underwent in-laboratory polysomnography (Alice 5, Philips Respironics, MA, USA) in a silent environment.29 (link) An apnea event was defined as a drop in the peak thermal sensor excursion by ≥90% of the baseline for at least 10 s. Hypopnea was defined as a decrease in the nasal pressure signal excursion by ≥30% for at least 10 s, accompanied by desaturation of 4% or more from the pre-event baseline or an arousal from sleep.30 (link) Apnea–hypopnea index (AHI), 3% oxygen desaturation index (ODI3), mean pulse oxygen saturation (SpO2), and minimal SpO2 were recorded. OSA was defined as obstructive AHI ≥5 events/h.
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7

Polysomnographic Assessment of OSA Patients

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We used Alice 5 (software Alice Sleepware, Respironics, Murrysville, USA) or Embla (software: Somnologica, Natus Enterprises, Middleton, USA) as the PSG system. We performed the polysomnography (PSG) in OSA patients according to the American Academy of Sleep Medicine (AASM) criteria (EEG electrodes: F3-M2, C3-M2, O1-M2, F4-M1, C4-M1, O2-M1, left and right electrooculogram, chin electromyogram, electrocardiogram, bilateral tibialis EMG, snoring signal, airflow, thoracic breathing and abdominal breathing, pulse oximetry, position sensor, audio and video recording).39 Controls were investigated by home sleep testing (Embletta). We analyzed the AHI, the hypopnea index per hour of sleep (HI), the oxygen desaturation index per hour of sleep (ODI), the number of obstructive and central apneas, and the number of hypopneas.
The following tests were performed the day after the PSG/ home sleep testing:
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8

Overnight Polysomnography for OSA Diagnosis

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The presence and severity of OSA were determined by overnight complete polysomnography using a computerized system (Alice 5, Philips Respironics, Herrsching, Germany). Standard techniques such as EEG, electrooculography, electromyography, electrocardiogram, thermistor measurements of air flow, thoracoabdominal motion, pulse oximetry of arterial oxyhemoglobin saturation (SPO2), and body position were used to monitor sleep disordered breathing. Bedtime was 10 p.m. to 6 a.m. Sleep stages were scored according to the standard criteria of the American Academy of Sleep Medicine [9 ]. Apnea was defined as an absence of airflow for >10 s. Hypopnea was defined as a more than 30% reduction in airflow accompanied by a decrease in SPO2 of >4%. AHI was calculated as the average number of apneas and hypopneas per hour of sleep. An AHI ≥15/h was defined as moderate to severe OSA.
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9

Comprehensive Sleep Apnea Monitoring Protocol

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All participants underwent standard PSG monitoring (ALICE 5; Philips Respironics, Pittsburgh, PA), including nose airflow transducers, mouth thermocouple, dynamic pulse oxygen saturation, dynamic electrocardiogram, thoraco-abdominal movement by inductance plethysmography, genioglossus electromyogram, electroencephalography, left and right electrooculogram, acoustic sensor (snore), and body position. In accordance with the American Academic Sleep Medicine criteria,28 (link) respiratory and apnea events (RDI, OAI, maximum apnea time, central apnea frequency, and obstructive apnea frequency), nocturnal hypoxemia (lowest SaO2, mean SaO2, SIT90%, ODI, ORF, MOR, and LORT), sleep quality (total sleep time, rapid eye movement stage sleep %, nonrapid eye movement stage sleep %, slow wave sleep %, and micro-arousal index), and HR were automatically recorded and proofread by an experienced respiratory physician.
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10

Effects of CPAP Withdrawal on Oxidative Stress

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Continuing abolition of OSA by CPAP at baseline was further confirmed on a home (Oxford) or hospital (Zurich) sleep study the night prior to randomization (Black Shadow, Stowood Scientific Instruments, Oxford, UK or Alice5, Philips Respironics AG, Zofingen, Switzerland), and the severity of any OSA after two weeks was similarly assessed with a repeat sleep study. The additional measurements made, including blood pressure, are described in the data supplement. The main outcome of this analysis was the change in plasma MDA levels over the two weeks, CPAP withdrawal subjects versus control subjects. In Oxford the primary outcome of the study was the change in plasma MDA levels, but in Zurich the identical protocol was run with a different primary outcome (hyperaemic myocardial blood flow); we took advantage of this and collected exactly similar samples to combine with the Oxford data. Secondary outcomes were plasma oxidized low-density-lipoprotein (OxLDL), serum total anti-oxidant capacity (TAC), urinary F2-isoprostanes (fresh morning urine sample), and NADPH oxidase-derived superoxide generation from peripheral blood mononuclear cells (PBMCs).
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