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. 2010 Feb;33(2):205-10.
doi: 10.1093/sleep/33.2.205.

Nocturnal cerebral hemodynamics in snorers and in patients with obstructive sleep apnea: a near-infrared spectroscopy study

Affiliations

Nocturnal cerebral hemodynamics in snorers and in patients with obstructive sleep apnea: a near-infrared spectroscopy study

Fabio Pizza et al. Sleep. 2010 Feb.

Abstract

Study objectives: Sleep disordered breathing (SDB) of the obstructive type causes hemodynamic consequences, leading to an increased cerebrovascular risk. The severity of SDB at which detrimental circulatory consequences appear is matter of controversy. Aim of the present study is the investigation of cerebral hemodynamics in patients with SDB of variable severity using near-infrared spectroscopy (NIRS).

Design: N/A.

Setting: Sleep laboratory.

Patients or participants: Nineteen patients with SDB.

Interventions: N/A.

Measurements and results: Patients underwent nocturnal videopolysomnography (VPSG) coupled with cerebral NIRS. NIRS data were averaged for each patient, and a new method (integral) was applied to quantify cerebral hemodynamic alterations. Nocturnal VPSG disclosed various severities of SDB: snoring (7 patients, apnea-hypopnea index [AHI] = 2 +/- 2/h, range: 0.5-4.5); mild SDB (7 patients, AHI = 14 +/- 8/h, range: 6.3-28.6); and severe obstructive sleep apnea syndrome (5 patients, AHI = 79 +/- 20/h, range: 39.6-92.9). Relative changes of NIRS parameters were significantly larger during obstructive apneas (compared with hypopneas; mean deoxygenated hemoglobin [HHb] change of 0.72 +/- 0.23 and 0.13 +/- 0.08 micromol/L per sec, p value = 0.048) and in patients with severe SDB (as compared with patients with mild SDB and simple snorers; mean HHb change of 0.84 +/- 0.24, 0.02 +/- 0.09, and 0.2 +/- 0.08 micromol/L per sec, respectively, p value = 0.020). In this group, NIRS and concomitant changes in peripheral oxygen saturation correlated.

Conclusions: The results of this study suggest that acute cerebral hemodynamic consequences of SDB lead to a failure of autoregulatory mechanisms with brain hypoxia only in the presence of frequent apneas (AHI > 30) and obstructive events.

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Figures

Figure 1
Figure 1
Light path of near-infrared (NIRS) light from the light source to the detector through the tissue (A) and positioning of the NIRS optode on the right forehead Figure 1A shows the light path of NIRS light from a single light source through superficial layers (skin and skull) to the cerebral tissue and back to the light detector. The multidistance approach uses different light sources at specified distances from a common light detector to allow the subtraction of the influence of superficial tissue from NIRS recording. The light path is bent and reaches a maximum depth of about 2 cm beneath the center of the multidistance sensor, defining the region of sensitivity of NIRS that originates at the light source and extends to the detector. Figure 1B shows an example of the position of the NIRS optode (i.e., a sensor with 4 light sources and 1 detector) on the right forehead. The NIRS optode is fixed to the head by a medical adhesive, before being shielded from external light with a cotton bend.
Figure 2
Figure 2
Averaged signals of (A) peripheral oxygen saturation (SpO2), and (B) oxygenated (O2Hb), deoxygenated (HHb), and total hemoglobin (tHb) concentrations during obstructive apneas in non-rapid eye movement (NREM) sleep of a patient with severe obstructive sleep apnea syndrome (OSAS). Figure 2A shows the average of the SpO2 signal occurring during obstructive apnea in NREM sleep in a patient with severe OSAS. The arrow marks the start of the respiratory event; the grey color depicts the area of the integral calculation between the maxima SpO2 levels (respiratory-event duration). Figure 2B shows the averages of O2Hb, HHb, and tHb concentration signals during obstructive apnea in NREM sleep of a patient with severe OSAS. The arrow marks the start of the integral calculation that is computed across the respiratory-event duration. After 5 seconds from the beginning of the obstructive apnea, the O2Hb decreases and the HHb increases abruptly (which corresponds with a severe tissue oxygen desaturation), whereas the tHb shows a concomitant transient increase. After 50 seconds from the beginning of the event, the O2Hb, HHb, and tHb concentrations are back to baseline values.
Figure 3
Figure 3
Averaged signals of oxygenated (O2Hb), deoxygenated (HHb), and total hemoglobin (tHb) concentrations during hypopneas in non-rapid eye movement (NREM) sleep of a patient with mild obstructive sleep apnea syndrome (OSAS). The O2Hb and tHb signals show parallel changes that are opposite to those of the HHb. After an initial decrease of O2Hb with a parallel increase of HHb (which corresponds to a tissue oxygen desaturation), a sudden increase of O2Hb and tHb with a decrease of HHb appears, consistent with an increase of local cerebral blood flow leading to a focal hyperoxygenation (i.e., a hemodynamic activation pattern).

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