Limits...
Reversal of functional changes in the brain associated with obstructive sleep apnoea following 6 months of CPAP.

Fatouleh RH, Lundblad LC, Macey PM, McKenzie DK, Henderson LA, Macefield VG - Neuroimage Clin (2015)

Bottom Line: MSNA was significantly elevated in newly diagnosed OSA patients compared to control subjects (55 ± 4 vs 26 ± 2 bursts/min).The reduction in resting MSNA was coupled with significant falls in signal intensity in precuneus bilaterally, the left and right insula, right medial prefrontal cortex, right anterior cingulate cortex, right parahippocampus and the left and right retrosplenial cortices.These data support our contention that functional changes in these suprabulbar sites are, via projections to the brainstem, driving the augmented sympathetic outflow to the muscle vascular bed in untreated OSA.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, University of Western Sydney, Sydney, Australia.

ABSTRACT
Obstructive sleep apnoea (OSA) is associated with an increase in the number of bursts of muscle sympathetic nerve activity (MSNA), leading to neurogenic hypertension. Continuous positive airway pressure (CPAP) is the most effective and widely used treatment for preventing collapse of the upper airway in OSA. In addition to improving sleep, CPAP decreases daytime MSNA towards control levels. It remains unknown how this restoration of MSNA occurs, in particular whether CPAP treatment results in a simple readjustment in activity of those brain regions responsible for the initial increase in MSNA or whether other brain regions are recruited to over-ride aberrant brain activity. By recording MSNA concurrently with functional Magnetic Resonance Imaging (fMRI), we aimed to assess brain activity associated with each individual subject's patterns of MSNA prior to and following 6 months of CPAP treatment. Spontaneous fluctuations in MSNA were recorded via tungsten microelectrodes inserted into the common peroneal nerve in 13 newly diagnosed patients with OSA before and after 6 months of treatment with CPAP and in 15 healthy control subjects while lying in a 3 T MRI scanner. Blood Oxygen Level Dependent (BOLD) contrast gradient echo, echo-planar images were continuously collected in a 4 s ON, 4 s OFF (200 volumes) sampling protocol. MSNA was significantly elevated in newly diagnosed OSA patients compared to control subjects (55 ± 4 vs 26 ± 2 bursts/min). Fluctuations in BOLD signal intensity in multiple regions covaried with the intensity of the concurrently recorded bursts of MSNA. There was a significant fall in MSNA after 6 months of CPAP (39 ± 2 bursts/min). The reduction in resting MSNA was coupled with significant falls in signal intensity in precuneus bilaterally, the left and right insula, right medial prefrontal cortex, right anterior cingulate cortex, right parahippocampus and the left and right retrosplenial cortices. These data support our contention that functional changes in these suprabulbar sites are, via projections to the brainstem, driving the augmented sympathetic outflow to the muscle vascular bed in untreated OSA.

No MeSH data available.


Related in: MedlinePlus

Brain regions in which fluctuations in BOLD signal intensity coupled to fluctuations in muscle sympathetic nerve activity (MSNA) were significantly different in subjects with obstructive sleep apnoea (OSA) prior to and following 6 months of continuous positive airway pressure (CPAP) treatment. Cool color scale represents regions in which changes in signal intensity during each burst of MSNA were significantly reduced following CPAP treatment. Significant clusters are overlaid onto a mean T1-weighted anatomical template image. Slice locations in Montreal Neurological Institute space are indicated at the lower right of each image. ACC: anterior cingulate cortex, mPFC: medial prefrontal cortex.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4459270&req=5

f0015: Brain regions in which fluctuations in BOLD signal intensity coupled to fluctuations in muscle sympathetic nerve activity (MSNA) were significantly different in subjects with obstructive sleep apnoea (OSA) prior to and following 6 months of continuous positive airway pressure (CPAP) treatment. Cool color scale represents regions in which changes in signal intensity during each burst of MSNA were significantly reduced following CPAP treatment. Significant clusters are overlaid onto a mean T1-weighted anatomical template image. Slice locations in Montreal Neurological Institute space are indicated at the lower right of each image. ACC: anterior cingulate cortex, mPFC: medial prefrontal cortex.

Mentions: Voxel-by-voxel comparison of MSNA-related BOLD signal intensity changes pre- and post-CPAP treatment revealed that the reduction in resting MSNA was coupled with significant changes in signal intensity in a number of brain regions (Fig. 3, Table 2). Significantly reduced signal-intensity changes post-CPAP compared with pre-CPAP occurred in the region of the precuneus bilaterally, the left and right insula, right medial prefrontal cortex (mPFC), right anterior cingulate cortex (ACC), right parahippocampus and the left and right retrosplenial cortices.


Reversal of functional changes in the brain associated with obstructive sleep apnoea following 6 months of CPAP.

Fatouleh RH, Lundblad LC, Macey PM, McKenzie DK, Henderson LA, Macefield VG - Neuroimage Clin (2015)

Brain regions in which fluctuations in BOLD signal intensity coupled to fluctuations in muscle sympathetic nerve activity (MSNA) were significantly different in subjects with obstructive sleep apnoea (OSA) prior to and following 6 months of continuous positive airway pressure (CPAP) treatment. Cool color scale represents regions in which changes in signal intensity during each burst of MSNA were significantly reduced following CPAP treatment. Significant clusters are overlaid onto a mean T1-weighted anatomical template image. Slice locations in Montreal Neurological Institute space are indicated at the lower right of each image. ACC: anterior cingulate cortex, mPFC: medial prefrontal cortex.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4459270&req=5

f0015: Brain regions in which fluctuations in BOLD signal intensity coupled to fluctuations in muscle sympathetic nerve activity (MSNA) were significantly different in subjects with obstructive sleep apnoea (OSA) prior to and following 6 months of continuous positive airway pressure (CPAP) treatment. Cool color scale represents regions in which changes in signal intensity during each burst of MSNA were significantly reduced following CPAP treatment. Significant clusters are overlaid onto a mean T1-weighted anatomical template image. Slice locations in Montreal Neurological Institute space are indicated at the lower right of each image. ACC: anterior cingulate cortex, mPFC: medial prefrontal cortex.
Mentions: Voxel-by-voxel comparison of MSNA-related BOLD signal intensity changes pre- and post-CPAP treatment revealed that the reduction in resting MSNA was coupled with significant changes in signal intensity in a number of brain regions (Fig. 3, Table 2). Significantly reduced signal-intensity changes post-CPAP compared with pre-CPAP occurred in the region of the precuneus bilaterally, the left and right insula, right medial prefrontal cortex (mPFC), right anterior cingulate cortex (ACC), right parahippocampus and the left and right retrosplenial cortices.

Bottom Line: MSNA was significantly elevated in newly diagnosed OSA patients compared to control subjects (55 ± 4 vs 26 ± 2 bursts/min).The reduction in resting MSNA was coupled with significant falls in signal intensity in precuneus bilaterally, the left and right insula, right medial prefrontal cortex, right anterior cingulate cortex, right parahippocampus and the left and right retrosplenial cortices.These data support our contention that functional changes in these suprabulbar sites are, via projections to the brainstem, driving the augmented sympathetic outflow to the muscle vascular bed in untreated OSA.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, University of Western Sydney, Sydney, Australia.

ABSTRACT
Obstructive sleep apnoea (OSA) is associated with an increase in the number of bursts of muscle sympathetic nerve activity (MSNA), leading to neurogenic hypertension. Continuous positive airway pressure (CPAP) is the most effective and widely used treatment for preventing collapse of the upper airway in OSA. In addition to improving sleep, CPAP decreases daytime MSNA towards control levels. It remains unknown how this restoration of MSNA occurs, in particular whether CPAP treatment results in a simple readjustment in activity of those brain regions responsible for the initial increase in MSNA or whether other brain regions are recruited to over-ride aberrant brain activity. By recording MSNA concurrently with functional Magnetic Resonance Imaging (fMRI), we aimed to assess brain activity associated with each individual subject's patterns of MSNA prior to and following 6 months of CPAP treatment. Spontaneous fluctuations in MSNA were recorded via tungsten microelectrodes inserted into the common peroneal nerve in 13 newly diagnosed patients with OSA before and after 6 months of treatment with CPAP and in 15 healthy control subjects while lying in a 3 T MRI scanner. Blood Oxygen Level Dependent (BOLD) contrast gradient echo, echo-planar images were continuously collected in a 4 s ON, 4 s OFF (200 volumes) sampling protocol. MSNA was significantly elevated in newly diagnosed OSA patients compared to control subjects (55 ± 4 vs 26 ± 2 bursts/min). Fluctuations in BOLD signal intensity in multiple regions covaried with the intensity of the concurrently recorded bursts of MSNA. There was a significant fall in MSNA after 6 months of CPAP (39 ± 2 bursts/min). The reduction in resting MSNA was coupled with significant falls in signal intensity in precuneus bilaterally, the left and right insula, right medial prefrontal cortex, right anterior cingulate cortex, right parahippocampus and the left and right retrosplenial cortices. These data support our contention that functional changes in these suprabulbar sites are, via projections to the brainstem, driving the augmented sympathetic outflow to the muscle vascular bed in untreated OSA.

No MeSH data available.


Related in: MedlinePlus