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In PD, altered upper airway musculature due to muscle stiffness at night and
bradykinesia may contribute to OSA development. However, there is no evidence to
support an increase in central sleep apnea in PD.A signicant decrease in muscle
tone increases the propensity for upper airway collapse, during REM sleep, possibly
worsening OSA.
The question then arises whether patients with REM sleep behavior disorder
(RDB) who increase muscle tone at night have a lower risk of OSA.In a study of
239 patients with AD, 28% had OSA (AHI>5), and logistic regression analysis
showed that RDB was a protective factor for OSA.In comparison, another with 46
patients showed PD comorbid with OSA was more frequent in the RDB (+) group
than in the RDB (−) group (51.4% vs. 9.1%). A greater decrease in nocturnal O2
saturation was found in the (+) group, and the increase in muscle tone in the chin did
not affect the severity of OSA.The proportion of patients with RDB was higher in
the group with PD+OSA [34]. The latest meta-analysis of PSG in patients with PD
shows that these patients have decreased total sleep time, sleep efciency, SWS,
REM sleep, increased AHI, time awake after falling asleep (WASO), and periodic
leg movements index (PLM-i), compared with normal controls. A supplementary
analysis showed increased AHI, REM sleep, and PLM-i in PD+RDB patients.
It has been shown that PD patients spend twice as much time in the supine position compared to normal controls. This position is related to a longer time of illness,
SED, and a high AHI.Additionally, an AHI>5 and low sleep efciency have been
related to cognitive impairment, specically in terms of attention, executive processes/working memory, and semantic memory [34].
K. J. Parejo
10.3.1 Possible Pathophysiological Mechanisms That Relate
PD andOSA
It has been suggested that the low incidence of OSA in patients with advanced
Parkinson’s is due to the low body mass index compared to the general population,
which in turn suggests that PD in these patients does not follow the same pattern.
However, some studies have shown no relationship between the severity of OSA
and BMI in patients with PD.But have found a relation between the severity of PD
with the severity of OSA, although causality cannot be inferred from these ndings [6].
OSA is not more common in PD than in the general population, although they
may coexist either because OSA is so common or PD-related changes predispose
to OSA or both. Biologically, there is a possibility that PD is involved in the
pathogenesis of OSA since the upper airway musculature may be affected by
involuntary movements. It may have abnormal spirometry consistent with upper
airway obstruction, which improves with levodopa. These alterations worsen during sleep, generating OSA.A decrease in sleep-disordered breathing has been
found in patients who use long-acting levodopa overnight, compared with those
who do not [32]. However, levodopa could generate respiratory alterations as a
form of dyskinesias.
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PD is also associated with autonomic dysfunction, which can alter respiratory
control during NREM sleep, where breathing is predominantly dependent on chemoreceptors. This mechanism could be related to the high incidence of sleepdisordered breathing in Shy–Drager syndrome, in which abnormal afferent feedback
to central respiratory centers has been implicated [6].
OSA itself can generate autonomic disturbances beyond sleep, particularly by
increasing sympathetic tone that is associated with changes in chemo and baroreceptors, damaging respiratory control, and promoting OSA. In PD, there is a
decrease in chemosensitivity to hypoxia despite adequate lung function, which
reduces dyspnea in hypoxic conditions. It has also been found that the respiratory
impulse to hypercapnia is reduced, probably related to the neurodegenerative process in the brain stem where the central chemoreceptors and respiratory centers are
located. An abnormal response to hypercapnia predisposes to hypoventilation.
Moreover, the activity of the dilator muscles of the upper airway is regulated by the
respiratory drive and CO2 levels, a key element in the pathophysiology of OSA.
Although this mechanism has not been studied directly in patients with PD,
another probable mechanism linked to OSA could be the fragmentation of sleep
generated by the dysfunction that occurs as part of PD, due partially to the alteration
of sleep circuits, medications, and comorbidities, increasing the possibility of upper
airway collapse during sleep. It might be a factor in the progression of OSA in this
disease [32].
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10.3.2 Cognitive Impairment inPD+OSA
The mechanisms by which OSA generates cognitive impairment were previously
explained when discussing AD; intermittent hypoxia has been implicated through
the mechanisms of ischemia/reperfusion and oxidative stress. In addition, evidence
of systemic inammation in OSA could contribute to neuroinammation that promotes neurodegeneration. However, these mechanisms could theoretically exacerbate the neuropathology of PD; they have not yet been studied in PD [6]. In PD,
OSA-related hypoxemia is less marked than in patients without PD; this is due to
the low body mass index (BMI) of patients with PD+OSA.
Sleep fragmentation has also been implicated in cognitive impairment in patients
with OSA and is the best predictor of alterations in episodic memory [32]. And
induce oxidative stress and inammation as well as hypoxia. Interestingly, in animal
models of OSA, decreased neuronal excitability has been found in the locus coeruleus (LC), an area involved in the pathophysiology of PD [6].
Regarding the glymphatic system, we know that it is a cleaning system that operates in the brain, transporting CSF through the perivascular spaces, connecting the
ow through the brain parenchyma to the cervical lymphatic system, removing proteins and soluble metabolites; its function declines with age, and it has been suggested that this contributes to the accumulation of abnormal proteins in the
extracellular space, such as amyloid-beta or alpha-synuclein, leaving the brain more
vulnerable to neurodegenerative pathologies. The peculiarity of this system is that it
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only acts during sleep, so any process that fragments sleep can alter it, generating
alterations in brain homeostasis. We also know that dementia in PD results from a
mixture of pathologies, including Lewy bodies, Alzheimer-related pathology, and a
small component of microvascular pathology. It could then be speculated that glymphatic abnormalities could predispose to cognitive dysfunction in PD by nonspecic mechanisms [6].
The development of dementia in PD has also been related in case series to the
role of noradrenergic defects on the LC.It has been implicated in cognitive impairment in the general population. In pathology studies in aging patients have been
found a decrease in neuronal density in this area that correlates with a low cognitive
level and faster cognitive deterioration [32], Intermittent hypoxia and fragmentation
of sleep in the LC and other specic areas of the brain could have signicant implications in PD [35].
In the pathophysiology of PD, the determining factor is the loss of dopaminergic
neurons in the substantia nigra that generates dopamine depletion in the basal ganglia. Still, other regions have been implicated in neurodegeneration that is more
associated with nonmotor symptoms. LC neurons specically have been implicated
in its pathophysiology, as the loss of their trophic inuences may increase the sensitivity of dopaminergic neurons to neurotoxic insults.
Currently, the pathology of PD involves a combination of genetic, cellular, and
environmental factors. There are no studies on humans, but animal studies show a
decrease in the noradrenergic neuronal population in the LC and its functional alteration. OSA could not only generate cognitive impairment but also globally accelerate the evolution of PD.Furthermore, recent epidemiological studies suggest that
OSA increases the risk of PD [36].
K. J. Parejo
10.3.3 Neuroimaging inRelation toCognitive Dysfunction
inOSA+PD
Structural and functional changes have been found in brain imaging of patients with
OSA, including decreased gray matter in the hippocampus and temporal lobe, anterior cingulate gyrus, and cerebellum, as well as in the frontal and parietal lobes, and
the CPAP treatment appears to increase gray matter volume in the hippocampus and
frontal structures.
In PD, cortical atrophy has been found in the hippocampus and frontal structures
in patients with MCI but not in cognitively intact patients [37]. Many studies associate atrophy of the temporal lobe with memory alterations in PD, others with frontal
or temporal regions. These variable ndings could be partly explained by the effects
of OSA [6]. Functional neuroimaging in OSA shows decreased activation of the
cingulate, frontal, and parietal regions during sustained attention and memory tasks.
In PD, poor performance in memory and executive functions was associated with
decreased metabolism in frontal and parietal association areas and increased in the
cerebellar vermis and caudate nucleus with PET-FDG. Other studies have found
other sites of hyperactivation, probably as a compensatory mechanism [6].
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10.3.4 Treatment ofOSA inPD
The general recommendation is the use of oral devices in mild cases of OSA and
CPAP in moderate to severe cases, as well as weight loss in obese patients. The
efcacy of the use of CPAP has been demonstrated in patients with advanced PD
with narcoleptic phenotype, the onset of sleep in the REM stage (SOREM) in the
multiple sleep latency test (MSLT), and OSA.In addition, a prospective study demonstrated improvement in OSA, and daytime sleepiness measured by MSLT in 38
patients with PD with a mean duration of 5.3years. Interestingly, improvement in
OSA has been shown with long-acting levodopa at bedtime [38].
Additionally, the benet has been seen in patients with PD with an average of 3h
36minutes of use with CPAP in terms of EDS, anxiety, and quality of sleep during
12 months of use. In patients with RDB +OSA, CPAP improved symptoms in
45.8% of those who used CPAP, which suggests that CPAP should be used rst in
this type of patient [34].
However, the long-term use of CPAP may be difcult due to the increase in
motor and nonmotor symptoms of PD, particularly in the more advanced stages.
Cognitive dysfunction, nocturia, RDB, and motor dysfunction are factors that could
inuence adherence to CPAP.
10.4 Small-Vessel Vascular Disease
Small-vessel vascular disease (SVVD) is a highly prevalent cerebral phenomenon
that refers to a group of pathological processes with various etiologies that affect the
small arteries, arterioles, venules, and capillaries of the brain. Age-related, arterial
hypertension-related, and amyloid angiopathies are the most common forms [39].
It is often considered an incidental nding on brain MRI that manifests with
white matter hyperintensities, silent cerebral infarcts, cerebral microhemorrhages,
and perivascular spaces. Recent meta-analyses have associated it with an increased
risk of stroke, cognitive impairment or dementia, and death. Reduced compliance in
the cerebral arterioles resulting from chronic dysregulated vascular remodeling has
been regarded as the fundamental pathomechanism of SVVD progression [39],
which causes damage to the blood–brain barrier (BBB). Intermittent hypoperfusion
alters the glymphatic system, which ultimately leads to chronic inammation and
subclinical ischemia in the brain parenchyma.
OSA is highly prevalent in the older population,, and shares common risk factors
with SVVD, such as age, hypertension, diabetes, and obesity, and is associated with
SVVD progression. In addition, it is involved in endothelial dysfunction and
decreased vascular compliance. A recent study suggests that endothelial dysfunction in OSA is related to the consequent generation of reactive oxygen species and
proinammatory molecules that produce microvascular damage [22].
However, the effect of OSA on the progression of SVVD is independent of these
cardiovascular risk factors. Its mechanism could be different from dysregulation of
vascular remodeling. Probably more related to the abrupt increase in intrathoracic
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pressure that interferes with adequate venous return and cardiac output, frequent
alerts, intermittent cerebral hypoxia, and provocation of arrhythmias [40].
Frequent alerts and intermittent hypoxia recurrently activate the sympathetic nervous system, generating oxidative stress and inducing inammation in the brain
parenchyma. Furthermore, increased intrathoracic pressure and frequent arousals
prevent activation of the glymphatic system. Although all these mechanisms are
interrelated, discrimination of the main mechanism underlying SVVD progression
in OSA patients could be important in predicting how appropriate OSA treatment
might also modify SVVD progression.
Ultrasonography or transcranial Doppler (TCD) is a noninvasive method widely
used to measure cerebral blood ow, and some parameters are helpful indicators to
measure cerebrovascular elasticity. The pulsatility index evaluates the vessel stiffness
and the resistance of the distal arterial bed. Recently, it has been reported that reducing
this index along the middle cerebral artery may be an indirect marker of the compliance of the small cerebral vessels. A recent study in 97 patients compared TCD with
PSG and SVVD markers in brain magnetic resonance imaging (MRI), such as volume
of white matter hyperintensities, measures of increased perivascular spaces, and the
presence of micro bleeding or lacunae, to determine the pathophysiological mechanisms that link OSA, impaired cerebrovascular compliance, and progression of
SVVD.The results of this study indicate that the severity of OSA is related to markers
of cerebrovascular compliance but not to other markers of vascular remodeling. The
AHI is signicantly related to the volume of subcortical white matter hyperintensities,
while the desaturation index (ODI) was to the volume of white matter hyperintensities
in deep structures [40]. This nding is consistent with a recent meta-analysis reporting
that moderate to severe OSA is positively associated with white matter hyperintensities and silent cerebral infarction but not with microbleeds [40].
Although most of these studies are cross-sectional and a relationship between
OSA and the progression of SVVD cannot be determined with complete certainty,
it can be inferred that OSA may contribute to the pathogenesis of SVVD, through
different mechanisms to vascular remodeling (chronic and irreversible process),
which could be reversible to a certain extent.
K. J. Parejo
10.4.1 Vascular Cognitive Impairment Associated
withSubcortical Small-Vessel Disease
The hallmark of SVVD is ischemic white matter lesions that can present as lacunar
infarcts, and global cerebral hypoperfusion in a common and homogeneous subtype
of vascular cognitive impairment (VCI). It is often unrecognized. The unique nature
and course of SVVD offer the opportunity to gather knowledge at all stages of its
pathogenicity. Atherosclerosis, hypoxic hypoperfusion, and inammation act synergistically, causing myelin degeneration and blood–brain barrier disruption. The
clinical diagnosis of SVVD includes early executive dysfunction manifested by a
diminished ability to use complex information, formulate strategies, and exercise
self-control [41].
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10.4.2 Regarding theTreatment ofSVVD inPatients withOSA
The use of CPAP in previous studies has shown reversal of white matter lesions and
increased gray matter volume in OSA patients, apparently due to amelioration of
early osmotic changes in cells induced by mild ischemia and inammation that
disrupt the integrity of the cell membrane [39]. Surgical treatment of OSA with
relocation pharyngoplasty, a UPP variant, also improves high-sensitivity C-reactive
protein and reduces cardiovascular risk in patients with OSA [42].
10.4.3 OSA asaRisk Factor forStroke andTransient Ischemic
Attack (TIA)
OSA is increasingly recognized as an independent risk factor for high blood pressure, diabetes, cardiovascular disease, and stroke.
OSA is common after a stroke, and stroke seems to be more common in people
with OSA.Also, there are shared risk factors for both. So, the question remains,
does stroke cause sleep apnea, or does sleep apnea lead to stroke, or are they both
caused by the same risk factors? This is important because it may have implications
for the prevention, acute treatment, and rehabilitation of patients with acute
stroke [43].
Stroke is a common disease, the second leading cause of death worldwide, generating high health costs. Recent studies suggest that OSA is common after stroke
with 50%–94% prevalence and is likewise recognized as a risk factor for stroke
[43]. At the same time, untreated OSA contributes to poor stroke outcome and is
also a risk factor for subsequent cardiovascular disease, including recurrent stroke.
Sleep apnea treatment improves recovery from stroke and decreases cardiovascular morbidity and mortality. However, underdiagnosis of OSA in stroke patients
is still common.
10.4.4 Relationship Between OSA andStroke
OSA creates a substrate for stroke vulnerability and is particularly hostile to brain
function. Exposure to intermittent hypoxia in rodents results in impaired executive
function, excessive sleepiness, and sensitivity to sleep deprivation. Mediating
mechanisms include free radical damage, lipid peroxidation, nitric oxide synthase
induction, platelet activation, and apoptosis.
However, oxidative stress, especially moderate hypoxia, may have a protective
effect on the brain and cardiovascular system by activating genetic programs that
induce vascular remodeling and other protective responses; thus, it builds resilience
in the brain (known as ischemic preconditioning) [44].
Moderate to severe OSA is associated with silent ischemic changes, including
white matter changes and lacunae, and cerebral microbleeds. Carotid and intracranial atherosclerosis is also accelerated in OSA.However, it is not clear whether the
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K. J. Parejo
use of CPAP has any effect on these changes. Arterial hypertension and insulin
resistance could mediate the development of stroke in OSA.Moderate-to-severe
OSA is signicantly associated with severity-dependent hypertension and is very
common in patients with resistant hypertension. Therefore, effective CPAP therapy,
alone or in addition to antihypertensive medication, substantially lowers blood
pressure.
OSA can also increase the risk of developing type 2 diabetes through increased
insulin resistance and elevated cortisol secretion. Continuously supervised CPAP
therapy (7.92h/night) improved glycemic control and insulin resistance. However,
the effect of CPAP on glycemic control is less consistent than its effect on blood
pressure. Therefore, concomitant obesity could have a more substantial impact than
OSA, not mitigated by CPAP therapy. OSA is also associated with the risk of
cardioembolism.
Nearly 40% of symptomatic atrial brillation events are seen between midnight
and 8:00AM.People with OSA are four times more likely to develop nocturnal
atrial brillation, and oxygen desaturation is an independent risk factor for newonset atrial brillation. In a recent cohort study of 6841 patients, the diagnosis and
severity of OSA were associated with atrial brillation during a 12-year follow-up.
Furthermore, OSA may potentiate the risk of cardioembolism or stroke in patients
with atrial brillation [45]. In addition, several observational studies found improvement or resolution of cardiac arrhythmia and atrial brillation after CPAP therapy.
Furthermore, sleep apnea is associated with inammation, endothelial dysfunction, hypercoagulability, and cerebral hemodynamic changes.
OSA is very common in acute stroke, with an estimated 50% to 70% of subjects
with acute stroke or TIA, a higher frequency than observed in control groups.
However, they share risk factors such as male sex, obesity, old age, hypertension,
and smoking. An independent association between the two conditions is hypothesized by large-scale epidemiologic studies, including the Sleep Heart Health Study
and the Wisconsin Sleep Cohort Study. In these studies, OSA with an apneahypopnea index (AHI) ≥20/h or>11/h was associated with prevalent stroke, with
an OR of 4.31 (95% CI: 1.31–14.15) and 1.58 (95% CI: 1.02–2.46), respectively,
when adjusted for age, sex, weight, blood pressure, smoking, and other confounding
factors [44].
It has been found that with an average nocturnal use of CPAP for at least 4h, the
risk of incident cardiovascular events among subjects with severe or symptomatic
OSA was comparable to that of controls or simple snorers (AHI<5/h). The cardiovascular effects of OSA are not limited to subjects with severe OSA burden. A
prospective observational study in a clinical population free of myocardial infarction or stroke at study entry found that the presence of OSA (AHI≥5/h) increased
the risks of events (stroke or death from any cause, during follow-up at 3.4years).
However, the treatment effect was not substantial.
In the SAVE and RIC-CADSA trials, a dose–response relationship was found
between adherence to CPAP and cardiovascular outcome, in which adherence to
CPAP was associated with a lower risk of stroke or cardiovascular events [46]. The
increased rates of stroke and death despite OSA treatment may be explained by
older age, long-term exposure to OSA prior to treatment, a relatively shorter
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duration of intervention, and changes in treatment efcacy (weight regain, reduced
adherence to CPAP, or loss of effect of surgery). The “healthy adherent” effect,
which describes a better outcome in subjects compliant with any given intervention
due to their health-conscious behavior or lifestyle, could bias the results in favor of
CPAP therapy. Adherence to CPAP has modied efcacy in previous trials: the
higher the adherence, the better the outcome.
Studies with randomized designs are required to provide a better understanding
of the causal relationship between OSA and stroke, and the therapeutic efcacy of
CPAP in stroke prevention [44]. OSA events during REM sleep are usually prolonged and associated with severe oxygen desaturation. Sleep apnea during REM
sleep, but not during NREM sleep, has been associated with hypertension, nondipping effect in nocturnal arterial pressure, and insulin resistance, even in subjects not
considered to have OSA (AHI<5/h). In a recent observational nding from the
Sleep Heart Health Study, severe REM OSA (AHI during REM sleep ≥30/h) was
associated with a higher incidence of cardiovascular events in the group with prevalent cardiovascular disease. The cardiovascular effects of REM OSA have several
important implications [44].
From a diagnostic standpoint, simple cardiorespiratory monitoring devices, for
example a portable device consisting of ow and oximetry, should not be used in
future trials. Such a kit cannot reliably detect REM OSA, central sleep apnea, and
periodic limb movements (PLM). The latter two conditions not only commonly
occur in populations at high risk for cardiovascular events (such as the elderly or
those with cardiovascular disease or stroke), but also increase the cardiovascular
risk of these individuals [44].
In conclusion, there is clear evidence that OSA is a complex pathophysiological
condition with multiple disease factors that often interact. The benet of CPAP therapy for the prevention of stroke and other cardiovascular events in OSA should be
considered based on the results of currently available clinical studies. The overall
ndings suggest that what matters is therapeutic effectiveness, which is determined by
CPAP adherence, CPAP efcacy, apnea burden, and possibly disease phenotype [44].
Take-Home Message
• Recent evidence suggests that OSA might be associated with the development or
worsening of neurodegenerative disorders as Alzheimer´s and Parkinson disease.
• OSA is comon in cerebrovascular disease and is associated with poor functional
outcomes.
• Treating OSA can improve the quality of live of patients with these
comorbidities.
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