What all neurologists should know about sleep apnea
Who has SDB in your neurology clinic?
Stroke and SDB.
While OSA affects 2%–4% of the general population, it is observed in 73.7% of ischemic stroke patients.e3 Sleep apnea may cause considerable nocturnal perturbations and has been identified as an independent risk factor for both cardiovascular and cerebrovascular disorders.5,e4 Aside from the direct effect on stroke risk, SDB can also predispose patients to develop other comorbid conditions commonly associated with increased risk of stroke, such as hypertension, diabetes, obesity, and cardiovascular diseases. Several studies have investigated the potential mechanisms underlying this relationship. Heart rate variability may be altered during sleep as well as wakefulness in patients with sleep apnea.e4 Atrial fibrillation and other autonomic and electrophysiologic cardiac dysfunction may also occur during sleep in patients with OSA, increasing the risk for stroke.5,e5 Further, sleep apnea patients who do not experience typical blood pressure “dipping” during sleep are at an increased risk for stroke.5,13,–,15,e6 Extreme dipper, nondipper, or reverse dipper patterns in patients with or without apnea have all been associated with intracranial hemorrhages, ischemic strokes, silent brain infarcts, and stroke deaths.5 Patients with OSA are also more likely to suffer their stroke event while sleeping, suggesting that factors specifically related to the dynamics of the SDB event itself may also play a role. For instance, during an obstructive apnea event there is a reduction in cerebral blood flow and impaired cerebral autoregulation.5,e7
While OSA is more commonly associated with stroke, it is important to remember that CSA has also been linked to stroke. CSA may be a consequence rather than a cause of stroke and can be a major symptom of vascular disease.e8 Development of CSA is heightened immediately following an acute stroke. It improves during the subacute phase and typically resolves within months after stroke.e8 CSA is also associated with congestive heart disease, a risk factor of cardioembolic strokes.e9
Headaches and SDB.
Rates of headaches are higher among patients with OSA than in the general population. Chronic daily headaches or frequent headaches upon awakening are more common in patients with OSA than the general population.e10 The relative risk of headache, especially daily headache, increases 2–3 times for those with SDB.e11 Patients with OSA are 8 times more likely to develop cluster headaches.e11 Patients with OSA who are overweight are 24 times more likely to develop cluster headaches.e11 Identification and treatment of OSA has been shown to improve cluster headaches.e12 Evidence also suggests that headaches may be a symptom of upper airway resistance,e13 and inadequate SDB treatment may result in morning headaches.e14 The frequency of SDB in migraine is reportedly comparable to the general population.e15 However, a small study suggests that treatment of OSA in those with migraine may improve migraine itself.e16
Epilepsy and SDB.
A bidirectional relationship has been demonstrated between seizure frequency/severity and presence of SDB.e17,e18Between 20% and 80% of patients with epilepsy have SDB (variation secondary to the degree of severity of epilepsy and criteria for SDB), with some evidence suggesting increased risk of seizures during sleep in those with apnea.e19Intermittent hypoxia and altered sympathetic activity experienced by patients with OSA is believed to activate epileptogenic regions of the brain, potentially lowering the seizure threshold.e18 Interestingly, treatment of OSA has been shown to reduce the frequency of seizures.e20,e21 Lastly, rates of central apnea in patients with epilepsy are comparable to the general population.e22
Neurodegenerative disorders and SBD.
The association between SDB and neurodegenerative disease has recently garnered increasing attention in the neuroscience research arena. The SDB prevalence varies depending on the specific neurodegenerative disorder. There is a particularly strong association between Alzheimer disease (AD) and OSA.e23,e24 Possible mechanisms underlying the SDB and neurodegenerative disorder relationship include cell loss in brainstem regions responsible for central respiratory regulation and diaphragmatic muscle control.e25
The evidence surrounding Parkinson disease (PD) as a direct risk factor for SDB is unclear. For one, patients with PD have other confounding risk factors, such as age, which increases risk of OSA. On the other hand, patients with PD may be at lower risk of sleep apnea since they have lower weights than controls.e26 Mechanisms potentially predisposing patients with PD to OSA may be related to the manifestation of hypokinesia and rigidity that may be associated with airway obstruction, restrictive lung disease, and autonomic dysfunction that subsequently results in SDB pathology.e27
Recognizing and treating SDB in patients with neurodegenerative diseases could improve quality of life.20 When considering all the relevant potential factors involved in this association, neurologists must also be aware of the potential effects on SBD of medications used in this patient population. For example, anxiolytics and pain medications may worsen SDB. Conversely, donepezil has been shown to improve OSA in patients with AD.e27
Neuromuscular disease and SDB.
Sleep-related ventilatory difficulties such as diaphragmatic weakness or restrictive lung disease also occur in patients with neuromuscular disease.e28 For example, 40%–60% of clinically stable patients with myasthenia gravis are diagnosed with SDB. Given the extraordinary prevalence of clinically significant but routinely underdiagnosed SDB, this figure may be an underestimate of the true prevalence of SDB in patients with neuromuscular disease. Oropharyngeal muscle weakness, tonsillar hypertrophy, obesity, and craniofacial dysmorphias may represent some of the underlying factors increasing risk for SDB.e28,e29
Similar to patients under management for neurodegenerative disease, patients with neuromuscular disease are often placed on medications that can indirectly affect their SDB. Thus, it is important to evaluate these patients for underlying SDB because not only can the SDB affect them clinically, but the medications used for their neurologic disorder may also further negatively affect manifestation and management of SDB.
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