Neurodegenerative diseases of the central nervous system and SDB 41 Alzheimer disease

Searching for links between Alzheimer's disease and sleep-disordered breathing has already started in the eighties. Cognitive deficits observed in individuals with SDB was seen as a preliminary stage in the development of dementia. Cognitive deficits in individuals with impaired respiratory function were found on both verbal, spatial and executive functions as well as short-term memory (Naegele, 1995; Alchanatis, 2005). A number of pathomechanisms may contribute to cognitive impairment in patients with respiratory disorders. The important part play episodes of hypoxia and subsequent oxidative stress resulting in impaired cholinergic transmission in the central nervous system (Gibson, 1981; Shimada, 1981). Another pathomechanism may be associated with changes in cerebral blood flow, observed during sleep -significant hypoperfusion after an episode of apnea. Studies using magnetic resonance spectroscopy showed a decrease in metabolism in the frontal lobes in people with severe respiratory problems during sleep (Alchanatis, 2004) and a decrease in metabolism in the white matter (Kamba, 1997). However, biochemical studies, concerning the biochemical markers of neuronal damage (S-100P protein), showed no significant differences between patients with impaired breathing during sleep and the control group (Jordan, 2002). Homocysteine levels did not differ in patients with apneas compared with the control group (Svatikova, 2004). The study of magnetic resonance and computed tomography show damage to white matter in patients with apneas (Kamba, 2001; Macey, 2006) and reduction of the total intracranial brain volume (O'Donoghue, 2005). Another argument in favor of the relationship between dementia and apneas was the discovery of frequent occurrence of apolipoprotein genotype ApoE4 in people with sleep apneas (Kadotani, 2001; Gottlieb, 2004). There were several studies conducted on the effects of sleep apnea treatment on improvement of cognitive functions. In most studies a positive effect of introducing CPAP therapy was found on improvement of cognitive functions (Feuerstein, 1997; Bliwise, 2002; Zimmerman, 2006). It was also observed a beneficial effect of donepezil treatment on reducing the number of apneas during sleep and improvement of sleep architecture (Moraes, 2008). The degree of cognitive impairment observed in patients with sleep-disordered breathing, however, is significantly lower and more slowly progressive than in those with Alzheimer's disease (Bliwise, 2002). Daytime sleepiness, which is a symptom of respiratory distress has a significant impact on cognitive impairment (Feuerstein, 1997). More and more evidence points to a potential relationship between vascular dementia and sleep-disordered breathing. Early studies showed a significantly higher incidence of respiratory distress in patients with vascular dementia (Hoch, 1986; Bliwise, 1989). The authors also showed a correlation between the severity of respiratory disorders and dementia (Reynolds, 1985). These studies, however, were performed on small groups of patients (up to 30 our participants). Newer studies show a similar incidence of sleep-disordered breathing in patients with Alzheimer's disease as in the general population of similar age (Bliwise, 2002). However, vascular dementia associated with lacunar strokes and damage to white matter, occurs more frequent in patients with obstructive sleep apneas (Bliwise, 2002; Matthews, 2003).

4.2 Parkinson's disease

Parkinson's disease is associated with many sleep disorders which include excessive daytime sleepiness, insomnia, abnormal sleep architecture, restless legs syndrome and sleep disorders associated with REM sleep stage (Dhawan, 2006; Postuma, 2009). It was thought that excessive daytime sleepiness is associated with concomitant breathing disorders during sleep. Most studies did not confirm this hypothesis. Sleep-disordered breathing in patients with Parkinson's disease are at a level similar to the prevalence in the population of people in middle age and older (Diederich, 2005; Jahan, 2009). The degree of severity of Parkinson's disease does not affect the frequency and severity of respiratory distress (Young, 2002). One publication noted a higher incidence of mild obstructive breathing disorders during sleep in patients with Parkinson's disease compared with controls (Maria, 2003). Parkinson's disease patients who present with symptoms of disordered breathing during sleep should be performed diagnostic tests and the treatment should be implemented immediately. It is known that excessive daytime sleepiness, cognitive impairment and depressive reactions, caused by sleep-disordered breathing, may exacerbate the non-motor symptoms of the Parkinson's disease (Monaca, 2006).

4.3 Multiple system atrophy (MSA)

In the course of the multiple system atrophy a number of types of SDB may occur (Gilman, 2003). Obstructive (Munschauer, 1990; Glass, 2006) central (Glass, 2006), and mixed disorders of breathing pattern (Guilleminault, 1981) were found. Respiratory disorders and respiratory failure may be the first sign of disease. Glass and colleagues (2006) described 6 cases of MSA beginning with respiratory disturbances. Leading respiratory symptoms were excessive daytime sleepiness, laryngeal stridor during sleep, and dyspnea on exertion. Polysomnographic studies have shown co-existing obstructive disorders associated with laryngeal stridor (caused by paralysis of vocal cords) and the numerous apneas and hypopneas of central type. Patomechanisms which links MSA with respiratory problems, concern both neural control of breathing rhytmogenesis and respiratory airways. It has been shown in postmortem studies reduced excitatory projection from the thalamus (behavioral respiratory rhythm drive) to the dorsal inspiratory neurons (Gilman 2003) and a significant loss of neurons in the brainstem chemoreceptive neurons (metabolic respiratory drive) (Benarroch, 2007). Loss of serotonergic neurons that stimulate the nucleus ambiguous, observed in MSA (Weston, 2004), causes weakening of negative throat pressure reflexes and may be responsible for laryngeal stridor and obstructive sleep apneas (Bennaroch, 2007). The loss of dopaminergic neurons in the periventricular gray matter, probably responsible for the maintenance of wakefulness, can affect both the respiratory rhythmogenesis, as well as excessive daytime sleepiness (Bennaroch, 2009).

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