Snoring Is Not That Simple: Snoring And Neurocognition

Chloe Jin -

Understanding Snoring

Have you ever shared a dorm room with someone else and been rudely awakened in the wee hours of the morning by your roommate’s snoring? If you've seen the TV sitcom Friends, Joey is one such annoying roommate. He snores like a decorator is working on their house, much to Chandler's annoyance. Even when Chandler yells Joey’s name at the top of his lungs, Joey doesn’t wake up and even starts making conversation in his sleep.

Chandler is not a rare victim to disruptions and annoyance from snoring; according to Statista, around 52% of people in the US reported that they or their partner snores. Of those people, the highest percentage of snoring people are aged 55-64 [1]. Many people snore, from a soft grumbling to a loud “symphony”. But why are you the one who snores? While anyone can snore, males and people who are obese may be genetically predisposed to snoring [2].

What causes people to snore? Snoring is the hoarse and noisy sound generated when air flows in and out of your throat. When you are slumbering, your tongue slips backward as your throat muscles relax, causing the airway of the throat to narrow. However, if something obstructs the airflow through this narrow pathway, the airflow will generate vibrations in relaxed throat muscles, creating the sounds of snoring.

Many people may assume that snoring is a sign of quality sleep when it may actually represent interrupted sleep and some serious conditions. Specifically, narrowing of the airway during snoring may have a significant impact on the snorer's cognitive functions that are related to neurological processing through areas of the brain involved in memory, language, learning, and perceptual-motor skills. For snoring with different triggers, it has different levels of neurocognitive effects. Considering this, snoring must be clarified and categorized in order to understand those health conditions.

Primary Snoring and its Effects

Generally, snoring can be categorized into two types: primary and obstructive sleep apnea (OSA)-induced snoring. Primary snoring occurs more than three nights per week. It is a type of sleep-disordered breathing (SDB) and is usually habitual, but it is not seen as a health concern and is not related to any diseases.

Primary snoring may cause sleep disruptions during non-rapid eye movement (NREM) sleep, a sleep state where the body repairs and consolidates declarative memories of conscious memory of particular facts or events, such as the date of your birthday, your credit card number, and who cooked for you last night [3]. This contrasts with rapid eye movement (REM) sleep, which is responsible for storing non-declarative memories like knowing how to ride a bike.

The mechanism by which primary snoring causes sleep disruption remains unclear, but studies show that snoring-related sleep disruption may change the physical features of certain brain structures over time. Research indicates that people with SDB conditions, particularly those with primary snoring, tend to have lower cortical thickness compared to those without. Cortical thickness represents the thickness of the cerebral cortex in the brain, varying between 1 to 4.5 mm thick. This reduction in cortical thickness is associated with a reduction in grey matter volume in several brain regions, including the precentral gyri, the supramarginal gyrus, and the orbital and the superior frontal gyri. A loss of grey matter in these regions may cause deficits in attention, working memory, perception and language processing, and behavioral inhibition [4].

Consequently, primary snoring may affect multiple aspects of neurocognition. A study that assessed the intelligence and attention-span of children who have primary snoring symptoms, showed that these children had more attention problems reported by their teachers and parents, but no intellectual disabilities [5]. Another study on children with primary snoring suggested that the cognitive scores for snoring children are lower than non-snoring children. Cognitive function was evaluated with the ability to recall past scenes like a photograph and the ability to process short term memory of linguistic terms like a person’s address, and vocabulary reading recognition tests [6]. Both of these studies showed that primary snoring may lead to neurocognitive deficits. However, some types of treatment, such as changing lifestyles, mouth exercises, and other medical treatment may help improve these deficits [7].

Besides neurocognition, primary snoring can also affect the nervous and circulatory systems. For example, one study found that in children with primary snoring, there is an over activation in the sympathetic nervous system for the N2 sleep stage of NREM sleep, the sleep stage where the body is relaxed, and the heart rate is lowered [8]. The over-activation of sympathetic nerves that occurs at this sleep stage can unintentionally speed up heart rate and cause hypertension [9].

Hypertension, or higher blood pressure, produces high vessel pressure and stress that can lead to damage of blood vessels in the brain. Blood clots can form when platelets come to fix the damage of blood vessels, suggesting that primary snoring people may have a higher risk of some cerebrovascular diseases, like strokes.

OSA Induced Snoring and its Effects

The second classification of snoring is obstructive sleep apnea (OSA) induced snoring, which is a more severe version of primary snoring and is usually accompanied by OSA. Common symptoms may include loud snoring, morning headache, and difficulty in paying attention while awake. OSA occurs when there is limited respiration, causing the chest wall to move abnormally inwards when inhaling and outwards when exhaling. This affliction is often accompanied by snoring [10].

Like primary snoring, OSA-induced snoring also has negative effects on neurocognitive function. Recent studies on adults investigated their performance on the Psychomotor Vigilance Task (PVT) and Motor Sequence Learning Task (MSL). PVT is a measure of vigilant attention with several simple tasks that require participants to respond to visual cues when different stimuli appear within a specific time interval. MSL requires participants to learn a set of sequences by typing or touching finger movements. In this study, sleep disordered patients scored lower in both PVT and MSL tasks, indicating difficulties with learning and memorizing skills [11]. Another study that examined the performance of finger-tapping tasks in patients with OSA showed that OSA patients have less frequency correctly typing the required digits, which indicates that OSA can cause impairment of motor skills [12]. This loss in learning and motor skills may indicate a higher risk of future neurocognitive dysfunction and are associated with dementia and other neurodegenerative diseases.

Aside from the impacts that OSA has on neurocognitive function, it can also influence brain structures similar to how primary snoring does, but through a different mechanism. Unlike primary snoring, this mechanism is relatively well-researched. There are two main models supported by neuroscientists: the hypoxia model and the sleep disruption model.

The hypoxia model states that when apnea occurs, the arterial oxygen pressure decreases while carbon dioxide pressure increases gradually. Consequently, arterial stress increases, indicating an imbalance in the relationship between oxygen and antioxidant species which help neutralize free radicals that can harm cells. Hypoxia plays a role in increased BBB permeability in OSA patients, but the mechanism behind its involvement is still unclear. One study indicates oxidative stress and hypoxia result in damage to the blood-brain barrier (BBB) [13]. The BBB serves to help restrict the diffusion and exchange of microscopic molecules into the brain, decreasing the likelihood of brain tissue damage. OSA, however, enhances BBB permeability, allowing more dangerous particles to enter brain tissue. This can cause significant brain injury. Research shows that this damage mostly occurs around the grey matter of different brain regions, like the superior frontal and prefrontal cortices and superior and lateral parietal cortices [14]. The damage to these brain regions leads to the reduction of memory and perceptual functions in patients with OSA. Although there is no clear explanation for the increased BBB permeability, one study hypothesized that the BBB permeability is modulated by an increase in the concentration of a serum called endothelin 1, which causes a decrease in neuronal myelin. Myelin is very important for most brain functions because it acts as a layer around nerves that insulate electrical pulses to increase the efficiency of impulse transmission. This reduction also leads to brain damage [15]. Regardless of if hypoxia affects the BBB or endothelin 1, it still plays a fundamental role in brain damage for patients with OSA. 

The sleep disruption hypothesis emphasizes the importance of sleep and suggests how sleep disruption can lead to impairment in the brain. When OSA occurs during sleep, the muscle behind the throat relaxes too much, which narrows an individual’s airway. This can lower the oxygen levels in the blood and thus increase the levels of carbon dioxide in the blood. The brain senses this impediment and will regularly wake the individual to get them to adjust their airway causing fragmentation of sleep. Some experiments using animal models suggest that sleep deprivation and fragmentation are associated with impairment of cognitive functions. One study experimentally inhibited the sleep of five lemur species. This experimental group of lemurs with the fragmented sleep condition had decreased memory consolidation and less sleep enhanced their foraging efficiency compared to control group lemurs with non-disrupted sleep [16]. Another experiment in mice specifically suggests that disrupted sleep intervals decrease a type of protein in the brain called cyclin D2, which decreases hippocampal plasticity, leading to a reduction in the memory storage functions of the hippocampus [17].

How OSA Induced-Snoring Affects Dreaming 

Now that primary and OSA induced snoring are well-defined, we can apply this knowledge to understanding how snoring can affect one's dreams. There is little research on the effects of primary snoring on dreams, but there are some studied effects of OSA induced snoring on dreaming.

One research study investigated this using electroencephalography (EEG), which measures the electrical activity of the brain by using electrodes placed on the scalp, suggesting that OSA patients are awake more during sleep. The researchers examined subjects with OSA and those without, and the results of the EEG showed a significant reduction of activity in the parietal cortex which is associated with receiving and processing sensory in the brain [18].  Similarly, one study compared EEG between patients with simple snoring and patients with OSA. Their results indicate that the patients with OSA have higher spectral density values in the bands associated with memory and deep sleep, called delta and beta bands, than in patients with simple snoring [19]. During NREM sleep, delta slow waves shown by EEG reflect the alterations between depolarization, in which neurons can send signals, and periods of hyperpolarization, in which neurons cease signaling. These interactions are necessary for patients to know that they are in dreams and to get general emotional feelings in dreams. Therefore, high activity in delta brands that alters the interactions may indicate the patient is unconscious about dreams happening and less dreaming occurs [20].

As a complement to physiological studies, some psychological studies also provide good evidence for the effects of OSA-induced snoring on dream content. A cross-sectional study on 4372 patients with OSA indicates that from the self-reported data in a questionnaire, violence and nightmarish content appear less frequently in the dreams of patients with OSA [21]. Additionally, one study compared the self-reported dream contents right after awakening between patients with OSA and normal people. Their results suggest that there is no significant difference in dream topics related to respiration [22]. These results suggest that patients with OSA might experience less violent and emotionally related dreams than normal people. However, the things they dream about are not affected by OSA.

EEG analysis of patients with OSA showed that they do not maintain conscious feelings during their sleep, and psychological research implies that the dreams of patients with OSA are less anxious and emotionally negative. However, since these psychological studies are based on self-reported data, the results might vary for different groups. These results cannot be generalized as a criterion for determining the content of dreams in patients with OSA. There are still many unanswered questions in the area of dream content.

Possible Treatments for OSA 

The effects of snoring, especially for patients with OSA, can be seriously detrimental to one's health. Fortunately, some modern treatments have been quite effective in targeting neurocognitive deficits in patients with OSA.

One of the traditional and most common treatments for OSA is Continuous Positive Airway Pressure (CPAP). In 1971, Gregory et al. discovered CPAP by applying the principle of infant breathing to create positive end-expiratory pressure. Conventional ventilators create CPAP by providing a constant flow of gas. By controlling the exhalation valve, the flow of gas can be monitored and used to improve oxygenation and reduce airway resistance to treat sleep apnea [23].

Recent research suggests that CPAP not only reduces sleep apnea, but also repairs neurocognitive function in patients with OSA. One study measured the changes in memory and cognitive processing speed in adults with OSA before and after one year of using CPAP. After CPAP, they observed statistically significant improvements in cognitive processing speed in patients with OSA though there was little improvement in memory and attention functions [24]. In general, the study concluded that effective CPAP may improve some aspects of neurocognitive functions for patients with OSA, but not all. Another study analyzed the neurobehavioral repair of 88 patients with OSA before and after a CPAP treatment lasting three months, and it showed similar results. The patient's cognitive processing improved after CPAP. Although there is significant improvement, the improvements are not comparable to people without sleep apnea [25].

Although CPAP is the common treatment for OSA, there are some downsides. CPAP can sometimes cause other problems in the body, including an increase in the nasal bacteria and inflammation which can further develop into rhinitis and worsen the conditions of OSA [26]. It may also cause CPAP belly syndrome, which is the distention of the belly after CPAP treatment, which can lead to continued pain for patients with OSA and may force the patients to discontinue treatment altogether [27]. However, talking with healthcare professionals on assisting the use of CPAP may help with these side effects.

Aside from CPAP, a recent study proposed an innovative treatment called hypoglossal nerve stimulation, which involved the use of a drug called rAAV5-hSyn-hM3(Gq)-mCherry (DREADD). DREADD is designed to activate certain receptors on neurons. Researchers first modify neuron receptors through a process called chemogenetics, which adds receptors that only work for the DREADD drug. Then, they inject the drug and activate the receptors. As a result, the drug binds to the receptor. This process was used to stimulate the hypoglossal nerve and markedly improved the opening of the upper airway, therefore improving the ventilation of the upper airway for OSA. Since the receptors that receive DREADD can modulate neuronal functions in sleep and memory, this drug may be useful for future research to investigate the improvement of neurocognitive deficits [28]. Compared with traditional treatments, hypoglossal nerve stimulation may have fewer harmful side effects on patients, but its effectiveness for treating OSA still requires further research. Meanwhile, whether the excitability of the hypoglossal nerve will have any effect on brain functions is still unknown.

Limitations

Although there is extensive research on snoring, there are limitations that some of the aforementioned studies in this article encounter. In particular, the neurocognitive effects of primary snoring cannot be generalized. The effects will vary for different severities of snoring.  For instance, the types of brain damage mentioned earlier may not occur in patients with mild symptoms. Also, the descriptions of EEG changes in patients with OSA are divergent between studies. More recent studies proposed in this article mostly agree with each other in regard to the results of EEG research on patients with OSA, but results have been contradictory which may arise from noise, varied experimental conditions, etc. In addition, the interpretations of dreams in patients with OSA are different between studies. For example, as mentioned above, patients with OSA have fewer dreams. However, one study on patients with both OSA and PTSD indicates OSA patients had higher dreams and nightmares frequency before treatment, and the frequency of nightmares was greatly reduced after treatment [29].

Summary & Conclusions 

Snoring is a surprisingly complex process that can be the cause of sleep-breathing disorders, lead to neurocognitive impairment, and modify an individual's dreaming.

Primary snoring alters the structure of one’s brain, thereby affecting neurocognition. However, its effects on dreams are still largely unknown. In contrast, OSA-induced snoring may affect brain structure through two mechanisms — hypoxia and sleep fragmentation. The resulting brain damage can impact several aspects of neurocognition such as memory, learning, and motor skills. OSA-induced snoring can also cause patients to dream differently than those without OSA, as the patient’s dreams are more often characterized by loss of consciousness and fewer nightmares.

Fortunately, treatments do exist for severe OSA symptoms. CPAP is more traditional and has been proven to enhance neurocognition for patients with OSA. Unfortunately, it also carries the risk of causing conditions such as nasal inflammation and CPAP belly syndrome. Hypoglossal nerve stimulation, on the other hand, is a more novel treatment that is less irritating to the nasal cavity than CPAP. However, its adverse effects on the brain are unknown.

In the future, more research on the mechanisms of neurocognition in response to primary snoring, as well as its effects on dreaming, is needed. Such research could lead to the development of novel therapeutic methods for neurocognitive declines in both patients with primary snoring and OSA-induced snoring.

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