The Mystery Of Rem Sleep And Its Exacerbated Issues

Sleep is divided into non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. During REM sleep, the eyes move rapidly in different directions, and the brain is active, resembling the activity during wakefulness. Dreams typically occur during this stage. REM sleep is important for learning, memory, concentration, and mood regulation.

REM sleep is associated with several physiological changes, particularly affecting breathing and airway functions. During this stage, muscle tone throughout the body decreases, including in the upper airway, which can lead to increased airway collapsibility and obstruction. This can result in reduced oxygen levels and strain on vital organs. The Apnea-Hypopnea Index (AHI) measures the severity of sleep apnea by counting the number of apneas and hypopneas per hour of sleep.

Factors such as airway collapsibility, oxygen desaturations, and the apnea-hypopnea index are typically exacerbated during REM sleep. This can lead to severe sleep apnea events and repeated cycles of desaturation and reoxygenation throughout the night. Therefore, individuals with obstructive sleep apnea may experience more frequent awakenings or disrupted sleep during the REM stage.

Airway collapsibility

Several techniques have been proposed to assess airway collapsibility, including:

• Negative pressure pulses (NPPs): This method involves applying negative pressure pulses during wakefulness to measure the pressure drop across the pharynx.
• Inspiratory resistive loading (IRL): This technique measures the resistance change in response to externally applied inspiratory resistive loading.
• Critical pressure (Pcrit): This is the pressure needed to induce a cessation of airflow and can be determined using various methods.

Research has shown that airway collapsibility during wakefulness, as measured by NPPs, is somewhat predictive of collapsibility during sleep. This suggests that certain properties of the pharyngeal airway may predispose individuals to airway collapse during sleep, even though other factors clearly contribute to OSA as well.

Furthermore, OSA patients tend to have greater airway collapsibility than control subjects during wakefulness. This indicates that there may be inherent pharyngeal properties that influence collapsibility during both wakefulness and sleep.

Additionally, therapeutic continuous positive airway pressure (CPAP) level has been found to be strongly associated with Pcrit. Lower therapeutic CPAP levels are linked to more negative Pcrit values, indicating less collapsible airways. This relationship may provide clinicians with valuable information for personalizing OSA treatments.

Oxygen desaturations

During REM sleep, the muscles that keep the airway open relax extensively, increasing the risk of obstructions. This is especially true for individuals with obesity or other anatomical risk factors. The relaxation of muscles during REM sleep can lead to increased airway collapsibility, making it more likely for the airway to close, particularly for those with OSA.

The decreased muscle tone during REM sleep can result in a higher occurrence of apneas (complete cessation of breath) and hypopneas (partial cessation of breath), as measured by the apnea-hypopnea index (AHI). This index quantifies the severity of sleep apnea by counting the number of apneas and hypopneas per hour of sleep. The increased frequency of these events during REM sleep contributes to a higher AHI.

Research has shown that individuals with OSA experience more frequent and severe oxygen desaturations during REM sleep. This is supported by studies that found a positive correlation between the severity of OSA, as measured by the apnea-hypopnea index (AHI), and the difference in oxygen saturation between REM and non-REM sleep. Specifically, as the AHI increases, the difference in oxygen saturation between REM and non-REM sleep becomes more pronounced, indicating more significant oxygen desaturations during REM sleep.

The oxygen desaturations during REM sleep can have important clinical implications. For example, the increased severity of hypoxia during REM sleep in individuals with severe OSA suggests that continuous positive airway pressure (CPAP) therapy may need to be adjusted to higher pressures to effectively control hypoxemia during this sleep stage.

Additionally, oxygen desaturations during REM sleep may be influenced by certain medications and substances. For instance, the discontinuation of serotonergic antidepressants has been associated with REM rebound, characterized by prolonged and intense dreams, which may be related to oxygen desaturations. Furthermore, the use of substances such as tetrahydrocannabinol, cocaine, heroin, and stimulants can lead to significant REM rebound, indicating a compensatory adjustment towards sleep homeostasis following their discontinuation.

Apnea-Hypopnea index

The Apnea-Hypopnea Index (AHI) is a diagnostic tool used to determine the presence and severity of Obstructive Sleep Apnea (OSA). OSA is a common sleep disorder that affects at least 2-4% of people. Those with OSA experience a collapse of their airways during sleep, resulting in hypopneas and apneas. Hypopneas occur when the airways partially collapse, leading to shallow breathing. On the other hand, apneas are periods when breathing stops entirely.

The AHI is calculated by dividing the total number of apneic and hypopneic events by the total number of hours of sleep. A normal AHI is less than 5 events per hour, while an AHI of 30 or more events per hour is considered severe. The AHI helps healthcare professionals diagnose OSA and determine the most effective treatment.

During REM sleep, the Apnea-Hypopnea Index is typically exacerbated due to muscle relaxation, which affects the airway. This increased airway resistance can lead to severe sleep apnea events, making them more likely during this stage.

REM rebound

REM (rapid eye movement) sleep is a critical phase of the sleep cycle, accounting for 20-25% of total sleep time in adults. It is marked by ocular saccadic movements, muscle atonia, and fast-wave electroencephalography (EEG) patterns resembling the waking state. During this stage, muscle tone throughout the body decreases significantly, which can lead to increased airway collapsibility and subsequent oxygen desaturation.

When individuals are deprived of REM sleep, they tend to experience REM rebound as their bodies attempt to restore a balanced sleep cycle. This compensatory mechanism is driven by neurophysiological and hormonal processes that are essential for maintaining normal sleep patterns and overall homeostasis.

Several factors can induce REM rebound, including sleep deprivation, withdrawal from REM-suppressing medications, substance withdrawal, depression, and the initiation of continuous positive airway pressure (CPAP) therapy. Stress is a significant contributor to REM rebound, as it increases the pressure to sleep and achieve REM rebound. Research suggests that the REM stage plays a crucial role in regulating emotions and processing negative experiences.

While REM rebound is generally not indicative of an underlying sleep disorder, it is often observed in individuals with parasomnias, narcolepsy, or obstructive sleep apnea (OSA) due to their disrupted sleep patterns.

To identify REM rebound, an electroencephalogram (EEG) can be used to measure brain waves during sleep. However, this information is typically not included in the results of a standard sleep study.

REM sleep behaviour disorder

RBD can be divided into three categories: idiopathic RBD, drug-induced RBD, and secondary RBD due to a medical condition. The diagnosis requires confirmation by an in-laboratory sleep study (polysomnography) with video recording, which helps to assert abnormal behaviours during REM sleep and exclude other sleep disorders.

The primary treatment goal of RBD is to reduce the risk of injury to the patient and their bed partners. This may involve changing routine sleep habits, such as lowering the bed closer to the floor, safeguarding firearms, cushioning sharp furniture surfaces, and separating the sleeping partner from the patient. The recommended pharmacological treatment of isolated RBD in adults includes immediate-release melatonin, clonazepam, or pramipexole.

The prognosis of RBD is dependent on its etiology. Idiopathic RBD and RBD associated with neurodegenerative diseases are often slowly progressive. In contrast, medication-induced RBD may occur acutely and improve upon discontinuing the medication. The prognosis of RBD with Parkinson's disease is associated with a higher risk of dementia, while RBD with Lewy-body dementia has a higher mortality risk.REM sleep behaviour disorder (RBD) is a parasomnia involving dream enactment behaviour associated with a loss of atonia during REM sleep. This can be extremely disturbing and cause injury to the individual or their sleeping partner. RBD is often associated with antidepressant use and narcolepsy. The strongest correlation is between RBD and comorbid neurodegenerative alpha-synucleinopathies, such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy.

RBD can be divided into three categories: idiopathic RBD, drug-induced RBD, and secondary RBD due to a medical condition. The diagnosis requires confirmation by an in-laboratory sleep study (polysomnography) with video recording, which helps to assert abnormal behaviours during REM sleep and exclude other sleep disorders.

The primary treatment goal of RBD is to reduce the risk of injury to the patient and their bed partners. This may involve changing routine sleep habits, such as lowering the bed closer to the floor, safeguarding firearms, cushioning sharp furniture surfaces, and separating the sleeping partner from the patient. The recommended pharmacological treatment of isolated RBD in adults includes immediate-release melatonin, clonazepam, or pramipexole.

The prognosis of RBD is dependent on its etiology. Idiopathic RBD and RBD associated with neurodegenerative diseases are often slowly progressive. In contrast, medication-induced RBD may occur acutely and improve upon discontinuing the medication. The prognosis of RBD with Parkinson's disease is associated with a higher risk of dementia, while RBD with Lewy-body dementia has a higher mortality risk.

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