Awake in orem needing release

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Try out PMC Labs and tell us what you think. Learn More. Cardiovascular and respiratory parameters change during sleep and wakefulness. This observation underscores an important, albeit incompletely understood, role for the central nervous system in the differential regulation of autonomic functions.

In this review, we examine the functional and anatomical ificance of hypothalamic, pontine, and medullary networks on sleep, cardiovascular function, and breathing. Seventeenth-century philosophers were fascinated with sleep [ 1 , 2 ]. Descartes grappled with an uncertain human existence during unconsciousness, concluding that the sleeping brain continues to think [ 1 ].

Locke separated the awake and sleeping minds, suggesting the latter state to be inactive and—by extension—with limited purpose [ 2 ]. By the s, however, discoveries about paradoxical sleep a sleep stage with rapid movements of the eyes and cortical activity resembling wakefulness challenged the notion that the sleeping brain was inactive [ 3 ]. Modern definitions acknowledge that many biologic processes are active during sleep, particularly networks regulating the autonomic nervous system ANS.

Understanding the neural mechanisms regulating sleep and autonomic function is important for defining the relationship between sleep disorders and cardiovascular CV morbidity. The purpose of this review was to examine neural networks differentially controlling the ANS during wakefulness versus sleep. Evidence from preclinical and clinical studies indicates that the modulation of ANS reflexes is dependent on behavioral state i. The key CNS nuclei associated with these functions are summarized in Table 1. During wakefulness, particularly during periods of physical activity, there are ificant fluctuations in cardiac output and respiratory flow.

The brainstem reflexively responds to afferent als communicating these changes from peripheral baroreceptors, chemoreceptors, and the cardiac sympathetic nerves. Baroreceptors in the aortic arch sense blood pressure BP changes and relay this information to the NTS via the vagus nerve [ 5 ]. When the BP is elevated, NTS efferents decrease sympathetic outflow to the heart while simultaneously increasing vagal tone [ 6 ]. NTS neurons project to gamma-aminobutyric acid GABA -ergic neurons in the caudal ventrolateral medulla, which provides inhibitory inputs to the RVLM, thereby reducing sympathetic outflow to the kidney [ 7 ].

Pre-motor neurons in the RVLM project to the intermediolateral column of the spinal cord, which synapse with renal post-ganglionic neurons [ 8 ]. Via this neural network, RVLM neurons regulate renal blood flow, sodium and water reabsorption, and excretion, as well as the activity of the renin—angiotensin system [ 9 ]. In the RVLM, sympathetic neurons are intermingled with respiratory-modulating neurons [ 7 ]. Chemoreceptors in the carotid body provide another afferent al to the NTS in response to hypoxia.

The chemoreflex enhances respiratory drive and sympathoexcitation. In addition, several modulatory CNS circuits exist to regulate wakefulness. A cholinergic pathway originating from the laterodorsal tegmentum and pedunculopontine tegmentum [PPT] promotes arousal. The cholinergic projections innervate the thalamus, promoting the transmission of sensory input to the cortex [ 12 ]. Monoaminergic neurons originating from the parabrachial nucleus, periaqueductal grey [PAG], locus coeruleus, and raphe nuclei project to the cortex, lateral hypothalamus, and basal forebrain and also modulate alertness [ 13 ].

Orexinergic neurons in the lateral hypothalamus represent another system promoting wakefulness; these neurons provide excitatory projections that activate the ascending monoaminergic system and brainstem cholinergic systems [ 14 ]. Collectively, these pathways activate the cortex and contribute to the low-voltage, high-frequency electroencephalogram EEG pattern occurring during wakefulness. Glutamatergic neurons in the parabrachial nucleus of the rostral pons are preferentially active during wakefulness [ 15 , 16 ]; projections from the parabrachial nucleus to the NTS may represent a mechanism for adjusting BP between wakefulness and sleep.

Increased parabrachial nucleus activity may inhibit the baroreflex [ 17 — 19 ], representing a mechanism for maintaining higher BP during wakefulness compared with sleep. During non-REM sleep, parasympathetic drive increases, with an associated reduction in cardiac sympathetic activity [ 20 ]. BP dipping represents a healthy cardiovascular response; non-dipping, rising, or extreme-dipping is associated with elevated CV disease risk [ 21 ]. Non-REM sleep is also accompanied by decreased muscle tone and reduced respiratory rate [ 22 ].

Hypothalamic nuclei, specifically the ventrolateral preoptic nucleus VLPO and median preoptic nucleus, promote non-REM sleep via descending GABAergic projections to the arousal systems of the hypothalamus and brainstem. These sleep-promoting pathways are regulated by neuromodulators, such as adenosine, that accumulate during wakefulness to increase the physiologic pressure to sleep [ 23 ].

Activity of the preoptic nuclei may also influence ANS functions. For example, anatomical evidence suggests that non-REM sleep-promoting neurons in the VLPO inhibit the hypothalamic structures with pressor and sympathoexcitatory functions. For example, Uschakov and colleagues demonstrated the presence of an inhibitory projection from the VLPO to the paraventricular nucleus of the hypothalamus in rats [ 24 , 25 ].

As a potent vasoconstrictor, vasopressin contributes to elevated BP, in addition to its role in increasing fluid reabsorption from the filtrate in the nephron [ 26 ]. The occurrence of non-REM sleep requires inhibition of the wake-promoting networks, which is dependent on neurotransmission involving GABA and galanin [ 12 ]. Inhibition of the networks exciting the cortex in a slower-frequency, higher-voltage EEG pattern during non-REM sleep, although slow waves are not uniformly distributed across the cortical surface [ 27 ].

The VLPO of the anterior hypothalamus plays an important role in promoting the transition from wake to sleep [ 28 ]. REM sleep is a paradoxical stage consisting of a high-frequency and low-amplitude EEG pattern similar to the EEG pattern observed during wakefulness with muscle atonia. The EEG features of REM sleep and the rapid eye movements are controlled by neurons in the sublaterodorsal region of the pons [ 12 ]. Skeletal muscle paralysis, a key feature of REM sleep, is associated with increased glutamatergic neuron activity in the dorsal pons [ 29 ]. Inhibition of REM sleep may also involve serotonergic input from the raphe nuclei, albeit this connection is incompletely understood [ 33 ].

Functional and anatomical data from rat studies support a role for the PPT in regulating sympathetic nerve activity. For example, studies in anesthetized rats demonstrated the ability to increase renal and splanchnic sympathetic nerve activity by stimulating neurons in the PPT [ 39 , 40 ], which also evoked respiratory dysrhythmia [ 39 ].

The irregular breathing patterns associated with REM sleep may be attributed to chemoreflex and baroreflex control [ 41 ]. During non-REM sleep, chemoreceptors promptly recognize small fluctuations in oxygen and carbon dioxide, which in minor adjustments in breathing rate and depth via NTS pathways [ 11 ]. For example, transitions from non-REM to REM sleep evoke increases in mean arterial pressure in humans [ 42 ] and in rats [ 43 , 44 ], and these BP fluctuations may lead to baroreflex instability.

These observations suggest that an increase in the loop gain of these feedback systems may accompany REM sleep. Loop gain measures the propensity for a feedback system to become unstable [ 45 , 46 ]. Although REM sleep is associated with skeletal muscle atonia, from several studies have challenged the notion that upper airway muscles lose tone during REM sleep.

For example, Fraigne and Orme demonstrated that genioglossus muscle activity increased in rats during REM sleep compared with non-REM sleep, suggesting the possibly that REM-specific muscle recruitment could contribute to changes in respiration [ 47 ]. In Fig. Both rodent and human sleep demonstrate alternating patterns of non-REM and REM sleep, which can be accompanied by fluctuations in BP, heart rate, ventilation, and arterial concentrations of oxygen and carbon dioxide. The latter is indicated by the very low EMG tone. Data were graphed using Igor Pro version 6.

In this example, the respiratory rate increased [from approx. BP remained relatively stable in this rat. Data were acquired using implantable telemetry system and analyzed using Neuroscore software Data Sciences International, Minneapolis, MN. Insomnia is accompanied by hyperarousal, elevated BP, and reduced heart rate variability [ 48 ]. In FFI, a progressive, inherited autosomal-dominant neurodegenerative disease, the inability to sleep le to unbalanced autonomic control, coma, and death [ 50 ].

FFI is characterized by severe sympathetic over-activity tachycardia, hypertension, and hyperthermia , which is hypothesized to involve impaired inhibition of the baroreflex, possibly resulting from over-excitation of the RVLM [ 51 ]. Sleep apnea involves a complex group of disorders causing adverse CV and metabolic consequences in addition to excessive daytime sleepiness. Sleep-disordered breathing can cause intermittent hypoxia and chronic activation of the sympathetic nervous system—two mechanisms hypothesized to link sleep apnea with an elevated risk for CV diseases, such as hypertension and stroke [ 52 ].

Patients experience frequent arousals from sleep, resulting from increased respiratory effort in response to hypoxia or hypercapnia [ 53 ]. The etiology of these respiratory events may be obstructive or central. Obstructive sleep apnea OSA involves repetitive airway blockage caused by the surrounding soft tissue and can be correlated with obesity; central sleep apneas result from reduced neural output of the brainstem neurons innervating the upper airway and thoracic inspiratory muscles [ 52 ].

Many patients, however, experience both obstructive and central events [ 54 ]. Interestingly, treating airway obstruction with positive airway pressure or tracheostomy in central apnea, suggesting that underlying CNS neural mechanisms are implicated in both types of apnea and contribute to complex sleep apnea phenotypes [ 55 , 56 ]. Sleep apnea disrupts sleep architecture, evoking frequent arousals and modifying sleep stage-dependent interactions between sympathetic and parasympathetic tone [ 57 ].

In OSA, hypoxia is a powerful stimulus for increasing sympathetic drive via the chemoreflex [ 58 — 60 ]. In humans, obstructive sleep apnea has been associated with an impaired nocturnal dipping pattern in BP. Mokhlesi and colleagues demonstrated a dose—response risk for developing systolic and diastolic non-dipping BP with increasing severity of sleep apnea [ 61 ].

Experiments in rats have demonstrated how repetitive apneas have an additive effect on widening pulse pressure and increasing BP; these responses activate CNS ascending arousal systems, increase respiratory muscle effort, cause changes in intrathoracic blood volume, and activate sympathetic activity [ 59 , 60 , 62 ]. Data from rat models of chronic intermittent hypoxia have also provided evidence for renal mechanisms in the development of chronically elevated BP. Plasma renin activity increased fourfold in the latter group but remained at baseline levels in denervated rats [ 63 ].

Awake in orem needing release

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