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mellitus, Guillain-Barré syndrome or porphyria can damage these nerves. Although pure sensory loss of these nerves is exceedingly rare, damage of these nerves is typically accompanied with loss of motor function. If pure sensory nerve loss did occur the peripheral feedback of information to the medulla would be diminished, and patients would rely upon central chemoceptors for feedback regulation.

At the level of the medulla, we find the first layers of respiratory cycle generators. Neurons in the nucleus solitarius, ambiguous, and retroambigualis work in concert to initially match ventilation to respiratory demand. The ventilatory cycle is composed of three phases: inspiration, postinspiration, and expiration. Respiratory neurons in the medulla and pons discharge in a pattern correlating to one of these phases. Together these neurons form the central pattern generator that orchestrates the cyclic activation of the respiratory musculature.

This central pattern generator is composed of predominately three neuronal groups. Nogues categorized these as dorsal respiratory group, ventral respiratory group, and pontine respiratory group (2). The dorsal respiratory group is in the ventrolateral subnucleus of the nucleus tractus solitarius. This neuronal group is primarily active during inspiration receiving input from pulmonary vagal afferents. Many of these neurons excite lower motor cranial nerves that dilate the upper airway prior to excitation of the contralateral phrenic and intercostal neurons in the spinal cord. This coordinated output must occur in the correct timed sequence to permit the movement of air through a patent airway. Other neurons in this same group receive input from baroreceptors and cardiac receptors influencing several other respiratory-related reflexes (e.g., coughing, sneezing).

The ventral respiratory group is located in the ventral lateral medulla from the top of the cervical cord to the level of the facial nerve. This group contains the Botzinger complex, the preBotzinger neurons, the rostral portion of nucleus ambiguous, and nucleus retroambigualis. The Botzinger complex contains neurons that are active during expiration and inhibit inspiration. The preBotzinger complex contains propriobulbar neurons that participate in generating the rhythm of respiration. The caudal portion of this group is primarily composed of expiratory neurons that project to intercostal, abdominal, and external sphincter motor neurons. Although these primary drivers form a rudimentary cycle, neurons in the ventral and midline medulla appear to have plasticity in response to intermittent hypox-emia to augment respiratory responses (3). Lesions in the medulla may produce ataxic breathing, agonal respiration or an absence of respiration.

The pontine respiratory group adds another layer of control. This group is localized to the dorsal lateral pons and is important in stabilizing the respiratory pattern. These neurons are influenced by both inspiratory and expiratory inputs and help determine the length of inspiration and expiration (1). Typically, the destruction of these neurons lengthens the duration of inspiration. Lesions of the caudal pons may also produce apneustic respiration, and lesions in the mid-brain or posterior hypothalamus may produce hyperventilatory responses. These types of respiratory abnormalities may result from strokes, tumors or demyelin-ating plaques.

The voluntary control over respiration primarily resides in the cerebral cortex and diencephalon. The cortex is responsible for initiating the intricate respiratory control involved in speech, eating, and singing. As an individual enters sleep, the cortical control over sleep is altered and may allow the emergence of SRBD. With cortical injury, patients may have prolonged posthyperventilatory apnea or Cheyne-Stokes respiration (CSR). The CSR may be more prominent or only present in sleep (4).

The output to the lower respiratory neurons requires transmission of the respiratory effort through the spinal cord to the peripheral nerves. The spinal cord respiratory motor output is divided into two components. The phrenic nerves emerge from the upper cervical cord region (C3-5) to maintain diaphragmatic function. The thoracic levels (T1-T12) innervate the intercostal muscles and the lower thoracic and upper lumbar levels (T6-L3) innervate the abdominal muscles. This division of labor adds a level of assurance of respiration despite the potential of spinal cord injury.

The peripheral nerves must deliver the sensory and motor signals. These peripheral nerves are generally well-myelinated, relatively protected from trauma by bone and have limited lengths. These characteristics assure these nerves are less vulnerable to damage compared to most nerves supplying the limbs. In general, nerves with longer courses have greater opportunity to incur injury from trauma, toxins or demyelination, and thus are more likely to demonstrate dysfunction. This may not be true for some etiologies such as porphyrias, or inflammatory polyradiculopathies, which can afflict more proximal nerves. Individuals with peripheral nerve disorders may demonstrate progressive nocturnal hypoventilation and respiratory failure requiring ventilatory assistance during the more severe portions of the disorder (5). In contrast, patients with multiple cranial neuropathies may also demonstrate features of upper airway obstruction.

The neuromuscular junction may also be associated with respiratory dysfunction. Respiratory muscles such as the diaphragm may require less depolarization to reach firing threshold and thus these muscles may not be the first affected by neuro-muscular dysfunction. The range of SRBDs affected by neuromuscular dysfunction is exemplified in myasthenia gravis (MG), as noted subsequently.

At the level of the muscle, respiration depends upon adequate contraction of these muscles no matter the sleep-wake state. These lower respiratory muscles include slow-twitch muscle, which generally require the less amount of energy to contract and thus are generally more stable with fatigue (6). Some inherited muscle conditions such as Pompe's disease (acid maltase deficiency) may primarily affect respiratory muscles causing hypoventilation. This hypoventilation may be more obvious in sleep.

Overall, respiration during sleep offers a unique window to view the neurological control over breathing. The entrance into each sleep state creates a change in the regulation over breathing and may allow the emergence of disordered breathing. This window may aid in the localization of neurological disease as well as bring insight into the potential causes of SRBD. We have included a table of typical breathing patterns and localization of neurological dysfunction (Table 1). As the reader reviews the variety of neurological disorders, the table may provide additional clarity to the secondary respiratory issues.

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