Sleep Disorders
A number of common types of sleep disorders have been identified and are summarized here.
Narcolepsy
Narcolepsy is commonly a disabling form of somnolence. The individual experiences attacks of sleep at times and places where sleep does not normally occur. For example, the individual may fall asleep in the car while driving or while giving a lecture. Such individuals may also be subject to a condition called cataplexy, which is a loss of muscle tone. Narcoleptic individuals may also display a sleep paralysis in which they remain awake at night, begin to hallucinate, and are unable to move. This disorder may be associated with abnormal functions of cholinergic neurons.
Insomnia
Insomnia is characterized by a chronic inability to fall asleep in spite of appropriate opportunities to do so. This disorder can either appear primarily as an abnormality in the sleep mechanism, or it can occur as a secondary phenomenon to a psychological or medical problem. In the first form of insomnia, there are no signs of a psychological or medical problem that could explain the disorder. The second form of insomnia is likely associated with pain, discomfort, or alcohol or drug abuse and is usually of short duration.
Somnambulism (Sleepwalking)
Somnambulism, a form of insomnia that occurs during non-REM sleep and is characterized by unusual autonomic and/or motor responses, typically takes place in the first few hours of sleep, and is more common in children than adults. The sleepwalker may get up out of bed, put on his or her clothes in an awkward way, open doors, or even have something to eat. He or she usually obeys instructions to go back to bed.
Night Terrors
Night terrors is a parasomnia that occurs mainly in children soon after falling asleep. The child awakens, is terrified, screams, and displays marked tachycardia and rapid respiration. These children can also be sleepwalkers. The entire episode lasts just a few minutes, and the child remembers nothing of the event when he or she awakens in the morning.
Restless Legs Syndrome
In the restless legs syndrome, the patient complains of drawing pains in the calves and thighs, which may include creeping or crawling feelings. They occur when the patient begins to rest and can be temporarily relieved by movement of the legs. This syndrome can easily delay the onset of sleep. The leg sensations can extend into the daytime and are worsened by fatigue. A related (or part of the same) disorder involves movements of the legs during sleep, which are slower than myoclonal jerks and which can occur every 20 to 90 seconds and last up to an hour. The cause of restless legs syndrome is unknown but, in some instances, has been associated with iron deficiency anemia. Various drug treatments have been given for this disorder. These include tricyclic antidepressants, L-3, 4-hydroxyphenylalanine, opiates, and serotonin reuptake inhibiting antidepressants.
Sleep Apnea
Sleep apnea is a condition characterized by an interruption of breathing. In individuals with this condition, there is a decline in the oxygen content of the blood. The interruption of breathing leads to arousal from sleep or results in lighter stages of non-REM sleep in order for breathing to be maintained. Muscle tone in individuals suffering from sleep apnea is further compromised by REM sleep, which, by itself, results in reduced muscle tone. The net effect in such individuals is that excessive reduction in muscle tone of the airway muscles leads to a further narrowing of the airway passages. In addition, patients with sleep apnea may show impaired performance in work-related functions and reduced intellectual capacity as well as excessive daytime sleepiness. This condition could be dangerous to the afflicted individual in such circumstances as driving a car or operating machines that may be lethal if misused. Sleep apnea is exacerbated in individuals who are obese because the added fatty tissue may further reduce the air passages. Although less common than the obstructive type (i.e., complete obstruction of the airway passages), sleep apnea can also occur as a result of a dysfunction of the central mechanisms regulating breathing. Such mechanisms may include sensory pathways, brainstem or the upper cervical spinal cord.
Sleep Disorders in Psychiatric Patients
In certain psychiatric conditions, there is a marked reduction in the amount of sleep that an individual may receive. These disorders include depression, in which the individual awakens very early or during the nighttime (in addition to the characteristic conditions of excessive guilt, depressed mood and appetite, and difficulties in concentrating on one’s work and remembering), and posttraumatic stress disorder, in which a life-threatening event in the distant past of the individual reappears in his or her memory during the daytime or in the evening in dreams. It is possible that this disorder may relate to the disruption of mechanisms that control REM sleep.
Coma
What are the consequences of lesions of the reticular formation? From the earlier discussion, it is not surprising that lesions of the brainstem reticular formation are associated with disturbances of consciousness. Damage (typically associated with a cerebrovascular accident) to the reticular formation of the pons or midbrain will produce coma in most instances. The EEG patterns resulting from lesions of different regions of the reticular formation may vary significantly. For example, lesions of the midbrain reticular formation result in the appearance of slow waves of large amplitude. In contrast, lesions of the pons are frequently characterized by an alpha rhythm typically seen in a normal drowsy person. With other lesions, the patient may display an EEG pattern characteristic of slow-wave sleep. In the case of a pontine lesion, the patient lies quietly and displays a variety of autonomic and somatomotor reflexes as well as normal eye movements. This constellation of responses is referred to as coma vigil or akinetic mutism. Lesions involving the lower brainstem also produce a loss of consciousness. However, lesions involving the lower brainstem are frequently fatal because of the severity of the accompanying cardiovascular respiratory disturbances.
History
Bill is a 23-year-old man who has had bouts of difficulty remaining awake for several years. Throughout high school, he was unable to remain awake during class and while taking tests. He would fall asleep while on the telephone, watching television, playing video games, and during driving instruction to such an extent that he was not permitted to obtain a driver’s license. If he heard a joke or reacted to another emotional stimulus, he would often have a loss of muscle tone in his head and jaw and, in severe cases, would fall to the floor. He required at least one nap during the day, which refreshed him even if it lasted only 15 or 20 minutes. He felt as though he had dreamed during these naps, although they were short. Although he had no trouble falling asleep at night, his nighttime sleep was fragmented, with frequent kicking and awakening. Upon falling asleep or awaking, he often felt paralyzed or had hallucinations similar to dreaming. He sought medical attention when it took him 6 years to complete college, despite having a superior intellectual ability.
Examination
A neurologist saw Bill and completed a history and physical examination. The neurologic examination was normal, except that when the lights were lowered to perform a fundoscopic examination, the neurologist observed the Bell effect, which involves the rolling back of the eyes, which is a normal response upon closing one’s eyes. A nighttime sleep study was ordered, followed by a test consisting of a series of naps called a multiple sleep latency test (MLST), in which Bill was asked to take a 20-minute nap every 2 hours. A magnetic resonance imaging scan of Bill’s head was ordered.
Explanation
Bill has narcolepsy, a neurologic disorder characterized by excessive daytime somnolence with frequent, uncontrollable napping, cataplexy (drop attacks, or loss of tone in the antigravity muscles), sleep paralysis (feeling paralyzed while falling asleep or awaking), and hypnagogic hallucinations (hallucinations upon falling asleep and awaking). One neurophysiological characteristic of narcolepsy is called sleep-onset REM (or REM sleep), which occurs in the first hour of nighttime sleep or anytime during daytime MLSTs. This provides evidence that narcolepsy is a disorder of the intrusion of REM sleep during inappropriate times, even wakefulness in response to an emotional stimulus (cataplexy—muscle tone is normally lost during REM sleep). Experimental evidence has been unable to pinpoint a precise lesion causing narcolepsy. Moreover, hypothalamic and brainstem tumors involving the reticular formation have been rarely found in new cases of narcolepsy. Most cases of narcolepsy are idiopathic and begin during the teenage years or even earlier.
SUMMARY TABLE
Input-Output Relationships of the Reticular Formation and Their Functional Relationships
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Process |
Anatomical Source/Distribution |
Function |
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Afferent Sources to Reticular Formation |
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Sensory Processes |
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Somatosensory signals from spinal cord |
Collaterals of spinothalamic fibers to reticular formation of medulla, pons,and midbrain PAG |
Pain and temperature inputs to reticular formation; affects cortical excitability and levels of consciousness; also part of circuit for pain inhibition (through the PAG) |
|
Cranial nerve nuclei |
Axons and dendrites of cranial nerve nuclei that encircle reticular formation provide multiple modalities of sensory input to reticular formation |
Provides multi-modal inputs associated with auditory, vestibular, and somatosensory sensations (from head region) |
|
Secondary sensory pathways |
Tertiary visual, auditory, and olfactory inputs via limbic structures to midbrain reticular formation |
Provides multi-modal inputs associated with olfactory, visual, and auditory sensations to midbrain reticular formation |
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Motor Processes |
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Cerebellum |
Afferent fibers from fastigial nucleus to motor nuclei of reticular formation of pons and medulla |
Outputs from fastigial nucleus provide feedback signals to regions of medulla and pons associated with descending reticulospinal pathways |
|
Cerebral cortex |
Afferent fibers from sensorimotor cortex to motor nuclei of reticular formation of pons and medulla |
Outputs from sensorimotor cortex regulate the activity of neurons in the pontine and medullary reticular formation whose axons form the reticulospinal pathways |
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Autonomic Processes |
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CN IX and X |
Primary afferents from both CN IX and CN X to reticular formation of medulla and pons |
CN IX and CN X provide baroreceptor and chemoreceptor signals to medullary and pontine reticular formation that mediate reflex regulation of blood pressure and respiration |
|
Limbic structures and hypothalamus |
Descending fibers from limbic system and hypothalamus to reticular formation (mainly of midbrain, but also to pons and upper medulla) |
Descending outputs from limbic system and hypothalamus powerfully regulate autonomic functions associated with reticular formation |
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Efferent Targets of Reticular Formation |
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|
Sensory Processes |
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To thalamus and cerebral cortex |
Projection from reticular formation: (1) to centromedian nucleus of thalamus and then to wide areas of cortex; or (2) from centromedian nucleus to specific thalamic nuclei which then project to different regions of cortex; or (3) monoaminergic fibers containing dopamine, norepinephrine, and serotonin from ventral tegmental area, locus ceruleus, and raphe nuclei to wide areas of cortex |
Reticular formation inputs to cerebral cortex regulate levels of cortical excitability related to many functions of cerebral cortex; examples include modulation of sensory perception, motor activity, and sleep and wakefulness |
|
To PAG |
Descending pathways passing through relays in raphe magnus of medulla and dorsal horn of spinal cord |
Descending pathways mediate inhibition of pain impulses at the level of the dorsal horn of spinal cord |
|
Process |
Anatomical Source/Distribution |
Function |
|
|
Efferent Targets of Reticular Formation |
|
|
Motor Processes |
||
|
To spinal cord |
Projections from nucleus reticularis pontis oralis and caudalis and nucleus gigantocellularis of medulla to alpha and gamma motor neurons of spinal cord ventral horn |
Reticulospinal fibers from pons facilitate extensor reflexes, whereas reticulospinal fibers from medulla inhibit extensor spinal reflexes; both descending fiber systems powerfully regulate postural reflexes |
|
To cerebellum |
Projections from lateral and paramedian nuclei of medulla and reticulotegmental nucleus of pons to anterior and posterior lobes of cerebellum |
Efferents to anterior and posterior lobes of cerebellum serve as part of a feedback circuit linking cerebellum with reticular formation; inputs from reticular formation provide continuous information to cerebellum concerning levels of excitability of reticular formation neurons that descend to spinal cord |
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Motor Processes |
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To CN VI and III |
Horizontal gaze center sends axons to CN VI (ipsilaterally) and CN III (contralateral^) |
Horizontal gaze center of pons integrates cortical and vestibular inputs and controls horizontal movement of the eyes by its connections with CNVI and CN III |
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Autonomic Processes |
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Regions, such as solitary nucleus and ventrolateral nucleus of medulla, project to dorsal motor nucleus of CN X and to intermediolateral cell column of thoracic and lumbar spinal cord, respectively; other projections from pontine and medullary reticular formation to cervical cord associated with phrenic nerve |
Solitary nucleus interactions with dorsal motor nucleus of CN X excites parasympathetic nervous system, whereas outputs from ventrolateral medulla to spinal cord mediate sympathetic activity; other descending fibers from reticular formation to spinal cord regulate respiration by acting upon neurons of the phrenic nerve |
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PAG = periaqueductal midbrain gray; CN = cranial nerve.
