QuestionHi,
We have a healthy, bright 11 year old son who has begun to develop sleep difficulties over the past 5- 6 weeks. Sunday nights are the worst nights. He has great difficulty falling asleep, and more often than not will also wake up during the night and have trouble returning to sleep. He gets very upset about this which only makes matters worse. This past Sunday night he started "getting the feeling" as he puts it an hour BEFORE bedtime- just anticipating that the problem would occur (and of course it did).
He denies any problems with school or freinds. He is an excellent student and we try not to put too much empaphasis on doing well in school.
He has always been a fairly "high-need" child and is very close to me. He tries getting back to sleep on his own (reading a book, listening to the radio, thinking of rote things) but (I think) always ends up coming in to wake me up to tell me about his problem. Sometimes I get up and rub his back. Sometimes he gets in our bed. These help a little.
It happens other nights too. We try to down-play the issue, not talking about it before bed time. The problem seems to be building and becoming a self-fulfilling prophecy.
We are both getting worn out and I don't know what else to do.
I would appreciate any suggestions you have.
Thank you.
Laura Simonds
AnswerYes, this is common at this age and is usually resolved by using good sleep hygiene. See below for a lot of information on insomnia. OK?
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Insomnia is the complaint of inadequate sleep; it can be classified according to the nature of sleep disruption and the duration of the complaint. The nature of the sleep disruption provides important information about the possible etiology of the insomnia and is also central to the selection of specific and appropriate treatment. Insomnia is subdivided into difficulty falling asleep (sleep onset insomnia), frequent or sustained awakenings (sleep maintenance insomnia), early morning awakenings (sleep offset insomnia), or persistent sleepiness despite sleep of adequate duration (nonrestorative sleep). Similarly, the duration of the symptom is an important determinant of the nature of appropriate treatment. An insomnia complaint lasting one to several nights (within a single episode) is termed transient insomnia. Transient insomnia is typically the result of situational stress or a change in sleep schedule or environment (e.g., jet lag). Short-term insomnia lasts from a few days to 3 weeks. Disruption of this duration is usually associated with more protracted stress, such as recovery from surgery or short-term illness. Long-term insomnia, or chronic insomnia, lasts for months or years and, in contrast with short-term insomnia, requires a thorough evaluation of underlying causes (see below). Chronic insomnia is often a waxing and waning disorder, with spontaneous or stressor-induced exacerbations.
While an occasional night of poor sleep, typically in the setting of stress or excitement about external events, is both common and without lasting consequences, persistent insomnia can have important adverse consequences in the form of impaired daytime function and increased risk of injury due to accidents. There is also clear evidence of increased risk of the development of major depression with insomnia of at least 1 year's duration. In addition, there is emerging evidence that individuals with chronic insomnia have increased utilization of health care resources, even after controlling for comorbid medical and psychiatric disorders.
Extrinsic Insomnia
A number of sleep disorders are the result of extrinsic factors that interfere with sleep. Transient situational insomnia can occur after a change in the sleeping environment (e.g., in an unfamiliar hotel or hospital bed) or before or after a significant life event, such as a change of occupation, loss of a loved one, illness, or anxiety over a deadline or examination. Increased sleep latency, frequent awakenings from sleep, and early morning awakening can all occur. Recovery generally occurs rapidly, usually within a few weeks. Treatment is usually symptomatic, with intermittent use of hypnotics and resolution of the underlying stress. Inadequate sleep hygiene is characterized by a behavior pattern prior to sleep and/or a bedroom environment that is not conducive to sleep. Noise and/or light in the bedroom can interfere with sleep, as can a bed partner with periodic limb movements during sleep or one who snores loudly. Clocks can heighten the anxiety about the time it has taken to fall asleep. Drugs that act on the central nervous system, large meals, vigorous exercise, or hot showers just before sleep may interfere with sleep onset. Many individuals participate in stressful work-related activities in the evening, producing a state incompatible with sleep onset. In preference to hypnotic medications, patients should be counseled to avoid stressful activities before bed, develop a soporific bedtime ritual, and to prepare and reserve the bedroom environment for sleeping. Consistent, regular rising times should be maintained daily, including weekends.
Psychophysiologic Insomnia
Persistent psychophysiologic insomnia is a behavioral disorder in which patients are preoccupied with a perceived inability to sleep adequately at night. The sleep disturbance is often triggered by an emotionally stressful event; however, the poor sleep habits and beliefs about sleep acquired during the stressful period persist long after the initial incident. Such patients become hyperaroused by their own persistent efforts to sleep and/or the sleep environment, and the insomnia is a conditioned or learned response. They may be able to fall asleep more easily at unscheduled times (when not trying) or outside the home environment. Polysomnographic recording in patients with psychophysiologic insomnia reveals an objective sleep disturbance, often with an abnormally long sleep latency; frequent nocturnal awakenings; and an increased amount of stage 1 transitional sleep. Rigorous attention should be paid to sleep hygiene and correction of counterproductive, arousing behaviors before bedtime. Behavioral therapies are the treatment modality of choice for psychophysiologic insomnia, with only intermittent use of medications. When patients are awake longer than 20 min, they should read or perform other relaxing activities to distract themselves from insomnia-related anxiety. In addition, bedtime and waketime should be scheduled to restrict time in bed to be equal to their perceived total sleep time. This will generally produce sleep deprivation, greater sleep drive, and, eventually, better sleep. Time in bed can then be gradually expanded.
Medication-, Drug-, or Alcohol-Dependent Insomnia
Disturbed sleep can result from ingestion of a wide variety of agents. Caffeine is perhaps the most common pharmacologic cause of insomnia. It produces increased latency to sleep onset, more frequent arousals during sleep, and a reduction in total sleep time for up to 8 to 14 h after ingestion. As few as three to five cups of coffee can significantly disturb sleep in some patients; therefore, a 1- to 2-month trial without caffeine should be attempted in patients with these symptoms. Similarly, alcohol and nicotine can interfere with sleep, despite the fact that many patients use them to relax and promote sleep. Although alcohol can increase drowsiness and shorten sleep latency, even moderate amounts of alcohol increase awakenings in the second half of the night. In addition, alcohol ingestion prior to sleep is contraindicated in patients with sleep apnea because of the inhibitory effects of alcohol on upper airway muscle tone. Acutely, amphetamines and cocaine suppress both REM sleep and total sleep time, which return to normal with chronic use. Withdrawal leads to a REM sleep rebound.
A number of prescribed medications can produce insomnia. Antidepressants, sympathomimetics, and glucocorticoids are common causes. In addition, severe rebound insomnia can result from the acute withdrawal of hypnotics, especially following the use of high doses of benzodiazepines with a short half-life. For this reason, hypnotic doses should be low to moderate, the total duration of hypnotic therapy should usually be limited to 2 to 3 weeks, and prolonged drug tapering is encouraged.
Altitude Insomnia
Sleep disturbance is a common consequence of exposure to high altitude. Periodic breathing of the Cheyne-Stokes type occurs during NREM sleep about half the time at high altitude, with restoration of a regular breathing pattern during REM sleep. Both hypoxia and hypocapnia are thought to be involved in the development of periodic breathing. Frequent awakenings and poor quality sleep characterize altitude insomnia, which is generally worst on the first few nights at high altitude but may persist. Treatment with acetazolamide can decrease time spent in periodic breathing and substantially reduce hypoxia during sleep.
Restless Legs Syndrome (RLS)
Patients with this sensory-motor disorder report a creeping or crawling dysesthesia deep within the calves or feet, or sometimes even in the upper extemities, that is associated with an irresistible urge to move the affected limbs. For most patients with RLS, the dysesthesias and restlessness are much worse in the evening or night compared to the daytime and frequently interfere with the ability to fall asleep. The disorder is exacerbated by inactivity and temporarily relieved by movement. In contrast, paresthesia secondary to peripheral neuropathy persists with activity. The severity of this chronic disorder may wax and wane with time and can be exacerbated by sleep deprivation, caffeine, and pregnancy. The prevalence is thought to be 5% of adults. Roughly one-third of patients will have multiple affected family members, possibly with an autosomal dominant pattern. Iron deficiency and renal failure may actually cause RLS, which is then considered secondary RLS. The symptoms of RLS are exquisitely sensitive to dopaminergic drugs (e.g., L-dopa or dopamine agonists). Narcotics, benzodiazepines, and certain anticonvulsants may also be of therapeutic value. Most patients with restless legs also experience periodic limb movement disorder during sleep, although the reverse is not the case.
Periodic Limb Movement Disorder
Periodic limb movement disorder, previously known as nocturnal myoclonus, is the principal objective polysomnographic finding in 17% of patients with insomnia and 11% of those with excessive daytime somnolence (Figure 27-2 ). It is often unclear whether it is an incidental finding or the cause of disturbed sleep. Stereotyped, 0.5- to 5.0-s extensions of the great toe and dorsiflexion of the foot recur every 20 to 40 s during NREM sleep, in episodes lasting from minutes to hours. Most such episodes occur during the first half of the night. The disorder occurs in a wide variety of sleep disorders (including narcolepsy, sleep apnea, REM sleep behavior disorder, and various forms of insomnia) and may be associated with frequent arousals and an increased number of sleep-stage transitions. The incidence increases with age: 44% of people over age 65 without a sleep complaint have >five periodic leg movements per hour of sleep. The pathophysiology is not well understood, though individuals with high spinal transections can exhibit periodic leg movements during sleep, suggesting the existence of a spinal generator. Polysomnography with bilateral surface EMG recording of the anterior tibialis is used to establish the diagnosis. Treatment options include dopaminergic medications or benzodiazepines.
Insomnia Associated with Mental Disorders
Approximately 80% of patients with psychiatric disorders describe sleep complaints. There is considerable heterogeneity, however, in the nature of the sleep disturbance both between conditions and among patients with the same condition.
Depression can be associated with sleep onset insomnia, sleep maintenance insomnia, and/or early morning wakefulness. However, hypersomnia occurs in some depressed patients, especially adolescents and those with either bipolar or seasonal (fall/winter) depression (Chapter 385 ). Indeed, sleep disturbance is an important vegetative sign of depression and may commence before any mood changes are perceived by the patient. Consistent polysomnographic findings in depression include decreased REM sleep latency, lengthened first REM sleep episode, and shortened first NREM sleep episode; however, these findings are not specific for depression, and the extent of these changes varies with age and symptomatology. Depressed patients also show decreased slow-wave sleep and reduced sleep continuity.
In mania and hypomania, sleep latency is increased and total sleep time can be reduced. Patients with anxiety disorders tend not to show the changes in REM sleep and slow-wave sleep seen in endogenously depressed patients. Finally, chronic alcoholics lack slow-wave sleep, have decreased amounts of REM sleep (as an acute response to alcohol), and have frequent arousals throughout the night. This is associated with impaired daytime alertness. The sleep of chronic alcoholics may remain disturbed for years after discontinuance of alcohol usage. Sleep architecture and physiology are disturbed in schizophrenia (with a decreased amount of stage 4 sleep and a lack of augmentation of REM sleep following REM sleep deprivation); chronic schizophrenics often show day-night reversal, sleep fragmentation, and insomnia.
Insomnia Associated with Neurologic Disorders
A variety of neurologic diseases result in sleep disruption through both indirect, nonspecific mechanisms (e.g., pain in cervical spondylosis or low back pain) or by impairment of central neural structures involved in the generation and control of sleep itself.
For example, dementia from any cause has long been associated with disturbances in the timing of the sleep-wake cycle, often characterized by nocturnal wandering and an exacerbation of symptomatology at night (so-called sundowning).
Epilepsy may rarely present as a sleep complaint (Chapter 360 ). Often the history is of abnormal behavior, at times with convulsive movements, during sleep, and the differential diagnosis includes REM sleep behavior disorder, sleep apnea syndrome, and periodic movements of sleep (see above). Diagnosis requires nocturnal EEG recording. Other neurologic diseases associated with abnormal movements, such as Parkinson's disease, hemiballismus, Huntington's chorea, and Gilles de la Tourette syndrome, are also associated with disrupted sleep, presumably through secondary mechanisms. However, the abnormal movements themselves are greatly reduced during sleep. Headache syndromes may show sleep-associated exacerbations (migraine or cluster headache) (Chapter 15 ) by unknown mechanisms.
Fatal familial insomnia is a rare hereditary disorder caused by bilateral degeneration of anterior and dorsomedial nuclei of the thalamus. Insomnia is a prominent early symptom. Progressively, the syndrome produces autonomic dysfunction, dysarthria, myoclonus, coma, and death. The pathogenesis is a mutation in the prion protein (Chapter 375 ).
Insomnia Associated with Other Medical Disorders
A number of medical conditions are associated with disruptions of sleep. The association is frequently nonspecific, e.g., that between sleep disruption and chronic pain from rheumatologic disorders. Attention to this association is important in that sleep-associated symptoms are the presenting complaint of many such patients. Treatment of the underlying medical disorder or symptom is the most useful approach to such patients. As noted above, sleep disruption can also result from the appropriate use of drugs such as glucocorticoids.
Among the most prominent associations is that between sleep disruption and asthma. In many asthmatics there is a prominent daily variation in airway resistance that results in marked increases in asthmatic symptoms at night, especially during sleep. In addition, treatment of asthma with theophylline-based compounds, adrenergic agonists, or glucocorticoids can independently disrupt sleep. When sleep disruption is a prominent side effect of asthma treatment, inhaled steroids (e.g., beclomethasone) that do not disrupt sleep may provide a useful alternative.
Cardiac ischemia may also be associated with sleep disruption. The ischemia itself may result from increases in sympathetic tone as a result of sleep apnea. Patients may present with complaints of nightmares or vivid, disturbing dreams, with or without awareness of the more classic symptoms of angina or of the sleep disordered breathing. Treatment of the sleep apnea may substantially improve the angina and the nocturnal sleep quality. Paroxysmal nocturnal dyspnea can also occur as a consequence of sleep-associated cardiac ischemia that causes pulmonary congestion exacerbated by the recumbent posture.
Chronic obstructive pulmonary disease is also associated with sleep disruption, as is cystic fibrosis, menopause, hyperthyroidism, gastroesophageal reflux, chronic renal failure, and liver failure.
