Insomnia

[daisy]

i dont have any problem with sleeping. each time i open my school books i go into deep sleep

[CtrlAltDel]

school books? how old are , or rather, what class/course r u studying?

[Sujatha]

Sorry Mr Igi First of all I apologise for my rude answer

I try to give some scientific answer

INSOMNIA



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 (Fig. 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 (Chap. 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 (Chap. 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) (Chap. 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 (Chap. 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.



EVALUATION OF DAYTIME SLEEPINESS



Daytime impairment due to sleep loss may be difficult to quantify in the clinical setting for several reasons. First, sleepiness is not necessarily proportional to subjectively assessed sleep deprivation. In obstructive sleep apnea, for example, the repeated brief interruptions of sleep associated with resumption of respiration at the end of apneic episodes result in significant waking impairment, despite the fact that the patient may be unaware of the sleep fragmentation. Second, subjective descriptions of waking impairment vary from patient to patient. Patients may describe themselves as "sleepy," "fatigued," or "tired" and may have a clear sense of the meaning of those terms, while others may use the same terms to describe a completely different condition. Third, sleepiness, particularly when profound, may affect judgment in a manner analogous to ethanol, such that subjective awareness of the condition and the consequent cognitive and motor impairment is reduced. Finally, patients may be reluctant to admit that sleepiness is a problem, both because they are generally unaware of what constitutes normal alertness and because sleepiness is generally viewed pejoratively, ascribed more often to a deficit in motivation than to an inadequately addressed physiologic sleep need.



In assessing sleepiness in the clinical setting, specific questioning about the occurrence of sleep episodes during normal waking hours, both intentional and unintentional, can overcome the inconsistencies among subjective characterizations and help to interpret the adverse impact of sleepiness on daytime function. Specific areas to be addressed include the occurrence of inadvertent sleep episodes while driving or in other safety-related settings, sleepiness while at work or school (and the relationship of sleepiness to work and school performance), and the effect of sleepiness on social and family life. Evidence for significant daytime impairment [in association either with the diagnosis of a primary sleep disorder, such as narcolepsy or sleep apnea, or with imposed or self-selected sleep-wake schedules (see "Shift-Work Sleep Disorder," below)] raises the question of the physician's responsibility to notify motor vehicle licensing authorities of the increased risk of sleepiness-related vehicle accidents. As with epilepsy, legal requirements vary from state to state, and existing legal precedents do not provide a consistent interpretation of the balance between the physician's responsibility and the patient's right to privacy. At a minimum, physicians should document discussions with the patient regarding the increased risk of operating a vehicle, as well as a recommendation that driving be suspended until successful treatment or schedule modification can be instituted.



The distinction between fatigue and sleepiness can be useful in the differentiation of patients with complaints of fatigue or tiredness in the setting of disorders such as fibromyalgia, chronic fatigue syndrome (Chap. 384), or endocrine deficiencies such as hypothyroidism or Addison's disease. While patients with these disorders can typically distinguish their daytime symptoms from the sleepiness that occurs with sleep deprivation, substantial overlap can occur. This is particularly true when the primary disorder also results in chronic sleep disruption (e.g., sleep apnea in hypothyroidism) or in abnormal sleep (e.g., fibromyalgia).



While clinical evaluation of the complaint of excessive sleepiness is usually adequate, objective quantification is sometimes necessary for diagnostic purposes or for the evaluation of treatment response. Assessment of daytime functioning as an index of the adequacy of sleep can be made with the multiple sleep latency test (MSLT), which involves repeated measurement of sleep latency (time to onset of sleep) under standardized conditions during a day following quantified nocturnal sleep. The average latency across four to six tests (administered every 2 h across the waking day) is taken as an objective measure of daytime sleep tendency. Disorders of sleep that result in pathologic daytime somnolence can be reliably distinguished with the MSLT. In addition, the multiple measurements of sleep onset may identify direct transitions from wakefulness to REM sleep that are suggestive of specific pathologic conditions (e.g., narcolepsy).



NARCOLEPSY



Narcolepsy is both a disorder of the ability to sustain wakefulness voluntarily and a disorder of REM sleep regulation (Table 27-2). The classic "narcolepsy tetrad" consists of excessive daytime somnolence plus three specific symptoms related to an intrusion of REM sleep characteristics (e.g., muscle atonia, vivid dream imagery) into the transition between wakefulness and sleep: (1) sudden weakness or loss of muscle tone without loss of consciousness, often elicited by emotion (cataplexy); (2) hallucinations at sleep onset (hypnogogic hallucinations) or upon awakening (hypnopompic hallucinations); and (3) muscular paralysis upon awakening (sleep paralysis). The severity of cataplexy varies, as patients may have two to three attacks per day or per decade. The extent and duration of an attack may also vary, from a transient sagging of the jaw lasting a few seconds to rare cases of flaccid paralysis of the entire voluntary musculature for up to 20 to 30 min. Symptoms of narcolepsy typically begin in the second decade, although the onset ranges from ages 5 to 50. Once established, the disease is chronic without remissions. Secondary forms of narcolepsy have been described (e.g., after head trauma).



Narcolepsy affects about 1 in 4000 people in the United States and appears to have a genetic basis. Recently, two independent discoveries have revealed that hypothalamic neurons containing the neuropeptide orexin (hypocretin) may play an important role in the regulation of sleep/wakefulness: (1) a mutation in the orexin (hypocretin) receptor 2 gene has been associated with canine narcolepsy; and (2) orexin "knockout" mice that are genetically unable to produce this neuropeptide exhibit a phenotype, as assessed by behavioral and electrophysiologic criteria, that is similar to human narcolepsy. In addition, modafinil, a drug recently approved by the U.S. Food and Drug Administration (FDA) for the treatment of narcolepsy, activates orexin-containing neurons. However, the inheritance pattern of narcolepsy in humans is more complex than that of the canine model. A high rate of discordance in identical twins indicates that one or more nonheritable factors contributes to its development. First-degree relatives of narcoleptic patients nonetheless have about a 1% incidence of narcolepsy, much higher than the general population but much lower than is seen in the animal models. Of note, nearly all narcoleptics with cataplexy are positive for the human leukocyte antigen DQB*0106 (ordinarly found in 20 to 30% of the general population) (Chap. 306).



Diagnosis Definition of the essential and distinctive features of narcolepsy has continued to evolve, and the diagnostic criteria continue to be a matter of debate. Certainly, objective verification of excessive daytime somnolence, typically with MSLT mean sleep latencies <8 min, is an essential if nonspecific diagnostic feature. Other conditions that cause excessive sleepiness, such as sleep apnea or chronic sleep restriction, must be rigorously excluded. The other objective diagnostic feature of narcolepsy is the presence of REM sleep in at least two of the naps during the MSLT. This excessive REM "pressure" is also manifested by the appearance of REM sleep immediately or within minutes after sleep onset in 50% of narcoleptic patients, a rarity in unaffected individuals maintaining a conventional sleep-wake schedule. The REM-related symptoms of the classic narcolepsy tetrad are variably present. There is increasing evidence that narcoleptics with cataplexy (one-half to two-thirds of patients) may represent a more homogeneous group than those without this symptom. However, a history of cataplexy can be difficult to establish reliably. Hypnogogic and hypnopompic hallucinations and sleep paralysis are often found in nonnarcoleptic individuals and may be present in only one-half of narcoleptics. Nocturnal sleep disruption is commonly observed in narcolepsy but is also a nonspecific symptom. Similarly, history of "automatic behavior" during wakefulness (a trancelike state during which simple motor behaviors persist) is not specific for narcolepsy and serves principally to corroborate the presence of daytime somnolence.



^TREATMENT



The treatment of narcolepsy is symptomatic. Somnolence is treated with stimulants. Methylphenidate has long been considered the drug of choice by most; the usual initial dose is 10 mg bid, increasing as needed to a maximum of 20 mg qid. Pemoline, frequently used as an alternative due to its longer half-life, may be less effective and has recently been associated with fatal hepatic failure in several children. Dextroamphetamine, 10 mg bid, and methamphetamine are also frequently used alternatives. Recently, modafinil, a novel wake-promoting agent, has been approved by the FDA for treatment of the excessive daytime somnolence in narcolepsy; the dose is 200-400 mg/d given as a single dose. It is a long-acting agent that may cause fewer side effects than other medications.

Treatment of the REM-related phenomena cataplexy, hypnogogic hallucinations, and sleep paralysis requires the potent REM sleep suppression produced by antidepressant medications. The tricyclic antidepressants [e.g., protriptyline (10-40 mg/d) and clomipramine (25-50 mg/d)] and the selective serotonin reuptake inhibitors (SSRIs) [e.g., fluoxetine (10-20 mg/d)] are commonly used for this purpose in the United States. Efficacy of the antidepressants is limited largely by anticholinergic side effects (tricyclics) and by sleep disturbance and sexual dysfunction (SSRIs). Adequate nocturnal sleep time and planned daytime naps (when possible) are important preventative measures in narcolepsy.^

[CtrlAltDel]

ok...i've finished reading that...when can i collect my MBBS degree...?

[The Jackal]

ok...i've finished reading that...when can i collect my MBBS degree...?

You have a lot of patience.

[Alexis]

ok...i've finished reading that...when can i collect my MBBS degree...?

[The Jackal]

school books? how old are , or rather, what class/course r u studying?

Well some people even call college work school sometimes(mostly in the states),its sometimes confusing for us.

[whyldchyld]

all u got to do is ...two tea spoons of nyquill or robitussin evry nite after dinner and zzzzzzz,u wake up fresh next day , dont actually try it...mite get addicted

[igiveadamn]

er, thanks sujatha for that wonderful and informative textbook extract (though honestly i did not understand everything).



nyquill sounds like a good idea wyld. but like you said, it can get addictive. will exercise help???

[daisy]

school books? how old are , or rather, what class/course r u studying?

Well some people even call college work school sometimes(mostly in the states),its sometimes confusing for us.

exactly

[daisy]

ok...i've finished reading that...when can i collect my MBBS degree...?

[Sujatha]

Hi Igi,

mainly i have experienced insomnia out of job related stress.

the stimulating factors like

bad incidents in the hospital

death of patients,

some sort of enmity with coworkers etc etc

afterthat whole night i will be sleepless/ in semisleep.

next day morning with terrible insomnic condition we have to see around 100 OPD patients.

Its terrible

will exercise help???

definitely

when stress happens, i walk for around 5 KMS

definitely there is some relief

I rank walking as the No 1 Remedy for insomnia

[igiveadamn]

hmm walking sounds good. so is insomnia mainly caused due to stress? that means it's more to do with psychology?

[Sujatha]

that means it's more to do with psychology?

You can try with non medical theraphy like psycho social counselling.



Never start with drugs.

[dethslut]

how many of the FHDB members are insomniacs? has anyone here ever experienced chronic insomnia? if yes how did you get out of it?

i have nt really7 been an insomniac, but had a change in my biological clock for about 1 year. used to be up all night and slept with sunrise for a few hours to wake up again.

the best advice i could give u is .... judt go do some rigorous physical activity, it should help u heaps.

[sleepfreak]

how many of the FHDB members are insomniacs? has anyone here ever experienced chronic insomnia? if yes how did you get out of it?

Man i really do pity.insomnia the worst thing that can happen to anyone.i have been insomniacal the last three days unable to sleep coz i was down with a fever and the leg pains were killing.



anyways i have had my bouts of 6 monthly insomnias and i do know the cure for it.u have to really sweat it out and tire yourself out at some point of the day.personally i feel insomnia hits u hardest when u r goin thru a stressful period. well go for a half hour jog and see to it that u sweat.sweat is the only cure for insomnia.yeah and the usual cut the nicotine alcohol and caffeiene also does apply.oh and yes after all this try and read urself to sleep by reading a good happy story.

[solosynergy]

Any insomniacs in the house