18.11.2014
Both the hypothyroidism and Non-24 unbranded ad campaigns are so general, they apply to almost everyone.
Sleep paralysis occurs when a person is falling asleep or waking up, and involves a person being fully conscious, but unable to move their body. Sleep eating, also called Sleep-Related Eating Disorder, is considered a parasomnia where people get up in the middle of the night to eat, and generally do not remember the episode in the morning.
Those with the disorder may have difficulty falling asleep or staying asleep, and may wake up groggy or feeling as if they need more rest. Although most people who are totally blind still can perceive light well enough to prevent non-24, there may be as many as 100,000 individuals in the United States with this condition, who can’t perceive enough light to establish a normal night sleep schedule. Needs Assessment: Circadian rhythm sleep disorders (CRSDs) should be considered in the differential diagnosis of patients presenting with symptoms of insomnia or daytime sleepiness. During the past decade, there have been major advances in understanding the role of the circadian clock in the regulation of sleep and wakefulness. The essential feature of a circadian rhythm sleep disorder (CRSD) is that the pattern of sleep disturbance is due primarily to alterations of the circadian time-keeping system or a misalignment between the endogenous circadian rhythm and exogenous factors that affect the timing or duration of sleep.
The circadian rhythm sleep phase disorders, delayed sleep phase (DSP) and advanced sleep phase (ASP), occur when the timing of the major sleep period is delayed or advanced in relation to 24-hour clock time or desired sleep and wake time.
DSP must be distinguished from normal sleep patterns, particularly in adolescents and young adults who exhibit delayed schedules without complaints of impaired function. Although the exact mechanisms responsible for DSP are unknown, several explanations, such as a longer-than-usual endogenous circadian period or alterations in the entrainment of the circadian system could account for a persistently delayed phase relationship between the endogenous circadian rhythm and the desired or conventional times for sleep and wake.9 It has been suggested that the advance portion of the phase response curve to light may be unusually small,23 or lack of early morning light exposure (due to prolonged sleep in the morning) may promote the delayed sleep phase under normal light-dark cycles. Approaches aimed at resetting circadian rhythms, such as chronotherapy, timed bright light, and melatonin administration have been employed for the treatment of DSP. Exposure to bright light for 1–2 hours in the morning results in an advance of the phase of circadian rhythms, whereas evening light exposure causes phase delays. Several studies have demonstrated the potential benefits of melatonin administered in the evening.44-47 However, because the timing of administration and dose varied between studies, as well as the relative lack of large-scale controlled clinical trials, clinical guidelines for the use of melatonin in the treatment of DSP are not available. ASP syndrome is a sleep disorder in which there is a stable advance of the major sleep period, characterized by early evening sleepiness and wake-up times that are several hours earlier relative to conventional and desired times (Figure 1). ASP should be distinguished from normal sleep patterns, particularly in the elderly who maintain advanced schedules without distress or impaired functioning (morning types or larks). Although the precise mechanisms underlying the pathophysiology of ASP are unknown, several circadian-based mechanisms, such as an unusually short endogenous circadian period that is <24 hours,55 or decreased exposure or weakened response to entraining agents such as light and physical activity,57-59 may impair phase delays and promote an advanced sleep phase. In addition to sleep history, actigraphy and sleep diaries can be very useful to confirm the ASP pattern. When the diagnosis is unclear, or when another sleep disorder may be in the differential diagnosis, PSG is indicated. Non-entrained circadian sleep-wake disorder (non-24 hour sleep and wake disorder, free-running) is characterized by a steady daily delay drift of the major sleep period in which the circadian clock is not entrained to the physical and social 24-hour cycle (Figure 1).
The diagnosis of a non-entrained circadian sleep-wake disorder requires that the periodic sleep disturbances are due to the lack of a stable entrainment of circadian rhythms to the 24-hour physical environment. The average endogenous period of oscillation of the human circadian clock is slightly longer than 24 hours.72 Therefore, the high prevalence of non-entrained circadian rhythms in blind people is most likely due to the lack of photic entrainment. Irregular sleep-wake disorder (no circadian rhythm, grossly disturbed sleep-wake rhythm, low amplitude circadian rhythm) is characterized by lack of a clearly defined circadian sleep and wake cycle.
In addition to the clinical history, continuous monitoring of sleep and wake activity with actigraphy for a minimum of 2 weeks is the most useful diagnostic tool.
In certain populations, like the institutionalized elderly and those with dementia, lack of regular exposure to bright light and social schedules have been postulated to influence the development and maintenance of irregular sleep-wake patterns.87,88 Therefore, both dysfunction of circadian regulation and weakened exposure to environmental signals are likely involved in the etiology of irregular or arrhythmic sleep and wake patterns. Clinical management approaches have been aimed at enhancing the amplitude of circadian rhythms and their alignment to the external physical environment.
Shift work-associated sleep disorder is characterized by complaints of insomnia or excessive sleepiness that occur in relation to work hours that are scheduled during the usual sleep period. Symptoms of insomnia or excessive sleepiness should be differentiated from that due to other primary sleep disorders such as other circadian rhythm sleep disorders, obstructive sleep apnea syndrome, narcolepsy, or insufficient sleep related to inadequate opportunity for sleep. Disturbance of sleep and alertness is due to a misalignment between the circadian alerting process with the time that the worker needs to sleep.
Most of the strategies developed for adjustment to shift work have focused on the night shift worker.
In summary, management of shift work sleep disorder requires multimodal strategies that address circadian alignment, sleep hygiene, improving sleep and alertness, and, very importantly, psychosocial factors.
Treatment of jet lag symptoms should address the sleep loss associated with the time zone change, as well as circadian re-entrainment.
Since the lab tests and clinical trials that would establish safety for a new condition haven’t been done, patients are guinea pigs.
Sleep talking can involve complete monologues and complicated dialogues, or gibberish and mumbling.
Because light and dark are environmental cues for sleeping and waking, many people with this syndrome are blind, though some sighted people also have this disorder.
Non-24 is a chronic circadian rhythm (body clock) disorder in the blind that causes problems with the timing of sleep.
People with non-24 may find their sleep patterns reversed -- needing to sleep during the day and to be awake at night.


Sleep and wake behaviors are generated by a complex interaction of endogenous circadian and sleep homeostatic processes, as well as social and environmental factors. The circadian-related sleep disruption leads to insomnia or excessive daytime sleepiness that causes functional impairment or distress. A diagnosis of DSP or ASP requires a complaint of inability to fall asleep or maintain sleep at the desired or conventional time. When allowed to follow their preferred schedule, circadian phase of sleep is delayed and sleep quality is normal. Social and behavioral factors play an important role in the development and maintenance of the delayed sleep patterns. However, diagnostic studies such as actigraphy and sleep diaries can be very useful to confirm the delayed sleep phase pattern. In addition to an earlier circadian phase, it has been postulated that an age-related decrease in the accumulation of the homeostatic drive for sleep could also contribute to the advanced sleep phase in older adults.60 Genetic factors have been shown to also play an important role in the pathogenesis of ASP. Chronotherapy was one of the earliest treatment approaches proposed for ASP,49 in which, a 3-hour advance in sleep time every 2 days allowed the individual to shift to the desired later sleep schedule.
Sleep and wake times are variable, so that a major sleep or wake period is not seen within the usual 24-hour period. Actigraphic recordings show disturbed or low amplitude circadian rhythm with loss of the normal diurnal sleep-wake pattern.
The relation between the occurrence of disturbed sleep and work hour distribution should provide sufficient information to indicate the correct diagnosis. The excessive sleepiness is most likely the result of both cumulative sleep loss and decreased circadian alertness during night and early morning work shifts. In addition to the history, sleep diaries and actigraphy are very useful in demonstrating a disrupted sleep-wake pattern consistent with shift work sleep disorder. Symptoms of jet leg typically consist of general malaise, daytime sleepiness, difficulty sleeping, impaired performance, and gastrointestinal complaints.110 These symptoms usually last for several days with resolution occurring as the traveler adapts to the new time zone. That most clinical practices do not have the tools to assess circadian rhythm profiles, coupled with a relative lack of standardized clinical treatment guidelines, are barriers to effective diagnosis and treatment of these disorders. Hetlioz is said to be chemically related to the sleeping pill marketed as Rozerem (Ramelteon).
Scientists have found that the phenomenon occurs due to a disconnect between the brain and body during REM sleep. Improved understanding of diagnosis and treatment approaches to these disorders will lead to improved care of patients with sleep disorders.
Circadian rhythm sleep disorders (CRSD) occur when there is an alteration of the internal circadian timing mechanisms or a misalignment between the timing of sleep and the 24-hour social and physical environments.
These self-sustaining rhythms are regulated at a molecular level and persist in the absence of any external time cues with a period of approximately 24 hours.1 In mammals, the suprachiasmatic nuclei, located in the hypothalamus, contains a master circadian clock2-5 that not only generates circadian rhythms, but also maintains the temporal organization of these internal circadian rhythms to the external physical environment as well as to social and work schedules. The diagnosis of CRSD is primarily based on published criteria using either the International Classification of Sleep Disorders or the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-Revised (DSM-IV-TR).21 In addition to physiologic and environmental factors, maladaptive behaviors often influence the presentation and clinical course of CRSDs.
Diagnostic criteria should also include a delayed or advanced stably entrained sleep and wake cycle for a minimum period of at least 1 month, though preferably 3 months. Patients with DSP often report feeling most alert in the evening and most sleepy in the early morning. Behaviors such as attempts to fall asleep earlier result in prolonged sleep latency and may promote and perpetuate features of conditioned insomnia and activities; exposure to bright light into the late evening may promote the inability to sleep and exacerbate the delayed circadian phase.
Recordings of sleep diaries and actigraphy over a period of at least 2 weeks demonstrate delayed sleep onset and sleep offset, with sleep typically delayed until 2–6AM and wake-up times in the late morning or even early afternoon. However, in adolescents, in which behavioral factors often contribute to the delayed sleep phase, enforcement of regular sleep and wake times together with sleep hygiene are important components of clinical management. However, if conventional later bed and wake times are enforced, the PSG recording may show decreased sleep latency, decreased total sleep time, and shortened rapid eye movement sleep latency.
As with the circadian sleep phase disorders, actigraphy and sleep diaries are useful diagnostic tools for evaluation of non-entrained circadian sleep-wake disorder. Irregular sleep-wake disorder should be distinguished from poor sleep hygiene and voluntary maintenance of irregular sleep schedules, as seen with shift work and frequent transmeridian travel. Sleep disturbance is most commonly reported in association with night and early morning shifts.
Use of sedative hypnotics and stimulants, as well as substance dependency, should be considered as contributing factors and may exacerbate the symptoms of shift work sleep disorder.
Polysomnographic recordings may be useful if the nature of the sleep disturbance is unclear, or to evaluate for comorbid conditions such as sleep disordered breathing. Family responsibilities such as childcare and household chores decrease the amount of time allotted for sleep. Bright light resets the human circadian pacemaker independent of the timing of the sleep-wake cycle. The human phase response curve (PRC) to melatonin is about 12 hours out of phase with the PRC to light. Paradoxical timing of the circadian rhythm of sleep propensity serves to consolidate sleep and wakefulness in humans. The dependence of onset and duration of sleep on the circadian rhythm of rectal temperature.


Chronotherapy: resetting the circadian clocks of patients with delayed sleep phase insomnia. A multicenter study of sleep-wake rhythm disorders: clinical features of sleep-wake rhythm disorders.
Poor compensatory function for sleep loss as a pathogenic factor in patients with delayed sleep phase syndrome.
Association of structural polymorphisms in the human period3 gene with delayed sleep phase syndrome. A length polymorphism in the circadian clock gene Per3 is linked to delayed sleep phase syndrome and extreme diurnal preference.
Significant association of the arylalkylamine N-acetyltransferase (AA-NAT) gene with delayed sleep phase syndrome. Phase-shifting effects of bright morning light as treatment for delayed sleep phase syndrome.
Delayed sleep phase syndrome: A placebo-controlled cross-over study on the effects of melatonin administered five hours before the individual dim light melatonin onset. Daily social and physical activity increases slow-wave sleep and daytime neuropsychological performance in the elderly. The effect of evening bright light in delaying the circadian rhythms and lengthening the sleep of early morning awakening insomniacs.
Circadian sleep regulation in the absence of light perception: chronic non-24-hour circadian rhythm sleep disorder in a blind man with a regular 24-hour sleep-wake schedule. Larger phase angle between sleep propensity and melatonin rhythms in sighted humans with non-24-hour sleep-wake syndrome.
Non-24-hour sleep-wake syndrome in a sighted man: circadian rhythm studies and efficacy of melatonin treatment.
Long-term melatonin treatment in blind children and young adults with circadian sleep-wake disturbances. Effect of SCN lesions on sleep in squirrel monkeys: evidence for opponent processes in sleep-wake regulation. Circadian rest-activity rhythms in demented and nondemented older community residents and their caregivers. Bright light therapy: improved sensitivity to its effects on rest-activity rhythms in Alzheimer patients by application of nonparametric methods. Circadian rhythm disorders in sleep-waking and body temperature in elderly patients with dementia and their treatment. Effect of light treatment on sleep and circadian rhythms in demented nursing home patients. Shift work sleep disorder: prevalence and consequences beyond that of symptomatic day workers. Soon there was an unbranded website called the Wake-Up Squad to sell the disease without ever mentioning the drug. However, physiologic sleepiness and alertness, not only varies with prior waking duration but also exhibits circadian variation. Polysomnographic (PSG) parameters of sleep architecture, when performed at the natural delayed sleep times, are essentially normal for patients 28–31 years of age. When recorded over 2–4 weeks, these measures typically show a progressive daily delay drift in the timing of sleep and wake.
The sleep environment needs to be optimized to decrease daytime noise, darkened room, and adherence to healthy sleep habits.
Eastward travel (requiring advancing circadian rhythms and sleep-wake hours) is usually more difficult to adjust than westward travel. Wearing loose clothing during the flight and ear plugs and eyeshades may be helpful even after arrival to promote sleep. In humans, daily variation in physiologic sleep tendency reveals a biphasic circadian rhythm of wake and sleep propensity,16,17 with an increase in sleep tendency occurring between 2–4 PM, followed by a decrease in sleep tendency and increase in alertness that lasts through the early to mid-evening hours.
Individuals may use alcohol and excessive caffeine to cope with symptoms of insomnia and excessive sleepiness, which in turn, may exacerbate the underlying CRSD or other comorbid psychiatric disorders, such as depression.
However, if a conventional bedtime and wake up time is scheduled, PSG recording will show prolonged sleep latency and decreased total sleep time.
Eastward travel generally results in difficulty falling asleep and westward travel in difficulty maintaining sleep.110 In addition, other factors such as the air quality, diminished physical activity level, and discomfort likely contribute to the severity of symptoms. In addition to good sleep habits, timed exposure to bright light and melatonin can be used for the treatment of CRSD.
Thus, in addition to providing timing information, a primary role of the circadian pacemaker is to promote wakefulness during the day, which in turn facilitates the consolidation of sleep during the nighttime hours.16,18-20 The interaction between circadian and homeostatic processes typically allows for approximately 16 hours of wakefulness and 8 hours of sleep.
Rapid advances in understanding the physiologic, cellular, and molecular basis of circadian rhythm and sleep regulation will likely lead to improved diagnostic tools and treatments for CRSDs.



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