Getting Off Track: How Government Actions and Interventions Caused, Prolonged, and Worsened the Fina

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Actigraphy measures physical activity with a portable device usually including an accelerometer worn on the wrist. Data recorded can be stored for weeks and then downloaded into a computer. Sleep and wake time can be analyzed by analyzing the movement data. This approach to estimating sleep and wake time has been shown to correlate with polysomnographic measures in normal sleepers, with reduced values noted in patients with insomnia. Investigations do not always correlate well with the patient's experience of insomnia and cannot replace a thorough clinical evaluation. Hence, it is important to recognize that insomnia is a subjective clinical diagnosis, and therefore, a patient's subjective report of sleep difficulties should play the most important role in directing management in most cases.

It is also important to ask questions about the range of symptoms experienced and changes over time. Because insomnia is a patient-reported symptom, rather than a polysomnographically defined disorder, referral to a sleep laboratory for polysomnographic diagnosis should be reserved for cases in which another primary sleep disorder, such as obstructive sleep apnea or periodic movement disorder, is suspected, because these may require greater expertise in sleep medicine.

The term "primary" indicates that the insomnia is independent of any known physical or mental condition.

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The International Classification of Sleep Disorders 2[ 26 ] codes insomnia under the broad heading of dyssomnias, either intrinsic or extrinsic sleep disorders. Based on the severity, it classifies insomnia into three types as follows. The treatment of chronic insomnia consists of initially diagnosing and treating the underlying medical or psychological problems.

The identification of behaviors that may worsen insomnia follows and stopping or reducing them would help eliminate insomnia. Next, a possible trial of pharmacology can be tried, although the long-term use of drugs for chronic insomnia is controversial. This is in spite of the fact that the US FDA has approved three medications for the treatment of insomnia with no limitation on the duration of their use.

A trial of behavioral techniques to improve sleep, such as relaxation therapy, sleep restriction therapy, and reconditioning, is however useful. Behavioral intervention combined with pharmacologic agents may be more effective than either approach alone. Non-pharmacologic interventions for insomnia consist primarily of short-term cognitive-behavioral therapies. These methods act primarily by reducing heightened autonomic and cognitive arousal, modifying self-perpetuating maladaptive sleep habits, altering dysfunctional beliefs and attitudes about sleep, and educating patients about healthier sleep practices.

Evidence suggests that stimulus control therapy is effective and well suited for the clinical management of insomnia in the elderly[ 30 ] with effect sizes ranging from 0. Sleep restriction therapy consists of restricting the amount of time spent in bed to nearly match the subjective amount of time spent sleeping.

Periodic adjustments are made usually on a weekly basis until an optimal sleep duration is achieved. Sleep restriction therefore creates a mild state of sleep deprivation and is said to "promote a more rapid sleep onset, more efficient sleep, and less inter-night variability.

Evidence suggests that sleep restriction therapy is moderately effective with effect sizes ranging from 0. Relaxation-based interventions are based on the observation that insomnia patients often display high levels of arousal physiological and cognitive , both at night and during daytime. Progressive muscle relaxation and biofeedback techniques seek to reduce somatic arousal, whereas attention focusing procedures such as imagery training and thought stopping are intended to lower presleep cognitive arousal e. Additional relaxation therapies e.

Cognitive therapy seeks to alter faulty beliefs and attitudes about sleep. Examples of treatment targets for cognitive therapy include having unrealistic sleep expectations e. The advocates of cognitive therapy believe that "it consists of identifying patient-specific dysfunctional sleep cognitions, challenging their validity, and replacing them with more adaptive substitutes through the use of restructuring techniques such as reattribution training, decatastrophizing, hypothesis testing, reappraisal, and attention shifting.

Paradoxical intention is a method that consists of persuading a patient to engage in his or her most feared behavior, i. Thus, if a patient stops trying to sleep and contrarily attempts to stay awake, performance anxiety will be reduced and sleep may come more easily. This procedure may be conceptualized as a form of cognitive restructuring technique to alleviate performance anxiety.

Effect sizes reported have been moderate in sleep latency 0. Sleep hygiene education targets health practices e. Additional recommendations, which tend to overlap with stimulus control and sleep restriction, may also include curtailing daytime napping and time spent in bed. While poor sleepers are generally better informed about sleep hygiene, they also engage in more unhealthy practices than good sleepers.

Thus, the objectives of sleep hygiene are to promote better health practices. In a meta-analysis of sleep hygiene, effect size observed was modest in all parameters. Having the patient keep a sleep diary for 2 weeks may be helpful. Depending on the findings in the sleep diary, a discussion of sleep hygiene may be beneficial to the patient. Adopting the practices of good sleep hygiene is often helpful regardless of whether the patient has primary insomnia or a sleep disturbance related to a medical condition. Patients can condition themselves to be insomniacs, and treatment focuses on de-conditioning the patient from associating the bedroom with a place of restlessness.

There are three recently published meta-analyses which serve to establish the efficacy of psychological and behavioral methods. Significant effect sizes in sleep latency 0. Drug treatment is indicated for patients as short-term alleviation of insomnia but is insufficient for long-term management of chronic insomnia. In combination with behavioral therapy, it however, yields the most durable improvements in sleep patterns. Although clinical trials of pharmacotherapeutic agents recently approved by the FDA have demonstrated their efficacy and safety, common general practice dictates that five basic principles be followed which characterize rational pharmacotherapy for insomnia, especially chronic insomnia, in both adult and geriatric patients: These drugs carry the highest level of evidence supporting efficacy and safety.

Benzodiazepines are frequently prescribed to treat insomnia. These hypnotics reduce latency to sleep onset and total awakenings by increasing total sleep duration. Benzodiazepines enhance the effect of the inhibitory neurotransmitter gamma-amino butyric acid GABA by increasing the affinity of GABA for its receptor. Benzodiazepines non-selectively bind to an allosteric site and affect the GABA-A receptor complex to allow a greater number of chloride ions to enter the cell when GABA interacts with the receptor and therefore enhance the inhibitory action of GABA.

This accounts for their sedative, anxiolytic, myorelaxant, and anticonvulsant properties. Five benzodiazepines estazolam, flurazepam, quazepam, temazepam, and triazolam have an FDA-approved indication for the management of insomnia. Dose, distinguishing pharmacokinetic properties absorption rate, distribution, and elimination half-life , and risk-benefit ratio should be considered when selecting the most appropriate medication. The lowest effective dose should be used to minimize side effects, and long-acting benzodiazepines with active metabolites should be avoided in the elderly.

Major side effects of short-acting benzodiazepines include rebound insomnia and anterograde amnesia. Intermediate-and longer-acting benzodiazepines are less effective for inducing sleep, but are indicated for sleep maintenance and decreasing nocturnal awakenings. Accumulation of active metabolites is problematic in elderly patients and in those patients with impaired liver function as it can cause confusion and cognitive dysfunction. Benzodiazepines are contraindicated in patients with acute alcohol intoxication with depressed vital signs, a history of substance abuse, and during pregnancy.

Benzodiazepines should be used cautiously in patients with chronic pulmonary insufficiency or untreated sleep apnea. They are frequently used in mood disorders but a worsening of the dysphoric symptoms and precipitation of suicide has been noted in depression, while hypomania or frank mania and paradoxical hyper-excited states can also occur.

Non-benzodiazepine hypnotics include zopiclone, zolpidem, and zaleplon. Zopiclone is a non-benzodiazepine hypnotic of the cyclopryrrolone class. It is effective for reducing sleep latency and nocturnal awakenings and increasing total sleep time. Zopiclone delays the onset of rapid eye movement REM sleep but does not reduce consistently the total duration of REM periods. Rebound effects have been reported but are minimal. The incidence of adverse effects is low at recommended doses 3. Zolpidem is a non-benzodiazepine hypnotic of the imidazopyridine class.

It exhibits hypnotic effects with minimal myorelaxant, anticonvulsant, and anxiolytic properties, as it preferentially binds with the GABA-A receptor complexes with an alpha-1 subtype. Zolpidem is effective for reducing sleep latency and nocturnal awakenings and increasing total sleep time. Rebound effects are minimal.

Common side effects include drowsiness, dizziness, and headache. Zaleplon, like zolpidem, belongs to the imidazopyridine class of non-benzodiazepine hypnotics. The pharmacology of these two drugs is similar; however, zaleplon has an ultra-brief duration of effect.

No next-day sedation or rebound insomnia is documented with zaleplon at recommended doses 5—10 mg. Eszopiclone, which is the active stereoisomer of zopiclone, acts as an agonist at benzodiazepine BNZ receptors. Well absorbed orally, about 3 mg of eszopiclone is equivalent to 10 mg of diazepam. It has also recently been approved for the treatment of insomnia and is the only non-scheduled prescription drug available in the United States for the treatment of insomnia.

It has been shown to be effective in the elderly.

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These drugs have moderate level of evidence supporting their efficacy and tolerability. Tricyclic antidepressants TCAs such as amitriptyline, doxepin, and nortriptyline are effective for inducing sleep and improving sleep continuity. The overdose potential of TCAs is greater than with other hypnotic agents, and daytime sedation can be significant. Trazodone is a potent sedating antidepressant. Trazodone improves sleep continuity and is an attractive option in persons prone to substance abuse, as addiction or tolerance is not a problem.

Adrenergic blockade can result in oversedation and orthostatic hypotension, especially in elderly patients. The risk of priapism, a condition of painful, prolonged erection in men, is rare. Other antidepressants used include Mirtazapine due to its sedative properties. Evidence for their efficacy when used alone is relatively weak and hence no specific agent within this group is recommended as preferable to the others in this group.

Antihistamines are found in many over-the-counter OTC sleep aids. These agents are effective for mild insomnia; however, next-day sedation may be a problem. Antihistamines commonly cause psychomotor impairment and anticholinergic effects. Tolerance may also develop with repeated use and evidence for their efficacy and safety is very limited. These are drugs with variable evidence and are useful only in individual cases. Valerian is a perennial plant that appears to increase GABA concentrations in animal studies, but its exact mechanism is not known.

Valerian should not be used for the acute management of insomnia because its hypnotic effect is delayed for 2—4 weeks. Valerian appears to be well tolerated; however, it can cause headache and daytime sedation[ 63 ] and is currently still being evaluated. Other herbs used to promote sleep include skullcap, passion flower, California poppy, and Lemon balm. The recommended drugs according to the level of clinical evidence are summarized in Table 3.

The prevalence of chronic insomnia is quite high, yet remains under-diagnosed. It is imperative to recognize it since it may result in increased healthcare utilization, lower quality of life and social relationships, and decrements in memory, mood, and cognitive function. Based on recommendations, an algorithm for treatment is proposed below. National Center for Biotechnology Information , U.

Ann Indian Acad Neurol. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Chronic, diagnosis, insomnia, treatment.

Oh sleep, Oh gentle sleep, Nature's soft nurse How have I frighted thee? That though no more will weigh mine eyelids down And sleep my senses in forgetfulness? Henry IV, William Shakespeare. Introduction The word "insomnia' originates from the Latin "in" no and "somnus" sleep. Results and Discussion Definition of chronic insomnia Although there are various definitions of chronic insomnia, the most widely accepted[ 16 ] is the one that defines it to be a condition characterized by "inadequate quantity or quality of sleep characterized by a subjective report of difficulty with sleep initiation, duration, consolidation, or quality that occurs despite adequate opportunity for sleep, and that results in some form of daytime impairment and has persisted for at least one month".

Evaluation of a patient with insomnia As insomnia is both a symptom and a disorder in itself, detailed evaluation of the problem is imperative before reaching a clinical diagnosis. The mandatory assessment of insomnia includes the following. Sleep history Sleep history is the first step in evaluation of primary insomnia, which provides the clinician with a structured approach to a diagnosis.

Primary area of focus Sample questions What is the nature and severity of the problem? What are the day time consequences of your sleep problem?

Book Review: Getting Off Track by John B. Taylor

Is it related to season, menstrual cycle or any other cyclical factors? Is the patient's environment disturbing? Is there anything in your home that disturbs your sleep such as loud TV, pets, infants, noise, lights, etc.? What is the patient's sleep routine?

Introduction

At what time do you get into bed and try to sleep? At what time do you get up in the morning? How many hours in the night do you actually sleep out of total time spent in bed? Is your occupation timings causing the sleep problems? Do you sleep during the day or evening? What do you do each night before going to bed?

Open in a separate window. Use of prescription drugs Various prescription drugs may be responsible for chronic insomnia. Sleep diary or sleep log A sleep diary helps in specifically estimating the severity of the problem, the night to night variability, and presence of maladaptive habits such as taking naps or spending excessive time in bed more than 8 hours. Sleep and psychological rating scale Epworth Sleepiness Scale ESS rates the chance of dozing in the following situations[ 21 ] which may be during sitting and reading, watching television, sitting inactively in a public place, being a passenger in a car for an hour without a break, during lying down to rest in the afternoon, sitting and talking to someone, sitting quietly after lunch without alcohol or while waiting at a traffic signal in a car.

The ESS is rated on a 4-point scale for each of the above factors based on the following scores: Focused physical examination A general physical examination may help assess certain organic pathologies such as chronic obstructive pulmonary diseases COPD , asthma, or restless leg syndrome which may disturb sleep. Blood tests Blood tests may help to rule out subtle manifestations of thyroid diseases, iron deficiency anemia, and vitamin B12 deficiency restless leg syndrome.

Polysomnography It is considered the gold standard for measuring sleep. Actigraphy Actigraphy measures physical activity with a portable device usually including an accelerometer worn on the wrist. Summary of investigations Investigations do not always correlate well with the patient's experience of insomnia and cannot replace a thorough clinical evaluation. Table 2 Diagnosis of primary insomnia.

The predominant complaint is difficulty initiating or maintaining sleep, or non-restorative sleep, for at least 1 month. The sleep disturbance or associated daytime fatigue causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. The sleep disturbance does not occur exclusively during the course of narcolepsy, breathing-related sleep disorder, a circadian rhythm sleep disorder or a parasomnia.

The disturbance does not occur exclusively during the course of another mental disorder e. The disturbance is not due to the direct physiological effects of a substance e. This term describes an almost nightly complaint of an insufficient amount of sleep or not feeling rested after the habitual sleep episode. It is accompanied by little or no evidence of impairment of social or occupational functioning. Mild insomnia is often associated with feelings of restlessness, irritability, mild anxiety, daytime fatigue, and tiredness. This term describes a nightly complaint of an insufficient amount of sleep or not feeling rested after the habitual sleep episode.

It is accompanied by mild or moderate impairment of social or occupational functioning. Moderate insomnia is always associated with feelings of restlessness, irritability, anxiety, daytime fatigue, and tiredness.

It is accompanied by severe impairment of social or occupational functioning. Severe insomnia is associated with feelings of restlessness, irritability, anxiety, daytime fatigue, and tiredness. Treatment of Chronic Insomnia The treatment of chronic insomnia consists of initially diagnosing and treating the underlying medical or psychological problems. Non-pharmacologic management strategies Non-pharmacologic interventions for insomnia consist primarily of short-term cognitive-behavioral therapies.

Sleep restriction Sleep restriction therapy consists of restricting the amount of time spent in bed to nearly match the subjective amount of time spent sleeping. Relaxation therapies Relaxation-based interventions are based on the observation that insomnia patients often display high levels of arousal physiological and cognitive , both at night and during daytime. Cognitive therapy Cognitive therapy seeks to alter faulty beliefs and attitudes about sleep. Paradoxical intention Paradoxical intention is a method that consists of persuading a patient to engage in his or her most feared behavior, i.

Sleep hygiene education Sleep hygiene education targets health practices e. Behavioral intervention Having the patient keep a sleep diary for 2 weeks may be helpful. Summary of non-pharmacologic strategies There are three recently published meta-analyses which serve to establish the efficacy of psychological and behavioral methods. Pharmacologic management strategies Drug treatment is indicated for patients as short-term alleviation of insomnia but is insufficient for long-term management of chronic insomnia.

The therapeutic options include the following.

First line pharmacotherapy These drugs carry the highest level of evidence supporting efficacy and safety. Arguably, the ideas and research behind the Taylor Rule are given some credit for the reduction in the volatility of both inflation and the growth rate of real GDP, and the reduction in the frequency of recessions between and For example, in the 20 years previous to this period there were recessions every 3 to 4 years while during this period there were only two recessions which were 8 years apart.

The first policy blunder can be laid at the feet of the Federal Reserve System and its fear that the U. According to the Taylor policy rule, the Federal Funds rate should have begun rising by the end of and increased at a relatively steady pace to 5. One can argue, therefore, that there exists explicit empirical evidence of the over-reaching of the Federal Reserve during this period of time. Similar evidence exists for countries within the European Union. The events leading up to this move by the Federal Reserve actually kicked off on August 9 and 10 of that year.

Late in and early in delinquencies and foreclosures started to shoot up in the housing sector. These problems became amplified because they connected directly with the adjustable-rate sub-prime mortgage market and mortgage-backed securities. The real difficulty was that there developed a lot of bad mortgages, but it was very, very difficult to identify where the bad mortgages were located. On August 9 and 10, , the interest rate spread between the three-month London Inter-bank Offered Rate Libor and the three-month overnight index swap OIS jumped from about 10 basis points where it had averaged for a long time to a range of roughly 60 to basis points.

An argument developed over the reason for this jump. To some, especially in the Fed, the increase in this spread represented a lack of liquidity. To others this increase was because of Counterparty risk: Taylor argues that this did not solve the problem, the spread remained high, and this move by the Fed only prolonged the crisis.

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