Fractured sleep, Ambien, dial wingin' and other things

General Discussion on any topic relating to CPAP and/or Sleep Apnea.
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robysue
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Re: Fractured sleep, Ambien, dial wingin' and other things

Post by robysue » Thu Mar 20, 2014 9:25 am

There's been some discussion about my hand and foot pain in this thread.

So I thought I'd clarify what I'm talking about.

For several years before starting CPAP I was waking up with moderate to severe pain in my hands and feet. I would describe the pain to my hubby as "It felt like I slept with my hands and feet in fists all night." The pain was confined to my hands and feet.

The pain in the feet was similar to what you get if you arch your foot and curve your toes towards the heels as far as you can and hold them in that position as long as you can. The pain in the hands was exactly like what you get if you make tight fists and hold them in that position long enough for them to start hurting.

I would wake up with my hands in actual fists much of the time. On the worst mornings, I'd actually have to pry my hands out of the "fist" shape. Both the hands and feet would hurt and be very, very stiff upon waking. As the day progress, the pain would dissipate and the stiffness would improve. By bedtime, usually the hands and feet were free of pain and stiffness, but the next morning the pain and stiffness were once again present and moderate to severe in intensity.

I complained to my PCP a number of times about this pain. At one point he did have some x-rays done and they may have shown some minor arthritis. He also ordered some kind of a test that measured some sort of inflammation as I vaguely recall. (We're talking about tests that were done over a decade ago, and I wasn't keeping track of all the medical stuff then, because other than the hand and foot pain, there wasn't any medical stuff to keep track of.) At any rate, the tests were inconclusive in that they indicated some mild inflammation, but nothing was far enough out of line to be diagnosed with anything. (At the time, the doc was thinking in terms of rheumatoid arthritis, lupus, and some other things I don't recall.) Eventually, the doc settled on a diagnosis of mild arthrities, type not specified. And I was told to take ibuprofen as needed for the pain.

During the First War on Insomnia, I was asked to track how I felt each morning upon rising, in addition to a whole bunch of other things. About 5 months into PAPing and 6 weeks into keeping the sleep log, the phrase, "I woke up without hand or foot pain this morning" started to appear in the sleep logs. By six months into PAPing, that phrase was appearing almost every morning in the sleep logs. By 8 or 9 months into PAPing, I was no longer keeping careful track of when the pain was ABSENT, because that had become the new norm. On the rare days where pain was around, that was what got noted.

And at the time that the pain first started disappearing, nothing much had changed except for starting PAP. (The pain started to disappear when I was between trials of migraine prophylatics meds that I could not tolerate.) Hence my conclusion that the PAP must have had some positive effect on the hand and foot pain.

This past summer, there were three nights where I did not sleep with my BiPAP. And after each one of those nights, the old "slept with my hands and feet in fists" pain came back big time. As soon as I returned to PAPing, the pain went away.

And so, regardless of whether it makes any sense or not, one of the main reasons I keep on PAPing is the fact that with PAP I wake up with NO hand or foot pain almost every single day. And that's a huge positive difference over how I used to wake up pre-CPAP.

***********
Other pain:

I also think that some other pain issues have gotten mixed up in the discussion. Since starting PAP I have had a serious break in my left pinky finger and a grade 2 MCL tear in my right knee. During the acute pain stage of each injury, pain definitely adversely affected the quality of my sleep. But as the pain subsided, the sleep also got better.

I injured my left knee last October in a fall and the limping then seriously aggravated my lower back. Over Veteran's Day weekend last November, I woke up in agony from the back pain. And yes, that pain definitely affected the sleep. I did a full course of PT for the back in Dec, Jan, and Feb, and the back is feeling better than it's felt in years (most days). The knee continued to give me problems and had some pain issues; a cortisone shot in Feb followed by (on-going) PT for the knee seems to be resolving this problem.

So perhaps this last round of bad sleep has been triggered by the knee/back pain that I've dealing with since late October and November. In that case, there's reason to hope that my sleep will get back to "sort of decent" as the last of the knee pain disappears.

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Re: Fractured sleep, Ambien, dial wingin' and other things

Post by avi123 » Thu Mar 20, 2014 2:08 pm

About those hands and feet you did mention:

Early rheumatoid arthritis tends to affect your smaller joints first — particularly the joints that attach your fingers to your hands and your toes to your feet. As the disease progresses, symptoms often spread to the knees, ankles, elbows, hips and shoulders. In most cases, symptoms occur in the same joints on both sides of your body.

Rheumatoid arthritis signs and symptoms may vary in severity and may even come and go. Periods of increased disease activity, called flares, alternate with periods of relative remission — when the swelling and pain fade or disappear. Over time, rheumatoid arthritis can cause joints to deform and shift out of place.

When to see a doctor

Make an appointment with your doctor if you have persistent discomfort and swelling in your joints.


In my case it is lack of circulation or/and Dupuytren's Disease and DeQuervain's Tendonitis in my hands and fingers.

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Re: Fractured sleep, Ambien, dial wingin' and other things

Post by robysue » Thu Mar 20, 2014 11:32 pm

avi123 wrote:About those hands and feet you did mention:

Early rheumatoid arthritis tends to affect your smaller joints first — particularly the joints that attach your fingers to your hands and your toes to your feet.
... In most cases, symptoms occur in the same joints on both sides of your body.
This was why the doc was thinking RA at the time I developed the hand and foot pain over a decade ago. He did testing for RA (both a series of blood tests and some xrays); the results were ambigious. Since there was very little to no redness or swelling in the joints I never did get a formal diagnosis.

Back in July 2010 at the physical exam where I got the referral for the sleep test, I also had a referral to a rheumatologist because I was complaining the pain was still around, was really bad during the first hour after waking (which is typical of RA) and was perhaps beginning to get worse. However, in the great Crash and Burn that followed the start of CPAP, calling a rheumatologist simply dropped off the radar screen---there were too many other more serious problems (in terms of the quality of my daily life) that took precedence. And by the time I got my head back above water and was beginning to function again, the hand and foot pain had disappeared. And it's not come back since, except on the handful of nights where the machine AHI has been excessively high (above 4.0) and the three nights last summer that I had no PAP.

The xrays done this fall when I fell and injured my left knee and my back started giving me so much trouble showed nothing in the knee, but there is some minor arthritis in the lower spine. The ultrasound done in Feb on the left knee indicated that there's some very mild OA in that joint. Since completing the PT for the back, I've got my full range of motion back and unless I sit too long, there's no back pain to speak of. The knee pain is still coming from the irritated bursa, but it's now down to very intermittent pain and I'm no longer constantly aware of the knee anymore---I'll finish up my PT for the knee next week most likely.

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Re: Fractured sleep, Ambien, dial wingin' and other things

Post by Sludge » Fri Mar 21, 2014 3:49 am

robysue wrote:We'll quit calling my problem insomnia.
OK, that'll make creating a plan far more simple ("you have to know...").
robysue wrote:So is it better to do the "sleep wingin" this summer or not?
If one knows what they're trying to fix, one does not have to resort to "wingin''" any more, one can move right to "doin'".

The 2 choices appear to be:
  • Let the DSPS settle where it wants to; and
  • Treat it.
What I'm hearing is that "settle where it wants to" does result in the DSPS creating a problem, so an attempt should be made to fix it. Referring to above Company Guidelines, you have 3 accepted approaches:
  • Prescribed Sleep Scheduling
  • Timed Light Exposure
  • Timed Melatonin Administration
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Re: Fractured sleep, Ambien, dial wingin' and other things

Post by Sludge » Fri Mar 21, 2014 4:17 am

Sludge wrote:
robysue wrote:We'll quit calling my problem insomnia.
OK, that'll make creating a plan far more simple ("you have to know...").
However, (and in "IMHO"), that does not mean that some degree is not present.
robysue wrote:...my already pretty good sleep hygiene...
Although it is very difficult for me to bring up anything that might result in controversy, I think I might disagree with this point (to some extent, anyway).

One of the most important concepts in sleep is don't think about it, just do it.

So I'm looking at March 18 where you put up 17 (SEVENTEEN!!) RS-sized posts, so I'm thinking, "Whoa, she's so wound up, she ain't sleeping a wink tonight!"

Of course, you might say that's a canoe full of bat crap cause
RS wrote:...I've now had the extremely rare occasion of two exceptionally good night's sleep in a row.
However, sleep is exceedingly complex, and the Company Line is still Do Not Spend A Lot of (Any)Time Concerned (Obsessed) About Sleep.
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Re: Fractured sleep, Ambien, dial wingin' and other things

Post by echo » Fri Mar 21, 2014 9:20 am

Sludge wrote: What I'm hearing is that "settle where it wants to" does result in the DSPS creating a problem, so an attempt should be made to fix it. Referring to above Company Guidelines, you have 3 accepted approaches:
  • Prescribed Sleep Scheduling
  • Timed Light Exposure
  • Timed Melatonin Administration
And light restriction at night, including blue-blocking glasses and/or filters for computer/phone screens to block the blue spectrum and reduce light intensity + red lightbulbs.

http://www.circadiansleepdisorders.org/treatments.php
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Re: Fractured sleep, Ambien, dial wingin' and other things

Post by avi123 » Fri Mar 21, 2014 10:30 am

Roby Sue, about those fists in the hands and feet which are clear indication of RA I am ready to ask Dr William St. Clair about it. I am with friendly relations with him. It seems to me that there is a straight forward test for RA:

http://www.rheumatology.org/about/newsr ... claire.asp

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Re: Fractured sleep, Ambien, dial wingin' and other things

Post by avi123 » Wed Oct 07, 2015 6:39 pm

A new report about insomnia:

http://www.nejm.org/doi/full/10.1056/NE ... ?query=TOC


"A 77-year-old overweight woman with hypertension and arthritis reports that she has had trouble sleeping for “as long as I can remember.” She has taken hypnotic medications nightly for almost 50 years; her medication was recently switched from lorazepam (1 mg), which had been successful, to trazodone (25 mg) by her primary care physician, who was concerned about her use of the former. She spends 9 hours in bed, from 11 p.m. to 8 a.m. She has only occasional difficulty falling asleep, but she awakens two to three times per night to urinate and lies in bed for over an hour at those times, “just worrying.” How should her case be managed?




The Clinical Problem

Dissatisfaction with sleep owing to difficulty falling asleep or staying asleep or to waking up too early is present in roughly one third of adults on a weekly basis.1 For most, such sleep difficulties are transient or of minor importance. However, prolonged sleeplessness is often associated with substantial distress, impairment in daytime functioning, or both. In such cases, a diagnosis of insomnia disorder is appropriate. Reductions in perceived health2 and quality of life,3 increases in workplace injuries and absenteeism,4 and even fatal injuries5 are all associated with chronic insomnia. Insomnia symptoms may also be an independent risk factor for suicide attempts and deaths from suicide, independent of depression.6 Neuropsychological testing reveals deficits in complex cognitive processes, including working memory and attention switching,7 which are not simply related to impaired alertness.




Key Clinical Points

Insomnia Disorder

Prolonged insomnia is associated with an increased risk of new-onset major depression and may be an independent risk factor for heart disease, hypertension, and diabetes, especially when combined with sleep times of less than 6 hours per night.


Evaluation of a patient with insomnia should include a complete medical and psychiatric history and a detailed assessment of sleep-related behaviors and symptoms.


Cognitive behavioral therapy, which includes setting realistic goals for sleep, limiting time spent in bed, addressing maladaptive beliefs about sleeplessness, and practicing relaxation techniques, is the first-line therapy for insomnia.


In those with acute insomnia due to a defined precipitant, use of Food and Drug Administration–approved hypnotic medications is indicated.


Long-term use of benzodiazepine-receptor agonists, low-dose antidepressants, melatonin agonists, or an orexin antagonist should be considered for patients with severe insomnia that is unresponsive to other approaches.



Older diagnostic systems attempted to distinguish “primary” from “secondary” insomnia on the basis of the inferred original cause of the sleeplessness. However, because causal relationships between different medical and psychiatric disorders and insomnia are often bidirectional, such conclusions are unreliable. In addition, owing to the poor reliability of insomnia subtyping8 based on phenotype or pathophysiology, the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders9 takes a purely descriptive approach that is based on the frequency and duration of symptoms (Table 1Table 1
Criteria for the Diagnosis of Insomnia Disorder.
), allowing a diagnosis of insomnia disorder independent of, and in addition to, any coexisting psychiatric or medical disorders. The clinician should monitor whether treatment of such coexisting disorders normalizes sleep, and if not, treat the insomnia disorder independently.


Coexisting Conditions

Insomnia is more common in women than in men, and its prevalence is increased in persons who work irregular shifts and in persons with disabilities.2 Although the elderly are more likely than younger people to report insomnia symptoms, actual insomnia diagnoses are not more frequent in the elderly, because the effects of sleeplessness on daytime functioning appear to be less dramatic. Roughly 50% of those with insomnia have a psychiatric disorder,10 most commonly a mood disorder (e.g., major depressive disorder) or an anxiety disorder (e.g., generalized anxiety disorder or post-traumatic stress disorder). Various medical illnesses are also associated with insomnia, particularly those that cause shortness of breath, pain, nocturia, gastrointestinal disturbance, or limitations in mobility.11

Although roughly 80% of those with major depressive disorder have insomnia, in nearly one half of those cases, the insomnia predated the onset of the mood disorder.12 A meta-analysis of more than 20 studies concluded that persistent insomnia is associated with a doubling of the risk of incident major depression.13 Associations have also been reported between insomnia and increased risks of acute myocardial infarction and coronary heart disease,14 heart failure,15 hypertension,16 diabetes,17 and death,18 particularly when insomnia is accompanied by short total sleep duration (<6 hours per night).19


Prevalence and Natural History

Insomnia is the most common sleep disorder, with a reported prevalence of 10 to 15%, depending on the diagnostic criteria used.1,2 Insomnia symptoms commonly wax and wane over time, though roughly 50% of those with more severe symptoms who meet criteria for insomnia disorder have a chronic course.20 The 1-year incidence of insomnia is approximately 5%. Difficulty maintaining sleep is the most common symptom (affecting 61% of persons with insomnia), followed by early-morning awakening (52%) and difficulty falling asleep (38%); nearly half of those with insomnia have two or more of these symptoms.11 Manifestations of insomnia often change over time; for example, a person may initially have difficulty falling asleep but subsequently have difficulty staying asleep, or vice versa.


Pathophysiology

Insomnia is commonly conceptualized as a disorder of nocturnal and daytime hyperarousal, which is both a consequence and a cause of insomnia and is expressed at cognitive and emotional as well as physiological levels.21 People with insomnia often describe excessive worry, racing thoughts, and selective attention to arousing stimuli. Hyperarousal is manifested physiologically in those with insomnia as an increased whole-body metabolic rate, elevations in cortisol level, increased whole-brain glucose consumption during both the waking and the sleeping states, and increased blood pressure and high-frequency electroencephalographic activity during sleep.21




Strategies and Evidence


Evaluation

The evaluation of insomnia requires assessment of nocturnal and daytime sleep-related symptoms, their duration, and their temporal association with psychological or physiological stressors. Because there are many pathways to insomnia, a full evaluation includes a complete medical and psychiatric history as well as assessment for the presence of specific sleep disorders (e.g., sleep apnea or the restless legs syndrome). Questioning the patient regarding thoughts and behaviors in the hours before bedtime, while in bed attempting to sleep, and at any nocturnal awakenings may provide insight into processes interfering with sleep. A daily sleep diary documenting bedtime, any awakenings during the night, and final wake time over a period of 2 to 4 weeks can identify excessive time in bed and irregular, phase-delayed, or phase-advanced sleep patterns.

There is often a mismatch between self-reported and polysomnographically recorded sleep in those with insomnia, in which the self-reported time to fall sleep is overestimated and total sleep time is underestimated.22 Because polysomnography cannot distinguish those with insomnia from those without it,23 the diagnosis of insomnia is made clinically. Polysomnography is not indicated in the evaluation of insomnia unless sleep apnea, periodic limb movement disorder, or an injurious parasomnia (e.g., rapid-eye-movement [REM] sleep behavior disorder) is suspected or unless usual treatment approaches fail.


Management

The choice of treatment of insomnia depends on the specific insomnia symptoms, their severity and expected duration, coexisting disorders, the willingness of the patient to engage in behavioral therapies, and the vulnerability of the patient to the adverse effects of medications. Patients with an acute onset of insomnia of short duration often have an identifiable precipitant (e.g., a medical illness or the loss of a loved one). In such cases, Food and Drug Administration (FDA)–approved pharmacologic agents (discussed below) are recommended for short-term use. In patients with chronic insomnia, appropriate treatment of coexisting medical, psychiatric, and sleep disorders that contribute to insomnia is essential for improving sleep. Nevertheless, insomnia is often persistent even with proper treatment of these coexisting disorders.24

Treatment for chronic insomnia includes two complementary approaches: cognitive behavioral therapy and pharmacologic treatments.


Cognitive Behavioral Therapy (CBT)

CBT addresses dysfunctional behaviors and beliefs about sleep that contribute to the perpetuation of insomnia (Table 2Table 2
Components of Cognitive Behavioral Therapy for Insomnia.
), and it is considered the first-line therapy for all patients with insomnia,25 including those with coexisting conditions.26 CBT is traditionally delivered in either individual or group settings over six to eight meetings. In a meta-analysis of randomized, controlled trials involving persons with insomnia without coexisting conditions, CBT had significant effects on time to sleep onset (mean difference [CBT group minus control group], −19 minutes) and time awake after sleep onset (mean difference, −26 minutes), though benefits with regard to total sleep time were small (mean difference, 8 minutes), a finding consistent with the restrictions on overall time spent in bed.27 The benefits were generally maintained in studies lasting 6 to 12 months. In short-term, randomized trials comparing behavioral treatments with benzodiazepine-receptor agonists (discussed below) in persons with insomnia without coexisting conditions, CBT had less immediate efficacy, but the intervention groups did not differ significantly in time to sleep onset or total sleep time at 4 to 8 weeks,28 and CBT was superior when assessed 6 to 12 months after treatment discontinuation.29 A barrier to the implementation of CBT is the lack of providers with expertise in its delivery. This limitation has begun to be addressed by the use of shorter therapies30 and Internet-based CBT,31 which have shown efficacy similar to that of longer and face-to-face delivery of CBT. However, sleep hygiene alone (Table 2), which is commonly recommended as an initial approach for insomnia, is not an effective treatment for insomnia.32

Adherence to CBT is less than optimal in clinical practice,33 probably as a result of the extensive behavioral changes required (e.g., reducing time spent in bed and getting out of bed when awake), the delay in efficacy (during which there are often short-term reductions in total sleep time),34 and pessimism that such approaches can be effective.


Pharmacologic Therapy

Several medications, with differing mechanisms of action, are used to treat insomnia, reflecting the multiple neural systems that regulate sleep (Table 3Table 3
Medications Commonly Used for Insomnia.
). Roughly 20% of U.S. adults use a medication for insomnia in a given month,35 and many others use alcohol for this purpose. Nearly 60% of medication use is with nonprescription sleep aids, primarily antihistamines. In the few existing placebo-controlled trials, however, diphenhydramine had at best modest benefit for either mild intermittent insomnia36 or insomnia in the elderly37 and caused daytime sedation and anticholinergic side effects (e.g., constipation and dry mouth) that are particularly problematic in older persons.


Benzodiazepine-Receptor Agonists

Benzodiazepine-receptor agonists include agents with a benzodiazepine chemical structure and “nonbenzodiazepines” without this structure. There is little convincing evidence from comparative trials that these two subtypes differ from each other in clinical efficacy or side effects. Because benzodiazepine-receptor agonists vary predominantly in their half-life, the specific choice of drug from this class is usually based on the insomnia symptom (e.g., difficulty initiating sleep vs. difficulty maintaining sleep). FDA approval of these medications is for bedtime use, with the exception of specifically formulated sublingual zolpidem (1.75 mg for women and 3.5 mg for men). Although not FDA-approved or rigorously studied for middle-of-the-night use, short-acting agents (e.g., zolpidem at a dose of 2.5 mg, and zaleplon at a dose of 5 mg) can also be used effectively to promote a return to sleep as long as 4 hours remain before the user plans to get up in the morning. The use of very-long-acting benzodiazepines (e.g., clonazepam, which has a half-life of 40 hours) for uncomplicated insomnia (i.e., in the absence of a daytime anxiety disorder) is not recommended owing to the risk of daytime side effects.

In a meta-analysis of randomized, controlled polysomnographic trials involving patients with chronic insomnia without coexisting conditions, benzodiazepine-receptor agonists showed significant effects on time to sleep onset (mean difference [group receiving benzodiazepine-receptor agonist minus control group], −22 minutes), time awake after sleep onset (mean difference, −13 minutes), and total sleep time (mean difference, 22 minutes).38 In placebo-controlled trials, persistent self-reported efficacy for insomnia was shown for nightly use of eszopiclone for 6 months39 and for intermittent use of extended-release zolpidem over a period of 6 months.40 A randomized, controlled trial involving patients with chronic insomnia showed that as compared with CBT alone, the combination of CBT and a benzodiazepine-receptor agonist was associated with a larger increase in total sleep time at 6 weeks as well as a higher remission rate at 6 months.29

Benzodiazepine-receptor agonists have a number of potential acute adverse effects, including daytime sedation, delirium, ataxia, anterograde memory disturbance, and complex sleep-related behaviors (e.g., sleepwalking and sleep-related eating, which are most common with the short-acting agents). As a result, they have been associated with an increase in motor-vehicle accidents41 and, in the elderly, falls (albeit inconsistently)42 and fractures. Recent longitudinal research suggests an association of long-term use of benzodiazepines with Alzheimer’s disease,43 but interpretation of these results is complicated by the possibility of confounding by indication, because anxiety and insomnia may be early manifestations of this disorder. Abuse of these agents is uncommon among persons with insomnia,44 but they should not be prescribed to persons with a history of substance or alcohol dependence or abuse.

Regular reassessment of the benefits and risks of benzodiazepine-receptor agonists is recommended. If discontinuation is indicated, gradual, supervised tapering (e.g., by 25% of the original dose every 2 weeks), in combination with CBT for insomnia, is strongly recommended for chronic users. Roughly one third of patients who used these discontinuation methods had resumed benzodiazepine use by 2 years of follow-up.45


Sedating Antidepressants

The use of sedating antidepressants to treat insomnia takes advantage of the antihistaminergic, anticholinergic, and serotonergic and adrenergic antagonistic activity of these agents. At the low doses commonly used for insomnia, most have little antidepressant or anxiolytic effect. Although data from controlled trials to support its use in insomnia are limited, trazodone is used as a hypnotic agent by roughly 1% of U.S. adults,35 generally at doses of 25 to 100 mg. Its side effects include morning sedation, orthostatic hypotension (at higher doses), and (in rare cases) priapism. Doxepin, a tricyclic antidepressant, is FDA-approved for the treatment of insomnia at doses of 3 to 6 mg. It has shown significant effects on sleep maintenance (time awake after sleep onset and total sleep time) but no significant benefit for sleep-onset latency beyond 2 days of treatment.46 Few side effects were observed at these doses. Mirtazapine has antidepressant and anxiolytic efficacy at doses used for insomnia and is a reasonable first option if patients have insomnia coexisting with those disorders, but it may cause substantial weight gain.


Other Agents

The orexin antagonist suvorexant, which was approved by the FDA in 2014 for the treatment of insomnia, showed decreased time to sleep onset, decreased time awake after sleep onset, and increased total sleep time in short-term randomized trials.47 At higher doses (30 to 40 mg, which were not approved by the FDA owing to a 10% rate of daytime sedation), suvorexant showed persistent efficacy for these measures after 1 year of nightly use48; lower doses have not been studied for more than 12 weeks. Its major side effect at lower doses is morning sleepiness (5% of patients).

Ramelteon is a melatonin-receptor agonist that is FDA-approved for the treatment of insomnia. Short-term studies as well as a controlled 6-month trial showed small-to-moderate benefits for time to sleep onset but no significant improvement in total sleep time or time awake after sleep onset.49 Side effects were limited to rare next-day sedation. A meta-analysis of trials of melatonin for insomnia (at a wide range of doses and in immediate-release and controlled-release forms) showed small benefits for time to sleep onset and total sleep time.50 However, the quality control of over-the-counter melatonin products is unclear.

Although controlled clinical trials to support its use are lacking, gabapentin is occasionally used for insomnia, predominantly in patients who have had an inadequate response to other agents, who have a contraindication to benzodiazepine-receptor agonists (e.g., a history of drug or alcohol abuse), or who have neuropathic pain or the restless legs syndrome. Potential side effects include daytime sedation, weight gain, and dizziness.




Areas of Uncertainty

Insomnia is an independent risk factor for depression, cardiovascular disease, and diabetes. Controlled studies are needed to determine whether long-term treatment of insomnia with CBT or medications (or both) can reduce the risk of these disorders.

Both sleeplessness and the pharmacologic therapies used to treat insomnia are associated with complications. In those who do not choose CBT or do not have a response to it, long-term randomized trials comparing benzodiazepine-receptor agonists, sedating antidepressants, and the orexin antagonist suvorexant to inform the choice of medications are lacking.




Guidelines

The American Academy of Sleep Medicine25 and the National Institutes of Health51 have published guidelines for the diagnosis and management of insomnia. The recommendations in this article are generally consistent with those guidelines.




Conclusions and Recommendations

The woman in the vignette has a long history of insomnia, now complicated by nocturia and pain. Recently, owing to her physician’s concerns about her benzodiazepine use, she was switched to a low dose of trazodone, but she reports frequent and prolonged awakenings. Attempting to discontinue lorazepam and replacing it with trazodone were reasonable, given the amnestic and psychomotor side effects of benzodiazepines, although data from studies that directly compare these agents are limited. I would strongly recommend a trial of CBT, including (but not limited to) educating her that 7 hours is an adequate amount of sleep, reducing the time from bedtime to final awakening to that amount, and advising her to get in bed only when sleepy and to get out of bed when not sleeping. Over time, these approaches should reduce the duration of nocturnal awakenings, although she should be cautioned initially about an increase in daytime sleepiness. Attention to her nocturia and nocturnal pain will further minimize her nocturnal awakenings and their duration. If these approaches are ineffective, I would consider an increase in the trazodone dose (if this does not cause unacceptable side effects) or a return to lorazepam, informing her of (and regularly reassessing) benefits and potential risks."


p.s. The tables are identical to those of Roby Sue

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Last edited by avi123 on Wed Oct 07, 2015 6:58 pm, edited 3 times in total.

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Re: Fractured sleep, Ambien, dial wingin' and other things

Post by Pugsy » Wed Oct 07, 2015 6:43 pm

avi123 wrote:A new report about insomnia:

http://www.nejm.org/doi/full/10.1056/NE ... ?query=TOC
Unavailable unless a subscriber to the publication.
Could you maybe copy/paste the relevant text?

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Re: Fractured sleep, Ambien, dial wingin' and other things

Post by avi123 » Wed Oct 07, 2015 7:19 pm

Pugsy wrote:
avi123 wrote:A new report about insomnia:

http://www.nejm.org/doi/full/10.1056/NE ... ?query=TOC
Unavailable unless a subscriber to the publication.
Could you maybe copy/paste the relevant text?
Reply: OK, but it might not be something new to most members.

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see my recent set-up and Statistics:
http://i.imgur.com/TewT8G9.png
see my recent ResScan treatment results:
http://i.imgur.com/3oia0EY.png
http://i.imgur.com/QEjvlVY.png

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Pugsy
Posts: 63941
Joined: Thu May 14, 2009 9:31 am
Location: Missouri, USA

Re: Fractured sleep, Ambien, dial wingin' and other things

Post by Pugsy » Wed Oct 07, 2015 7:28 pm

avi123 wrote: Reply: OK, but it might not be something new to most members.
Go ahead anyway. If we got right down to splitting hairs about something being new or not to most members .....pretty much everything we post now is old news. Certainly the questions and problems have all been asked hundreds of time before. There are no new problems...just new people with same old problems.
It's very rare that I see a question or a problem that I have never seen here.

How have you been feeling lately? We've missed you.

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Macpage
Posts: 226
Joined: Thu Jul 24, 2014 10:48 am
Location: Kentucky, USA

Re: Fractured sleep, Ambien, dial wingin' and other things

Post by Macpage » Fri Oct 09, 2015 9:55 am

I think its great that we bring some of these really good threads back up from time to time for all of us and especially new users. We all know it's sometimes hard to find these jewels with the search function.

I think it serves a purpose if some of the veterans picked really good threads over the years and placed them in the sticky section. Everyone could make suggestions and we could post the ones agreed upon. Just a thought. I know I'm still finding great information in threads, and I've been around for a while now.

Best,

Mike

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