AHI still erratic, time to wingding?

General Discussion on any topic relating to CPAP and/or Sleep Apnea.
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Sludge
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Re: AHI still erratic, time to wingding?

Post by Sludge » Mon Jun 09, 2014 4:28 am

robysue wrote:... what I'm noticing indicates a possible problem with the high pressures triggering or contributing to the unstable breathing.
I would certainly consider that to be pretty high on the list of possibilities.

I think it would be really helpful to go through breath-by-breath on the download, preferably in ResScan, so you would need to upload the SD files:
  • Open account with 3rd party depository (Google Docs, Dropbox, etc).
  • Upload the following files from SD card (basically all of them) to depository:
    • DATALOG
    • SETTINGS
    • Identification.tgt
    • Identification.crc
    • STR.edf
    • STR.crc
Also, all the pertinent patient info (in a review of posts, given an 86 year old with an HST thrown on an APAP, this isn't wingdingin', this is wingdingin' in the dark!).

Also, which HST did she have? It would be helpful to try to get a hold of that raw data (although some of that is proprietary to the point of being inaccessible).

It may be that a single change would magically solve all the problems, but this could also turn into some significant time/expense wingdingin' .

(On a side note, please be aware that The Sludge does not/cannot/will not participate in actual wingdingin' .)
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Re: AHI still erratic, time to wingding?

Post by robysue » Mon Jun 09, 2014 9:08 am

Sludge wrote:
robysue wrote:... what I'm noticing indicates a possible problem with the high pressures triggering or contributing to the unstable breathing.
I would certainly consider that to be pretty high on the list of possibilities.
Thanks! It's good to know I'm not totally off base with my observations here.
I think it would be really helpful to go through breath-by-breath on the download, preferably in ResScan, so you would need to upload the SD files:
I agree that looking at things on a breath-by-breath basis would be useful. I've got both an older version of ResScan and the current SleepyHead installed in case College3girls prefers to email me the files. Curiosity, why would you prefer ResScan?
Also, all the pertinent patient info (in a review of posts, given an 86 year old with an HST thrown on an APAP, this isn't wingdingin', this is wingdingin' in the dark!).
Even though I thought I'd gone back and looked at every thing, I didn't pick up on the home sleep test as the diagnostic tool. Thanks for pointing this out to me.

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Re: AHI still erratic, time to wingding?

Post by College3girls » Mon Jun 09, 2014 3:28 pm

I just spoke to Mom. Last night was the first night of the lowered IPAP and increased EPAP. Her AHI was 7 something, which is half what it has been running. One night is not enough to go on, I know, but hopefully this is all going in the right direction.

Mom is going to call and request a complete report of her over-night titration, and also try to get the HST results from last year.

I'll attempt to learn how to get all her SD card data to Robysue and Sludge. I'll be going to Mom's on Thursday. Feel free to share the data and post it on the forum.

This will only be the data from her BIPAP. When she received the BIPAP set-up, it was just under 13 months of time on the APAP, so that was taken back along with the SD card.

Thank you Robysue and Sludge, (and Pugsy from earlier posts). I know this takes a lot of your time.

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Re: AHI still erratic, time to wingding?

Post by robysue » Mon Jun 09, 2014 6:02 pm

College3girls wrote:I just spoke to Mom. Last night was the first night of the lowered IPAP and increased EPAP. Her AHI was 7 something, which is half what it has been running. One night is not enough to go on, I know, but hopefully this is all going in the right direction.
That is good news. Yes, one night is not enough to go on, but even so, it's better to have the first night go well than be a disaster. I'm keeping my fingers crossed for your mom.
Mom is going to call and request a complete report of her over-night titration, and also try to get the HST results from last year.
This is an excellent idea.
I'll attempt to learn how to get all her SD card data to Robysue and Sludge. I'll be going to Mom's on Thursday. Feel free to share the data and post it on the forum.
Check your PMs.
This will only be the data from her BIPAP. When she received the BIPAP set-up, it was just under 13 months of time on the APAP, so that was taken back along with the SD card.
How long has your mom been using the BiPAP again?
Thank you Robysue and Sludge, (and Pugsy from earlier posts). I know this takes a lot of your time.
You're welcome!

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Re: AHI still erratic, time to wingding?

Post by College3girls » Mon Jun 09, 2014 8:22 pm

Mom has been on the BiPAP since May 21. I'm trying to address issues right away this time. She doesn't have a recheck with the sleep clinic scheduled yet.

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Re: AHI still erratic, time to wingding?

Post by Sludge » Tue Jun 10, 2014 2:53 am

robysue wrote:Curiosity, why would you prefer ResScan?
  • More comfortable with it.
  • The SD files could be looked at in either application.
  • SH is buggy, including misplacing the -0- line (which delineates inspiration vs expiration) in Flow Rate.
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Re: AHI still erratic, time to wingding?

Post by Sludge » Tue Jun 10, 2014 3:19 am

College3girls wrote:...and also try to get the HST results from last year.
And specifically, try to get the actual raw data file.

If we are adopting the philosophy of

Image

then everything becomes suspect, and we need to find primary data wherever possible.

In this case, I believe the premi (plural of premus)(oh wait, NM) are:
  • Most/all the events are central, or at least have a central flavor; and
  • Some/most/all of the events are in SWJ (you guys are presuming an 86 year old lady has uninterrupted asleep. "IMHO", the safer bet would be she does not).
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Re: AHI still erratic, time to wingding?

Post by Sludge » Tue Jun 10, 2014 3:37 am

Sludge wrote:Some/most/all of the events are in SWJ ...
Or perhaps even plain ol' "W".
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Re: AHI still erratic, time to wingding?

Post by robysue » Tue Jun 10, 2014 8:14 am

Sludge wrote:...

then everything becomes suspect, and we need to find primary data wherever possible.
But how does one get the raw data from the sleep center or doctor? This is a real question for me: Back in 2011 when I was still having extreme difficulties it was suggested by either you or -SWS that I get the full raw data from my sleep studies. I tried and hubby tried, but the sleep doc whose clinic did the testing simply refused to burn a CD with the raw data on it and give or sell it to me. We had made it clear that we were willing to pay a fee for obtaining that raw data. Still no dice.
In this case, I believe the premi (plural of premus)(oh wait, NM) are:
  • Most/all the events are central, or at least have a central flavor; and
  • Some/most/all of the events are in SWJ (you guys are presuming an 86 year old lady has uninterrupted asleep. "IMHO", the safer bet would be she does not).
You are right SWJ or W is a real possibility. But in that case, is allowing the machine to keep the pressure above 21/17 for as long as two hours of SWJ a good idea or a bad idea? In other words, if many or most of those 30-minute to 2 hour long clusters are predominately SWJ "events", is there any chance that discomfort from the extremely high pressure could be prolonging the SWJ periods?

Another question: I've been told by several sleep docs that a typical adult does not remember a W that lasts less than 5 minutes. As you get older, does that change? In other words, for an 86 year old to remember a wake, is it likely that the wake has to be longer than 5 minutes? If so, how much longer on average?

Finally, If these events are mostly SWJ, would the mom be better off with a pressure capped at 21/17? Or is it more that the mom would be no worse off with a pressure capped at 21/17?

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Re: AHI still erratic, time to wingding?

Post by bavinck » Tue Jun 10, 2014 10:10 am

Can one of you explain what SWJ is? This conversation is very interesting, but I am unfamiliar with this.
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Re: AHI still erratic, time to wingding?

Post by robysue » Tue Jun 10, 2014 3:30 pm

bavinck wrote:Can one of you explain what SWJ is? This conversation is very interesting, but I am unfamiliar with this.
SWJ = Sleep-Wake-Junk

When you are half awake, half asleep and repeatedly going between (barely) WAKE and Stage 1 sleep, the breathing can get pretty irregular. Wake breathing itself is very irregular compared to normal sleep breathing, once you are in persistent sleep---i.e. not dozing off and on.

And when there's a lot of this half-wake, half-sleep stuff going on, the control of the breathing is going back and and forth between the voluntary and autonomous nervous systems. And all of that makes the breathing irregular (compared to normal sleep breathing). And our machines, smart as they are, can mis-iterpret all that SWJ breathing and score events that would not be scored on a sleep study because they're not occurring during sleep as sleep disordered breathing events.

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Re: AHI still erratic, time to wingding?

Post by Sludge » Wed Jun 11, 2014 2:43 am

robysue wrote:
Sludge wrote:...

then everything becomes suspect, and we need to find primary data wherever possible.
But how does one get the raw data from the sleep center or doctor? This is a real question for me: Back in 2011 when I was still having extreme difficulties it was suggested by either you or -SWS that I get the full raw data from my sleep studies. I tried and hubby tried, but the sleep doc whose clinic did the testing simply refused to burn a CD with the raw data on it and give or sell it to me. We had made it clear that we were willing to pay a fee for obtaining that raw data. Still no dice.
Review mantra above.

What are they hiding?

"IMHO" more than a few HST reviewers hit the AutoScore button, but more importantly, given the incidence of co-morbidity in the elderly, one must ask if HST was appropriate in the first place (plenty of people cite the incidence of insomnia in the elderly at 40-50%) and one must interpret the results very carefully (if AHI is like 10, what does that mean? And did they use the Medicare Rules for scoring? If they didn't, then no, we ain't getting the data.)

But while HST should be used with great caution, it was CMS that said it's OK to use it, so that opened up the can of worms for the elderly (the patient group that shouldn't be getting blanket HST is the one that got initial approval).
robysue wrote:I've been told by several sleep docs that a typical adult does not remember a W that lasts less than 5 minutes. As you get older, does that change? In other words, for an 86 year old to remember a wake, is it likely that the wake has to be longer than 5 minutes? If so, how much longer on average?
I don't think you can make a one size fits all rule. Perhaps ask "How often do you lose your keys?" (cause that might be memorable. If you ask "How often do you forget to take your medication?" the answer will undoubted be "How should I know? I forgot, duhhhhh!!!")

Anyway:

http://www.sciencedirect.com/science/ar ... 5713001408
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Re: AHI still erratic, time to wingding?

Post by Sludge » Wed Jun 11, 2014 2:56 am

bavinck wrote:Can one of you explain what SWJ is?
Sure.

SWJ means one should spend less time looking at AHI and more time and considering this:
Aging is often associated with complaints of difficulties with sleep, as evidenced by reports that up to 50% of older US adults complain of chronic trouble with sleep.1 Research has found that a number of normal changes in sleep occur with aging, which may explain some of these complaints.2 However, there are a variety of conditions that may account for the sleep difficulties experienced by many older adults, including specific sleep disorders, circadian rhythm disturbances, and medical and psychiatric comorbidities.

With age, it is normal for a number of changes to occur in sleep architecture and sleep patterns. Compared with younger adults, older adults sleep less despite spending more time in bed, spend more time awake during the night, wake up earlier in the morning, nap more, and take longer to fall asleep. Findings from a meta-analysis that included more than 3500 participants showed that after age 60, sleep efficiency (defined as the ratio of total sleep time to nocturnal time in bed, normally defined as 85% or greater), which is considered a measure of sleep continuity, decreases with further increases in age.2 Older adults experience more fragmented sleep, as evidenced by an increase in the number of sleep stage shifts, arousals, and awakenings.2

Older adults' need for sleep does not decrease with age. Their actual ability to sleep, however, does.3 When tested for daytime sleepiness (considered one marker of insufficient sleep), older adults were sleepier than their young counterparts, which may in part be due to their difficulty in obtaining enough sleep at night.

Insufficient sleep is associated with significant morbidity and increased mortality. Increased symptoms of depression and anxiety and decreased quality of life have been reported in patients who experience difficulty in sleeping. Sleep problems in older adults are associated with an increased risk of falls and difficulty with ambulation, balance, and vision—even after controlling for medication use.4 Chronic sleep difficulties and lack of sleep can lead to deficits in attention, response times, short-term memory, and performance level. Poorly maintained sleep, as reflected in low sleep efficiency, is also associated with increased mortality; a longitudinal study of healthy older adults reported that lower sleep efficiency (less than 80%) nearly doubled the risk of all-cause mortality.5

Insomnia
Insomnia is the most commonly reported sleep disturbance in older adults and is defined as the inability to initiate or maintain sleep resulting in daytime consequences. Complaints, which are more common in older women than in older men, can vary from difficulty in falling asleep to difficulty in maintaining sleep to frequent arousals from sleep and early morning awakenings. In a study of more than 9000 older adults (older than 65 years), 42% had difficulty in falling asleep and staying asleep.6 Three years later, insomnia complaints had resolved in 15% of the patients, although there was a 5% incidence of new sleep complaints.6

Insomnia may be a primary sleep disorder. In the older adult, however, it is important to recognize that complaints of insomnia may coexist with many chronic medical and/or psychiatric conditions including depression, chronic pain, cancer, chronic obstructive pulmonary disease, congestive heart failure, and stroke. In a survey of insomnia, 28% of older adults complained of chronic insomnia, but fewer than 10% of the new cases occurred in the absence of one of these related conditions.6 In addition to any underlying medical/ psychiatric condition, a number of medications used in the treatment of these conditions, including β-blockers, bronchodilators, corticosteroids, decongestants, diuretics, and antidepressants, can contribute to or even cause sleep difficulties.

Research has found that behavioral therapy, specifically cognitive-behavioral therapy (CBT), is as effective as or more effective than medications for insomnia. Based on head-to-head trials of CBT versus medications, the 2005 NIH State-of-the-Science Conference on Insomnia concluded that CBT is as effective as prescription medications for the treatment of chronic insomnia in older adults.7 A variety of medications have been used to treat insomnia in older adults but, as concluded by the conference, there is no systematic evidence for the effectiveness of the following classes of medications in the treatment of insomnia: antihistamines, antidepressants, antipsychotics, and anticonvulsants.7 Furthermore, the panel of experts stated that the risks associated with the use of these medications, especially among the elderly, largely outweigh any benefits.

Sedative-hypnotic medications are effective and appropriate at times for the management of insomnia. Studies have shown, however, that these medications should be accompanied by behavioral therapy and should no longer be considered first-line agents in the treatment of insomnia.7 To use this class of medications effectively and safely, clinicians must select the sedative-hypnotic that best fits the specific type of insomnia (eg, an agent with a long onset of action is not appropriate for a patient with sleep-onset insomnia).

New medications with different mechanisms of action are now available and should be consid-ered the first-line agents for the treatment of insomnia (Table 1). The selective short-acting nonbenzodiazepines, including eszopiclone, zaleplon, zolpidem, and zolpidem MR, are safe and effective for older adults. The melatonin agonist, ramelteon, is the only sleep-related medication not controlled by the Drug Enforcement Administration, and it is safe and effective in the treatment of sleep-onset insomnia in the elderly. In general, both pharmacological and behavioral treatments should be combined for the most effective treatment of insomnia. Patients should receive short-term relief with medications while learning the techniques of CBT, which should provide long-term treatment of insomnia.

Circadian rhythm sleep disorders
The sleep-wake cycle in humans is controlled by an endogenous clock located in the suprachiasmatic nucleus of the hypothalamus, which generates a circadian rhythm that is synchronized by external time cues (zeitgebers). The light-dark cycle is the major cue in humans. Circadian rhythm sleep disorders may develop if a lack of synchrony occurs between the endogenous clock and external environmental zeitgebers.

A number of factors associated with aging may contribute to the development of circadian rhythm sleep disorders. The circadian pacemaker itself degenerates with age, which may result in a weaker rhythm. Melatonin is important in the sleep-wake cycle, but its nocturnal secretion decreases with age, which may contribute to disrupted or weakened circadian rhythms. In addition, the environmental cues needed to synchronize the circadian rhythm of sleep-wake (ie, daily exposure to light) may be absent or weak in older patients. A study found that daily bright light exposure averaged 60 minutes for healthy elderly persons, 30 min-utes for patients with Alzheimer disease living at home, and no exposure for nursing home patients.8,9

Advanced sleep phase syndrome is by far the most common circadian rhythm sleep disorder, and its prevalence increases with age. Advanced sleep phase syndrome is characterized by routine and involuntary sleep and wake times that are several hours earlier than societal norms. Individuals with advanced sleep phase syndrome feel sleepy in the early evening and wake up in the early morning. Sleep architecture itself is normal and if patients follow their natural rhythms, they do not typically complain of daytime sleepiness. However, as these individuals experience an early morning wake time regardless of what time they go to sleep, delays in sleep onset often result in insufficient sleep time and complaints of excessive daytime sleepiness. A careful and detailed sleep history, sleep diaries, and activity monitoring with wrist actigraphy can be useful in making the diagnosis.

Patients with advanced sleep phase syndrome should be reassured that this condition is not a medical disorder, does not require treatment, and is a natural, often expected shift in circadian rhythm. If patients are happy with their sleep/wake times and are getting enough sleep, treatment is not necessary. For those patients who prefer a more "normal" sleep/wake time, however, therapy to delay circadian rhythm should be offered.

Treatment of advanced sleep phase syndrome focuses on strengthening and synchronizing the sleep-wake cycle; because bright light is the strongest cue for circadian entrainment, it is the most common and the most effective treatment. Exposure to bright light in the evening strengthens the sleep-wake cycle and delays circadian rhythms in patients with advanced sleep phase syndrome, including those who reside in nursing homes. Patients with advanced sleep phase syndrome should be advised to avoid bright light during the morning and should be educated on sleep hygiene practices, including maintaining a regular sleep schedule. Supplemental exogenous melatonin administered in the morning could, in theory, result in a phase delay in older adults with advanced sleep phase syndrome. The effectiveness and safety of this therapy has not been well studied in advanced sleep phase syndrome, however, and the sedating properties of melatonin may limit its clinical utility.

Obstructive sleep apnea
Obstructive sleep apnea is characterized by the complete cessation of respiration (apnea) and/or partial or reduced respiration (hypopnea) during sleep. Most patients with obstructive sleep apnea experience some combination of these events.

Obstructive sleep apnea appears to be more common in older than in younger adults, more common in older men than older women, and more common in institutionalized older adults than in those living independently. The reported prevalence of obstructive sleep apnea in older adults ranges from 20% to 81%, and most longitudinal and cross-sectional studies have found that its prevalence increases or stabilizes with increasing age.10-12 In a large study of community-dwelling adults aged 65 to 95 years, researchers found that 81% of the subjects had an apnea-hypopnea index (AHI) of at least 5.10 Patients with dementia experience high rates of obstructive sleep apnea, probably related to degeneration in the areas of the brain stem responsible for regulating respiration and other autonomic functions. In a review of 7 studies examining the prevalence of obstructive sleep apnea in older adults with and without dementia, prevalence rates ranged from 33% to 70% in those with dementia compared with 5.6% to 45% in those without dementia.13

Risk factors for obstructive sleep apnea include increasing age, sex, obesity, use of sedating medications, consumption of alcohol, family history/ genetic factors, race, smoking, and craniofacial anatomy. Snoring and excessive daytime sleepiness are typical clinical manifestations of obstructive sleep apnea, although clinicians should be aware that less common presentations may include insomnia and nocturnal confusion. Excessive daytime sleepiness can have a significantly negative affect on quality of life and may lead to unintentional napping, social and/or occupational difficulties, and cognitive dysfunction, which is of particular relevance for those patients with baseline cognitive impairment.14

In general, the presence of untreated obstructive sleep apnea is associated with significant morbidity. Although there is clear evidence that untreated obstructive sleep apnea in younger adults is an independent risk factor for the development of systemic hypertension, the relationship between obstructive sleep apnea and hypertension remains less clear in the older adult. Recent data from the Sleep Heart Health Study found that in adults aged 60 years or older, there was no association between obstructive sleep apnea and systolic/diastolic hypertension.15 The exact relationship between obstructive sleep apnea and other forms of cardiovascular disease in the older adult remains somewhat unclear, although recent studies have found positive associations between the severity of obstructive sleep apnea and the risk of developing coronary artery disease, congestive heart failure, and stroke.16 In addition to these possible cardiovascular effects, older patients with severe obstructive sleep apnea (defined as an AHI of 30 or higher) have consistently been found to have evidence of cognitive dysfunction including impairment in vigilance, memory, executive tasks, and manual dexterity.

When evaluating an older adult with suspected obstructive sleep apnea, clinicians should obtain a thorough sleep history focused on symptoms of obstructive sleep apnea (excessive daytime sleepiness, unintentional napping, cognitive dysfunction, and snoring), preferably in the presence of a bed partner or caregiver. The patient's medical history should be reviewed with particular attention to conditions associated with obstructive sleep apnea (eg, stroke, ischemic heart disease), medications (especially sedatives), and the use of alcohol. The diagnosis should be confirmed with an overnight sleep recording.

The first line of treatment of obstructive sleep apnea is continuous positive airway pressure, provided by a device that creates a pneumatic splint to keep the airway open during inspiration. If used appropriately, continuous positive airway pressure can safely and effectively treat obstructive sleep apnea at night with minimal adverse effects,17 and its use results in improvements in nocturia, excessive daytime sleepiness, depression, quality of life, and cognition.18,19 Less effective treatments include oral appliances and surgery. All patients should be counseled on weight loss, smoking cessation, and abstaining from alcohol, if applicable. Clinicians should avoid prescribing medications such as benzodiazepines and narcotics, which worsen obstructive sleep apnea.

Despite its effectiveness, continuous positive airway pressure adherence can be an issue for a patient with obstructive sleep apnea, regardless of age, and clinicians should not assume that older adults will be nonadherent simply because they are older. On the contrary, in a study of patients with dementia, our laboratory reported that most patients used continuous positive airway pressure for about 5 hours a night, and the only factor associated with poor adherence was depression—not age, severity of dementia, or severity of obstructive sleep apnea.20

The debate regarding the significance of obstructive sleep apnea in older adults is ongoing, although at the present time most experts agree that the initiation of obstructive sleep apnea treatment should be guided by the significance of the patient's symptoms, the severity of the obstructive sleep apnea, and the presence of other comorbid conditions, and not by age alone.21

Periodic limb movements in sleep and restless legs syndrome
Like obstructive sleep apnea, periodic limb movements (PLMS) in sleep and restless legs syndrome (RLS) are commonly found in older adults. PLMS are characterized by clusters of repetitive leg movements during sleep with jerks or kicks typically occurring every 20 to 40 seconds and recurring throughout the night. Each jerk may cause an awakening, resulting in sleep fragmentation, and therefore patients with PLMS may experience excessive daytime sleepiness. The diagnosis of PLMS requires an overnight sleep study. The cause of PLMS is unknown, although it can be seen in patients with a number of neurological disorders and in combination with other sleep disorders including obstructive sleep apnea.

RLS is a disorder strongly linked to PLMS and is characterized by leg dysesthesia (a "creepy crawling" or "aching" sensation) occurring while the patient is in an awake/relaxed state and is relieved by movement. The uncomfortable sensation can prevent patients from falling asleep or can awaken patients. Unlike PLMS, the diagnosis of RLS is purely clinical and based on history alone—polysomnography has no role in the diagnosis. The cause of RLS is also unknown, but the disorder is associated with a number of other conditions including anemia, uremia, peripheral neuropathy, and rheumatoid arthritis.

The prevalence of both disorders increases dramatically with age. The prevalence of PLMS can be as high as 45% in community-dwelling adults older than 65 years,22 while the prevalence of RLS in older adults ranges from 9% to 20%.23 PLMS are equally prevalent in older men and women, while RLS appears to occur more commonly in older women than in older men.23

Medications that suppress the leg movements and/or the related arousals are the therapies currently recommended for both RLS and PLMS. Dopamine agonists (specifically, ropinirole and pramipexole) are the first-line treatments for both disorders in the older adult because these agents effectively decrease the number of leg jerks and associated arousals. PLMS in the absence of associated arousals from sleep and in the absence of significant symptoms do not require treatment.

Rapid eye movement sleep-behavior disorder
Rapid eye movement (REM) sleep-behavior disorder is another sleep disorder found more commonly in older adults, especially in older men. Patients with REM sleep-behavior disorder display complex motor activities during REM sleep caused by the loss of normal skeletal muscle atonia during this stage of sleep. Patients with REM sleep-behavior disorder appear to act out their dreams and may punch, kick, yell, or jump out of bed in response to dream imagery. Vivid dreams that are consistent with the patient's aggressive and/or violent behavior may be recalled on waking. The reported prevalence is 0.5%, with the highest incidence occurring after the age of 50 years.24 Approximately 40% of the cases are associated with an underlying neurodegenerative disorder such as synucleinopathies including diffuse Lewy body disease and Parkinson disease. REM sleep-behavior disorder may actually be the first manifestation of these disorders, preceding the clinical symptoms of the underlying neurological disorder by more than 10 years.25

The diagnosis of REM sleep-behavior disorder requires a complete sleep history in the presence of the bed partner if possible and an overnight polysomnogram with video recording. The mainstays of treatment for REM sleep-behavior disorder are environmental safety, patient education, and the long-acting benzodiazepine clonazepam, which may suppress or simply reduce the increased movements during sleep.

Sleep in dementia
Patients with dementia, whether they live independently or are institutionalized, are especially prone to experiencing fragmented and disrupted sleep. While the underlying neurodegenerative process of dementia itself may cause these sleep disturbances, patients with dementia may also have primary sleep disorders, such as obstructive sleep apnea, PLMS, RLS, or REM sleep-behavior disorder, or have disturbed sleep related to pain, medications, circadian rhythm changes, or depression. Disturbed sleep related to dementia should be a diagnosis of exclusion. Consequences of this disrupted sleep may include napping (intentional and unintentional) and abnormal nighttime behavior such as wandering or confusion. Such behavior at night can significantly add to caregiver stress and may contribute to the need for institutionalization.

As with patients without dementia, treatment of specific sleep disorders in the older patient with dementia should be guided by the specific sleep disorder. For example, patients with obstructive sleep apnea should be treated with continuous positive airway pressure if appropriate; patients with circadian rhythm disturbances should be treated with bright light therapy if appropriate. In this patient population, the risk-to-benefit ratio does not favor the use of many of the pharmacological treatments. In general, nonpharmacological interventions, such as regular physical activity and good sleep hygiene like restricting time in bed and maintaining regular sleep-wake times (Table 2), should always be used and medications added only when indicated. Many of the medications prescribed as sleeping aids such as sedative-hypnotics, antihistamines, and antipsychotics have significant potential adverse effects, particularly residual daytime sleepiness, which may be magnified in the older adult and result in impaired motor and/or cognitive function.

Sleep in institutionalized older adults
Older adults with dementia who reside in nursing homes experience even more fragmented and disturbed sleep than those living in the community. Reports show that during any 24-hour period, institutionalized patients with severe dementia may not spend a single hour completely awake or completely asleep.26 Nursing-home patients have been found to have more advanced sleep-wake cycles and worse overall sleep quality. Furthermore, they are treated with sedative-hypnotics more frequently than older patients living at home or in an assisted-living facility.27

The poor sleep experienced by many nursing-home residents is probably caused by a variety of factors, including excessive noise at night28 and inadequate light exposure (less than 10 minutes of bright light per day).9 These patients also tend to spend large amounts of time in bed, which may disrupt circadian rhythms and contribute to further disruptions in sleep. As with community living older adults with dementia, nonpharmacological inventions, such as reducing nighttime noise and improving sleep hygiene, especially restricting time in bed, should be instituted first. In addition, increased light exposure has been shown to consolidate sleep and strengthen circadian rhythms in this population of patients.29

Summary
For many older adults, the aging process is associated with difficulty in getting a good night's sleep. Potential contributors to poor sleep include primary sleep disorders, circadian rhythm disturbances, insomnia, medications, and the presence of comorbid conditions such as depression and chronic diseases. Older adults with sleep complaints should be evaluated with a thorough sleep history and an overnight sleep recording or sleep diary when indicated. Treatment should focus on the underlying sleep disorder and should take into account some of the unique and special issues found in older adults. A good night's sleep can be achieved in older adults with some patience and the proper interventions and can result in significant improvements in their quality of life and daytime functioning.
http://www.psychiatrictimes.com/sleep-d ... rs-elderly
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Sludge
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Re: AHI still erratic, time to wingding?

Post by Sludge » Wed Jun 11, 2014 3:02 am

robysue wrote:Finally, If these events are mostly SWJ, would the mom be better off with a pressure capped at 21/17? Or is it more that the mom would be no worse off with a pressure capped at 21/17?
IDK, but "IMHO", I'd want to be real sure that an 86 year-old really needed 21/17 before I was part of a crowd that said we should pound her for a hefty chunk of the night with it.
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Re: AHI still erratic, time to wingding?

Post by Sludge » Wed Jun 11, 2014 3:13 am

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