| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Guest Access | Sign In via User Name/Password
|
|
|
|||||||
Guest Access | Sign In via User Name/Password |
|||||||||
* From the Sleep and Human Health Institute (Dr. Krakow, Mr. Melendrez, Ms. Ferreira, Mr. Clark, and Ms. Sisley), Albuquerque; and Departments of Psychiatry (Dr. Warner), and Emergency Medicine (Dr. Sklar), University of New Mexico School of Medicine, Albuquerque, NM.
Correspondence to: Barry Krakow, MD, Sleep and Human Health Institute, 4775 Indian School Rd NE, Suite 305, Albuquerque, New Mexico, 87110; e-mail: bkrakow{at}salud.unm.edu
 |
Abstract |
|---|
 TOP Abstract IntroductionMaterials and MethodsResultsDiscussionAppendix 1References |
|---|
Design: Retrospective medical chart review of a representative sample of patients with SDB.
Setting: University sleep-disorders clinic and laboratory.
Patients: Two hundred thirty-one patients with SDB were selected from a pool of approximately 2,000 patients with sleep disorders.
Measurements: Data were extracted from intake questionnaires and polysomnographic studies.
Results: Of 231 patients with SDB diagnoses, 115 patients reported no insomnia complaints (SDB-only patients) and 116 patients reported clinically meaningful insomnia complaints (SDB-plus patients). Compared to SDB-only patients, SDB-plus patients reported significantly worse mean sleep characteristics consistent with insomnia, including sleep latency (17 min vs 65 min), total sleep time (7.2 h vs 5.6 h), and sleep efficiency (92% vs 75%). SDB-plus patients experienced significantly more psychiatric disorders, cognitive-emotional symptoms, and physical and mental symptoms that disrupted or prevented sleep. SDB-plus patients also reported greater use of sedative and psychotropic medications and had significantly more primary complaints of insomnia, restless legs or leg jerks, and poor sleep quality despite having relatively similar referral rates for sleep apnea or complaints of loud snoring.
Conclusions: Problematic insomnia symptoms were reported by 50% of a representative sample of patients with objectively diagnosed SDB. Research is needed to determine the degree to which insomnia and related symptoms and behaviors interfere with SDB treatment.
Key Words: insomnia • obstructive sleep apnea • sleep-disordered breathing • upper airway resistance syndrome
|
Introduction |
|---|
|
TOPAbstractIntroductionMaterials and MethodsResultsDiscussionAppendix 1References |
|---|
The dearth of research in this area may arise from the assumption that SDB patients experience sleep maintenance insomnia or recurrent awakenings11 without concomitant difficulty returning to sleep. As such, "insomnia" associated with SDB appears to be clinically irrelevant. Current American Academy of Sleep Medicine practice parameters for the diagnosis of SDB11 in fact depart from an earlier version of the International Classification of Sleep Disorders construct12 by no longer using the term insomnia in the diagnostic criteria.11 Most studies or reviews on this topic have attempted primarily to clarify the role of polysomnography in assessing insomnia,3 13 14 15 and a few of these works have assessed SDB prevalence rates in insomniacs. Generally, these studies3 14 concluded that the evaluation of insomnia does not routinely require polysomnography. Parenthetically, the studies from which these practice parameters were derived were absent the use of nasal pressure transducer technology, which assesses subtle airflow irregularities.16 Preliminary research suggests that insomnia and SDB have a more complex relationship than previously observed.17 18 One uncontrolled study18 recently documented an SDB prevalence of 91% in crime victims seeking treatment for insomnia.
Regardless of how these two common sleep disorders are related, it may prove worthwhile to consider their relationship as a "two-way street," particularly if insomnia symptoms in SDB patients manifest as primary comorbid conditions, requiring treatments distinct from and supplemental to sleep breathing therapies.15 19 Speculatively, comorbid insomnia could influence compliance with SDB therapies, such as continuous positive airway pressure (CPAP) or oral airway devices.4 20 21 22 And, with the growing influence of managed care,23 a patient with complex sleep disorders (such as comorbid insomnia and SDB) might not receive the level of follow-up required to maximize treatment outcomes. As a preliminary step in learning more about this clinical presentation, the current study focused on the frequency of insomnia complaints in patients with obstructive sleep apnea (OSA) and upper airway resistance syndrome (UARS). The study included a representative sample of SDB patients treated at a university sleep-disorders clinic. We hypothesized that a sizeable proportion of patients with objectively diagnosed SDB would report clinically important insomnia symptoms, and that SDB patients who reported comorbid insomnia would report greater symptom distress compared with SDB patients without complications.
|
Materials and Methods |
|---|
|
TOPAbstractIntroductionMaterials and MethodsResultsDiscussionAppendix 1References |
|---|
SDB Diagnoses
Diagnoses were made in all 231 patients by standard
polysomnography (97%), or an EdenTrace II Plus Digital Recorder (model
37111; EdenTec; Eden Prairie, MN) [3%]. EdenTrace monitors were used
in grossly apparent OSA cases to expedite care. Polysomnography was
performed in the University Hospital Sleep Disorders Center Laboratory.
Technicians prepared the patients using the international 10–20 system
of electrode placement and the collodian set-up. The recording had a
14-channel montage: left outer canthus-A2; right
outer canthus-A1;
C3-A2;
C4-A1;
O1-A2; chin; ECG; left
leg-right leg; snore; oral-nasal thermistor; chest effort; abdominal
effort; arterial oxygen saturation; and position. Polysomnography
was scored manually according to Rechtschaffen and
Kales24
by a registered polysomnographic
technician. Two types of events were scored. An apnea was a 
75%
decrease in airflow for at least 10 s. Hypopnea was a 50 to 75%
decrease in airflow coupled with either a 4% oxygen desaturation or an
arousal. Minimum arterial oxygen saturation
(minSaO2) was recorded by pulse
oximetry. Snoring patterns were assessed qualitatively by the reviewer
based on observations from the snore channel and assigned to one of
four categories (constant, frequent, intermittent, infrequent).
Self-reported sleep complaints reported on the sleep history and
objective sleep study data were used to determine OSA diagnoses based
on current American Academy of Sleep Medicine research
criteria,11
including sleepiness (criteria A), or at least
two of five sleep-related symptoms (criteria B) [sleep breathing
difficulties, recurrent awakenings, unrefreshing sleep, daytime
fatigue, and impaired concentration], and an apnea-hypopnea index
(AHI) of 5/h (criteria C). Criteria A or B were also used for UARS
diagnoses, but criteria C was determined differently because
thermistors were used on polysomnography. UARS diagnoses were
established with polysomnographic findings of airflow irregularities
(subcriteria hypopneas) coupled with EEG microarousal activity or the
presence of intermittent or frequent crescendo snoring culminating in
an EEG microarousal.25
26
27
On average, this abnormal
airflow and arousal activity was present on at least 30% of all
recorded 30-s epochs of sleep. In all patients with UARS, the AHI was
< 5/h. However, because of the lack of actual indexes for respiratory
effort-related arousals in these patients, UARS diagnoses were deemed
valid only when objective resolution of subcriteria hypopneas (presumed
respiratory effort-related arousals) was demonstrated during CPAP
titrations. A board-certified sleep specialist examined all
polysomnographic records to determine final SDB diagnoses; for most
UARS diagnoses, the patient’s sleep clinic physician also reviewed the
recording for clinical correlation.
Insomnia Complaints
Insomnia symptoms were based on a three-item scale (Cronbach’s
= 0.52) in which patients were asked if they usually (1)
take > 30 min to fall asleep, (2) wake up a lot, and (3) if
awakened, have difficulty returning to sleep. The patients answered
each question categorically (0 or 1), and then the scores were summed
(range, 0 to 3). Patients with an insomnia score of 0 or 1 were
considered to be without insomnia because they experienced one of three
conditions: no insomnia complaints, recurrent awakenings but no
difficulty returning to sleep, or rare awakenings associated with
difficulty returning to sleep. Comparison of groups with an insomnia
score of 0 (n = 40) vs an insomnia score of 1 (n = 75) yielded no
statistically significant differences for demographic, objective, or
outcome variables. Thus, the group of patients with insomnia scores of
0 to 1 was designated as "SDB-only" (n = 115). Patients with an
insomnia score of 2 or 3 reported clinically apparent insomnia,
including difficulties with falling asleep, staying asleep, and
returning to sleep. Comparison of groups with an insomnia score of 2
(n = 63) vs an insomnia score of 3 (n = 53) yielded no
statistically significant difference for demographic, objective, or
outcome variables. Thus, the group of patients with insomnia scores of
2 to 3 group was designated "SDB-plus" (n = 116). SDB-only and
SDB-plus patients were the primary focus of the analysis.
Procedures and Measures
From the sleep medicine history, data were extracted on patient
responses regarding chief complaints, sleep history, past mental
health, and review of systems. For chief complaints, patients selected
from a list of eight primary sleep disorders or symptoms that best
described their current problems with sleep. These included sleep apnea
referral, loud snoring, difficulty falling asleep, difficulty staying
asleep, nightmares, restless legs or leg jerks, daytime fatigue or
sleepiness, and poor sleep quality. Patients were instructed to select
all applicable items. The section on sleep history provided information
on sleep latency, total sleep time, total hours in bed, and other
symptoms related to SDB and insomnia. The sections on past mental
health and review of systems provided information on past psychiatric
disorders, medication use, and cognitive-emotional complaints. To
compare patients with uncomplicated SDB (SDB-only group) with those who
suffered insomnia and SDB (SDB-plus group), five brief scales were
devised based on extracted data. Scales were comprised of a few
clinical questions to which patients responded categorically (0 = no,
or 1 = yes). Their responses were summed to provide a total score in
which higher scores reflected greater severity in all instances:
1. Sleep breathing scale (range, 0 to 5): (1) loud snoring; (2) moving from a bed or bedroom due to loud snoring; (3) witnessed breathing cessation; (4) choking, gasping, or struggling for breath; and (5) other sleep breathing complaints.
2. Physical symptom scale (range, 0 to 4): (1) trouble breathing, (2) restless legs, (3) indigestion, and (4) pain, any of which the patient associated with prevention or disruption of sleep.
3. Mental symptom scale (range, 0 to 2): (1) racing thoughts and ruminations, and (2) anxiety and fear, each of which the patient associated with prevention or disruption of sleep.
4. Psychiatric disorders scale (range, 0 to 4): (1) anxiety, (2) depression, (3) posttraumatic stress disorder, and (4) panic attacks, which were reported in the past mental health history.
5. Cognitive-emotional scale (range, 0 to 8): (1) attention or concentration, (2) memory, (3) depressed feelings, (4) anxious feelings, (5) irritability, (6) hostility, (7) frustration, and (8) claustrophobia, which were reported as problematic on review of systems.
Statistical analysis was conducted using analysis of variance to
compare means, and 
2 was used to compare
frequencies between SDB-only and SDB-plus groupings. Statistical
significance was set at 0.05. Effect sizes between groups for pertinent
variables were calculated with Cohen’s d or differences in
group proportions.
|
Results |
|---|
|
TOPAbstractIntroductionMaterials and MethodsResultsDiscussionAppendix 1References |
|---|
Comparison of the demographics between these two primary groups
(SDB-only and SDB-plus) revealed no differences in age, gender, and
BMI. Work status (homemaker, student, working vs disabled, retired) and
marital status (married, cohabitation vs single, widowed, divorced)
were collapsed into dichotomous variables. There were no significant
differences between groups for work status, but the SDB-only group had
significantly more single individuals
(2 = 10.36, p = 0.001). For ethnicity,
the sample was sufficient for comparing non-Hispanic whites and
Hispanics; SDB-plus comprised a significantly greater proportion of
non-Hispanic whites (2 = 4.60, p = 0.03).
Objective sleep findings revealed no differences between SDB-only and
SDB-plus groups for
minSaO2, snoring pattern,
OSA or UARS diagnosis; AHI was 58/h in the SDB-only group compared with
46/h in the SDB-plus group (F[1,227] =4.67, p = 0.03).
The two groups described their primary sleep problems (chief complaints) at similar rates for sleep apnea referral, loud snoring, daytime fatigue or sleepiness, and nightmares; however, parallel with their insomnia scale scores, SDB-plus patients reported significantly more chief complaints of difficulty falling asleep and difficulty staying asleep than SDB-only patients. SDB-plus patients also complained somewhat more of restless legs or leg jerks and of poor sleep quality (Table 1 ).
|
|
|
|
Discussion |
|---|
|
TOPAbstractIntroductionMaterials and MethodsResultsDiscussionAppendix 1References |
|---|
It is worth noting that SDB processes may also cause, exacerbate, or otherwise contribute to insomnia.3 4 8 9 10 11 12 13 14 15 17 18 19 20 21 31 32 33 34 This may occur through the development of psycho-physiologic conditioning in response to repeated awakenings, which in turn could lead to frustration and dissatisfaction with sleep behaviors.1 31 This may promote further ruminations about sleep and subsequent sleep onset or maintenance insomnia.1 31 Interestingly, a study employing nasal pressure transducer technology16 reported a surprisingly high rate of SDB in a select group of crime victims seeking treatment for insomnia,18 and subsequent CPAP treatment yielded marked insomnia improvement in some of these patients.34 Nonetheless, "CPAP for insomnia" would seem like a nonstarter. In our clinical and research experience, insomniacs can successfully adapt to CPAP, but the resources needed to facilitate the use of the breathing mask in an insomniac with SDB requires a threefold increase in time and effort compared to a classic OSA case.
The relationship between insomnia and SDB remains unclear. It is important to clarify why some patients with recurrent SDB awakenings suffer from insomnia whereas others do not. A thorough chronology of the inception of sleep disorders in such patients may provide clues to a potential bidirectional relationship between SDB and insomnia. Or, perhaps SDB patients with greater symptom distress from whatever causes are simply at greater risk for developing comorbid insomnia. While it seems probable that SDB could exacerbate insomnia complaints through varying patient response to sleep fragmentation and poor sleep quality, it is less certain how insomnia might exacerbate SDB. Speculatively, sleep fragmentation that is commonly associated with insomnia may worsen SDB through greater exposure to less stable, lighter stages of non-rapid eye movement sleep (stage 1) or through fragmentation effects on upper-airway muscle tone.35 Conversely, decreased REM sleep, also commonly observed in insomnia, may protect this type of patient from even worse SDB by decreasing exposure to the greater airway collapsibility associated with REM physiology.36
It is noteworthy that the two groups were very similar in their sleep breathing complaints and averaged similar BMIs, minSaO2, snoring patterns, and AHIs (both groups averaged severe indexes). Thus, to identify SDB-plus patients prior to polysomnographic evaluation requires a complete sleep history to evaluate insomnia symptoms and their impact on overall sleep dysfunction. Furthermore, in light of the markedly reduced mean sleep efficiencies reported in the SDB-plus group, it may be prudent to address sleep consolidation needs with behavioral methods before such patients undertake a CPAP titration or prior to their subsequent use of CPAP or oral appliances. Failing to educate or treat the patient with sleep hygiene maneuvers or advanced cognitive-behavioral therapies to consolidate sleep might be associated with CPAP noncompliance. Admittedly, treating such patients is time-consuming and difficult in a managed-care setting, particularly if there is an expectation that most SDB cases would follow the classic textbook description in which the patient is sleepy and has no insomnia complaints.
While the preceding discussion may seem axiomatic to some sleep specialists, more pulmonary medicine and critical care specialists are becoming involved in clinical sleep medicine,37 and it is unknown to what extent such providers receive training in the treatment of insomnia. Our objective is not to impugn the work of pulmonologists, a specialty group that brings substantial expertise and perspective to the field of sleep-disorders medicine. However, it has been noted38 that pulmonary sleep specialists may have greater difficulty in managing nonpulmonary cases, although, there is no extant literature on pulmonologists’ capacity to treat insomnia symptoms. To be sure, a university environment might attract more complex sleep-disorders patients. Notwithstanding, if SDB treatment compliance were linked inversely with comorbid insomnia in some proportion of patients, sleep medicine practitioners, including pulmonologists, will need proper training or experience in the use of sleep hygiene and other cognitive-behavioral strategies in the management of insomnia. As sleep medicine continues its evolution toward a multidisciplinary specialty, such expertise will be required routinely.10 39
Primary care physicians also have an important role to play in this process because they must be able to distinguish insomnia patients with SDB who need referral for polysomnography from insomnia patients without SDB who require other forms of treatment. Similarly, mental health practitioners who treat insomnia patients referred by other physicians must also consider the potential for undiagnosed SDB in their patients, particularly when pharmacotherapy or psychotherapy are ineffective in ameliorating insomnia symptoms. As such, it would be equally important to determine whether practicing psychiatrists and psychologists, specializing in insomnia treatment, receive appropriate training and experience in the assessment of SDB. These complex symptom presentations may be especially difficult to assess because certain SDB patients with severe insomnia, like the subset of 20 patients in our sample, describe such overarching episodes of sleeplessness that attention is diverted away from a potential SDB diagnosis. More active consideration of SDB in the differential diagnosis of insomnia will improve the capacity of all clinicians to identify these complex cases and to distinguish those who need polysomnography.
Generalizability of these findings to other environments is limited because data were collected from a single university sleep clinic, which may have disproportionately attracted more complex cases. The clinic also does not employ standardized insomnia instruments to measure insomnia severity. Therefore, it is unknown from this study the extent to which these comorbid insomnia symptoms were clinically relevant in these patients and how they might affect SDB treatment and other patient outcomes. The temptation may be to assume that these findings are epiphenomenal or coincidental and therefore clinically insignificant; however, such perspectives are probably a function of so little research having been conducted on patients with both insomnia and SDB. Regardless, no definitive practice parameters can be offered based on this study, although we anticipate that additional research in this area will confirm that SDB and insomnia co-occur frequently, and that each disorder has important influences on the other condition and on overall treatment success. Treatment studies measuring CPAP or oral airway device compliance with and without concurrent insomnia treatment for this type of SDB patient will provide greater clinical insights into these complex sleep-disorders cases.
In summary, 50% of a representative sample of SDB patients appeared to have clinically substantive insomnia symptoms; of these 116 cases, 20 patients presented with chief complaints of insomnia only. For patients with insomnia and SDB, assessment and treatment is likely to be more time intensive if appropriate therapeutic regimens were to be provided for both sleep disorders. In the current climate of managed-care medicine and its impact on sleep-disorders centers and laboratories, it remains to be seen whether or not these complex patients are receiving the proper amount and quality of care.
|
Appendix 1 |
|---|
|
TOPAbstractIntroductionMaterials and MethodsResultsDiscussionAppendix 1References |
|---|
Sleep-Wake Schedule
1. On average, how long does it usually take you to FALL
ASLEEP?
2. On average, how many HOURS OF SLEEP do you usually get?
3. On average, how many HOURS IN BED do you usually spend?
4. What is your usual bedtime?
5. What is your usual wake-up time?
Sleep and Breathing
1. Would you or others say that you SNORE LOUDLY?
2. Have you or others ever MOVED from your bed/bedroom because of your snoring?
3. Would you or others say that you STOP BREATHING while you sleep?
4. Would you or others say that you CHOKE, GASP, or STRUGGLE for breath in your sleep?
5. Do you have any other TROUBLE BREATHING while you sleep?
Sleep and Insomnia
1. Does it usually take you longer than 30 MINUTES to fall
asleep?
2. Do you WAKE UP a lot during your sleep?
3. If awakened, do you have trouble RETURNING to sleep?
|
Acknowledgements |
|---|
|
Footnotes |
|---|
This research was conducted at the Sleep and Human Health
Institute and the University Hospital Sleep Disorders Center.
Received for publication January 25, 2001. Accepted for publication July 17, 2001.
|
References |
|---|
|
TOPAbstractIntroductionMaterials and MethodsResultsDiscussionAppendix 1References |
|---|
This article has been cited by other articles:
|
|
 |
|
  S. P. Patil, H. Schneider, A. R. Schwartz, and P. L. Smith Adult Obstructive Sleep Apnea: Pathophysiology and Diagnosis Chest, July 1, 2007; 132(1): 325 - 337. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. A. Bradshaw, G. A. Ruff, and D. P. Murphy An oral hypnotic medication does not improve continuous positive airway pressure compliance in men with obstructive sleep apnea. Chest, November 1, 2006; 130(5): 1369 - 1376. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. S. Gooneratne, P. R. Gehrman, J. E. Nkwuo, S. L. Bellamy, S. Schutte-Rodin, D. F. Dinges, and A. I. Pack Consequences of comorbid insomnia symptoms and sleep-related breathing disorder in elderly subjects. Arch Intern Med, September 18, 2006; 166(16): 1732 - 1738. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. D. Wells, R. C. Day, R. M. Carney, K. E. Freedland, and S. P. Duntley Depression Predicts Self-reported Sleep Quality in Patients With Obstructive Sleep Apnea Psychosom Med, September 1, 2004; 66(5): 692 - 697. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K.-F. Chung, B. Krakow, D. Melendrez, T. D. Warner, and B. N. Sisley Relationships Between Insomnia and Sleep-Disordered Breathing Chest, January 1, 2003; 123(1): 310 - 313. [Full Text] [PDF]
|
|
|
|
|
|
D. Posner and N. A. Collop Need for Broader Training in Sleep? Chest, August 1, 2002; 122(2): 751 - 751. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
