Im confused and new.  Well, I have my report or what the Doc gave me when I asked. Doesn't look like anything that ya'll have been posting. Does say I have something and Doc is scheduling me to go back to try the c-pap. Was referred here by a very wise post on another board dealing with COPD which I also have. I am a 37 year old female. I feel like once I learn everything thats wrong with me I could be a Doc. Except right now Im tooooo tired to get off the couch. Anyway please someone explain to me what this is I got the short version. Didn't get all the numbers to compare to everyone else. Am I really bad, fair or what?

The study demonstrates severe snore arousal in addition to severe sleep fragmentation with multiple awakenings and arousals throughout the night with significantly decreased sleep efficiency of only 80%  after prolonged sleep latency of 26 minutes. There were on average 5.2 apneas per hour. Oxygensaturation is dropped to a close 90% from a normal awaking baseline of 97%. There was some tachycardia with heart rate as high as 110 with a low of 70. there were a number of periodic limb movements, but these did not lead to seperate arousals. There were no EEG or EKG abnormalities seen.

Interpretation:
This study does indeed show significant sleep disordered breathing with primarily severe snore arousal syndrome. She demonstrates severe pathologic hypersomnia with an Epworth Sleepiness Scale score of 20, normal being less than 10.  Given all these factors then, a repeat study with CPAP titration is suggested, followed then by clinical follow up and consideration for home trial treatment of CPAP if the patient is able to tolerate that treatment.

The only thing that I could figure out is that it took me 26 minutes to fall asleep at the lab. Although I was falling asleep when he was sticking the electrode on my head. At least I think thats what that # means.  

Please some info on my study????? Thanks!!!!

H Nette!
Sounds like UARS, here's a good summary, taken from the Cleveland Clinic:

Quote:

UPPER AIRWAY RESISTANCE SYNDROME
UARS can cause symptoms similar to those found in OSA, yet this syndrome is considerably different due to the lack of oxygen desaturations found during sleep studies. UARS was a term first applied to patients who were found to have excessive daytime sleepiness without a clear cause on a multiple sleep latency test, which was further documented by an overnight polysomnogram. These patients were often labeled as having idiopathic hypersomnia. After many of these individuals were further tested with "invasive polysomnography" (including an esophageal balloon transducer and full pneumotachograph), these patients were found to have increased upper airway resistance. Resistance was indicated by increased negative esophageal inspiratory pressure.
DEFINITION
UARS is characterized by repeated arousals due to upper airway resistance that lead to excessive daytime sleepiness. This disorder often produces a snoring pattern termed crescendo snoring. When the crescendo snoring episode ends, an arousal occurs with rapid decrease in upper airway resistance; the snoring then disappears and stops for a period. UARS events are noted to be typically short—one to three breaths in duration. These events have recently been termed respiratory effort-related arousals (RERAs). In UARS, unlike in OSAHS, there is no evidence of oxygen desaturations.2 For the measurement criteria to be classified as a RERA, there must be a pattern of progressively increased negative esophageal pressure that is terminated by a sudden change in the pressure to a less negative level and a sleep arousal. Furthermore, the event must last 10 seconds or longer.
Recognition of UARS has led to a more conservative use of the term snoring. Patients who snore and have no daytime symptoms or excessive daytime sleepiness are called primary snorers. Patients who snore and have daytime sleepiness symptoms may have UARS.
 
PREVALENCE
The prevalence of UARS in the general adult population is unknown, yet it has been estimated to be as high as 10% to 15% when the definition is applied to adults that suffer from snoring and excessive daytime sleepiness. It has been suggested that UARS occurs in a less obese younger population and more frequently in females than does OSAHS.
PATHOPHYSIOLOGY
Guilleminault and coworkers demonstrated that many nonapneic patients show a reduction in cross-sectional area of the pharynx during sleep. Reduction in airway area is sufficient enough to avoid hypopneas and apnea but enough to increase upper airway resistance. Patients with UARS suffer from increased airway resistance, which generates snoring, then leads to arousal episodes and ultimately to excessive daytime sleepiness. The physiologic basis of arousals is based on the generation of negative intrathoracic pressure as detected by various mechanoreceptors located in the upper airway. After arousal, an immediate reduction in airway resistance is noted, accounting for the cessation of snoring for a period. The American Academy of Sleep Medicine Task Force published a report that notes the key role that RERA plays in the pathophysiology of UARS in the absence of apnea or hypopnea.
SIGNS AND SYMPTOMS
Although patients with UARS share no standard clinical presentation, the cardinal symptom of UARS is excessive daytime sleepiness or fatigue. Patients also may complain of difficulty with concentration, morning headaches, impotence, difficulty sleeping, or restless sleep. They often report having repetitive nightmares, such as choking or being buried alive, which may suggest difficulty with breathing. Abnormal oronasal-maxillomandibular features are noted on visual examination, including deviated nasal septum, enlarged turbinates, crooked teeth, laxity of the temporo-mandibular joint with an audible click, or a narrow face with a high hard palate or enlarged or elongated uvula.28 Bed partners may complain about the cycle of the crescendo snoring pattern, with short arousals and abrupt cessation of snoring only to reoccur later. Again, snoring is not a necessary feature of this syndrome because the upper airway resistance is due to a partial decrease in airway cross-sectional area; therefore, the airway walls do not have to vibrate to produce a snoring sound.
DIAGNOSIS
UARS should not be overdiagnosed. Three essential clinical features consistently have been used by investigators and authors to diagnose UARS:

excessive daytime somnolence;
an elevated EEG arousal index, with the arousal related to increased respiratory efforts; and
a normal respiratory disturbance index (RDI) of less than five events per hour of sleep.
UARS is present only if there are documented elevations in upper airway resistance, sleep fragmentation, and daytime dysfunction or excessive daytime sleepiness. The clinical complaint of fatigue or daytime sleepiness can be documented by an abnormal increase in the Epworth Sleepiness Scale score to a value greater than 10 or by use of another validated sleep questionnaire. In addition, a low RDI is needed to distinguish UARS from OSAHS. The elevated EEG arousal index related to increased respiratory efforts is the specific measurement that distinguishes UARS from idiopathic hypersomnolence.27 The clinical complaint of snoring (including crescendo snoring), increase in snoring intensity before EEG arousals, and clinical improvement with a short-term trial of nasal CPAP can be regarded as supportive features of UARS.

The diagnosis of UARS requires full polysomnography. Although measurements of upper airway resistance were first used, based on the original definition of UARS, substitute measurements of effort and ventilation may be used as long as no evidence of hypopneas or apneas are present. A normal apnea/hypopnea index (AHI) of less than five events per hour of sleep should be seen on the polysomnograph. Additionally, EEG arousals should occur at a rate of more than 10 per hour of sleep and must be associated with increased respiratory effort (usually made by use of nocturnal esophageal pressure monitoring).

Current literature supports that esophageal pressures greater than -10 cm H20 are abnormal. The measurement of esophageal pressure is the gold standard for measuring respiratory effort and is the only consistent measurement reported for the diagnosis of UARS. Substitute measurements can include inductive plethysmography, strain gauges, oronasal temperature measurements, nasal pressures, and the carbon monoxide levels in exhaled gas. Arousals are documented from the EEG tracings and electromyography, although changes in heart rate, ventilation, and other measurements of autonomic activity may play some role in the future.
 
TREATMENT
CPAP, surgery, oral appliances, and weight loss are possible treatment options for UARS. Ideally, the recommended treatment of UARS should be effective, relieve symptoms, and produce normalized studies posttherapy. These therapies also should be covered by health insurance and have long-term effectiveness. Thus far, however, none of the proposed treatments have fully met these criteria.
Although currently available data supports the use of nasal CPAP as a treatment option for UARS, compliance may be an issue, making this treatment modality less practical. Also, the safety and efficacy of surgical interventions have been poorly documented in the literature. Surgical intervention in the UARS population includes LAUP, which has been shown in small studies to improve sleep quality and daytime somnolence. Palatal tissue reduction by radiofrequency ablation and the use of oral appliances may be safer and very effective, although further study of these modalities is needed.

Another approach to the treatment of UARS is to create a more-negative esophageal pressure and delay arousal times through the application of topical anesthetics to the mechanical receptors responsible for arousals in the upper airway.
 
OUTCOMES
Data in the sleep literature are not yet clear-cut regarding the efficacy, safety, and compliance of UARS treatment modalities, including weight loss, nasal CPAP, oral appliances, and surgery

The whole article with references is at:
The Cleveland Clinic
sleepydave

Thanks Sleepydave- That sure is alot of information to digest.  I'm still not sure if I understand the severity. I'll have to do more research I guess to understand it all. I know if I go by how I feel through the day, I can hardly stay awake. I need a nap that can last from 3-6 hours,  sometimes more than one. I can't watch a movie without falling asleep. I'm  asleep by 10 or 11 pm and I wake up at 3,4,or5am. I have never slept well as long as I can remember. But I thought this was a progression of the COPD I have. Im glad its not. But Im ready to get something done. I'm sleeping my life away....


P.S.  If you get a chance, until Im a little more up on things, can it be dumbed down a little bit?  And what I should ask the Doctor.  I know so much about COPD & Emphysema because I spent months researching it. I just don't know if I have the energy. Thanks

Hi Nette!
Well, the best thing to do would be to get the long report, and look for the number of arousals you had during all respiratory events- apneas, hypopneas, and RERAs.  If that's a big number (>5.0 really, to start considering UARS), then CPAP has a shot at addressing your sleepiness.  Then you can get the CPAP report and objectively measure how the UARS was addressed.
Also, there's plenty of other reasons why one would be sleepy, and if you're only getting 4 hours of sleep per night, and that sleep is poor quality, yeah, it's gonna be tough getting through the day.  Get all the sleep stage% and other info that you can, that might be helpful.
If I may ask, how severe is the COPD?  Does that affect your sleep quality, do you sleep with pillows, have trouble breathing supine?
Check back.
sleepydave