Excessive daytime sleepiness: Diagnosing the causes
Although poor energy, hypersomnia, amotivation, irritability, and frustration often suggest a depressive disorder or chemical dependency, these symptoms also may point to one or more sleep disorders. The author reviews assessment, diagnostic possibilities, and treatment options for the sleepy patient.
Untreated excessive daytime sleepiness (EDS) results in compromised quality of life, reduced productivity, and public safety concerns.1 Obstructive sleep apnea (OSA), restless legs syndrome, circadian rhythm disorders, and narcolepsy are frequently underdiagnosed sleep disorders that can cause EDS. These conditions commonly go undetected and untreated for several reasons:
- Patients may not recognize sleepiness as a legitimate medical concern.
- Physicians, with few exceptions, typically have little training in sleep disorders and limited time to diagnose them.2 Screening questions regarding sleep are typically absent.
- Definitive diagnostic tests are costly.
As a result, many patients go without appropriate sleep evaluations. Instead a depressive or other psychiatric disorder may be suspected because of the sleepy patient’s poor energy, hypersomnia, amotivation, irritability, and frustration. Because of ongoing behavioral symptoms, patients with an undiagnosed primary sleep disorder are often referred to psychiatrists. Thus, a clear understanding of the differential diagnosis of EDS is crucial.
Patients with sleep issues fall into three major categories:
- Patients with EDS.
- Individuals with insomnia, another large group often seen by psychiatrists. Generally, these patients are less hesitant than patients with EDS to seek help because of the marked distress they suffer nightly when trying to sleep. Insomniacs typically experience minimal EDS.
- Patients with unusual behaviors at night that range from arm waving to violent behaviors.
Assessing the sleepy patient
When evaluating a patient with sleep complaints, several valuable sources of data come into play.
Initially, observe the patient in the waiting room or office before starting the interview. Did the patient nod off while waiting for his or her appointment? Pay attention to any patient who appears sleepy—even if he or she denies having trouble staying awake. Over time, sleepy patients may have lost their perspective on alertness. Some patients have had EDS for so many years that they no longer recall what it is like to feel fully awake.
Collateral history is often important because family members generally observe the sleeping patient. The bed partner often provides valuable information about snoring, irregular breathing leg kicks, unplanned naps, and strained interpersonal relationships due to EDS. For the patient who does not have a bed partner, ask his or her travel companion, with whom the patient may have shared accommodations.
Unfortunately, few useful screening tests exist. Most questionnaires about sleepiness are neither very reliable nor valid. One of the better questionnaires, the Epworth Sleepiness Scale, helps confirm the presence of sleepiness with a score <8, differentiating the inability to stay awake from fatigue. (Box 1 can be cut out, copied, and handed to patients). This brief questionnaire also provides a useful measure of severity.3
The value of the Epworth scale is limited, however, because patient answers often are based on a specific time and context that may not be representative. Additional validated surveys include the Pittsburgh Sleep Quality Inventory and several that focus on OSA.4
EPWORTH SLEEPINESS SCALE
How likely are you to doze off or fall asleep in the following situations, in contrast to feeling just tired? Even if you have not done some of these things recently, try to work out how each situation would affect you now. Use the scale below to choose the most appropriate number for each situation:
- 0 no chance of dozing
- 1 slight chance of dozing
- 2 moderate chance of dozing
- 3 high chance of dozing
Chance of dozing
Sitting and reading
Sitting inactive in a public place (e.g., a theater or a meeting)
Sitting as a passenger in a car for an hour without a break
Lying down to rest in the afternoon when circumstances permit
Sitting and talking to someone
Sitting quietly after a lunch without alcohol
In a car, while stopped for a few minutes in traffic
Johns, M. Sleep 14:540-545, 1991.
Electroencephalographic (EEG) monitoring can accurately measure the patient’s degree of sleep disruption. This information is critical in understanding if a patient’s EDS is caused by a physiologic condition that prevents quality nocturnal sleep. At this time, however, no portable devices that employ EEG technology are used in clinical settings.
Additionally, none of the widely used screening devices that assess leg kicks indicate the presence of possible periodic limb movements.
Even though overnight pulse oximetry has been used to screen for sleep-disordered breathing,5 the technology has limitations. For one, most pulse oximeters do not provide information about sleep stage or body position. Some patients with significant sleep-disordered breathing lack adequate oxygen desaturations but have frequent EEG arousals due to sleep issues. In this case, pulse oximetry would generate a false negative result because EEG data is not collected. The inadequate sensitivity is most likely to occur with females and thin patients.
Oximetry provides only one or two types of data (oxygen saturation plus possibly heart rate), while other physiologic processes, e.g., body movement or sleep architecture, can repetitively be disrupted during sleep.
The most critical steps in detecting sleep disorders do not require technology or specialized expertise, but rather intuition and common sense. The psychiatrist should consider the possibility of a sleep disorder and incorporate pertinent questions into the clinical interview. Figure 1 lists sequential questions that might uncover specific sleep disorders. Once suspected, the decision whether to refer the patient to a sleep disorder center for diagnostic testing depends on the type of sleep disorder detected.
Diagnosing and treating OSA
Recent epidemiologic studies show that OSA affects at least 4% of men and 2% of women in the United States.6 Psychiatrists are virtually assured of seeing patients with undiagnosed OSA. The condition is caused by repeated collapse of the soft tissues surrounding the upper airway, decreasing airflow that is restored when the patient briefly awakens. Patients develop EDS because of sleep fragmented by frequent arousals.
Figure 1 THE SLEEPY PATIENT: Possible medical and psychiatric explanations
Obese patients are at higher risk than are patients at normal weight because of their body habitus. Alcohol or sedative medication use close to bedtime can aggravate OSA. These substances promote muscle relaxation and increase the arousal threshold, meaning that patients do not wake readily when apneas occur.
Long-term complications of untreated OSA include sleepiness leading to accidents, hypertension, cerebrovascular disease, and progressive obesity. New data associate OSA with multiple potential cardiovascular complications (arrhythmias, congestive heart failure, and myocardial infarction).7 Therefore, recognition and treatment are paramount.
The physical examination should focus on detecting nasal obstruction (having the patient sniff separately through each nostril can be helpful), big neck, crowded oropharynx (a low-hanging palate, reddened uvula, enlarged tonsils, large tongue size relative to oropharynx diameter) and jaw structure (particularly a small retrognathic mandible).
Referral for nocturnal polysomnography might be the next step. During a comprehensive sleep study, data is collected about respiratory, cardiovascular, and muscle activity at night, as well as the sounds the patient makes (e.g., snoring, coughing) when asleep. EEG monitoring also is performed. OSA may be diagnosed if repeated episodes of reduced airflow and oxygen desaturation are observed; these typically result in brief shifts in EEG frequency called arousals.
First-line interventions for OSA include avoidance of alcohol within 1 to 2 hours of bedtime, sleeping on the side instead of the back, weight loss (ideally with a regular exercise program), and nasal sprays for allergies.
If the first-line treatments for OSA are ineffective, nasal continuous positive airway pressure (CPAP) works well for almost all patients who adhere to the regimen.8 CPAP requires the patient to wear a nasal mask that delivers room air, splinting open the nasopharynx and the upper airway (Box 2). Some patients benefit from a brief trial of a sleeping medication, e.g., zolpidem or trazodone, for the first 1 to 2 weeks of nasal CPAP usage.
HOW CPAP WORKS
Nasal continuous positive airway pressure (CPAP) must be started in an observed setting so that the clinician can determine the optimal amount of positive pressure needed to keep the upper airway patent. CPAP can be started during the second half of a “split-night” sleep study after obstructive sleep apnea (OSA) has been diagnosed. Alternatively, the sleep laboratory might ask the patient to return for a second night for a trial of nasal CPAP.
Patients with severe OSA might notice improved sleep quality and reduced EDS, even after only a few hours of use. Such patients sometimes wish to start CPAP treatment immediately.
Overall, advances in masks and equipment have improved patient adherence to CPAP. Such innovations include auto-titrating machines, in which the pressure level can be varied depending on sleep state or body position. Many newer machines also have a data microchip that allows the clinician to determine the duration of usage, then use that information to counsel the patient about adherence if necessary.
Patient education also can promote CPAP adherence. Upon being first told they might need to sleep each night wearing a nasal mask, patients often voice well-founded concerns about comfort, claustrophobia, or sexual activity.
As part of a comprehensive approach at the Mayo Sleep Disorders Center, patients watch an educational videotape, tour the sleep laboratory bedrooms before the sleep study, and are carefully fitted for masks. Ideally, the technologists interact with the patient during the sleep study to adjust the headgear and fine-tune other aspects of the equipment. The sleep specialist meets with the patient to compare the baseline diagnostic study results with changes in breathing patterns after a trial of nasal CPAP.
Other useful patient compliance tools include a CPAP informational handout, telephone access to nursing staff, and a 30-day follow-up visit.
Obtaining the support of the bed partner by welcoming her or him to all appointments, including educational activities, is optimal. The bed partner was likely the impetus for the appointment in the first place because of concerns about excessive snoring or apneas.
Image reprinted from Oct. 2001 Mayo Clinic Health Letter with permission of Mayo Foundation for Medical Education and Research, Rochester, MN 55905
Surgical options exist for OSA. The most common procedures are uvulopalatopharyngoplasty (UPPP) and laser-assisted uvulopalatoplasty (LAUP). Other procedures in use include tongue reduction and mandibular advancement.
The response rate to OSA surgery averages around 50% but varies on the patient’s characteristics and procedure selected.9 Positive outcomes are most likely for thin patients with obvious upper airway obstruction, including a deviated nasal septum, large tonsils, a low-hanging palate, and large uvula. Potential complications include nasal regurgitation, voice change, postoperative pain, bleeding, infection, tongue numbness, and snoring without apnea (silent apnea).
Oral appliances have a vital niche in OSA treatment. Multiple devices have been developed that open the oropharynx by moving the mandible and tongue out of way. A growing body of data shows that oral appliances improve sleep and reduce EDS and promote patient satisfaction more effectively than nasal CPAP.10 Several studies also show that patients with mild to moderate OSA accept these devices well.
Oral devices do have drawbacks, however. In most settings, effectiveness cannot be observed during a “split-night” laboratory sleep study because the patient has not yet purchased the device. Also, multiple visits sometimes are required to custom fit the oral appliance; this can pose a hardship to patients who live a distance from the provider.
Restless legs syndrome, periodic limb movement disorder
The patient with restless legs syndrome typically reports a restless painful feeling in the limbs that occurs in the evening and at night, disrupting sleep. This condition, which affects 10% of the population, is associated with aging, blood loss, anemia, peripheral neuropathies, and pregnancy.11 Patients can have childhood onset and in some cases there is a familial tendency.
Most patients with restless legs syndrome have periodic limb movements (repetitive leg jerks or twitches). The clinical significance of periodic limb movements with no subjective disagreeable feelings in the limbs is controversial. Typically, treatment is not instituted in these cases.
The history usually confirms the diagnosis without a sleep study. Sleep studies are used only if a co-existing sleep problem is suspected or if the diagnosis is not clear-cut.
One suspected mechanism of restless legs syndrome is a dopamine-deficient state. A serum ferritin level can help detect a relative iron deficiency, iron being a cofactor for dopamine synthesis.12