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Evidence-Based Reviews


Struggling not to nap: Causes of daytime sleepiness

Depressive symptoms may mask a sleep disorder.

Vol. 5, No. 12 / December 2006
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Poor energy, hypersomnia, amotivation, irritability, and frustration can suggest depression or other psychiatric disorders to busy primary care physicians. As a result, psychiatrists often are referred patients with excessive daytime sleepiness (EDS) caused by undiagnosed primary sleep disorders.

Physicians may miss obstructive sleep apnea (OSA), restless legs syndrome, circadian rhythm disorders, or narcolepsy because:

  • many have little training in sleep disorders and limited time to diagnose them1
  • patients do not report sleepiness or recognize it as a legitimate medical concern
  • definitive diagnostic tests are expensive and usually are not ordered.

Psychiatrists, therefore, need a clear understanding of the EDS differential diagnosis to determine whether a patient’s behavioral symptoms are a sleep or psychiatric issue.

Box 1

Epworth Sleepiness Scale

How likely are you to doze off or fall asleep in the following situations, in contrast to feeling just tired? This refers to your usual way of life in recent times. 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  Situation

             Sitting and reading

             Watching TV

             Sitting inactive in a public place (such as in a theater or a meeting)

             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

Scoring key

1 to 6        Getting enough sleep

7 to 8        Average

>8          Seek a sleep specialist’s advice without delay

Assessing the sleepy patient

Sleepiness is an inability to stay awake at appropriate times. Fatigue, by comparison, does not involve sleepiness but very low energy associated with wakefulness. In general, sleepy patients get transient relief from napping, whereas fatigued patients report they cannot fall asleep.

Untreated EDS results in compromised quality of life, reduced productivity, and public safety concerns such as falling asleep while driving.2 Sleep complaints fall into three major categories:

  • EDS
  • insomnia (marked by distress because of poor sleep, but usually with minimal EDS)
  • unusual nocturnal behaviors (ranging from arm waving to violent behaviors.

When you evaluate a patient with sleep complaints, valuable sources of data include observation, questionnaires, and screening devices. The most important may be common sense.

Observation. Observe the patient in the waiting room or office before starting the interview. Did he or she nod off while waiting to see you? Pay attention to anyone who appears sleepy—even those who deny having trouble staying awake. Over time, sleepy patients can lose their perspective on alertness. Some have had EDS so long that they no longer recall what it is like to feel fully awake.

Collateral history often is important because family members probably have observed the sleeping patient. The bed partner can provide information about snoring, irregular breathing, leg kicks, unplanned naps, and strained interpersonal relationships because of EDS. For the patient without a bed partner, consider interviewing a travel companion.

Questionnaires. Few useful screening tests exist for sleepiness; most are neither reliable nor valid. One of the better questionnaires—the Epworth Sleepiness Scale (Box 1)—helps confirm the presence of sleepiness with a score >8, differentiating the inability to stay awake from fatigue. This brief questionnaire also provides a useful measure of sleepiness severity.3

The Epworth scale’s value is limited because its questions of specific time and context might not represent a patient’s experiences. Additional validated surveys include the Pittsburgh Sleep Quality Inventory and several for sleep apnea.4

Screening. Electroencephalographic (EEG) monitoring can accurately measure the patient’s degree of sleep disruption. This information is key to understanding if a patient’s EDS is caused by a physiologic condition that prevents quality nocturnal sleep.

None of the widely used screening devices that assess leg kicks indicate the presence of possible periodic limb movements.

Overnight pulse oximetry has been used to screen for sleep-disordered breathing5 but also has limitations:

  • Most pulse oximeters do not provide information about sleep stage or body position.
  • Patients with sleep-disordered breathing can lack adequate oxygen desaturations but have frequent EEG arousals related to sleep issues. Because EEG data are not collected during arousals, pulse oximetry would generate a false-negative result in this scenario, which occurs most often in female and thin patients.
  • Oximetry provides only oxygen saturation data and possibly heart rate, whereas other physiologic processes such as body movement or sleep architecture can be disrupted repetitively during sleep.

Common sense. The most productive tools for detecting sleep disorders are intuition and common sense. The Figure suggests sequential questions that might uncover specific sleep disorders. Then the decision whether to refer the patient to a sleep disorder center for diagnostic testing depends on the type of sleep disorder you detect.

Box 2

How to help sleep apnea patients adjust to using ‘CPAP’ machines

Nasal continuous positive airway pressure

(CPAP) should 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.

For some patients, CPAP is started in the second half of a “split-night” sleep study after a diagnosis of obstructive sleep apnea (OSA) is made. Other patients return a second night for a nasal CPAP trial. Those with severe OSA might notice improved sleep quality and reduced EDS after only a few hours of CPAP use. Some wish to start CPAP treatment immediately.

Advances in masks and equipment have improved patient adherence to CPAP. Innovations include auto-titrating machines, in which the pressure level can be varied depending on sleep state or body position. Many machines include a data microchip that allows the clinician to determine duration of usage, then use that information to counsel the patient about adherence, if necessary.

Patient education also can promote CPAP adherence. When patients are first told they might need to sleep each night wearing a nasal mask, they often voice well-founded concerns about comfort, claustrophobia, or sexual activity.

Obtaining the support of the bed partner by welcoming her or him to all appointments, including educational activities, is optimal. The bed partner’s concerns about the patient’s excessive snoring or apneas probably were the impetus for the appointment in the first place.

Medication. Some patients benefit from 1 to 2 weeks of a sleeping medication such as zolpidem or trazodone while they acclimate to using nasal CPAP.

Figure The sleepy patient: Possible medical and psychiatric explanations



* Supportive factors: Persuasive if present, but if absent do not exclude possible conditions

Obstructive sleep apnea

Because OSA affects at least 4% of men and 2% of women,6 you are virtually assured of seeing undiagnosed patients. OSA 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 sleep is fragmented by frequent arousals.

Obese patients, because of their body habitus, are at higher risk for OSA than patients at normal weight. Carefully screen patients for OSA if they develop weight problems while taking psychotropics, such as antipsychotics.

Alcohol or sedatives used at bedtime can aggravate OSA. These substances promote muscle relaxation and increase the arousal threshold so that patients do not awaken readily when apneas occur.

Long-term complications of untreated OSA include sleepiness leading to accidents, hypertension, cerebrovascular disease, and progressive obesity. Data also associate OSA with cardiovascular complications such as arrhythmias, congestive heart failure, and myocardial infarction.7

Physical examination focuses on detecting:

  • nasal obstruction (have patient sniff separately through each nostril)
  • large neck
  • crowded oropharynx (low-hanging palate, reddened uvula, enlarged tonsils, large tongue relative to oropharynx diameter)
  • jaw structure (particularly a small, retrognathic mandible).

Sleep studies. Referral for nocturnal polysomnography might be the next step. A comprehensive sleep study collects data about respiratory, cardiovascular, and muscle activity at night, as well as the sounds the patient makes—such as snoring or coughing—when asleep. EEG monitoring also is performed. OSA may be diagnosed if repeated episodes of reduced airflow and oxygen desaturation (arousals) are observed as brief shifts in EEG frequency.

Treatment. First-line interventions for the patient with OSA include:

  • no alcohol 1 to 2 hours before bedtime
  • sleeping on the side instead of the back
  • weight loss (ideally with exercise)
  • nasal sprays for allergies.

If first-line treatments are ineffective, nasal continuous positive airway pressure (CPAP) works well for most 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 upper airway (Box 2).

Surgical options. The most common surgeries for OSA are uvulopalatopharyngoplasty and laser-assisted uvulopalatoplasty. Others include tongue reduction and mandibular advancement.

The response rate to surgery averages 50%, depending on patient characteristics and procedure.9 Positive outcomes are most likely for thin patients with obvious upper airway obstruction, including deviated nasal septum, large tonsils, low-hanging palate, and large uvula. Postsurgical complications include nasal regurgitation, voice change, pain, bleeding, infection, tongue numbness, and snoring without apnea (silent apnea).

Oral appliances open the oropharynx by moving the mandible and tongue out of way. Patients with mild to moderate OSA accept these devices well. Evidence suggests that oral appliances improve sleep and reduce EDS more effectively than nasal CPAP and are preferred by patients.10

Oral devices have drawbacks, however. In most settings, their 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 appliance; this can pose a hardship for patients who live a distance from the provider.

Restless legs syndrome

Patients with restless legs syndrome (RLS) typically report 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 Onset can occur in childhood, and in some cases there is a familial tendency.

Most patients with RLS 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, and these cases usually are not treated.

The history usually confirms RLS. Order sleep studies only if you suspect a coexisting sleep problem or the diagnosis is unclear.

A suspected mechanism of restless legs is dopamine deficiency. Low serum ferritin levels have been associated with RLS—presumably because iron is a cofactor necessary for dopamine synthesis12—and may be diagnostically helpful.

Box 3

2 techniques to modify patients’ abnormal sleep schedules

The most common technique is to ask the patient to establish a consistent awakening time and a regular bedtime. Initially this could be unconventional by societal standards—such as bedtime at 5 AM and arising at 2 PM. After this pattern is in place, the patient gradually shifts the timing by 1 hour per day. Most patients find it easier to delay rather than advance the bedtime until it conforms to the desired time.

Reinforce this new sleep pattern with a structured daytime schedule that includes predictable mealtimes, regular exercise, social activities, and possibly bright light exposure. Provide reinforcement in the morning for patients with delayed sleep phase disorder and in the evening for advanced sleep phase disorder. These interventions take time and discipline.

Another approach is for the patient to skip sleep one night and, in a sleep-deprived state, establish a new bedtime at the desired time. Use the same modalities listed above to reinforce (“entrain”) this schedule; otherwise the patient will slip back into the previous abnormal sleep-wake rhythm.

Treatment can include iron repletion when indicated. Medications include dopaminergic agents, most notably pramipexole and levodopa/carbidopa. Other options include gabapentin, benzodiazepines, and narcotics.

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