| Hypersomnia | |
|---|---|
| Classification and external resources | |
| MeSH | D006970 |
The term hypersomnia (not to be confused with the disease idiopathic hypersomnia) refers to a large group of disorders characterized by excessive daytime sleepiness (EDS). As per the revised International Classification of Sleep Disorders, this group of disorders includes numerous different etiologies. Hypersomnia can be primary (of central/brain origin), or it can be secondary to another medical condition (see Differential Diagnosis). Both hypersomnia and EDS "are complex traits whose formal study is in its infancy, and whose socioeconomic burden is enormous."
In the proposed 5th edition of the Diagnostic and Statistical Manual of Mental Disorders, due for publication in May 2013, hypersomnia appears under sleep-wake disorders as hypersomnolence, of which there are several subtypes.
The main symptom of hypersomnia is excessive daytime sleepiness (EDS), which has occurred for at least 3 months prior to diagnosis.
Hypersomnia affects approximately 5% of the general population, "with a higher prevalence for men due to the sleep apnea syndromes."
"The severity of daytime sleepiness needs to be quantified by subjective scales (at least the Epworth Sleepiness Scale) and objective tests such as the multiple sleep latency test (MSLT)." After it is determined that EDS is present, a complete medical examination and full evaluation of potential disorders in the differential diagnosis should be undertaken. For the patient, the process can be tedious, expensive and time-consuming.
Hypersomnia can be primary (of central/brain origin), or it can be secondary to any of numerous medical conditions. However, it is very important to keep in mind that more than one type of hypersomnia can coexist in a single patient. Even in the presence of a known cause of hypersomnia, one should assess the contribution of this cause to the complaint of EDS. When specific treatments of the known condition do not fully suppress EDS, additional causes of hypersomnia should be sought. For example, if a patient with sleep apnea has resolution of their apneas, but not their EDS, upon treatment with CPAP (continuous positive airway pressure), it is necessary to seek other causes for the EDS. Obstructive sleep apnea “occurs frequently in narcolepsy and may delay the diagnosis of narcolepsy by several years and interfere with its proper management.”
The true primary hypersomnias include: narcolepsy (with and without cataplexy); idiopathic hypersomnia; and recurrent hypersomnias (like Klein-Levin syndrome).
There are also several genetic disorders that may be associated with primary/central hypersomnia. These include: Prader-Willi syndrome; Norrie disease; Niemann–Pick disease, type C; and myotonic dystrophy). However, hypersomnia in these syndromes may also be associated with other secondary causes, so it is important to complete a full evaluation. Interestingly, myotonic dystrophy is often associated with SOREMPs (sleep onset REM periods, such as occur in narcolepsy).
There are many neurological disorders that may mimic the primary hypersomnias narcolepsy and idiopathic hypersomnia: brain tumors; stroke-provoking lesions; and dysfunction in the thalamus, hypothalamus, or brainstem. Also, neurodegenerative conditions such as Alzheimer's disease, Parkinson's disease, or multiple system atrophy are frequency associated with primary hypersomnia. However, in these cases, one must still rule out other secondary causes.
Early hydrocephalus can also cause severe EDS. Additionally, head trauma can be associated with a primary/central hypersomnia, and symptoms similar to those of idiopathic hypersomnia can be seen within 6-18 months following the trauma. However, the associated symptoms of headaches, memory loss, and lack of concentration may be more frequent in head trauma than in idiopathic hypersomnia. "The possibility of secondary narcolepsy following head injury in previously asymptomatic individuals has also been reported."
Secondary hypersomnias are extremely numerous.
Hypersomnia can be secondary to disorders such as clinical depression, bipolar disorder, celiac disease, uremia, chronic fatigue syndrome, and fibromyalgia. Hypersomnia can also be a symptom of other sleep disorders such as narcolepsy, sleep apnea, restless leg syndrome and periodic limb movement disorder. It may also occur as an adverse effect of taking certain medications (e.g. some psychotropics for depression, anxiety, or bipolar disorder), of withdrawal from some medications, or of drug or alcohol abuse. A genetic predisposition may also be a factor.
Sleep apnea is the most frequent cause of secondary hypersomnia, affecting up to 4% of middle-aged adults, mostly men. Upper airway resistance syndrome is a clinical variant of sleep apnea that can also cause hypersomnia. Just as other sleep disorders (like narcolepsy) can coexist with sleep apnea, the same is true for UARS. There are many cases of UARS in which EDS persists after CPAP treatment, indicating an additional cause, or causes, of the hypersomnia and requiring further evaluation.
Regarding periodic limb movement disorder (PLMS), there is actually no evidence that it plays “a role in the etiology of daytime sleepiness. In fact, two studies showed no correlation between PLMS and objective measures of EDS. In addition, EDS in these patients is best treated with psychostimulants and not with dopaminergic agents known to suppress PLMS.”
Regarding chronic fatigue syndrome, it is “characterized by persistent or relapsing fatigue that does not resolve with sleep or rest. Polysomnography shows reduced sleep efficiency and may include alpha intrusion into sleep EEG. It is likely that a number of cases labeled as chronic fatigue syndrome are unrecognized cases of upper airway resistance syndrome” or other sleep disorders.
Similarly to chronic fatigue syndrome, fibromyalgia also may be associated with anomalous alpha wave activity (typically associated with arousal states) during NREM sleep. Also, researchers have shown that disrupting stage IV sleep consistently in young, healthy subjects causes a significant increase in muscle tenderness similar to that experienced in "neurasthenic musculoskeletal pain syndrome." This pain resolved when the subjects were able to resume their normal sleep patterns.
Hypothyroidism and iron deficiency with or without (iron-deficiency anemia) can also cause secondary hypersomnia. Blood tests for these disorders are done so they can be treated. Hypersomnia can also develop within months after viral infections such as Whipple's disease, mononucleosis, HIV, and Guillain–Barré syndrome.
Primary hypersomnia in diabetes, hepatic encephalopathy, and acromegaly is rarely reported, but these medical conditions may be associated with the secondary hypersomnias sleep apnea and periodic limb movement disorder (PLMD).
Behaviorally induced insufficient sleep syndrome must also be considered in the differential diagnosis of secondary hypersomnia. This disorder occurs in individuals who fail to get sufficient sleep for at least three months. In this case, the patient has chronic sleep deprivation although he or she is not necessarily aware of it. This situation is becoming more prevelant in western society due to the modern demands and expectations placed upon the individual.
Many medications can also lead to secondary hypersomnia. Therefore, a patient's complete medication list should be carefully reviewed for sleepiness or fatigue as side effects. In these cases, careful withdrawal from the possibly offending medication(s) is needed; then, medication substitution can be undertaken.
Mood disorders can also be associated with hypersomnia. The complaint of EDS in these conditions is often associated with poor sleep at night. "In that sense, insomnia and EDS are frequently associated, especially in cases of depression." Hypersomnia in mood disorders seems to be primarily related to "lack of interest and decreased energy inherent in the depressed condition rather than an increase in sleep or REM sleep propensity." In all cases with these mood disorders, the MSLT is normal (not too short and no SOREMPs)."
Appropriate treatment will depend on the specific cause or causes of hypersomnia that are diagnosed.
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