Excessive Sleepiness By. Ahmad Younis Professor of Thoracic Medicine Mansoura Faculty of Medicine. Excessive Sleepiness.
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Professor of Thoracic Medicine
Mansoura Faculty of Medicine
Demographics Excessive sleepiness is the most common complaint of patients presenting to sleep disorders centers.Excessive sleepiness is estimated to affect 5% of the general population. more prevalent among persons employed full-time compared with those who are employed part-time or unemployed.
Severity of sleepiness Mild Sleepiness occurs during times of rest or when little attention is required (eg, reading or watching television)Sleepiness is associated with minor impairment of social and occupational functioning Moderate Sleepiness occurs daily and during mild physical activities that involve some degree of attention (eg, group meetings).Sleepiness is associated with moderate impairment of social or occupational functioning Severe Sleepiness occurs daily and during physical activities that involve mild to moderate degree of attention (eg, conversation, eating or driving). Sleepiness is associated with marked impairment of social or occupational functioning.
Severity of sleepiness Epworth score
1- Inadequate sleep duration
2-Frequent awakenings and fragmented sleep
3- Pathology of the central nervous system sleep-wake apparatus
4- Disturbance of the endogenous circadian rhythm influencing the timing of wakefulness and sleep
5- Drug or substance use
6- Other conditions
Most wake circuits originate in the Brain stem arousal nuclei (BAN), which stimulate the thalamus, hypothalamus (Hyp) and basal forebrain.These projections also inhibit sleep centers
The nuclei (BAN), which stimulate the thalamus, hypothalamus (ventrolateralpreoptic nucleus (VLPO) in the hypothalamus inhibits the BAN and the parts of the hypothalamus involved in wakefulness. This leads to inhibition of other wake-centers including the thalamus, basal forebrain, and the cortex, and thus the initiation and maintenance of sleep.
serotonin and gammaaminobutyric acid (GABA).
Other neurotransmitters include adenosine, norepinephrine,
Brainstem reticular formation, especially oral pontine reticular formation ,Other brainstem (lower medullary) and spinal cord neurons
The main REM sleep neurotransmitter is acetylcholine.
Other neurotransmitters include GABA and glycine.
Narcolepsy with cataplexy
A Sleep onset REM periods and excessive sleepiness persist after adequate therapy of sleep apnea.
Clinical Features of Narcolepsy nuclei (BAN), which stimulate the thalamus, hypothalamus (
Onset of narcolepsy is generally (between 15 and 25years of age).
Excessive sleepiness is often the first symptom to appear, followed one to several years later by cataplexy, sleep paralysis, and sleep hallucinations.
The classic clinical tetrad of narcolepsy consists of:
Associated sleep disorders
1-Excessive sleepiness. 100% 2-Cataplexy. 70%to80% 3- Hypnagogic
Hypnopompic hallucinations. 8% to 70%
4- Sleep paralysis. 5% to 65%
Excessive Sleepiness nuclei (BAN), which stimulate the thalamus, hypothalamus (
Cataplexy nuclei (BAN), which stimulate the thalamus, hypothalamus (
Status cataplecticusdescribes repetitive episodes of cataplexy occurring in succession that may last from several minutes to an hour; this may occur following abrupt withdrawal of REM sleep suppressants. Episodes of cataplexy may give rise to REM sleep with hypnagogic hallucinations and dreaming.
Demonstrates wakefulness during brief attacks and REM sleep during more prolonged attacks.
1- Narcolepsy with cataplexy with normal hypocretin-1 levels inCSF of cases Normal CSF hypocretin-1 levels are present in 10%
2-Narcolepsy without cataplexy with low hypocretin-1 levels Low CSF hypocretin-1 levels (< 110 pg/mL) are present in the CSF up to 10% to 20%
3-Narcolepsy with cataplexy-like or atypical episodes Low CSF hypocretin-1 levels are present in up to 20%
3- Isolated cataplexy Rare familial cases with early onset
4- Hypocretin gene mutations Early-onset (6 months of age) narcolepsy with cataplexy
NB:Narcolepsy with cataplexy can be diagnosed by clinical history alone.
A thorough evaluation of medication and substance use as well as sleep, medical, neurologic and psychiatric history is mandatory.
Cerebrospinal Fluid Hypocretin-1
Differential diagnosis of sleepiness condition
Differential diagnosis of cataplexy condition
Transient ischemic attacks
Conversion disorder (pseudocataplexy)
Pharmacologic therapy of narcolepsy condition
1- Excessive sleepiness and sleep attacks
2- Cataplexy, sleep paralysis and sleep hallucinations
3- Sleep disruption
Behavioral therapy for narcolepsy condition
Definition sleepiness occurs after sufficient or even increased amounts of nighttime sleep and without any identifiable cause.
Types of idiopathic conditionhypersomnia
1- Idiopathic hypersomnia with long sleep time:
2- Idiopathic hypersomnia without long sleep time:
Multiple sleep latency test
24-hour continuous polysomnography
MSLT: mean sleep latency is reduced (approximately 3 to 9 minutes), without sleep onset REM periods.
Characteristics Narcolepsy Idiopathic hypersomnia
Short sleep latency Normal architecture Short REM sleep latency
SOREM periods present SOREM periods absent
Definition Insufficient sleep syndrome is a chronic voluntary but unintentional failure to obtain nighttime sleep that is sufficient in duration to achieve and maintain normal alertness while awake. If desired, individuals have no difficulty sleeping longer.
Note:Ideally, MSLT should be performed after several days of adequate amounts of nocturnal sleep
Neurologic evaluation, including EEG, imaging studies and, occasionally, Doppler tests of cerebral blood flow, is indicated.
Polysomnography reveals normal sleep duration and quality.
Treatment There is no specific treatment.
1-Hypersomniaonly (mono-symptomatic type)
2- Hypersomnia accompanied by binge eating and hypersexuality (Kleine-Levin syndrome).
The differential diagnosis includes menstrual-related hypersomnia, non–24-hour circadian sleep-phase disorder, and psychiatric conditions such as seasonal affective disorder, bipolar disorder, psychosis, and somatoform disorder.
Polysomnographicfeatures condition: include decreased sleep efficiency, sleep latency and REM sleep latency, and diminished stages 3 and 4 of NREM sleep.
Course is usually self-limited.The frequency, severity, and duration of episodes may decrease over time.
Therapy with lithium or valproic acid has been described.
Counseling regarding safety issues is recommended.
Consequences of Kleine-Levin syndrome include significant weight gain as well as social and academic/occupational impairment.
1-Adjustment sleep disorder Daytime sleepiness secondary to sleep disruption related to stress or unfamiliar sleep environments
2-Limit-setting sleep disorder Sleep onset disruption resulting in a decrease in total sleep time.
3-Inadequate sleep hygiene Excessive sleepiness resulting from acquired habits that are incongruous with sleep
1- Delayed sleep-phase syndrome:- An inability to arise until late morning or early afternoon is typical. Morning sleepiness attempts develops if a person to arise at times closer to socially accepted norms
2- Advanced sleep-phase syndrome:-There is a severe inability to delay sleep time beyond 6 to 8 PM. Excessive sleepiness may develop in the early evening hours if the person is forced to stay awake beyond the customary bedtime
3-Irregular sleep-wake pattern Disorganization of sleep and wake times, with three or more short “naps”constituting the fragmentary remnants of the major sleep episode, can lead to excessive daytime sleepiness
4-Non–24-hoursleep-phase Sleep-wake patterns are entirely dependent on intrinsic biologic rhythms. Because free-running internal rhythms have a periodicity of slightly over 24 hours, the person’s sleep onset and arising times are delayed by about 1 hour or more each day.
Desynchrony between the external 24-hour world and internal rhythms can give rise to excessive daytime sleepiness.
5- Jet lag Excessive sleepiness can develop following rapid travel across multiple time zones.
Delay in nighttime sleep after a westward flight and the earlier-than-customary arising times following eastward flights can result sleep deprivation and diminished daytime alertness.
6- Shift work sleep disorder Mismatch between the requirements of nighttime work and the demands for sleep, as well as the decreased efficiency of sleep taken during the daytime, produces excessive sleepiness and diminished vigilance among shift workers.
1- OSAS:- Respiratory events and arousals can recur throughout the evening, to produce sleep fragmentation and subsequent daytime sleepiness. Naps are generally unrefreshing.
2- CSAS:- Persons can present with complaints of daytime sleepiness and cognitive impairment.
3- Central alveolar hypoventilation:-Hypoventilation during sleep leads to ABG abnormalities (hypercapnia and hypoxemia), repetitive arousals, sleep fragmentation and, possibly, excessive daytime sleepiness.
4- RLS:-When sufficiently severe, restless legs syndrome can increase sleep onset latency and cause sleep disruption, which can, in turn, lead to excessive daytime sleepiness.
5-PLMD:- Sleep fragmentation from repetitive limb movement-related arousals can result in excessive sleepiness. Diagnosis requires polysomnography.
Polysomnographyshould always be performed on the evening preceding an Multiple Sleep Latency Test. It may demonstrate specific sleep disorders, such as obstructive sleep apnea or period limb movements of sleep, which may account for the patient’s complaint of excessive sleepiness.
Maintenance of wakefulness test (MWT) measures a person’s ability to stay awake.
It consists of four nap periods each lasting 40 minutes in which the patient is asked to try to stay awake.
Most normal persons without excessive sleepiness can remain awake during these naps.
MWT is sensitive to sleep deprivation and the effects of circadian sleep-wake rhythms
Performance vigilance testing Teststhat involve repetitive tasks, such as driving simulators, which measure performance, attention, and alertness, can be used to assess excessive sleepiness.
Actigraphy ScaleA person’s periods of rest/sleep and activity can be discerned using wrist actigraphs. These devices produce a signal whenever movement is detected. Because of its portability, it permits extended monitoring over several days to weeks.
The diameter and stability of the pupil can be evaluated using pupillometry.
Lack of a reference standard limits its clinical application.
Depending on the clinical presentation, laboratory testing for restless legs syndrome (eg, serum ferritin) and hypothyroidism may be indicated as well.