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Clinical application of polysomnography: Polysomnography began as a tool of discovery, but its primary use quickly evolved into a clinical procedure for diagnosing sleep disorders. (Hirshkowitz, 2016)
- 1- Hypersomnia: defined as Sleepiness not explained by volitional sleep deprivation. It is almost due to an underlying sleep disorder, most commonly obstructive sleep apnea or narcolepsy.
- A- Obstructive sleep apnea: apnea-hypopnea index (AHI) will be used as a marker of sleep-related breathing disorder (SRBD) severity in children, which will be graded as mild (14.9/h), moderate primary (59.9/h), or severe (>10/h) It is seen primarily in people who are loud snorers and is characterized by the collapse of the upper airway during sleep. (Caples et al, 2005) This upper airway collapse may be associated with a fall in blood oxygen level & results in repetitive arousals (up to 100 per hour of sleep) to reestablish upper airway airflow. These brief arousals are not perceived by individuals but result in excessive daytime secondary sleepiness. OSA is not confined to middle-aged, overweight males but may be seen in children (3% of all children), women, and thin individuals. (Roland et al, 2011). apnea requires more than 90 % drop in airflow for more than 10 seconds & hypopnea requires more than 30% drop in airflow for more than 10 seconds followed by either e 3% oxygen desaturation or arousal. (Berry et al, 2012)
- B- Narcolepsy: it is a relatively rare neurological disorder affecting 1 in 2,000 individuals. It is characterized by the tendency to fall asleep inappropriately during the daytime, particularly during sedentary or non-stimulating activities, despite having obtained an adequate amount of sleep during the timeline preceding night. Other symptoms of narcolepsy include: first, cataplexy (sudden brief spells of muscle weakness), often triggered by emotions; second, hypnagogic (occurring at sleep onset) or hypnopompic (occurring at sleep offset) hallucinations; third, sleep paralysis (awakening to find entire body paralyzed, with exception of being able to breathe & move eyes); fourth, automatic behavior; and last, disrupted night-time sleep. Patients with narcolepsy may show abnormalities on PSG that include a decrease in TST, short sleep-onset latency or sleep onset REM, sleep fragmentation, and periodic limb movement (PLM). (Guillemiault & Framherz, 2005)
There is a relationship between hypocretin-1 and narcolepsy. Hypocretin-1 is a neuropeptide confined to a small number of cells in the hypothalamus. It seems that patients with narcolepsy have lost these hypocretin-producing cells, possibly through an immune-primary with the secondary mediated mechanism. (Taheri et al, 2002) Undetectable levels of hypocretin-1 in cerebrospinal fluid (CSF) are very specific for patients with narcolepsy who have cataplexy. Absent CSF hypocretin-1 levels have not been found in any other conditions that could be confused clinically with narcolepsy, and this suggests that CSF hypocretin determinations may be of value in the diagnosis of narcolepsy in difficult cases. (Mignot et al, 2002)
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