Table 4.

Sleep Disorder Syndromes. Shown are common sleep disorder syndromes and their diagnoses, evaluations, treatments, and clinical findings.

	Diagnosis	Evaluation	Treatment	Clinical Findings
Primary Snoring	Prevalence: 3–16% [21,22] Snoring without apnea or hypopnea, hypercapnia, hypoxemia, high arousal index, disruption of normal sleep architecture or daytime symptoms [22]	Sleep study if severe to rule/out apnea or hypopnea, hypercapnia, hypoxemia, high arousal index, disruption of normal sleep	Sleep hygiene counseling	Decrease in mean verbal intelligence quotient (IQ) scores, global IQ scores, selective attention scores, sustained attention scores, memory index [23]. Direct correlation between number of mild desaturations (3%)/arousals & severity of neurocognitive deficits [23] Characterized as benign; linked to neuropsychological impairments.
Restless leg syndrome (RLS)	Insomnia with “creepy or crawling” feeling in the arms and legs at night Insomnia accompanied by an urge to move the limbs [21]	Diagnosis of exclusion No single test can diagnose RLS Low iron levels are suggestive Electromyography (EMG) and possible muscle biopsy to rule out other neuro-muscular disease [21,22]	Sleep hygiene counseling Dopamine agonists Oral iron Clonazepam Gabapentin [21,22]	Autosomal dominant, sensorimotor disorder 2/3 of children may have low levels of serum ferritin; iron is a cofactor in synthesis of dopamine. Restless legs syndrome and attention deficit disorder are associated. Interferes with going to sleep and staying asleep May be accompanied by daytime fatigue, inattentiveness, or frank sleepiness. Dopamine deficiency implicated in the pathogenesis [21,22]
Delayed Sleep Phase Syndrome	Habitually unable to fall asleep before 2–3 am Neurological sleep disorder in which a person's sleep/wake cycle is delayed with respect to the external day/night cycle Normal sleep if sleeps freely but very sleepy if conforming to conventional sleep-wake schedules [21,22]	History of circadian sleep pattern Perform sleep logs and wrist actigraphy Evaluate for secondary effects of chronically poor sleep [21,22]	“Bright light” therapy: provide 2700–10 000 lux of bright light via a light box for 20–30 minutes immediately after waking leading to a gradual phase advancement (shifting back) of the sleep onset time at night. 0.5–1 mg melatonin about 5.5 hours before sleep onset Stimulant drugs to counter residual daytime sleepiness [21,22]	Habitually unable to fall asleep before 2–3 am Prefer to wake in the late morning or early afternoon. Higher likelihood of the presence of the Human Leukocyte Antigen (HLA) DR1 on chromosome 6, and the occasional familial clustering of delayed sleep phase syndrome suggest a genetic predisposition. Delayed sleep phase syndrome linked to polymorphisms in Period (Per) gene. Onset: typically, adolescence, boys > girls [21,22]
Obesity Hypoventilation Syndrome (OHS)	Awake chronic hypercapnia; partial pressure carbon dioxide (PaCO2) >45 ​mm Hg) ​+ ​Obesity Excessive work of breathing and increased carbon dioxide (CO2) production Abnormal central ventilatory drive and obesity Other disorders should be ruled out Also known as Pickwickian Syndrome [21,22,24,25]	Evaluate for concurrent obstructive sleep apnea (OSA) (90% chance) Sleep study: Oxygen (O2) Saturation levels, CO2 levels, and apnea episodes Cardiac and pulmonary work up if symptomatic [21,22,24,25]	Weight loss Respiratory support as indicated, including continuous positive airway pressure (CPAP) [21,22,24,25]	May have central respiratory control system abnormality with decreased responsiveness to CO2 rebreathing, hypoxia, or both. Inspiratory muscle strength and resting tidal volumes decreased Leptin deficiency/resistance may contribute to OHS by reducing ventilatory responsiveness leading to CO2 retention. Pulmonary hypertension (HTN) more common & severe than in OSA. [21,22,24,25]