Journal of Sleep Disorders & Therapy
Open Access

Sleep-Onset Insomnia and Its Association with Suicidality in Youth Populations

Ned Baraeon^{* *}Correspondence: Ned Baraeon, Department of Pediatric Sleep Disorders, Great Ormond Street Hospital, London, United Kingdom, Email:

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Description

Sleep-onset insomnia represents one of the most distressing forms of sleep disturbance, characterized by the persistent difficulty in initiating sleep. Unlike other subtypes of insomnia that involve difficulty staying asleep or waking up too early, sleep-onset insomnia specifically refers to prolonged sleep latency the time it takes to transition from full wakefulness to sleep. In clinical settings, individuals with this condition often report lying awake for hours despite being fatigued, mentally prepared, and in a conducive environment for sleep. The implications of this issue are both extensive and profound, affecting cognitive performance, emotional regulation, physical health, and overall quality of life.

A defining feature of sleep-onset insomnia is its chronic nature. While occasional difficulty in falling asleep is a universal experience linked to situational stressors or lifestyle choices, sleep-onset insomnia is typically diagnosed when sleep difficulties occur at least three nights per week for a minimum of three months. This temporal persistence makes it a clinical concern rather than a passing inconvenience. Furthermore, sleep-onset insomnia does not merely reflect a sleep issue; it often signals broader physiological or psychological imbalances. These can include hyperarousal of the central nervous system, elevated stress hormone levels, circadian rhythm disruptions, and maladaptive cognitive associations with the sleep environment.

The psychological and neurobiological mechanisms underlying sleep-onset insomnia are multifactorial. One of the most prominent theories is the hyperarousal model, which posits that individuals with insomnia experience heightened levels of cognitive and physiological arousal not only at night but also throughout the day. Neuroimaging studies have shown that the brains of people with insomnia remain in a heightened state of alertness, even when they appear to be at rest. This state of hypervigilance is marked by increased metabolic activity in regions of the brain associated with wakefulness, such as the ascending reticular activating system. These findings suggest that sleep-onset insomnia may not be a passive failure to fall asleep but an active interference by the brain's wake-promoting mechanisms.

Another key contributing factor to sleep-onset insomnia is cognitive rumination. Individuals struggling to fall asleep often report racing thoughts, excessive worry about their inability to sleep, and anxiety related to daytime functioning. This mental state leads to a vicious cycle: the more a person worries about not sleeping, the more difficult sleep becomes. This performance anxiety around sleep, sometimes called “sleep effort,” causes the bed and bedtime to become associated with stress rather than rest. Behavioral conditioning plays a crucial role in perpetuating this cycle, as individuals may begin to unconsciously associate their sleep environment with wakefulness and frustration.

Pharmacological interventions for sleep-onset insomnia typically include short-term use of hypnotic agents such as benzodiazepines and non-benzodiazepine sedative-hypnotics like zolpidem. While these medications can be effective in reducing sleep latency, they carry risks of dependency, tolerance, and rebound insomnia when discontinued. Melatonin supplements and melatonin receptor agonists such as ramelteon have also been used to address circadian-related components of sleep-onset difficulties. However, their efficacy varies among individuals, and their effects are often modest compared to behavioral interventions. As a result, clinical guidelines increasingly recommend Cognitive Behavioral Therapy for Insomnia (CBT-I) as the first-line treatment.

Adolescents and young adults appear to be particularly vulnerable to sleep-onset insomnia. Developmental changes in circadian rhythms during puberty naturally predispose teenagers to later sleep and wake times. However, societal demands such as early school start times, academic pressures, and increased screen use clash with these biological tendencies, leading to widespread sleep-onset issues among youth. In this population, untreated sleep-onset insomnia can have profound consequences on academic performance, emotional regulation, and even the risk of substance use or suicidal ideation.