Insomnia is a highly prevalent symptom associated with SARS-CoV-2 infection, affecting individuals during the acute illness and persisting for months afterward as part of Long COVID. Sleep disturbances are reported by a significant portion of those who have had the virus, with estimates suggesting up to 40% of post-COVID survivors experience poor sleep quality. This phenomenon, sometimes called “coronasomnia,” involves difficulty falling or staying asleep, as well as changes in sleep architecture, such as reduced deep sleep. Understanding the complex biological and psychological causes is essential for addressing this common consequence of the infection.
The Role of Systemic Inflammation in Sleep Disruption
The body’s immediate defense against the SARS-CoV-2 virus is a robust inflammatory response that directly interferes with the finely tuned processes of sleep regulation. This systemic inflammation involves the rapid release of signaling molecules known as pro-inflammatory cytokines, such as Interleukin-6 (IL-6), Tumor Necrosis Factor-alpha (TNF-α), and Interleukin-1 beta (IL-1β). These molecules induce “sickness behavior,” which includes symptoms like fatigue and changes in sleep patterns, often resulting in fragmented or poor-quality sleep.
Cytokines communicate with the brain through complex neuroimmune cross-talk. These inflammatory signals disrupt normal sleep homeostasis by crossing the blood-brain barrier or signaling the brain through other pathways. Elevated levels of IL-6 and TNF-A are consistently linked to sleeping difficulties because they modulate the activity of brain regions controlling the sleep-wake cycle.
The inflammatory surge induces a state of hyperarousal that prevents the brain from entering restorative sleep. Even after the acute infection subsides, persistent, low-grade inflammation is implicated in the prolonged sleep disturbances seen in Long COVID. This ongoing inflammatory state sustains the disruption of the central nervous system’s sleep mechanisms.
Central Nervous System Effects and Stress Hormone Imbalance
Beyond general inflammation, the virus can directly affect the central nervous system, a concept known as viral neurotropism. SARS-CoV-2 gains entry into cells by binding to the Angiotensin-Converting Enzyme 2 (ACE2) receptor, which is present in brain areas that regulate the sleep-wake cycle. The virus may invade the brain directly, potentially via the olfactory nerve, or indirectly by disrupting the blood-brain barrier, allowing inflammatory factors to perturb sleep-regulating structures.
A major biological pathway affected is the Hypothalamic-Pituitary-Adrenal (HPA) axis, which governs the stress response and the release of hormones like cortisol. The physiological stress of a COVID-19 infection, combined with systemic inflammation, can dysregulate the HPA axis. The chronic nature of the stressor and the direct viral impact on the hypothalamus, pituitary, and adrenal glands (all expressing ACE2 receptors) contribute to this dysfunction.
This dysregulation often manifests as chronic physiological hyperarousal, where the body’s fight-or-flight system is constantly activated. High levels of stress hormones, including adrenaline, prevent the brain from quieting down to initiate or maintain restorative sleep. Conversely, some Long COVID patients experience hypocortisolism (low cortisol), which is associated with chronic fatigue and fragmented sleep. Regardless of whether the HPA axis is over- or under-responsive, the resulting hormonal imbalance compromises the brain’s capacity to achieve deep, restful sleep.
Psychological and Environmental Factors Perpetuating Insomnia
Insomnia is not solely a biological issue; psychological and environmental factors significantly contribute to its development and persistence. The fear of contracting the virus, anxiety about the illness’s trajectory, and the emotional distress of isolation all act as powerful stressors that disrupt sleep. This health-related anxiety leads to cognitive arousal, causing the mind to remain excessively active and worried at bedtime, which makes sleep onset difficult.
Environmental changes imposed by the pandemic, such as stay-at-home orders, altered work schedules, and reduced physical activity, disrupted the body’s natural circadian rhythm. For those who were hospitalized, the constant noise and medical interventions further fractured normal sleep patterns. Loneliness due to social isolation has also been strongly linked to increased insomnia symptoms.
These factors often lead to a learned behavior of insomnia, where the bedroom becomes associated with wakefulness and frustration rather than rest. Even after the initial illness resolves, the behavioral and cognitive patterns established during the acute phase can perpetuate chronic insomnia. The reciprocal relationship between anxiety, depression, and poor sleep ensures that psychological distress is both caused and worsened by continued sleep deprivation.
Strategies for Managing COVID-Related Sleep Disturbances
Managing persistent sleep issues following a COVID-19 infection requires a structured approach focused on restoring healthy sleep habits. The first line of defense involves strict adherence to sleep hygiene principles:
- Maintain a consistent sleep-wake schedule seven days a week.
- Ensure the bedroom environment is cool, dark, and quiet.
- Reserve the bed only for sleep and intimacy.
- Avoid activities like working or watching television in bed.
Behavioral interventions are the most effective long-term solution for chronic insomnia. Cognitive Behavioral Therapy for Insomnia (CBT-I) is an evidence-based treatment that addresses the learned and cognitive factors perpetuating poor sleep. CBT-I techniques include stimulus control, which breaks the negative association between the bed and wakefulness, and cognitive restructuring, which challenges unhelpful thoughts about sleep.
Relaxation techniques, such as mindfulness or deep breathing exercises, can help reduce the physiological hyperarousal state that prevents sleep. Physical activity during the day can also improve sleep quality, though intense exercise should be avoided close to bedtime. While medications may be considered, non-pharmacological methods like CBT-I are the preferred strategy for lasting relief.