Trauma-induced insomnia: A novel model for trauma and sleep research

Traumatic events have been increasingly recognized as important precipitants of clinically significant insomnia. Trauma is an extreme form of stressful life event that generates a sustained neurobiological response triggering the onset and maintenance of insomnia. Trauma may disrupt the normal sleep-wake regulatory mechanism by sensitizing the central nervous system's arousal centers, leading to pronounced central and physiological hyperarousal. The central concept of hyperarousal has been linked to both the pathogenesis of insomnia and to the neurobiological changes in the aftermath of traumatic events, and may be a neurobiological commonality underlying trauma and insomnia. This paper presents evidence for trauma-induced insomnia and advances a model of it as an important nosological and neurobiological entity. Trauma-induced insomnia may occur in the absence of full-blown posttraumatic stress disorder (PTSD), and may also be a precursor of subsequent PTSD development. Converging lines of evidence from the neuroscience of insomnia with the neurobiology and psychophysiology of stress, fear, trauma and PTSD will be integrated to advance understanding of the condition. Preclinical and clinical stress and fear paradigms have informed the neurobiological pathways mediating the production of insomnia by trauma. Elucidating the underlying neurobiological substrates can establish novel biological markers to identify persons at risk for the condition, and help optimize treatment of the trauma-insomnia interface. Early identification and treatment of trauma-induced insomnia may prevent the development of PTSD, as well as other important sequelae such as depression, substance dependence, and other medical conditions.