Insomnia: Predisposition, Precipitation, Perpetuation

Clinical Professor, Department of Psychiatry, University of California San Diego School of Medicine, Staff Scientist, Scripps Research Institute Department of Neuropharmacology, President, Pacific Sleep Medicine Services

Spielman and colleagues’ lucid model for understanding how insomnia may develop, commonly referred to as the “3-P model,” incorporates the impact of various traits (predisposing factors) and life stresses (precipitating factors) in the development of insomnia. It also recognizes that chronic insomnia is maintained (unintentionally) by maladaptive coping strategies (perpetuating factors).

Predisposing Factors of Insomnia

Age is a factor in development of insomnia, and the presence of concomitant medical illnesses is the largest contributing factor to increased rates of insomnia seen with increased age. Personality traits may also play a significant contributory role in the development of insomnia, based on this model. Insomnia patients are often anxious, and may develop fixations about the amount and quality of sleep that they obtain and the impact they believe it will have on daytime function.

Precipitating Factors of Insomnia

Insomnia can clearly be provoked in virtually everyone by the effects of stress. An example of a stress that would be expected to be relatively “universal” would be the impact of living near “Ground Zero” on September 11, 2001. Susceptible individuals have an increased risk for developing insomnia, even in association with stimuli that would not be problematic for “better sleepers.” These individuals are also at risk for the recurrence of insomnia episodes whenever levels of stress are increased.

Perpetuating Factors of Insomnia

To stop the development of insomnia, patients may make various changes in their habits and routines to try to compensate for their sleep loss and greater difficulties falling asleep. They may try to fall asleep at an earlier hour (ie, 8 p.m.), not appreciating that their level of alertness at that hour, controlled by their circadian sleep rhythms, will prevent premature entry into sleep. They will try harder to “fall asleep,” not recognizing that sleep occurs when levels of alertness and arousal are diminished and that the effort to try to fall asleep raises levels of arousal and further interferes with the capacity to fall asleep. They may nap in the daytime, not appreciating that their daytime hours of sleep will reduce sleep drive at bedtime. A state of conditioned arousal to the bed and bedroom may then develop. As sleep becomes more elusive, efforts to fall asleep may become more intense. The bed and bedroom, which ideally are associated with comfort, pleasure, and relaxation, become increasing associated with pain, arousal, and anxiety. Other efforts or strategies to promote sleep may ensue, further disrupting normal sleep patterns and habits. Alcohol or over-the-counter sleep aids may be used. When they fail, or lead to side effects or residual morning sleepiness, sleep is further physiologically disrupted and the intensity of distress is increased.

Disclosure: Dr. Erman is a consultant to Cephalon, Mallinckrodt, Neurocrine Sanofi-Aventis, and Takeda; has received grant/research support from Arena, Cephalon, Eli Lilly, GlaxoSmithKline, Mallinckrodt, Merck, Organon, Pfizer, Pharmacia, ResMed, Sanofi-Aventis, Schwarz Pharma, and Takeda; is on the advisory boards of Cephalon, Neurocrine, Sanofi-Aventis, and Takeda; is on the speakers bureaus of Forest, Sanofi-Aventis, and Takeda; and is a stock/shareholder in Cephalon, Forest, Merck, Neurocrine, Pfizer, Sanofi-Aventis, and Sepracor.