About Insomnia

Everyone has had difficulty sleeping at one time or another. But insomnia involves more than just the inability to sleep at night-it is when an individual experiences daytime consequences as a result of a difficulty in initiating or maintaining sleep or having sleep that is not refreshing. And the severity of these consequences is directly related to the type of insomnia the individual is experiencing.1

Types of insomnia and their consequences

Transient Insomnia

Intermittent Insomnia

Chronic Insomnia

Insomnia can be described as short-term, or transient, and typically lasts from a few nights to a few weeks. Transient insomnia may cause next-day sleepiness, changes in mood, and psychomotor performance impairment.1,2

Having periods of transient insomnia that occur on and off is considered intermittent insomnia. Intermittent insomnia can lead to chronic insomnia.2

Long-term, or chronic, insomnia occurs when an individual has difficulty sleeping that persists for more than a month. Chronic insomnia is often related to more serious manifestations including depression, memory impairment, accidents, absenteeism, and increased healthcare utilization.1,2


Several factors contribute to insomnia

Predisposing factors

Precipitating factors

Perpetuating factors

may be present in a person long before symptoms appear. These factors include physiological hyperarousal, cognitive arousal, emotional arousal, and decreased homeostatic sleep drive.1

increase the propensity for insomnia over a threshold, causing insomnia to appear. Medical or psychiatric illness, drug use, shift work, stressful life events, and sleep disorders like sleep apnea are all types of precipitating factors.1

are those that exacerbate insomnia. These factors can prolong the insomnia even after the initial cause is eliminated. Perpetuating factors include a sedentary lifestyle, poor sleep hygiene, and excessive worry about sleeping.1

 
 
Treatment goals
Recent research suggests that several bouts of transient insomnia can lead to chronic insomnia, and one of the current treatment goals is to prevent this evolution. New understandings about the sleep cycle and the role of the sleep switch may provide opportunities for novel treatments. 3,4



Rozerem™ is indicated for the treatment of insomnia characterized by difficulty with sleep onset. Rozerem should not be used in patients with hypersensitivity to ramelteon or any components of the formulation. Rozerem can be prescribed for long-term use. However, failure of insomnia to remit after a reasonable period of time, worsening of insomnia, or the emergence of new cognitive or behavioral abnormalities after taking Rozerem should be evaluated, as such symptoms may be the result of an unrecognized underlying medical disorder. In primarily depressed patients, worsening of depression, including suicidal ideation, has been reported in association with the use of hypnotics.

Rozerem should not be used by patients with severe hepatic impairment, or in patients in combination with fluvoxamine.

Rozerem has not been studied in subjects with severe sleep apnea or severe COPD and is not recommended for use in those populations. Patients should be advised to exercise caution if they consume alcohol in combination with Rozerem.

Rozerem has been associated with decreased testosterone levels and increased prolactin levels. As a result, healthcare professionals should be mindful of any unexplained symptoms possibly associated with such changes in these hormone levels. Rozerem has not been studied in children or adolescents, and the effects in these populations are unknown.

Rozerem should be taken within 30 minutes before going to bed and activities should be confined to those necessary to prepare for bed. Rozerem should not be taken with or immediately after a high-fat meal. Engaging in hazardous activities that require concentration (such as operating a motor vehicle or heavy machinery) after taking Rozerem should be avoided.

The most common adverse events seen with Rozerem that had greater than 2% incidence difference from placebo were somnolence, dizziness, and fatigue.

References: 1. Turek FW, Dugovic C, Zee PC. Current understanding of the circadian clock and the clinical implications for neurological disorders. Arch Neurol. 2001;58:1781-1787. 2. Edgar DM, Dement WC, Fuller CA. Effect of SCN lesions on sleep in squirrel monkeys: evidence for opponent processes in sleep-wake regulation. J Neurosci. 1993;13:1065-1079. 3. Roth T, Roehrs T. Insomnia: epidemiology, characteristics, and consequences. Clin Cornerstone. 2003;5:5-15.




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