Short-Term Insomnia

Etiology

The cause of short-term insomnia is not well understood and is not attributable to one single etiology. The etiology of insomnia involves many factors, including environmental, genetic, psychological, and behavioral, which lead to a state of hyperarousal.[3]

Epidemiology

Up to one-third of the world’s population reports dissatisfaction with their sleep. Amongst the elderly and women, this percentage would be on the higher end. As high as 50% of older adults report sleep disturbances and insomnia. Using the DSM-5 criteria, up to 10% to 15% of adults would be classified as having short-term insomnia.[4] Women are two times as likely to have insomnia than age-matched men.[3][4]

Pathophysiology

The exact mechanism causing short-term insomnia remains unknown, even though there are many proposed models. There is an emerging consensus that short-term insomnia is a disorder of hyperarousal.

Hyperarousal is a state of increased somatic, cortical, and cognitive activation. Measured in physiologic terms, this would mean that patients with short-term insomnia would demonstrate increases in cortisol levels, body temperature, 24-hour metabolic rate, and heart rate.[5] 

There is also a growing body of knowledge that links short-term insomnia to the upregulation of wake-promoting chemicals of orexin (also known as hypocretin), histamine, and catecholamines. The presence of these chemicals couples with the downregulation of the sleep-promoting chemicals adenosine, serotonin, melatonin, and GABA. More research is necessary regarding the precise molecular mechanism responsible for hyperarousal.[6]

History and Physical

Patients with short-term insomnia have a constellation of symptoms and perceived issues with the quantity or quality of sleep. Symptoms include difficulty initiating and maintaining sleep, early morning awakenings, and difficulty going back to sleep. It is important to note that these symptoms exist even though the patient has the opportunity to get adequate sleep. The evaluation should include a thorough medical and psychiatric history. A sleep diary kept over a 2 to 4 week period may be helpful to assess sleep patterns.[7]

Another vital aspect of a patient’s history is that the nighttime issues with sleep contribute to daytime consequences such as:

• Decreased functioning/productivity in the academic or work setting.
• Fatigue or low energy
• Frequent napping
• Difficulty concentrating
• Susceptibility to errors and accidents
• Impaired attention, concentration, or memory
• Mood disturbances or irritability
• Impaired interpersonal or social functioning
• General feelings of poor quality of life

Evaluators should also perform questioning to rule out sleep-related disorders such as sleep apnea, narcolepsy, or restless leg syndrome.[7]

New research also indicates that there may be an independent association of insomnia contributing to major depression, and patients may present with depressed mood and complaints of anhedonia.[8]

Evaluation

Evaluating for short-term insomnia hinges on obtaining a robust sleep history as the diagnosis is made clinically. It is also essential to rule out other causes of insomnia, including but not limited to medication or substance use, or medical or mental disorders. Polysomnography testing plays a very limited role, but it can help differentiate sleep apnea and other sleep disorders from short-term insomnia. The use of sleep diaries and sleep logs have an essential role in helping to diagnose short-term insomnia. Patients are generally asked to note their sleep patterns such as time in bed, nighttime awakenings, sleep satisfaction, sleep onset latency, and total sleep time. These are measured from two to four weeks and are brought in for the clinician to review.[7] 

The two main classifications systems that define insomnia disorders are the International Classification of Sleep Disorders, 3rd edition (ICSD-III), and the Diagnostic and Statistical Manual-5 (DSM-5). The ICSD-III classifies insomnia into three categories: Chronic Insomnia Disorder, Short-term Insomnia Disorder, and Other Insomnia Disorder.[9] The DSM-5 criteria take a descriptive approach based on the frequency and duration of symptoms.[7] 

Questionnaires such as the Insomnia Severity Index (ISI) and the Pittsburgh Sleep Quality Index (PSQI) is a tool to aid in the diagnosis of insomnia. The Insomnia Severity Index consists of seven questions with a score of 1-4. The maximum score is 28, and the higher the score, the worse insomnia. A score of greater than 14 indicates clinical insomnia. The questionnaire can be self-administered by patients and brought in for evaluation by the provider. The PSQI was developed to help differentiate between different sleep-related disorders. It consists of 19 questions and measures different domains of sleep (quality, latency, duration, efficacy, medication use, daytime symptoms, and disturbances) over a month.[10]

Currently, two modalities help with objectively measuring sleep activity: actigraphy and polysomnography. Actigraphy is a technique for measuring limb movement activity with actigraphic devices that are wearable on wrists or ankles. The data for movement activity is then gathered over a period, ultimately giving us patterns for wakefulness and sleep. With the patterns, general sleep parameters, including sleep latency, sleep efficiency, total sleep time, and wake after sleep onset, can be obtained. These parameters would greatly aid in evaluating insomnia. Non-REM and REM sleep cycles, however, can not be gathered and need polysomnography to assess.[11] Although polysomnography is the golden standard in measuring sleep-related disorders, it should not be used routinely for diagnosing insomnia. In insomnia cases, it is usually indicated when there is suspicion that another sleep-related disorder is possible. Such conditions would include breathing disorders such as obstructive sleep apnea, central sleep apnea, or sleep-related movement disorders (i.e., periodic limb movement disorder).[12]

Treatment / Management

Treatment of short-term insomnia divides into two sections: nonpharmacologic and pharmacologic. Nonpharmacologic treatment is the first line as it is more cost-effective with a less side effect profile. Studies have shown nonpharmacologic therapy to be as effective as pharmacologic treatments. In more complicated patients with long histories of insomnia, it is permissible to combine pharmacologic and nonpharmacologic therapies.

Nonpharmacologic methods include cognitive therapies, sleep restriction, stimulus control, and sleep hygiene education.[3][13][14](B3)

• Cognitive therapies help patients link their ideas/attitudes, such as excessive worrying, emotional distress, and dysfunctional thoughts as the cause for short-term insomnia. It helps exchange beliefs such as overestimating needed hours of sleep to feel rested, being anxious about missing sleep time and worrying about the effects of insomnia on daytime functioning with more reassuring beliefs and attitudes.
• Sleep restriction therapy is exactly as it sounds. The simple objective of this therapy is to limit the amount of bedtime to the actual total sleep time (derived from sleep logs/diaries), which is usually less than that to which the patient has become accustomed. This approach helps increase the drive to sleep and creates sleep inertia aiding with sleep efficiency, decreasing early-morning awakenings, and decreasing sleep onset latency. Of note, sleep restriction should not be less than 5 to 6 hours per day.[15]
• Stimulus control therapy is where the patient tries to associate the bed with sleep. The time spent in bed should only be for sleeping and sexual activity. To implement this therapy, patients should to only go to bed when sleepy, not to stay in bed for more than 15 minutes before falling asleep, and to have rigid wake and sleep times.
• Sleep hygiene education supports the patient in understanding certain behaviors that are causing issues with sleep. These factors include limiting caffeine use during the daytime, decreasing daytime napping, and avoiding eating, vigorous exercise, alcohol, and smoking near bedtime.
(A1)

There is an abundance of pharmacologic therapies that exist for treating insomnia. These consist of herbs and over the counter melatonin pills and prescription drugs. Melatonin is an endogenous hormone produced by our pineal gland when stimulated by the suprachiasmatic nuclei in response to light, or lack thereof. The response of melatonin on our body is complex, but in essence, it regulates the circadian rhythm and aids in sleep onset. Over the counter, melatonin tablets are available in 1 mg to 10 mg dosages and have demonstrated modest effects on sleep onset.

Herbs have been used for centuries to induce sleep and aid in relaxation. Some of the popular herbs used include valerian root, kava-kava, chamomile, and lavender. Valerian root is a well-known herb that works on the GABA-A receptor to help with insomnia. Kava-kava is an extract from the herb Piper methysticum used in the South Pacific for insomnia and anxiety. It also works on the GABA receptor.[16] Another popular herb that has its effect by modulating the GABA receptor is chamomile, a flower native to Europe and Western Asia. Recent data shows that it has a modest impact on daytime functioning in patients who have insomnia.[17] Lavender is a familiar flower whose essential oil is often used in aromatherapy. Research on the effect of aromatherapy with lavender indicates that it raises the serum melatonin levels in the blood, thus promoting sleep.[18] These herbs are only the tip of the iceberg as many other herbs have been used for centuries to treat insomnia and anxiety, including Chinese herbs not mentioned in this article.(B3)

Regarding prescribed drugs, although there are no agreed-upon guidelines for prescribing, the American Academy for Sleep Medicine (AASM) assigned a task force of four experts in sleep medicine. It published a practice guideline for chronic insomnia in 2017. This guideline gives recommendations for each of the prescription drugs. Below is a concise list of medications along with their starting doses used in insomnia disorders. If one medication does not work or has a side effect profile not conducive to a patient’s lifestyle or physiology, clinicians can always switch to other medications. Clinicians are also encouraged to look up the side effect profile of each drug and its interactions. It is also important to note that all prescription drugs have adverse effects including but not limited to addiction, withdrawal, and tolerance, and should be used for a short duration if not effective.[19][20][21](A1)

• Benzodiazepine receptor agonist drugs (not to be used more than 2 to 4 weeks)
• GABA-A receptor- temazepam (7.5 mg), triazolam (0.125 mg)
• GABA-A alpha1 receptor- zolpidem (5 mg), zaleplon (5 mg), eszopiclone (2 mg)
• Antihistamine drugs- diphenhydramine (25 mg)
• Tricyclic antidepressant (TCA) drug- doxepin (3 mg), amitriptyline (10 mg)
• Melatonin receptor agonist- ramelteon (8 mg)
• Sedating antipsychotics- quetiapine (25 mg)
• Anticonvulsants- gabapentin (100 mg)
• Antidepressants- trazodone (25 mg)
• Orexin (hypocretin)-antagonist- suvorexant (10 mg)

In the elderly, it becomes important to consider the Beers criteria for proper prescribing. Drugs to be avoided include benzodiazepines, antihistamine drugs, TCAs, among other drugs.

Differential Diagnosis

The following is a list of diagnoses to rule out before the diagnosis of short term insomnia can be made:

• Insomnia disorder due to substance or medication use
• Insomnia disorder due to medical condition (i.e., pain, psychiatric illness, etc.)
• Obstructive or central sleep apnea
• Restless leg syndrome
• Narcolepsy
• Sleepwalking or sleep terror disorder
• Depression and anxiety
• Circadian misalignment from delayed sleep phase disorder
• Shift work sleep disorder

Prognosis

Sleep is vital to a patient’s overall health and feeling of well-being. There is emerging evidence tying sleep disturbances and insomnia disorders to increased cardiometabolic morbidity and mortality. Due to the hyperarousal state, patients with insomnia have a higher incidence of hypertension, type 2 diabetes, and acute myocardial infarction. These states mostly relate to the hypercortisolemia effect of insomnia by way of causing stress. Other studies show a correlation between insomnia and neurocognitive decline; this includes impairments in memory, executive functions, and attention. These impairments over time give way to developing psychiatric disorders such as depression, anxiety, and even suicide. The long-term prognosis, however, of short-term insomnia is very good if interventions and treatments are made appropriately and promptly.[22]

Complications

Untreated and unrecognized short-term insomnia can lead to a host of complications. Thus, in treating patients, it would be prudent for a provider to be aware of these complications. Below is a list of the following known complications:[22][23]

• Dependence on medication to sleep
• Psychiatric disorders such as anxiety and depression
• Cardiovascular disease
• Hypertension
• Type 2 diabetes