**7.2 Cognitive behavior therapy for insomnia (CBT-I)/disturbed sleep**

Regarding sleep, cognitive behavior therapy for insomnia (CBT-I) proved to be superior to pharmacotherapy in several outcome studies [71, 72]. CBT-I consists of psychoeducation about sleep and insomnia, stimulus control, sleep restriction, sleep hygiene, relaxing training, and cognitive therapy.

*Stimulus control techniques* pretend to associate bed with a rapid sleep onset by teaching the patient to avoid habits other than sex and sleep in bed. Naps should also be avoided and regular sleep-wake schedules must be encouraged. Another important aspect is that the patient should learn only to go to bed when feeling sleepy and get out of bed if not asleep after 20 min [73].

*Sleep restriction* pretends to limit the amount of time spent in bed in relation to the actual time asleep. In the first days, this will lead to a mild sleep deprivation which soon will increase the sleep drive and afterwards to a more consolidated sleep with better rest and efficiency. When the patient improves, time in bed will increase again [74].

*Sleep hygiene* contributes to more adequate behaviors near bedtime as avoiding caffeine or tobacco, intense exercise, or too much light, noise, and use of electronic devices [75].

Relaxation training will reduce cognitive and physical tension prior to bedtime. Techniques like hypnosis, meditation, and guided imagery can be used with more or less efficacy depending of personality and circumstances [76].

*Cognitive therapy* will help patient to have real beliefs regarding sleep and to adopt attitudes that will favor sleep. For instance, many patients lie in bed and think they will not sleep the whole night, making them worried about this. This technique also pretends to eliminate excessive rumination and negative thoughts, mainly in the bedtime [77].

*Cognitive behavioral therapy* is also available for other sleep disturbances such as sleep apnea, narcolepsy, sleep-wake circadian mismatch, and several pediatric disorders. Therefore, it could be used in several domains [78–80].

#### **7.3 Cognitive behavioral therapy for pain (CBT-P)**

Several psychological- and behavioral-related options showed to be effective for chronic pain, including CBT-P, acceptance and commitment, mindfulness, progressive muscle relaxation training, motivational interviewing, and goal setting to behavioral activation. CBT-P is effective in a manner that its principles are associated to identify and approach those negative or dysfunctional thoughts and behaviors that usually worsen patient's adjustment to chronic mechanisms of pain. It was shown to effectively reduce patient distress in patients with pain-associated conditions. Although it is expected that CBT-P also has impact on sleep in those patients, there are only few studies addressing this.

#### **7.4 Combined cognitive behavioral therapy directed to both sleep and pain**

A synergistic (CBT-I + CBT-P) approach was associated with significant greater improvements either in pain and sleep when compared with each isolated strategy. Fatigue, depression, and overall improvement in quality of live with less pain interference were observed in patients treated with this combination [81].

### **7.5 Pharmacological therapy**

Reciprocal interaction between pain and sleep disturbance makes it important to concurrently address and treat both conditions in order to succeed. In some

**99**

dose in females.

*Sleep and Orofacial Pain: Physiological Interactions and Clinical Management*

patients, in which CBT is not successful or effective, pharmacological therapy is often required. Sometimes, also in the beginning of the therapeutic process, some classes of drugs are useful to optimize therapeutic adherence in both sleep and pain.

Opioids may improve subjective sleep quality in some patients with chronic pain, but can also interfere with sleep in others, mainly if they have sleep related breathing disorders which may be aggravated by this class of analgesic drugs. Other well-known potential adverse effects are hyperalgesia, tolerance, and dependence. That is the reason to support the recommendation *against* the use of opioids for insomnia, although it could be effective in highly selected pain patients [82].

This class of drugs binds to GABA (gamma aminobutyric acid)-A receptors and has sedative/hypnotic, amnestic, anxiolytic, muscle relaxant, and anticonvulsant effects. Many studies show that this GABA-mediated pharmacological activity favors sleep quality, reduces sleep latency, and wakefulness after sleep onset and improve total sleep time. Half-lives of BzRAS vary from short and intermediate to long, and therefore indications for sleep disturbance and insomnia depends of its clinical aspect (onset, maintenance, or end-stage insomnia) as well as their expected adverse effects (cognitive impairment, low attention levels, anterograde amnesia). Some controversies persist however regarding clinical improvements using these drugs on the long term. Long-term adverse reactions involve the increase in depressive symptoms, cognitive and psychomotor slowing. Its abrupt stop should not happen as rebound insomnia and seizures could appear or increase in intensity. Tolerance and dependence are also issues important to consider and in clinical practice it should be avoided to prescribe more than one benzodiazepine at the time since metabolites can combine and prolong sedation time. BzRAS should not be a first option in non-controlled patients with sleep disordered breathing as they can disturb respiratory responses and therefore increase severity of sleep-related respiratory disturbances. Finally, it is crucial to appropriately taper the BzRA in order to prevent associated deleterious effects in comparison of their

*DOI: http://dx.doi.org/10.5772/intechopen.86770*

**7.7 Benzodiazepine receptor agonists**

probable short time advantage [83].

**7.8 Non-benzodiazepine benzodiazepine receptor agonists**

The agents from this pharmacological class are active at the benzodiazepine GABA complex, particularly on receptors in the ventrolateral preoptic nucleus. Due to their proven efficacy, reduced side effects and less risk for addiction, non-benzodiazepine receptor agonists (non-BzRAs) became the most commonly prescribed hypnotic agents for onset and maintenance insomnia in the recent years [84]. Zolpidem, zaleplon, and eszopiclone belong to this newest class of FDAapproved hypnotics. They improve sleep latency with fewer side effects given their shorter half-lives and receptor binding profile. While Zolpidem is currently the most prescribed drug for insomnia with no evidence of tolerance or rebound effect [85], Eszopiclone seems to have a similar safety profile but higher antidepressant and anxiolytic effects in patients with comorbid insomnia [86]. Regarding safety, behavioral effects of zolpidem, and zaleplon are much similar to triazolam and include sleep eating, sleep walking, and sleep driving. As recent data from zolpidem showed some negative cognitive impact on women, FDA recommended to lower the

**7.6 Opioids analgesics**

patients, in which CBT is not successful or effective, pharmacological therapy is often required. Sometimes, also in the beginning of the therapeutic process, some classes of drugs are useful to optimize therapeutic adherence in both sleep and pain.
