Confusional arousals are characterized by recurrent mental confusion or confusional behavior during arousals or awakenings. There is disorientation and diminished mentation for several minutes. The behavior can be aggressive or even violent. In adolescents or adults, confusional arousals can present as severe morning sleep inertia or sleep-related sexual behaviors (sexsomnia) (1,2). This latter behavior can also present with sleepwalking.

Generally, a conservative approach is sufficient for the treatment of confusional arousals. Reassuring the patient and their family of the benign nature of this condition and the tendency for episodes to decrease and/or completely resolve over time is an important aspect of the management. Caretakers should also be
alerted that interacting with the patient during an episode could prolong its duration and even cause the event to take a violent tone. The patient should keep a regular sleep-wake schedule, and avoid sleep deprivation as well as alcohol and other substances that can depress the central nervous system. Escitalopram, a serotonin uptake inhibitor, at a dose of 10 mg has been reported as effective therapy for the treatment of sexsomnia (2).

Sleepwalking is characterized by a series of behaviors that emerge from slow wave sleep terminating in ambulation with an altered state consciousness or impaired judgement (1). The event can vary from simple walking to movements with violent behavior resulting in injury.

Precipitating factors include sleep deprivation, fever, stress (physical or emotional), hyperthyroidism (3), and some medications. Avoidance of variation in sleep-wake schedules, sleep curtailment, and agents such as nonbenzodiazepine receptor agonists (4,5), lithium (6), and other psychotropic substances is recommended. Additionally, other sleep disorders such as obstructive sleep apnea can cause interruptions of slow wave sleep and precipitate sleepwalking episodes. Therefore, therapy for other underlying sleep disorders is advised. Educating patients and families about safeguarding the sleep environment is paramount. Simple maneuvers such as removing sharp or dangerous objects near the bed, locking windows, blocking stairways, and having the patient sleep on the ground floor whenever possible is key in preventing injury. Anticipatory awakenings have been reported as a treatment modality for sleepwalking. It is believed that with this intervention the underlying electrophysiological changes during sleepwalking are prevented. The
patient should be fully awakened for at least 5 minutes approximately 30 minutes before the usual time of the events. In one particular case described in the literature, the patient did not have further episodes of sleep walking after anticipatory awakenings were instituted for five consecutive nights (7). Pharmacologic treatment is usually not necessary. However, if the episodes are severe or refractory, benzodiazepines or tricyclic antidepressants can be initiated. For adults, clonazepam 0.5 to 1 mg has been the most commonly prescribed medication (8, 9 and 10). The dose of clonazepam can be increased by 0.25 mg every few nights until the episodes of sleepwalking resolve or side effects from the medication arise. Other benzodiazepines taken at bedtime like diazepam (10 mg at bedtime) and triazolam (0.25 mg at bedtime) have been reported to be effective in the treatment of somnambulism (8). Dose adjustment is required for the pediatric population. Alternatively, the use of tricyclic antidepressants, like imipramine (10 to 25 mg for children, 50 to 300 mg in adults) has been described in the literature (9).

Sleep terrors are characterized by a sudden episode of terror during slow wave sleep (SWS). The episodes usually commence with a loud scream or cry and are accompanied by manifestations of extreme fear as evident by alterations in the autonomic nervous system (tachycardia, tachypnea, mydriasis, diaphoresis, and increased muscle tone) and in the person’s behavior. In some adults these episodes are associated with partial dream recall. In children there is no association between sleep terrors and psychiatric disorders, while in adults this relationship has not yet been well established. The precipitating factors for sleep terrors are similar to the ones for sleepwalking and include fever, sleep deprivation, certain medications, and obstructive sleep apnea. Sleep terrors typically present between ages 4 and 12 and tend to disappear during adolescence. Their recurrence during adulthood is usually associated with emotional stress.

Pharmacologic treatment is typically not necessary. If the episodes are intense or frequent, then a pharmacologic intervention can be considered. Paroxetine at a dose of 20 to 40 mg daily has been shown to be effective in adults (11,12). It appears that its mechanism of action is directly related to its ability to increase 5-hydroxytryptamine (5-HT) concentrations in the brainstem by blocking reuptake (12). Other treatment alternatives include benzodiazepines (13) (clonazepam or diazepam), trazodone (14), and tricyclic antidepressants (15). Cognitive-behavioral therapy (16) may be implemented and can aid in the treatment of this condition by itself or in combination with medication.

Currently, clear-cut recommendations for the management of NREM parasomnias remain elusive for reasons previously stated. The overall low quality of evidence—comprised primarily of case series, retrospective analyses, and anecdotal reports—does not readily lend itself to systematic review. However, given the potential for serious injuries and the legal implications definitive guidelines for treatment are warranted.

Nightmare disorder is characterized by recurrent awakenings from disturbing dreams with recall of the dreams and dysphoric emotions, little or no confusion, difficulty returning to sleep, and/or occurrence of the awakenings in the latter half of the habitual sleep period (1). The full alertness and the late occurrence of the episodes distinguish nightmare disorder from NREM parasomnias. Nightmare disorder is
generally classified as idiopathic versus posttraumatic; however, there is a long list of medications known to cause nightmares, particularly those affecting the norepinephrine, serotonin, and dopamine systems, of which beta-blockers, dopaminergic agonists, and SSRIs are prominent examples (17). Thus, the initial evaluation should include a medication history and, if appropriate, an attempt at switching to an alternative medication if medication-induced nightmares are suspected.

The treatment of idiopathic and posttraumatic nightmares involves pharmacotherapy and/or cognitive-behavioral therapies. Most of the published literature consists of treatment of nightmares associated with posttraumatic stress disorder (PTSD) although some of the studies include subjects with idiopathic nightmares. It is unknown whether certain therapies would be more applicable to one patient group over another or whether these therapies are equally efficacious in patients who have bad dreams that do not result in significant sleep disruption. In general, the literature supporting different medications is weaker than that demonstrating efficacy of behavioral therapies. The numbers of subjects in the pharmacotherapy literature are usually small and these studies are mostly case series, with the exception of the data supporting prazosin (see below). In addition, many of the subjects are on additional psychoactive medications, which may potentially worsen the nightmare disorder or have a potentiating effect on the study medication that was not controlled for in all studies. In contrast, the literature on behavioral therapies surveys larger patient populations with the primary weakness being the use of waitlist control groups rather than a placebo-therapy control group.

Medications demonstrating efficacy in the treatment of nightmare disorder include prazosin, clonidine, trazodone, and nefazodone, with preliminary data suggesting that the atypical antipsychotics, topiramate, and gabapentin may prove to be effective therapies with further study. Interestingly, although venlafaxine is effective in treating many symptoms of PTSD, it was not statistically significantly better than placebo in the treatment of nightmares (18). Clonazepam, a drug effective in decreasing the nightmares associated with REM sleep behavior disorder, did not demonstrate efficacy in a very small single-blind, placebo-controlled, crossover clinical trial for treatment of PTSD-associated nightmares (19).

Prazosin is the drug with the most developed body of pharmacologic data demonstrating efficacy, including three small placebo-controlled studies involving both veterans and civilians generated by the same group of investigators (20, 21 and 22). Prazosin is an α₁-adrenergic receptor antagonist with a presumptive therapeutic effect through decreasing CNS noradrenergic activity, which is elevated in PTSD (23). The trials demonstrated a fall in a combined frequency and severity scale (Clinician-Administered PTSD Scale [CAPS] (24) item “recurrent distressing dreams”) from an average pretreatment severity rating of 4.8 to 6.9 (maximum score of 8 on the CAPS) to 3.2 to 3.6 posttreatment. Treatment was generally started at 1 mg at bedtime and increased by 1 to 2 mg every 3 to 7 nights until an effective dose was reached. The average effective dose ranged from 3.1 mg to 13.3 mg, with orthostatic dizziness as the most common side effect. The rationale for clonidine use is similar but there are only two case series demonstrating efficacy of this α₂-adrenergic receptor agonist at doses of 0.2 to 0.6 mg total daily dose (twice daily dosing) (25,26), with subjects being co-treated with either imipramine or desipramine for depression in one study (25). As with prazosin, the clinician needs to monitor the patient for orthostatic hypotension.

The two serotonin-potentiating non-SSRI medications, trazodone and nefazodone, have also demonstrated efficacy in the treatment of PTSD-associated nightmares; however, both have significant side effects. Trazodone decreased nightmare frequency in a group of hospitalized veterans, but 19% discontinued therapy because of side effects (priapism, daytime sedation, more vivid nightmares, severe dry mouth or dry sinuses) and 60% of those who continued on therapy also complained
of side effects (daytime sedation, dizziness, headache, priapism, and orthostatic hypotension) (27). Dose ranged from 25 to 600 mg with a mean of 212 mg. Three small uncontrolled studies of nefazodone reported efficacy in veterans and civilians with PTSD-associated nightmares with doses between 400 mg and 600 mg (28, 29 and 30). Treatment effects ranged from a 30% drop in nightmare frequency (28) to a 50% or greater fall in the nightmare score on the Structured Interview for PTSD in half of the study population at week 12 (30).

Small, open-label studies of the atypical antipsychotics suggest that they might be effective for the treatment of nightmares. The data are limited and in some studies the subjects are on multiple neuropsychiatric medications so further studies are needed to determine more robustly whether they are truly efficacious, either as monotherapy or as adjunctive therapy. Nonetheless, there are small case series suggesting that risperidone, aripiprazole, and olanzapine may be helpful. Risperidone has α₁-noradrenergic antagonistic properties (31), and two case series suggest efficacy in doses ranging from 0.5 to 3 mg nightly. One study demonstrated a statistically significant fall in CAPS score of recurrent distressing dreams (32) but the other study did not provide a quantitative analysis and just reported improvement in nightmares (33). Aripiprazole was added to therapy in one small (n = 5) case series and the authors reported that four subjects experienced a reduction in nightmare frequency and one subject had paradoxical hyperexcitation with insomnia at doses ranging from 15 to 30 mg (34). Olanzapine was also used to augment current psychotropic pharmacotherapy in a small case series because of its ability to improve sleep. The authors noted that it resulted in improvement of nightmares at doses of 10 or 20 mg with improvement often seen within a few days (35).

Topiramate was noted to be effective in one small case series (36) of civilian PTSD-associated nightmares with complete suppression of nightmares in 50% and reduction in nightmare frequency in 79% of the 35 subjects. The effective dose ranged from 12.5 to 500 mg/day but was 100 mg/day or less in 91% of the full responders. Dosage began at 12.5 to 25 mg daily and was increased in 25 to 50 mg increments every 3 to 4 days as tolerated until effective. Treatment was discontinued for the following side effects: urticaria, eating cessation, acute narrow-angle glaucoma, severe headaches, overstimulation or panic, emergent suicidal ideation, and memory concerns. A retrospective open-label clinical series of adjunctive gabapentin administered to 30 veterans on different combinations of antidepressants, antipsychotics, and anxiolytics suggested efficacy in decreasing nightmares, although the measure was a simple clinical global improvement scale with 77% of the subjects showing moderate to marked improvement in the symptom of insomnia and “most” of these also demonstrating improvement in nightmare disorder (37). Dose ranged from 300 to 3600 mg of gabapentin, with the greater effect seen with higher doses.

There are many behavioral therapies for nightmare disorder, of which four are supported by randomized controlled trials (RCTs): image rehearsal therapy (IRT), systematic desensitization (SD), self-exposure therapy (SET), and progressive deep muscle relaxation (PMR). While there are RCTs for each of these therapies, those for IRT are from a single site (although there are case series from other investigators), there are only two small ones for SD, one for SET, and one small one for PMR. Other behavioral therapies that have been used for treating nightmares include exposure, relaxation, and rescripting therapy (a variant of IRT) (38), sleep dynamic therapy (39), lucid dreaming therapy (another variant of IRT) (40,41), hypnosis (42,43), eye-movement desensitization and reprocessing (44,45), testimony method (46), and individual psychotherapy (47). These therapies await larger controlled trials to better substantiate efficacy.

IRT is a cognitive-behavioral therapy that addresses preconceptions about the role of nightmares (particularly posttraumatic nightmares), educates the patient about the value of treating nightmares as a disorder as opposed to a symptom, and provides instruction on rescripting the nightmares through daytime imagery practice
(see Appendix 11.1) (48)

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