Medication for Sleep Problems in Posttraumatic Stress Disorder


Drug

Study

Type of study

Duration and follow-up

N

Outcome sleep; insomnia (p value if given in publication)

Outcome sleep; nightmares (p value if given in publication)

Outcome sleep; objective parameters (p value if given in publication)

Paroxetine

Stein et al. (2003) [157]

Pooled analyses

Placebo controlled 12 wks

1180

Less disturbed sleep

Not mentioned

Not mentioned

Sertraline

Davidson et al. (2001) [41]

Placebo controlled 12 wks

208

Impr PSQI, but placebo = sertraline

Not performed

Fluoxetine

Meltzer-Brody et al. (2000) [103]

Placebo controlled

5 wks

53

Self: Impr.

Interview: NI

Self: trend

Interview: NI

Not performed

Fluvoxamine

De Boer et al. (1992) [47]

Open label

12 wks

24

13 DO

Impr

Impr

Not performed

Neylan et al. (2001) [113]

Open label

10 wks

21 (18 for sleep analysis)

Impr for staying asleep; NI for falling asleep

Impr

Not performed

Venlafaxine

Stein et al. (2009) [158]

Pooled analysis placebo controlled

12 wks

687

DO not reported (LOCF)

NI

NI (trend)

Not performed

Duloxetine

Walderhaug et al. (2010) [167]

Open label

8 wks

21

1 DO

Unknown

Impr (not specified)

Not performed

Villareal et al. (2010) [166]

Open label

12 wks

20

5 DO

PSQI impr. Duration longer, but NI with Bonferroni correction

Not performed

Imipramine

Burstein and Burstein (1983) [25]

Case reports

4 months

5

“Deepening” of sleep
 
Not performed

Burstein (1984) [24]

Open label

2–3 wks

N = 15; 5 DO

Less insomnia p = 0.001

Less dreams about trauma

P < 0.01

Not performed

Kinzie and Leung (1989) [79]

Open label

12

4 of 12 Impr; not specified

5 of 12 Impr; not specified

Not performed

Tranylcypromine

Shen and Park (1983) [150]

Case report

1

No information

Improved

Not performed

Phenelzine

Shen and Park (1983) [150]

Case reports

2

No information

Improved

Not performed

Hogben and Cornfield (1981) [72]

Case reports

5

No information

Improved

Not performed

Lerer et al. (1987) [93]

Open label

8–18 wks

25

Improved

Improved

Not performed

Davidson et al. [39]

Open label

4–6 wks

11

Improved

Improved

Not performed

Shestatzky et al. (1988) [151]

Randomized, crossover

4–5 wks

13

3 DO

NI

NI

Not performed

Moclobemide

Neal et al. (1997) [112]

Open label

12 wks

10

Impr

P = 0.001

Impr

P = 0.014

Not performed

Trazodon

Hertzberg et al. (1996) [65]

Open label

16 wks

6

Impr

Not specified

Not performed

Warner et al. (2001) [169]

Open label

8 wks

74

14 DO

Impr

Impr

Not performed

Ashford and Miller (1996) [7]

Open label

Cases

57 patients (30 with PTSD)

Impr

Impr

Not performed

Mirtazapine

Lewis (2002) [94]

Open label report

Period not reported

>300

? DO

Impr

Impr

Not performed

Schneier et al. (2015) [145]

Plac control RCT

36

NI

NI

Not performed

24 wks

17 DO (1st 12 wks)

10 DO (2nd 12 week)

Nefazodone

Davidson et al. (1998) [40]

Open label

12 wks

17

Impr

Impr

Not performed

Hertzberg et al. (1998) [66]

Open label

16 wks

10

Impr

Not specified

Not performed

Hidalgo et al. (1999) [70]

Pooled analysis of 6 open-label studiesa

105

Impr

Impr

Not performed

Mellman et al. [101]

Open label

12 wks

15

4DO

Impr

Impr

Less awakenings

Zisook et al. (2000) [180]

Open label

12 wks

19

Impr

Impr

Not performed

Gillin et al. (2001) [54]

Open label

12

Impr

Impr

PSG didn’t change

12 wks

Hertzberg et al. (2002) [68]

Open label

3–4 years

10

Impr

Not specified

Not performed

Neylan et al. (2003) [114]

Open label

12 wks

10

Impr

Impr

Increase TST (0.001)

Increase Sleep maintenance (0.016) Increase delta sleep (0.001)

McRae et al. (2004) [100]

RCT (with sertraline)

26 for analysis

13 nefazodone

Impr (PSQI) but the same as sertraline

Not performed

Agomelatine

De Berardis et al. (2012) [46]

Case report

7 months

1

Impr

Impr

Not performed

Gabapentine

Hamner et al. (2001) [61]

Retrospective chart review

1–36 months

30

Impr

Impr

Not performed

Divalproex

Hamner et al. (2009) [62]

RCT

10 wks

29 (13 plc)

DO 14 (7plc)

No difference with placebo

Not performed

Tiagabine

Taylor (2003) [160]

Case reports

1–4 months

7

DO 1

Impr

Impr

Not performed

Connor (2006) [35]

2-phase study with first open label (OL) then plc-controlled phase

Open label: 29

DO 10

Plcc-part: 18

DO: 5 (1plc)

OL: Impr

Plcc-part: tiagabine = plc

OL: Impr

Plcc-part: tiagabine = plc

Not performed

Davidson et al. (2007) [43]

Double-blind plcc RCT

232 (116 each arm)

No difference with placebo

Not performed

12 wks

Krystal et al. [84]

Open-label

3 wks

20

Impr

Impr

Less WASO (0.03)

Less NAW (0.01)

More SWS (0.01)

Less stage 1 (0.01)

Topiramate

Berlant (2001) [13]

Case reports

1–5 months

3

Impr

Impr

Not performed

Berlant and Van Kammen (2002) [15]

Open label

1–119 wks

Mean 33 wks

35

DO 5.

Not specified

Impr

Not performed

Berlant (2004) [14]

Open label

Duration unknown, study parameters at 4 wks

33

DO 12

Not specified

Impr

Not performed

Alderman et al. (2009) [5]

Open label

8 wks

43

NI (p = 0.08)

Impr

Not performed

Pregabaline

Strawn et al. (2008) [159]

Case report

At least 4 months

1

Impr

Impr

Not performed

Paslakis et al. (2011) [122]

Case report

Not reported

1

Impr

Impr

Not performed

Risperidone

Leyba and Wampler (1998) [95]

Case report

4

Impr

Impr

Not performed

Stanovic et al. (2001) [155]

Retrospective chart review

Unknown how long

10

Impr

Impr

Not performed

David et al. (2006) [36]

Open label study

At least 6 wks

17 completed at least 6 wks

DO 1 (lost in follow-up)

Impr

Impr

Not performed

Rothbaum et al. (2008) [138]

Plc controlled randomized augmentation study

8 wks

25 (14 risp and 11 plc)

DO 5 (all risp)

Impr

NI (although trend p = 0.09)

Not performed

Krystal et al. (2016)[86]; See as well Krystal et al. (2011) [85]

Plc controlled randomized augmentation study

24 wks

267 for secondary analysis

Impr (p = 0.03)

Impr (p = 0.03)

Not performed

Olanzapine

Labbate and Douglas (2000) [88]

Case report

4 months

1

Impr

Impr

Not performed

Jakovljević et al. (2003) [75]

Case reports

5

Impr

Impr

Not performed

Stein et al. (2002) [156]

Double-blind, placebo-controlled augmentation study

19

Impr

Not reported

Levomepromazine

Aukst-Margetić et al. (2004) [8]

Open-label study

4 wks

23

DO 2

Impr

Impr

Not performed

Thioridazine

Dillard et al. (1993) [50]

Case report

3 wks

1

Impr

Impr

Not performed

Aripiprazole

Lambert (2006) [89]

Case reports

Not reported

5

DO 1

Impr

Impr

Not performed

Villarreal et al. (2007) [165]

Open label study

12 wks

22

DO 8

Duration of sleep and PSQI improvements were not significant after Bonferroni

Not performed

Quetiapine

Robert et al. (2005) [132]

Open-label study

6 wks

20

DO 2

Impr

Impr

Not performed

Byers et al. (2010) [26]

Retrospective chart review

0.5–6 years

324 (237 included)

DO not clear

Impr

Impr

Not performed

Clonidine

Kinzie and Leung (1989) [79]

Open-label pilot

Not reported

9

Impr

Impr

Not performed

Kinzie et al. (1994) [80]

Case reports

Not reported

4

Impr

Impr

Results not conclusive

Guanfacine

Neylan et al. (2006) [115]

Double-blind

RCT

8 wks

63

DO 10

NI

NI

Not performed

Davis et al. (2008) [44]

Double-blind RCT with open-label study

8 wks + 2 months

35 randomized

DO 6

Open label extension period N = 24

NI

NI

Not performed

Clonazepam

Cates et al. (2004) [30]

Randomized, single-blind plc-controlled crossover study

2 wks

6 pts. with PTSD

Impr

NI

Not performed

Zolpidem

Dieperink and Drogemuller (1999) [49]

Case reports up to 20 months

32

DO 7

Impr

Impr

Not performed

Abramowitz et al. (2008) [1]

Randomized study comparing zolpidem with hypnotherapy

2 wks

32; 15 received zolpidem of which DO 1

Hardly Impr and hypnoth was better

Not performed

Eszopiclone

Pollack et al. (2001) [124]

Double-blind plc-controlled

Crossover RCT

3 wks each arm

24

Subjective improvement in sleep quality (PSQI), total sleep time, and sleep latency

Not performed

Buspirone

Wells et al. (1991) [170]

Case reports

At least half to 1 year

3

Impr

Impr

Not performed

Hamner et al. (1997) [60]

Open label case series

Not reported

15

DO 2 (side effects)

Impr

Impr

Not performed

Cyproheptadine

Harsch (1986) [64]

Case reports

Not clear

2

Not reported

Impr

Not performed

Brophy (1991) [20]

Case reports

Not reported

5

DO 2

Not reported

Improved

Not performed

Rijnders et al. (2000) [130]

Case report

Not reported

1

Impr

Impr

More deep sleep and less REM sleep

Clark et al. (1999) [32]

Open label

At least 1 week

36 baseline

DO 9

16 for statistics of which another DO 3

Not impr

0,26 for number of awakenings

Not impr

0.07 for disturbance of dreams

Not performed

Gupta et al. (1998) [58]

Case reports

Not clearly reported

9

Impr

Impr

Not performed

Jacobs-Rebhun et al. (2000) [74]

A double-blind, plc-controlled RCT

69

60 for analysis

NI

PSQI worse in treatment group, but p = 0.06)

NI

p = 0.17 (worse in treatment group)

Not performed


Impr improvement, NI no improvement, DO dropout, Plc placebo, Plcc-part placebo-controlled part of study, wks weeks





Agomelatine


Agomelatine was developed as a melatonergic receptor agonist and 5-HT2C antagonist antidepressant. Quera Salva et al. [126] performed an open study with 15 patients with MDD who received 25 mg agomelatine a day for 42 days; there was an increase in sleep efficiency, time awake after sleep onset, and the total amount of slow-wave sleep (SWS). The increase of SWS was predominant during the first sleep cycle. There was no change in REM latency, amount of REM, or REM density. No trials focusing on PTSD and use of agomelatine are available. The only publication is a case report by De Berardis et al. [46] describing one patient with PTSD who improved after 25 mg for 2 weeks, with improvement in sleep quality after only 1 week. After 2 weeks the patient started taking 50 mg/day and improved further until full remission, which still persisted after 7 months follow-up.


Vortioxetine


Vortioxetine has multiple effects that probably derive from the interaction with 5-HT-receptor-mediated feedback and appear to increase serotonergic, noradrenergic, dopaminergic, cholinergic, histaminergic, and glutamatergic neurotransmission in brain structures associated with MDD. The FDA and the European Medicines Agency have approved vortioxetine for the treatment of MDD. Concerning sleep, the effect can be better than with SSRI or SNRI as the sleep problems found as side effects are comparable with placebos, which are different than with the use of SSRIs or SNRIs.

There is some evidence that the HT7 receptor antagonism of vortioxetine might influence sleep fragmentation, but more research is needed concerning the effect on sleep [142] as PTSD is known to be related to sleep fragmentation.



Anticonvulsants


Anticonvulsants are thought to have anti-kindling effects, and several have been used to improve PTSD symptoms [16]. It is possible that they act via inhibition of glutamate neurotransmission . The effect on sleep and PTSD has been studied in a few small studies.

Legros and Bazil [92] performed a prospective study in patients with localization-related epilepsy by comparing sleep parameters of patients with and without antiepileptic drugs (AEDs). They found that gabapentin improved sleep by increasing SWS, valproic acid disrupted sleep by increasing stage 1 sleep, and lamotrigine had no significant effects. Vigo and Baldessarini [164] performed a review on AED for MDD. However, they found very few studies, and these differed in size and design and had uncontrolled use of antidepressants. The authors concluded that there was suggestive evidence of effects of carbamazepine, lamotrigine, and valproate for MDD and especially for long-term adjunctive use and for patients with recurring MDD with prominent irritability or agitation.


Gabapentin


Hamner et al. [61] retrospectively reviewed the files of 30 patients with PTSD (and 67% MDD) who received gabapentin as adjunctive medication. Gabapentin was mainly prescribed first to facilitate sleep; with a dose of 300–3600 mg/day, the majority (77%) showed moderate or greater improvement in the duration of sleep and a decrease in frequency of nightmares. The improvement appeared to be dose dependent; the group with moderate or marked improvement received 1344 ± 701 mg, and the group with mild or no improvement received 685 ± 227 mg.


Lamotrigine


There is some evidence that lamotrigine is helpful for PTSD; however, posttraumatic sleep disturbance or sleep difficulties caused by nightmares were not measured in studies such as that performed by Hertzberg et al. [67]. Their study included 15 patients with PTSD enrolled in a 12-week double-blind study of lamotrigine (start 25 mg and titration up to 500 mg if possible) and placebo. One patient dropped out, ten were on lamotrigine, and four on placebo; more patients on lamotrigine responded (50–25%), and patients on lamotrigine improved more on reexperiencing and avoidance/numbing symptoms.


Divalproex


Schneider et al. [144] studied the effect of di-n-propylacetic acid (DPA) (valproic acid) on sleep in 11 healthy volunteers. After short-term application (2 days), a shortening of the time to fall asleep and of the waking time was found, whereas under long-term administration (2 weeks), a decrease in deep synchronous sleep was observed. No marked influence on REM sleep was observed. Subjective sleep experiences did not change. Hamner et al. [62] performed a placebo-controlled study with divalproex in 29 chronic PTSD patients of whom most used other medication (antidepressants, anxiolytics); the authors found no difference compared with placebo concerning the sleep-related measures and even found a decrease in avoidance/numbing scores and improvement in the Clinical Global Impression Scale favoring placebo.


Tiagabine


Tiagabine is a GABAergic anticonvulsant. Mathias et al. [98] conducted a double-blind, placebo-controlled study of a single oral dose of 5 mg tiagabine on nocturnal sleep in ten healthy elderly volunteers (mean age 68 years) and found tiagabine to increase sleep efficiency, tendentially decreased wakefulness, and prominently increased both SWS and low-frequency activity in the EEG within non-REM sleep. Except for self-rated sleep intensity, there was no significant change in subjectively assessed sleep parameters nor perceived state upon awakening. Taylor [160] did a case series on seven patients with PTSD and reported positive findings on sleep disturbance, especially nightmares; the mean dose was 8 mg tiagabine . Connor et al. [34] performed an open-label tiagabine for 12 weeks with tiagabine (initiated at 2 mg bid and up to 16 mg daily max, mean dose 10.8 mg) in 29 outpatients with PTSD; those who showed significant improvement (n = 19) continued with placebo or tiagabine , and there was a greater trend toward a likelihood of further remission but no significant differences. Distressing dreams, nightmares, and PSQI improved significantly during the open-label part, but, in the placebo-controlled phase, the improvements stayed the same in both the placebo and tiagabine group. Walsh et al. [168], in a placebo-controlled, randomized, double-blind, parallel-group study in insomnia patients (n = 232) with different dosages of tiagabine, found a significant dose-dependent increase of slow-wave sleep and a decrease in stage 1 sleep but no change in WASO, sleep latency, or total sleep compared to placebo.

Davidson et al. [43] performed a 12-week, double-blind, randomized, multicenter study and included 232 patients with PTSD (tiagabine and placebo; both n = 116). There was no difference in change by tiagabine (mean dosage 11.2 mg/day) and placebo concerning PTSD symptoms (CAPS) (p = 0.85) baseline vs. final visit. There were no differences in sleep ratings between the tiagabine and placebo groups. Krystal et al. [83] performed an open-label 3-week study on 20 adults with PTSD who took 2–12 mg tiagabine daily (two times) with polysomnography measures. Contrary to the findings of Davidson et al. [58], there appeared to be an improvement in different sleep parameters such as the WASO (effect size 0.49; p0.033) and nightmares (e.g., PSQI item 5 h gave an effect size of 0.44; p = 0.008).

They also concluded that the first treatment night predicted PTSD response at 3 weeks. A decrease in self-reported and objective time awake after onset of sleep and an increase of SWS accounted for 94% of the week 3 PTSD score. More important, they found positive and significant correlations between changes in sleep parameters and total PTSD scores, such as WASO with PSG (r = 0.6; p < 0.001) or self-reported (r = 0.82; p < 0.001). This means that improvements in sleep can lead to improvements in PTSD symptoms.


Topiramate


In several case and open-label studies on topiramate [1315], some effect of topiramate on PTSD was found, especially on sleep problems . The study of Berlant [14] was an open-label study with topiramate as monotherapy or augmentation (median dosage 50 mg/day); this led to a decline of PTSD symptoms in median 9 days, and 94% of the patients with nightmares reported full cessation after 4 weeks. Tucker et al. [162] conducted a double-blind, placebo-controlled study on topiramate monotherapy (median final dose 150 mg/day) in 38 patients with PTSD; the authors found no significant reduction in the CAPS score, but there was a significant decrease in reexperiencing symptoms and the treatment outcome PTSD scale. No separate sleep measures were reported.

Alderman et al. [5] performed an 8-week open-label pilot study of topiramate in 43 patients with PTSD; they found reductions in several scales and a significant reduction of PTSD symptoms (CAPS). The Stanford sleepiness scale tendentially improved (p = 0.08). There was a significant reduction in nightmares and a reduction in the number of patients who were anxious to fall asleep and the number of patients with high-risk drinking patterns.


Levetiracetam


Kinrys et al. [78] performed a retrospective chart review on 40 patients who have taken 9.3 weeks (sd 5.1) adjunctive levetiracetam . There was improvement, but change of severity was measured by use of clinical global inventory (CGI) only, and no information about sleep or nightmares was given.


Pregabalin


Hindmarch et al. [71] performed a randomized, double-blind, placebo- and active-controlled, 3-way crossover study with 24 volunteers (23 completers) who took pregabalin 150 mg t.i.d., alprazolam 1 mg t.i.d., and placebo t.i.d. for 3 days. Pregabalin increased slow-wave sleep and reduced sleep latency. REM sleep was reduced, but REM sleep latency appeared to be equal to placebo. Pregabalin reduced the number of awakenings. Subjective sleep improved, but ratings of behavior after awakening showed impairments.

Strawn et al. [159] wrote a case report about a patient with PTSD who took 75 mg b.i.d. in addition to her other medication; her nightmares stopped and insomnia improved within 2 weeks. Pae et al. [120] conducted an open-label study with nine patients with PTSD who were on stable doses of antidepressants. They were treated with flexibly dosed pregabalin [mean dose 200 mg/day (range 150–300 mg/day)] for 6 weeks and improved on PTSD complaints; however, but no sleep measures were made. Paslakis et al. [122] published a case report about a patient with PTSD who previously used different kinds of medication but improved on pregabalin with later addition of quetiapine because of an additional bipolar disorder. The patient reported improvement in sleep and nightmares within the first week.


Antipsychotics


Giménez et al. [55] compared effects on (subjective) sleep activity due to typical and atypical antipsychotic drugs; they performed a randomized, double-blind, placebo-controlled, four-period crossover clinical trial on 20 healthy young volunteers who took a single oral morning dose of olanzapine 5 mg, risperidone 1 mg, haloperidol 3 mg, or placebo. The drugs resulted in different changes in sleep patterns. Olanzapine led to an increase in TST, sleep efficiency, SWS, and REM sleep with a decrease in wake time and also resulted in a significant improvement in subjective sleep quality compared with risperidone and haloperidol and a tendency compared with placebo. Risperidone resulted in a decrease in wake time and REM sleep, whereas stage 2 increased. Haloperidol tended to increase sleep efficiency and stage 2, with a decrease of wake time. Neither haloperidol nor risperidone improved subjective sleep quality.


Risperidone


Risperidone was used in a study which consisted of two parts [148]. The first was a placebo-controlled, double-blind, crossover study on eight volunteers who took risperidone 1 mg for one night; this resulted in a significantly decreased REM sleep. The second part was an open-label study on eight patients with MDD who did not respond to a therapeutic dose of antidepressants and received 2 weeks of risperidone 0.5–1 mg (final mean 0.7 mg) daily. The depressed patients had significantly less wake and REM sleep as well as a significant decline in depressive symptoms.

There are a few case reports about the positive outcome when using risperidone for PTSD, e.g., the study of Leyba and Wampler [95]. Stanovic et al. [155] performed a retrospective chart study in acutely burned hospitalized patients with distressing acute stress symptoms that probably would not respond to brief psychotherapeutic interventions. Patients received 0.5–2 mg risperidone (mean 1 mg) at bedtime and had less sleep disturbances, nightmares/flashbacks, and hyperarousal. David et al. [36] conducted an open-label study of flexible dose adjunctive risperidone (1–3 mg) in patients who partially responded to medication (different use of AD, AED, and anxiolytics). A total of 17 Vietnam veterans completed at least 6 weeks and showed improvement of sleep disturbance measured by self-report sleep measures. Less awakenings and reduction in trauma-related dreams (CAPS item) were found, but improvement was especially found in sleep log data and not in retrospective scales, such as the PSQI .

Rothbaum et al. [138] performed a randomized augmentation study with risperidone and sertraline . The patients who did not remit during 8 weeks treatment with open-label sertraline received risperidone or placebo for 16 weeks. Of the 45 patients that started, 34 completed the sertraline part and 25 went on to the second part, of whom 20 completed. All patients improved, with no group differences. Post hoc analyses showed that the group that received risperidone improved more on the sleep item of the Davidson Trauma Scale (p = 0.03) and the sleep item of the CAPS Scale (trend p = 0.09). Krystal et al. [85] conducted a 6-month, randomized, double-blind, placebo-controlled multicenter trial with 367 screened patients, of which 296 were diagnosed with military-related PTSD and ongoing symptoms after at least two SRI treatments. Risperidone (up to 4 mg) or placebo was given to 247, and there was no significant change in total CAPS score. Post hoc analyses [86] showed a significant but small reduction in reexperiencing and hyperarousal symptoms, perhaps clinically not detectable. Risperidone use resulted in more adverse events than placebo, such as weight gain, fatigue, and somnolence. Sleep was measured by means of the PSQI, and risperidone provided some improvement (p = 0.034) as well as less severe nightmares (measured by means of CAPS item and p = 0.033). The improvements in sleep correlated with PTSD symptom reductions as a whole (measured by the CAPS; r-0.28, p = 0.001) and improvement in general mental health measured by means of the SF-36 V subscale (r = 0.26, p = 0.003). The scores became significantly different from placebo in week 24; before that time, the differences were not significant, and the positive effect was not seen in measures for global clinical status and general measures of quality of life. This gave the authors reason to conclude that the results have some, but limited, clinical significance.


Olanzapine


Sharpley et al. [149] studied olanzapine and its effects on sleep when used as augmentation to ineffective treatment with SSRIs in depression . In an open trial, 12 patients with SSRI-resistant depressive disorder took 2.5–10 mg olanzapine (mean 4.8 mg) for 3 weeks; the depressive symptoms decreased, while sleep efficiency increased, as did the subjective sleep quality and SWS. In general, the improvements occurred after the first week.

Labbate and Douglas [88] and Jakovljević et al. [75] reported on patients with PTSD given olanzapine 5–20 mg as augmentation; they described improvements in symptoms (e.g., nightmares and sleep disturbance) starting after 1–4 days. Stein et al. [156] performed a double-blind, placebo-controlled study with augmentation of olanzapine (15 mg/day) or placebo in 19 patients with PTSD who hardly responded to an SSRI; the authors found a significant clinical improvement of PTSD and depressive and sleep measures. The enhanced sleep accounted for much of the reported improvement. They concluded that the overall clinical magnitude of effects was modest for most of the patients but clinically meaningful for some. Carey et al. [28] performed a randomized 8-week placebo-controlled study with olanzapine (flexible dosage; ending at mean 9.3 mg/day) as monotherapy in 34 patients with PTSD (ten dropped out, and four of them were included in the analysis) and found more improvement on the CAPS compared with placebo. There were no special measurements on insomnia or nightmares.

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Feb 25, 2018 | Posted by in PSYCHOLOGY | Comments Off on Medication for Sleep Problems in Posttraumatic Stress Disorder
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