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Chronic sleep disruption and the reexperiencing cluster of posttraumatic stress disorder symptoms are improved by olanzapine: brief review of the literature and a case-based series

Chronic Sleep Disruption and the Reexperiencing Cluster
of Posttraumatic Stress Disorder Symptoms
Are Improved by Olanzapine: Brief Review of
the Literature and a Case-Based Series
James H. States, M.D., and Clarke D. St.Dennis, Ph.D., B.C.P.P.
osttraumatic stress disorder (PTSD) is a serious Panxiety disorder with a lifetime prevalence of 5.0%
Background: Posttraumatic stress disorder
to 13.8%.1 Most people will experience or be exposed to (PTSD) is one of the most prevalent psychiatric a traumatic event at some point in their life, with 15% disorders in young adults. Early diagnosis and to 24% developing PTSD. This connotes to about 1 in 12 treatment of PTSD are essential to avoid possible adults being affected by PTSD during their lifespan and long-term neuropsychiatric changes in brain makes the disorder one of the most prevalent psychiatric physiology and function. A cardinal symptom ofPTSD is chronic sleep disruption, often with re- disorders in young adults, after depression, phobia, and curring nightmares. If untreated, PTSD symptoms alcohol and substance abuse.1 A cardinal symptom of often contribute to substance abuse and the devel- PTSD that should alert the clinician is the complaint of opment of other comorbid psychiatric disorders.
chronic sleep disruption. On further questioning about the Once PTSD is diagnosed, drug treatment should onset of this problem, some PTSD patients may provide begin with antidepressant therapy. If antidepres-sants do not correct the sleep disruption, adjunc- vivid descriptions of recurring nightmares about a pre- tive treatment with the atypical antipsychotic cipitating traumatic event. Others may not remember spe- olanzapine or other agents should be considered.
cific nightmares replaying the event, but will complain Method: This case series reviews 7 cases of
that they cannot remember the last time they experienced patients with PTSD (DSM-IV criteria) seen in a restful night’s sleep. If patients of this type can identify primary care clinics who were successfullytreated with olanzapine. In most cases, olanzapine an abrupt onset of their sleep disturbance, then the clini- therapy was adjunctive and followed failed treat- cian should try to identify a precipitating event and con- ment with antidepressant monotherapy for sleep sider a more in-depth diagnostic workup for PTSD.
In light of the recent attacks on the World Trade Cen- Results: All patients reported improved sleep
ter, clinicians will need to be more aware of PTSD symp- with decreased or absent nightmares, as well asimprovements in other PTSD symptom clusters.
toms and treatment. A follow-up survey of Manhattan, Conclusion: Further controlled studies are
N.Y., residents 5 to 8 weeks after Sept. 11, 2001, indicated needed to better characterize and validate this a prevalence of symptoms consistent with the diagnoses of PTSD and depression that was more than twice the ac- (Primary Care Companion J Clin Psychiatry 2003;5:74–79) cepted baseline values for this population.2 Received July 18, 2002; accepted Feb. 5, 2003. From Adolescent and Young Adult Medicine, Bellevue, Wash. (Dr. States); the College of PTSD is characterized by 3 core symptom clusters3,4: Pharmacy, Washington State University, Spokane (Dr. St.Dennis); and theDepartment of Psychiatry, School of Medicine, University of Washington,Seattle (Dr. St.Dennis). 1. Reexperiencing: unwanted recollections of the Dr. States has been a member of the speakers board for Eli Lilly, event in the form of intrusive and distressing Pfizer, Wyeth, Pharmacia, and Bristol-Myers Squibb. Dr. St.Dennis has images, nightmares, flashbacks, or emotional and received honoraria from AstraZeneca, Eli Lilly, Pfizer, Wyeth, Forest,Janssen, and GlaxoSmithKline and has been a member of a speakers/ physical distress at exposure to reminders (trig- advisory board for AstraZeneca, Eli Lilly, Pfizer, Wyeth, Forest, Janssen, gers) of the event. Reexperiencing the trauma Corresponding author and reprints: Clarke D. St.Dennis, Ph.D., in the form of chronic nightmares often leads to Washington State University, Spokane, Department of Pharmacotherapy, chronic sleep disruption, which may further pre- 310 N. Riverpoint Blvd., P.O. Box 1495, Spokane, WA 99212-1495(e-mail: dispose the patient to cognitive dysfunction.
2. Avoidance: attempts to avoid reminders associ- ated with the experience, together with diminished COPYRIGHT 2003 PHYSICIANS POSTGRADUATE
Primary Care Companion J Clin Psychiatry 2003;5(2) PRESS, INC. COPYRIGHT 2003 PHYSICIANS POSTGRADUATE PRESS, INC.
responsiveness to the external world (psychic that the development of PTSD is facilitated by a failure to control the biological stress response at the time of the 3. Hyperarousal: physiologic manifestations of the trauma, resulting in a cascade of alterations in brain disorder that may occur persistently and that functioning that lead to the core symptom complexes.4 are manifested as insomnia, irritability, hypervigi- One consequence of these alterations appears to be higher lance, increased startle response, and impaired circulating norepinephrine levels and an increased reac- tivity of adrenergic receptors.4 These findings, plus theobservation that thyroid levels may be increased in PTSD Diagnosis of PTSD is often complicated by a high patients,4 help to account for many of the somatic symp- degree of psychiatric comorbidity that may approach 80%.5 Concurrent depression occurs in 30% to 50% ofPTSD patients.6 Other concomitant disorders commonly seen in PTSD include bipolar disorder, substance or alco-hol abuse, and other anxiety disorders, notably, panic dis- As our understanding of PTSD increases, it is apparent that early treatment and intervention are critical and thatthere is an urgent need for effective treatments that can control and reverse the potentially destructive patho-physiologic processes described above.13 Treatment strat- If diagnosis and treatment are not initiated soon after egies to date have focused on the use of antidepressants the trauma, PTSD may persist for years with definite neu- combined with psychotherapy.4,14 Antidepressants that ropsychiatric changes noted in brain physiology and have been shown in randomized trials to control at least function. Mid-adolescence is an age at which major some of the symptoms of PTSD include tricyclics, mono- structural changes occur naturally in the brain.7 Trauma amine oxidase inhibitors, and selective serotonin reup- during this period of rapid brain change and growth may take inhibitors (SSRIs).4 Antidepressants reported to con- arrest development or produce a regression to an earlier trol some PTSD symptoms in open-label trials include stage of neural structure.7 Adults diagnosed with PTSD trazodone, nefazodone, venlafaxine, and mirtazapine.
typically demonstrate a reduction in the volume of the Only sertraline and paroxetine have received U.S.
hippocampus as measured by magnetic resonance imag- Food and Drug Administration–approved indications for ing, with associated memory deficits.8,9 However, neuro- PTSD. The Expert Consensus Guidelines recommend imaging of children and adolescents with PTSD reported switching to either nefazodone or venlafaxine if there is lower corpus callosum volume, greater cerebrospinal and no response to an SSRI after an 8-week trial.14 In addi- ventricular fluid volumes, and lower overall cerebral vol- tion, mood stabilizers have been shown in open-label ume, all results consistent with an underdeveloped or trials to help control certain symptoms, to reduce irritabil- ity, and to improve impulse control. These drugs include Symptom provocation studies utilizing positron emis- lithium and valproate products, which demonstrate some sion tomography scanning have demonstrated disrupted efficacy against avoidance/numbing and arousal symp- cerebral blood flow in brain areas associated with fear re- toms, and carbamazepine, which has been reported to re- sponse.4,8,11 Results to date point to increased reactivity of duce reexperiencing and arousal symptoms.13 The Expert the amygdala and anterior paralimbic region to trauma- Consensus Guidelines also recommend adding dival- related stimuli, whereas activities of the anterior cingu- proex to an SSRI if there is only partial response.14 Pre- late and orbitofrontal areas are decreased.8 The amygdala liminary reports with topiramate indicate rapid and effec- and paralimbic areas are associated with processing tive reduction of reexperiencing symptoms associated negative emotions and the ensuing expression of auto- with trauma-related nightmares or intrusive memories/ nomic arousal, whereas the anterior cingulate and asso- flashbacks.13 Similarly, the use of prazosin, a centrally ciated medial frontal cortex are thought to play a role acting α -antagonist, has been shown to reduce night- in the extinction of conditioned fear responses.8 Thus, it mares in up to 75% of combat veterans, usually the most appears that the brains of PTSD patients continue to unresponsive group of PTSD patients to most accepted overrespond to negative emotions with autonomic arousal, while lacking the stimulation of the medial pre-frontal cortex to perform its compensatory role in the Patients with PTSD have chronically low serum corti- In our practice, we have noted that not all patients have sol levels and high levels of corticotropin-releasing fac- resolution of nightmares and sleep disruption when tor, indicative of major disruption of the hypothalamic- treated with SSRIs. In fact, sertraline actually failed to pituitary axis.4,12 Current theory supports the hypothesis significantly separate from placebo on the reexperiencing COPYRIGHT 2003 PHYSICIANS POSTGRADUATE PRESS, INC. COPYRIGHT 2003 PHYSICIANS POSTGRADUATE PRESS, INC.
Primary Care Companion J Clin Psychiatry 2003;5(2) symptom cluster during pre-marketing trials.16 On the stabilized. She felt positive about the decreased night- basis of preliminary reports, its demonstrated efficacy for mares and improved sleep, reporting that her concen- restoration of sleep architecture in bipolar and psychotic tration was better when she slept soundly. She indicated disorders, and its positive effects on cognition, olanzapine that she was experiencing her first uninterrupted sleep in was tried as an adjunctive agent when SSRI treatments failed to reverse the reexperiencing symptom cluster or On day 11 after starting olanzapine, the patient re- other symptom clusters.17,18 To date, we have treated over ported that she had no nightmares and was sleeping 20 adolescent and adult outpatients meeting DSM-IV through the night. She reported only “a little bit of intru- criteria for PTSD in this manner. Patients were between sive thoughts.” She was still experiencing recall of some the ages of 17 and 46 years and were identified during vis- the events surrounding the trauma, but without physi- its with the primary author (J.H.S.) at 1 of 3 sites: a uni- ologic reactivation symptoms or anxiety. She indicated versity counseling service, a rural health clinic, or a pri- that the improved sleep and mood stabilization were help- vate practice, outpatient medical clinic. All psychiatric ing her to experience psychotherapy more effectively, be- diagnoses were made according to DSM-IV criteria.
cause her recall of adverse events was improved without Patients were initially test-dosed with olanzapine, 1.25 triggering reactivation symptoms. After 3 weeks of treat- mg p.o., given 12 hours before their usual awakening ment, Ms. A indicated that she was feeling less avoidance time. If tolerated, doses were titrated to a level that per- and had started to schedule recreational and social time mitted 7 to 10 hours of sleep per night. Doses were de- creased if daytime lethargy persisted. Patients were ques-tioned at follow-up interview about nightmares, intrusive thoughts, and quality and duration of sleep. Final daily Ms. B is a 19-year-old white woman with a diagnosis doses ranged from 2.5 to 15 mg, usually dosed 12 hours of bipolar disorder not otherwise specified (NOS) and before the patient’s usual awakening time.
PTSD. Her past history included 3 episodes of rape and In this article, we review in detail the medical histories 1 hospitalization for suicidal ideation. Ms. B reported of 7 patients from this sample and their responses to previous treatment trials with paroxetine, quetiapine, and olanzapine and other adjunctive therapies. These 7 pa- nefazodone, with minimal improvement in her PTSD tients were chosen because the other patients had serious comorbidities that required concomitant use of other After 12 days of therapy with olanzapine, 5 mg/day, she reported a 75% improvement in sleep and nearly com-plete resolution of nightmares replaying her episodes of abuse, although she still experienced some daytime Ms. A is a 44-year-old white woman who presented intrusive thoughts. The emergence of panic attacks with with a past history of trauma, depression, anxiety, and obsessive-compulsive features resulted in the addition of PTSD. She had been treated previously with paroxetine, sertraline, 25 mg/day, to her regimen.
20 mg/day. After 2 weeks, she discontinued paroxetine On day 24, Ms. B demonstrated no further mood cy- due to distress over an increase in nightmares in which cling, panic attacks, or symptoms of diffuse anxiety and she relived the trauma in a symbolic manner. The intru- reported feeling less aggressive due to the decrease in sive thoughts and nightmares were based on a childhood nightmares and intrusive thoughts. She stated that she felt assault and left her with a sense of helplessness. Her pri- “a lot better” and was better able to finish her goals and mary symptoms at intake were severe early, middle, and tasks. Due to concerns over weight gain and to further op- late insomnia. She reported sleeping no more than 45 timize sleep patterns, topiramate, 25 mg/day for 7 days, minutes at a time and waking up from “weird and terrify- followed by an increase to 50 mg/day, was initiated on ing” dreams. In each situation, Ms. A felt “helpless and day 24. Both the sertraline and topiramate doses were vulnerable.” Her childhood was also complicated by her eventually increased over the next 2 months, with excel- mother’s auditory and visual hallucinations and frequent lent resolution of the nightmares, intrusive thoughts, and paranoid thinking, leading to unprovoked attacks with knives and other weapons. Her sister was diagnosed with Over 3 months later (day 124), the patient was receiv- ing a regimen of olanzapine, 5 mg/day; sertraline, 150 Ms. A was treated initially with sertraline, 25 mg/day, mg/day; and topiramate, 200 mg/day. She discontinued but discontinued it after she felt like she was “in a cloud olanzapine due to weight gain concerns. Rapid-cycling of confusion.” She was then placed on treatment with hypomanic symptoms, panic attacks, and nightmares olanzapine, 2.5 mg/day, combined with outpatient coun- returned 1 to 2 weeks post-discontinuation, leading to ma- seling. On day 7 of treatment, she reported that her sleep jor sleep disturbance. On day 132, lithium, 300 mg t.i.d., had improved, with no nightmares or night terrors. Her was started and titrated to a serum level of 0.7 mg/dL. By depressive symptoms were improved, and her mood had day 139, the patient’s hypomania had diminished and she COPYRIGHT 2003 PHYSICIANS POSTGRADUATE
Primary Care Companion J Clin Psychiatry 2003;5(2) PRESS, INC. COPYRIGHT 2003 PHYSICIANS POSTGRADUATE PRESS, INC.
had stabilized on a regimen of sertraline, 25 mg/day; lith- She was started on treatment with olanzapine, 2.5 mg ium, 300 mg t.i.d.; and topiramate, 100 mg b.i.d. Several q.h.s., and was tapered off trazodone during the first week weeks later, Ms. B began reexperiencing nightmares of treatment. The patient’s nightmares rapidly resolved when she accidentally met the perpetrator of her abuse. At over a period of 2 weeks, but then slowly returned. The that point, she elected to reinitiate olanzapine, 2.5 mg patient’s olanzapine dose was then increased to 5 mg q.h.s., in her drug regimen. The patient reported that her q.h.s. on day 14. Two weeks later (day 28), her venlafax- nightmares had decreased significantly by day 4 of her ine XR dose was decreased to 300 mg/day in response second course of olanzapine therapy.
to mild hypertension. On day 35, Ms. D reported thatolanzapine, 5 mg q.h.s., had stopped the nightmares, stat- ing, “It is totally under control; I don’t wake up with a Ms. C is a 30-year-old Native American woman who sense of doom or terror.” The patient was sleeping well presented with depression with mood swings and full di- and reported remembering traumatic events, but without agnostic criteria for PTSD, as well as a history of asthma, physical abuse resulting in multiple head injuries withloss of consciousness, and substance dependence, includ- ing seizures secondary to amphetamine abuse. She had a Ms. E is a 31-year-old white woman who was sexually positive family history for bipolar disorder.
molested at 10 years of age. She had experienced distress- Initial treatment consisted of continuing venlafaxine, ing symptoms since the trauma and met full diagnostic 300 mg/day; discontinuing trazodone for sleep; and add- criteria for PTSD. In addition to PTSD, her presenting ing olanzapine, 5 mg q.h.s. One week after starting olan- symptoms included depression and early and middle zapine treatment, she experienced a seizure. She discon- insomnia. She had had previous trials with paroxetine, tinued olanzapine after 5 weeks due to weight concerns, fluoxetine, bupropion, nefazodone, and sertraline. Ms. E reported that fluoxetine caused manic symptoms, that ser- A later electroencephalogram revealed paroxysmal ab- traline and paroxetine increased her anxiety, that bupro- normalities, most likely epileptiform and mild focal sei- pion did not alleviate her depression, and that nefazodone zures, resulting in a diagnosis of partial seizure disorder made her forgetful. She was taking trazodone at bedtime (both focal and generalized) secondary to multiple head for sleep; gabapentin, 900 mg/day; and venlafaxine, 75 injuries. Ms. C was started on treatment with divalproex mg/day, at the time of the first interview. The patient sodium, which was titrated to 500 mg b.i.d. Due to con- reported that trazodone was not helping her insomnia.
cerns over increased nausea on day 55 after discon- Her initial diagnoses included PTSD, alcohol abuse, and tinuation of olanzapine, the patient discontinued venla- faxine. She was then started on treatment with sertraline, During the first week of treatment, trazodone was dis- 25 mg/day, with the dose being slowly increased over the continued and the patient was started on treatment with olanzapine, 2.5 mg q.h.s., which was increased incremen- Eight months after discontinuation of olanzapine, tally until she achieved adequate sleep with 10 mg q.h.s.
she reported a more stable mood with the divalproex- She initially remained on treatment with gabapentin, but sertraline combination, but was concerned about increas- was tapered off this medication by the end of week 3.
ing nightmares and other PTSD symptoms related to her Over the next several weeks, Ms. E required 10 to 15 mg incidents of abuse. Continuing problems with nightmares of olanzapine q.h.s. to maintain normal sleep without and severe sleep disruption led to her restarting olanza- nightmares. By week 8, her mood had stabilized and her pine, 2.5 mg q.h.s. One month later, Ms. C reported that nightmares had resolved completely with olanzapine, 15 her nightmares had resolved. Her mood was stable, with mg q.h.s., and venlafaxine, 75 mg/day.
Mr. F is a 36-year-old white man who reported a his- Ms. D is a 22-year-old white woman who presented tory of depressed and irritable mood that had been present with a history of chronic nightmares and depression stem- since childhood. At the first interview, the patient met ming from multiple episodes of sexual abuse. Ms. D met DSM-IV criteria for PTSD, bipolar disorder NOS with full criteria for PTSD and had been on treatment with current episode depressed, and developmental learning venlafaxine extended release (XR), 375 mg/day, for over disorder. The patient was diagnosed with a developmental 2 years. In addition, she was receiving trazodone, 150 mg, reading disorder via psychological testing in 1995. Mr. F at bedtime for sleep and had escalated the dose to 300 mg had experienced multiple family traumas, physical and previously. Her nightmares and sleep disturbance contin- emotional neglect, and sexual abuse from family mem- ued despite medication compliance with venlafaxine XR bers. Current stressors included recent loss of a relation- ship with a female friend and academic problems.
Primary Care Companion J Clin Psychiatry 2003;5(2) Other symptoms noted at intake included early and middle insomnia that had lasted 2 years and was notresponding to trazodone taken at bedtime, fatigue not re- All 7 patients demonstrated rapid and significant reduc- lieved by rest, and nightmares and intrusive thoughts tion in PTSD-related insomnia and nightmares with olan- associated with childhood abuse and neglect. He com- zapine in the range of 2.5 to 15 mg/day, typically dosed plained of intermittent mood irritability with rapid and 12 hours before the person’s normal “alert” time after pressured speech and grandiose plans lasting a few hours.
awakening. Six of 7 patients demonstrated improvement The irritability alternated with depression lasting 2 to 3 of these symptoms after failing to adequately respond to days. Mr. F reported no 2-month reprieve in symptoms standard SSRI monotherapy. Other beneficial olanzapine during the last 2 years. He also complained of anhedonia actions included rapid mood stabilization, especially in the and impaired concentration. He had been taking citalo- 3 patients with diagnosed bipolar disorder. Olanzapine pram, 40 mg b.i.d., for 2 to 3 months and reported that it was generally well tolerated, with 2 patients initially dis- seemed to help his depression but not his nightmares or continuing therapy due to concerns about weight gain.
Both elected to restart treatment due to recurrence of In the past, Mr. F had been treated unsuccessfully with nightmares. A third patient concerned about weight gain thiothixene, diazepam, sertraline, paroxetine, and fluoxe- was successfully treated with adjunctive topiramate. Olan- tine. Fluoxetine worsened his insomnia and made the pa- zapine appears to be an effective and rational adjunctive tient “super-irritable.” Sertraline at a dose of 200 mg/day agent for treating the reexperiencing cluster of PTSD for 1 year was judged “OK,” helping with the patient’s symptoms, especially sleep disturbance secondary to nightmares. Future controlled studies are needed to better Olanzapine was added to citalopram at an initial dose characterize and quantify this therapeutic indication.
of 5 mg/day. This addition was associated with a 50% The importance of recognizing and treating chronic reduction in nightmares and intrusive thoughts during sleep disruption in potential PTSD patients cannot be the first week of treatment. A further dose increase to 7.5 overemphasized. This symptom may be the only symptom mg/day by week 5 of treatment led to resolution of night- patients will volunteer, and it should trigger a more in-depth PTSD workup on the part of the clinician. IfPTSD is identified, treatment with SSRI antidepressants is warranted as baseline treatment, with or without psy- Ms. G is a 29-year-old African American woman with chotherapy. If antidepressant therapy does not adequately a history of repeated rape and abuse that occurred in her improve sleep or stop nightmares, then adjunctive treat- own home, beginning at 5 years of age. She met full crite- ment with olanzapine, topiramate, or prazosin should be ria for PTSD, presenting with complaints of recurrent nightmares, intrusive thoughts, and disrupted sleep thataveraged 4 hours or less per night. She indicated that even Drug names: bupropion (Wellbutrin and others), carbamazepine(Tegretol and others), citalopram (Celexa), diazepam (Valium and returning to her current residence after school precipitated others), divalproex sodium (Depakote), fluoxetine (Prozac and others), her PTSD symptoms. The case was further complicated gabapentin (Neurontin), lithium (Eskalith, Lithobid, and others), by the death of a surrogate parent the day of her initial in- mirtazapine (Remeron), nefazodone (Serzone), olanzapine (Zyprexa),paroxetine (Paxil), prazosin (Minipress and others), quetiapine (Sero- terview. She was receiving no medications at the time of quel), sertraline (Zoloft), thiothixene (Navane and others), topiramate (Topamax), trazodone (Desyrel and others), venlafaxine (Effexor).
Ms. G was started on treatment with olanzapine, 2.5 mg 12 hours before awakening, and reported complete resolution of nightmares at follow-up on day 7. Her sleepthat week improved to 8.5 hours per night. During her 1. Breslau N. The epidemiology of posttraumatic stress disorder: what is third visit (day 24), she indicated that her nightmares had the extent of the problem? J Clin Psychiatry 2001;62(suppl 17):16–22 2. Galea S, Ahern J, Resnick H, et al. Psychological sequelae of the not returned. Because of a family history of diabetes and September 11 terrorist attacks in New York City. N Engl J Med concerns over carbohydrate craving and recent weight gain, topiramate, 25 mg p.o. t.i.d., 1 to 2 hours before 3. Miller MC. Disaster and trauma. Harv Ment Health Letter 2002;18:1–5 4. Yehuda R. Review article: post-traumatic stress disorder. N Engl J Med meals was added to the patient’s regimen on day 24. At the next clinic visit (day 81), Ms. G indicated that she had 5. Breslau N, Davis GC, Andreski P, et al. Traumatic events and PTSD in an lost 5 lb (2 kg) and was feeling very much improved. Her urban population of young adults. Arch Gen Psychiatry 1990;47:259–266 6. Shalev AY. What is posttraumatic stress disorder? J Clin Psychiatry 2001; intrusive thoughts, nightmares, and sleep disturbance had resolved, with an “even mood” and good concentration 7. Pynoos RS, Steinberg AM, Ornitz EM, et al. Issues in the developmental until around 9:00 p.m. She still displayed avoidance of neurobiology of traumatic stress. Ann N Y Acad Sci 1997;821:176–193 8. Pitman RK, Shin LM, Rauch SL. Investigating the pathogenesis of post- bathrooms (a site of early abuse) and significant psychic traumatic stress disorder with neuroimaging. J Clin Psychiatry 2001;62 COPYRIGHT 2003 PHYSICIANS POSTGRADUATE
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9. Weller EB. Symposium 14. Presented at the 46th annual meeting of the Disorder. J Clin Psychiatry 1999;60(suppl 16):1–76 American Academy of Child and Adolescent Psychiatry; Oct 19–24, 15. Raskind MA, Thompson C, Petrie EC, et al. Prazosin reduces nightmares in combat veterans with posttraumatic stress disorder. J Clin Psychiatry 10. De Bellis MD, Keshavan MS, Clark DB, et al. Developmental trauma- tology, 2: brain development. Biol Psychiatry 1999;45:1271–1284 16. Brady K, Pearlstein T, Asnis GM, et al. Efficacy and safety of sertraline 11. Shin L, McNally R, Kosslyn S, et al. Regional cerebral blood flow during treatment of posttraumatic stress disorder: a randomized controlled trial. script-driven imagery in childhood sexual abuse–related PTSD: a PET investigation. Am J Psychiatry 1999;156:575–584 17. Labbate LA, Douglas S. Olanzapine for nightmares and sleep disturbance 12. Yehuda R. Biology of posttraumatic stress disorder. J Clin Psychiatry in posttraumatic stress disorder (PTSD). Can J Psychiatry 2000;45: 13. Berlant JL. Topiramate in posttraumatic stress disorder: preliminary 18. Petty F, Brannan S, Casada J, et al. Olanzapine treatment for post- clinical observations. J Clin Psychiatry 2001;62(suppl 17):60–63 traumatic stress disorder: an open-label study. Int Clin Psychopharmacol 14. Expert Consensus Guideline Series: Treatment of Posttraumatic Stress COPYRIGHT 2003 PHYSICIANS POSTGRADUATE PRESS, INC. COPYRIGHT 2003 PHYSICIANS POSTGRADUATE PRESS, INC.
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