Journal of Psychosomatic Research 76 (2014) 485–488

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Journal of Psychosomatic Research

Letters to the Editor Prevalence of posttraumatic stress disorder (PTSD) in women with breast cancer ☆

Studies on posttraumatic stress disorder (PTSD) in patients with medical diagnoses are increasingly common, particularly since the inclusion in DSM-IV of a diagnosis with a life-threatening illness as a traumatic event that could precipitate PTSD [1]. Concerns have been raised, however, about whether a PTSD diagnosis is the best way to capture emotional distress in patients with medical diagnoses, such as cancer [2–4]. Rather than a single traumatic event with a defined end point, cancer diagnosis, treatment, and survivorship comprise interconnected, ongoing experiences involving significant stress, including anxiety and worry related to realistic future-oriented health concerns [2–4]. In this context, it is important to understand the prevalence of PTSD in breast cancer. Estimates vary widely [5], with published estimates as high as 32% [4]. However, most prevalence estimates are based on the proportion of patients above cutoffs on symptom questionnaires rather than actual PTSD diagnoses [4]. Symptom questionnaires pick up cancer-related distress or ‘subsyndromal PTSD’ symptoms [6], but they tend to cast a wide net and identify far more patients as possible cases than the proportion who meet diagnostic criteria, and, thus, overestimate PTSD rates. A questionnaire with sensitivity and specificity of 80%, for instance, would identify 20% of patients as cases, even if there were no actual cases. Only 5 studies with ≥100 women with breast or gynecological cancer (range 102–506) have reported the prevalence of PTSD using a validated diagnostic interview. All used the Structured Clinical Interview for DSM-IV (SCID) [7] and reported that 2.4% to 5.9% of patients met diagnostic criteria for current PTSD [2,3,8–10]. In this study, we assessed the current prevalence of PTSD in a large sample of women with breast cancer close to the time of initial diagnosis who received treatment at the Rowan Breast Center of the University of Pennsylvania Comprehensive Cancer Center between December 2003 and April 2009. Eligible patients were 18 to 85 years of age, within 5 months of their index diagnosis, had not yet started chemotherapy, and were fluent in English. Exclusion criteria were a recurrence of cancer within 5 years, current substance abuse, and a history of bipolar or psychotic disorders. Patients were invited after their first medical oncology or postoperative surgical visit to participate in a longitudinal study on the psychosocial impact of breast cancer. Within 2 weeks after patients returned their baseline questionnaires and at 3 months follow-up, the SCID-I/NP module for PTSD [7] was administered in a telephone interview, conducted by interviewers with certified SCID training. The study was approved by the Institutional Review Board of the University of

☆ Financial support: Supported by Grant Number R01MH63172 from the National Institute of Mental Health and the National Cancer Institute. Dr. Kwakkenbos is supported by a Fonds de la Recherche en Santé Québec (FRSQ) postdoctoral fellowship. Dr. Thombs is supported by an Investigator Salary Award from the Arthritis Society. No conflicts of interest exist.

Pennsylvania and the Clinical Trials and Scientific Monitoring Committee of the Abramson Cancer Center. Written informed consent was obtained from all patients. Baseline data as well as the SCID at 3-month follow-up were included in the present study, since symptoms of PTSD should be present at least 1 month post-trauma (DSM-IV criterion E), and baseline interviews took place within 1 month of diagnosis for some patients in the sample. At baseline, participants were asked to respond to symptom-level criteria in the module based on their experience with breast cancer specifically. At 3 months, they were asked to respond based on their worst lifetime traumatic experience, if one had been experienced. Of 652 women who were invited to participate, 588 provided informed consent, 539 completed the baseline questionnaire assessment and of these, 437 completed the structured interview for PTSD and were included in the present study. The mean age was 54.2 (SD = 11.6), and the majority were white (72.4%), had at least a college education (54.2%), and were married or living as married (66.8%). The mean time since diagnosis was 65.4 days (SD = 30.9, range = 1–150 days). At baseline, 13 patients (3.0%, 95% CI 1.8–5.1%) met the criteria for PTSD. At 3-month follow-up (N = 363), 9 patients (2.5%, 95% CI 1.3– 4.6%) met PTSD criteria. In summary, the prevalence of women who met criteria for PTSD in our sample was similar to prevalence estimates found in other studies that utilized a clinical interview [2,3,8–10]. These prevalence estimates are generally similar to what might be expected in the general population, given that the estimated 12-month prevalence of PTSD in women in the US general population has been reported as 5% [11]. Thus, although cancer is distressing and frightening to many patients, it is uncommon that symptoms meet criteria for PTSD. Cancer patients have substantial psychosocial needs that should be addressed, but PTSD is not a specific need among most patients beyond what would be the case in the general population.

References [1] American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington: American Psychiatric Association; 2000. [2] Mehnert A, Koch U. Prevalence of acute and post-traumatic stress disorder and comorbid mental disorders in breast cancer patients during primary cancer care: a prospective study. Psychooncology 2007;16:181–8. [3] Greimel E, Dorfer M, Lambauer M, et al. Posttraumatic stress disorder in female cancer patients: an inappropriate diagnosis in oncology? Psychother Psychosom 2013;82:271–2. [4] Kangas M, Henry JL, Bryant RA. Posttraumatic stress disorder following cancer. A conceptual and empirical review. Clin Psychol Rev 2002;22:499–524. [5] Koutrouli N, Anagnostopoulos F, Potamianos G. Posttraumatic stress disorder and posttraumatic growth in breast cancer patients: a systematic review. Women Health 2012;52:503–16. [6] Shelby RA, Golden-Kreutz DM, Andersen BL. PTSD diagnoses, subsyndromal symptoms, and comorbidities contribute to impairments for breast cancer survivors. J Trauma Stress 2008;21:165–72. [7] First MB, Spitzer RL, Gibbon M, et al. Structured clinical interview for DSM-IV-TR Axis I disorders. New York: Biometrics Research, New York State Psychiatric Institute; 2001. [8] Palmer SC, Kagee A, Coyne JC, et al. Experience of trauma, distress, and posttraumatic stress disorder among breast cancer patients. Psychosom Med 2004;66:258–64.

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Letters to the Editor

[9] Green BL, Rowland JH, Krupnick JL, et al. Prevalence of posttraumatic stress disorder in women with breast cancer. Psychosomatics 1998;39:102–11. [10] Widows MR, Jacobsen PB, Fields KK. Relation of psychological vulnerability factors to posttraumatic stress disorder symptomatology in bone marrow transplant recipients. Psychosom Med 2000;62:873–82. [11] Kessler RC, Chiu WT, Demler O, et al. Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry 2005;62:617–27.

Linda Kwakkenbos Department of Psychiatry, McGill University, Montréal, Québec, Canada Lady Davis Institute for Medical Research, Jewish General Hospital, Montréal, Québec, CanadaCorresponding author at: Jewish General Hospital; 4333 Cote Ste Catherine Road; Montreal, Quebec H3T 1E4. Tel.: +1 514 340 8222x8578. E-mail addresses: [email protected] James C Coyne University of Groningen, Groningen, the Netherlands Institute for Health, Health Care Policy and Aging Research, Rutgers University, USA Brett D Thombs Department of Psychiatry, McGill University, Montréal, Québec, Canada Lady Davis Institute for Medical Research, Jewish General Hospital, Montréal, Québec, Canada Department of Medicine (Division of Rheumatology), McGill University, Montréal, Québec, Canada Epidemiology, Biostatistics, and Occupational Health, McGill University, Montréal, Québec, Canada Educational and Counselling Psychology, McGill University, Montréal, Québec, Canada School of Nursing, McGill University, Montréal, Québec, Canada 24 March 2014 http://dx.doi.org/10.1016/j.jpsychores.2014.03.103 0022 – 3999/$ – see front matter © 2014 Elsevier Inc. All rights reserved.

The role of the inferior frontal cortex in hyperkinetic movement disorders

dystonia and Huntington's disease, are caused by maladaptive synaptic plasticity that can be expressed by functional changes such as an increase in transmitter release, receptor regulation and synaptic plasticity or anatomical modifications such as axonal regeneration, sprouting, synaptogenesis and neurogenesis. With this in mind, one may suppose similar neurodegenerative mechanisms underlying pathophysiological processes of GTS. Considering, PD patients, the development of LIDs has been attributed to dysfunctional brain plasticity triggered by the combined effects of dopamine denervation and chronic pharmacological dopamine replacement [7]. Our recent neuroimaging studies have shed new light on the pathophysiological mechanisms underlying LIDs [8]. Indeed, we demonstrated that these patients are characterised by abnormal grey matter volume in the IFC. This finding has been confirmed using different population [9] and neuroimaging metrics [10], and has already raised an interesting scientific debate on the toxic effects of levodopa on brain morphometry [11]. Interesting, similar evidence highlighting the presence of neural abnormalities in the IFC, has also been provided in psychiatric realm: TDs. Originally, the term TDs referred to abnormal movements produced by long-term dopamine receptor antagonist therapy, mainly characterised by rapid, repetitive, stereotypic movements affecting mainly the oral, buccal and lingual areas and less the limb and the trunk. A recent neuroimaging study [12] investigating the neuroanatomical differences between schizophrenic patients with TDs with respect to patients without TDs (closely matched for age at onset of illness, duration of illness, or antipsychotic chlorpromazine equivalent dose) demonstrated the presence of volumetric abnormalities in the same prefrontal region described in LIDs patients. The merit of this work [12] was to demonstrate that chronic psychotropic treatment in schizophrenic patients might result in maladaptive neural rearrangements. To establish whether IFC neural abnormalities detected in GTS, LIDs and TDs have a causative effect (or whether this might be only considered as a consequence of having hyperkinetic movements for a long time) represents an exciting new challenge for future studies. We retain that studies designed to stimulate this region could become more useful. Indeed, the effectiveness (or non-effectiveness) of the repetitive transcranial stimulation (rTMS) over the IFC can help us to refute this hypothesis, as well as to provide a possible therapeutic target for improving motor disorders, as already proposed by our group on PD patients with LIDs [13]. Conflict of interest

To the Editor: We read with interest the article by Ganos et al., Prefrontal cortex volume reductions and tic inhibition are unrelated in uncomplicated GTS adults. J Psychosom Res. 2014; 76: 84-7 [1] who, upon investigation of the neural basis of Tics in Gilles de la Tourette syndrome (GTS), demonstrated the presence of anatomical abnormalities in a specific frontal region, the right inferior frontal cortex (IFC), which was unrelated to clinical symptoms. The IFC is part of a well-known neural network involved in response inhibition [2]. Previous functional magnetic resonance imaging (fMRI) studies have demonstrated that this network is fundamentally right-lateralised and comprised of: the IFC, supplementary motor areas, primary motor cortex, subthalamic nucleus and striatum [2,3]. The fact that GTS patients are associated with anatomical changes in the IFC might stimulate an exciting hypothesis. Indeed, the same pattern of neural abnormalities has been also described in other hyperkinetic movement disorders: in Parkinson's disease (PD) patients with levodopa-induced dyskinesias (LIDs) and schizophrenic patients affected by tardive dyskinesias (TDs). In the last years, several influential authors [4–6] proposed that some hyperkinetic movement disorders, in the neurological and psychiatric realms, such as: LIDs, TDs, primary

The authors declare no conflicts of interest. References [1] Ganos C, Kühn S, Kahl U, Schunke O, Brandt V, Bäumer T, et al. Prefrontal cortex volume reductions and tic inhibition are unrelated in uncomplicated GTS adults. J Psychosom Res 2014;76:84–7. [2] Aron AR, Poldrack RA. Cortical and subcortical contributions to stop signal response inhibition: role of the subthalamic nucleus. J Neurosci 2006;26:2424e33. [3] King AV, Linke J, Gass A, Hennerici MG, Tost H, Poupon C, et al. Microstructure of a three-way anatomical network predicts individual differences in response inhibition: a tractography study. Neuroimage 2012;59:1949–59. [4] Breakefield XO, Blood AJ, Li Y, Hallett M, Hanson PI, Standaert DG. The pathophysiological basis of dystonias. Nat Rev Neurosci 2008;9:222–34. [5] Teo JT, Edwards MJ, Bhatia K. Tardive dyskinesia is caused by maladaptive synaptic plasticity: a hypothesis. Mov Disord 2012;27:1205–15. [6] Cenci MA. Dopamine dysregulation of movement control in L-DOPA-induced dyskinesia. Trends Neurosci 2007;30:236–43. [7] Calabresi P, Giacomini P, Centonze D, Bernardi G. Levodopa-induced dyskinesia: a pathological form of striatal synaptic plasticity? Ann Neurol 2000;47:S60–8. [8] Cerasa A, Pugliese P, Messina D, Morelli M, Gioia MC, Salsone M, et al. Prefrontal alterations in Parkinson's disease with levodopa-induced dyskinesia during fMRI motor task. Mov Disord 2012;27:364–71. [9] Cerasa A, Salsone M, Morelli M, Pugliese P, Arabia G, Gioia MC, et al. Age at onset influences neurodegenerative processes underlying PD with levodopa-induced dyskinesias. Parkinsonism Relat Disord 2013;19:883–8.

Prevalence of posttraumatic stress disorder (PTSD) in women with breast cancer.

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