Prospective risk factors for new-onset post-traumatic stress disorder in National Guard soldiers deployed to Iraq.

BACKGROUND: National Guard troops are at increased risk for post-traumatic stress disorder (PTSD); however, little is known about risk and resilience in this population. METHOD: The Readiness and Resilience in National Guard Soldiers Study is a prospective, longitudinal investigation of 522 Army National Guard troops deployed to Iraq from March 2006 to July 2007. Participants completed measures of PTSD symptoms and potential risk/protective factors 1 month before deployment. Of these, 81% (n=424) completed measures of PTSD, deployment stressor exposure and post-deployment outcomes 2-3 months after returning from Iraq. New onset of probable PTSD 'diagnosis' was measured by the PTSD Checklist - Military (PCL-M). Independent predictors of new-onset probable PTSD were identified using hierarchical logistic regression analyses. RESULTS: At baseline prior to deployment, 3.7% had probable PTSD. Among soldiers without PTSD symptoms at baseline, 13.8% reported post-deployment new-onset probable PTSD. Hierarchical logistic regression adjusted for gender, age, race/ethnicity and military rank showed that reporting more stressors prior to deployment predicted new-onset probable PTSD [odds ratio (OR) 2.20] as did feeling less prepared for deployment (OR 0.58). After accounting for pre-deployment factors, new-onset probable PTSD was predicted by exposure to combat (OR 2.19) and to combat's aftermath (OR 1.62). Reporting more stressful life events after deployment (OR 1.96) was associated with increased odds of new-onset probable PTSD, while post-deployment social support (OR 0.31) was a significant protective factor in the etiology of PTSD. CONCLUSIONS: Combat exposure may be unavoidable in military service members, but other vulnerability and protective factors also predict PTSD and could be targets for prevention strategies.

Eating-related anxiety in individuals with eating disorders.

Although previous research has supported the importance of anxiety as an etiological and maintenance factor for eating disorders, the specific mechanisms are not well understood. The role of anxiety in the context of eating behavior is especially unclear. The purpose of this study was to identify anxiety-eliciting eating situations and anxiety management strategies patients use to mitigate anxiety experienced in the context of eating as determined by diagnostic groups and symptom patterns. Fifty-three eating disorder outpatients were administered the Eating and Anxiety Questionnaire (EAQ) and the Eating Disorder Diagnostic Scale. Ratings indicated significant anxiety in most eating situations, whereas management strategies were more limited yet regularly employed. Factor analysis of the EAQ revealed a 6-factor solution for anxiety management strategies and a 4-factor solution for anxiety-eliciting situations. These results indicate patients with eating disorders report high levels of anxiety associated with eating behaviors but utilize limited yet consistent anxiety management strategies. Effective intervention strategies for managing eating-related anxiety should be incorporated into treatment and may need to be specified for different diagnostic subgroups.

Drinking to cope with negative emotions moderates alcohol use disorder treatment response in patients with co-occurring anxiety disorder.

BACKGROUND: Epidemiological studies and theory implicate drinking to cope (DTC) with anxiety as a potent moderator of the association between anxiety disorder (AnxD) and problematic alcohol use. However, the relevance of DTC to the treatment of alcohol use disorder (AUD) in those with a co-occurring AnxD has not been well studied. To address this, we examined whether DTC moderates the impact of two therapies: (1) a cognitive behavioral therapy (CBT) designed to reduce DTC and anxiety symptoms; (2) a progressive muscle relaxation training (PMRT) program designed to reduce anxiety symptoms only. METHODS: Patients undergoing a standard AUD residential treatment with a co-occurring AnxD (N=218) were randomly assigned to also receive either the CBT or PMRT. DTC in the 30 days prior to treatment was measured using the Unpleasant Emotions subscale of the Inventory of Drinking Situations. RESULTS: Confirming the predicted moderator model, the results indicated a significant interaction between treatment group and level of pre-treatment DTC behavior. Probing this interaction revealed that for those reporting more pre-treatment DTC behavior, 4-month alcohol outcomes were superior in the CBT group relative to the PMRT group. For those reporting less pre-treatment DTC behavior, however, 4-month alcohol outcomes were similar and relatively good in both treatment groups. CONCLUSIONS: These findings establish a meaningful clinical distinction among those with co-occurring AUD-AnxD based on the degree to which the symptoms of the two disorders are functionally linked through DTC. Those whose co-occurring AUD-AnxD is more versus less strongly linked via DTC are especially likely to benefit from standard AUD treatment that is augmented by a brief CBT designed to disrupt this functional link.

Leptin in anorexia nervosa.

Serum leptin levels are low in untreated anorexia nervosa, but studies of the exact relationship between leptin and body weight and the impact of refeeding in anorectics are limited. Therefore, we studied serum leptin, insulin-like growth factor I, and other endocrine parameters in female anorectics before and after gaining weight and in female normal body weight controls. Leptin levels in untreated anorectics were significantly lower than those in normal body weight controls (3.6 +/- 1.6 vs. 12.0 +/- 6.9 ng/mL; P < 0.001), and they uncoupled from body weight in a nonlinear relationship, suggesting a threshold effect at lowest body weights. Leptin increased significantly with refeeding (5.6 +/- 3.8 ng/mL; P < 0.01). The significant linear correlations of leptin with body mass index in the anorectics after weight gain and in normal body weight controls (r = 0.69; P < 0.001 and r = 0.76; P < 0.001, respectively) are consistent with a normal physiological increase in leptin with weight gain. Leptin and insulin-like growth factor I were highly correlated, even after controlling for body weight (r = 0.63; P = 0.001) during starvation, but were no longer significantly correlated after body weight gain in the anorectics or the normal body weight controls. Further studies are necessary to elucidate the relationship of leptin to neuroendrocrine abnormalities seen in starvation and to determine a possible contribution of leptin to difficulties with weight restoration in anorexia nervosa.

Elevated pain threshold in anorexia nervosa subjects.

BACKGROUND: Conflicting data have been published regarding pain threshold in subjects with anorexia nervosa (AN), with some studies indicating elevated pain threshold and others indicating normal thresholds. Previous research has indicated the presence of elevated pain threshold in eating disorder subjects with binge-eating behavior. METHODS: In this study pressure pain detection thresholds (PDT) (assessed by a pressure analgesiometer) in binge-eating/purging and restricting subtypes of AN subjects were compared to control subjects. RESULTS: PDT was elevated in AN compared to control subjects at baseline. There was no difference in PDT between the subgroups of AN subjects. CONCLUSIONS: The etiology of elevated PDT in AN subjects is most likely different from the etiology of elevated PDT in bulimia nervosa subjects.

Lamotrigine in rapid-cycling bipolar disorder.

BACKGROUND: We evaluated the antidepressant and mood-stabilizing effects of lamotrigine, a novel anticonvulsant, in a group of rapid-cycling bipolar patients. Most were already nonresponders or poor partial responders to other conventional mood-stabilizing agents. METHODS: This open, naturalistic, and prospective study was conducted with five rapid-cycling bipolar patients (DSM-IV). Each received lamotrigine titrated to a minimum dose of 150 mg/day as monotherapy or in combination with other psychotropic agents. Patients were assessed with the Global Assessment Scale (GAS), Beck Depression Inventory (BDI), and Young Mania Rating Scale (YMRS) for evidence of cycling mood. RESULTS: Lamotrigine was used at a mean +/- SD dose of 185.0 +/- 33.5 mg/day for 225.8 +/- 28.0 days. Random regression modeling of data showed significant dose- and time-dependent improvements in depressive symptoms and social function of patients taking lamotrigine (Dose: z = 2.17, p < .03 for BDI, z = 4.44, p < .001 for GAS; Time: z = -3.79, p < .001 for BDI, z = 2.16, p < .03 for GAS). Further random regression modeling analysis of change over time in symptoms prior to lamotrigine compared with symptoms during lamotrigine treatment showed a significant treatment by time effect for GAS (z = 2.40, p < .016) and a trend for BDI scores (z = -1.79, p < .073). No significant time or dosage effect or time by treatment effect was observed for YMRS. Finally, t statistics showed a significant reduction in mean BDI scores following treatment with lamotrigine (t = -5.26, p < .006). Lamotrigine was well tolerated by all patients; only one patient experienced several side effects, which were probably due to interaction between several psychotropic medications. CONCLUSION: Lamotrigine augmentation therapy and monotherapy appeared to have mood-stabilizing and antidepressant efficacy in the treatment of five rapid-cycling bipolar patients. The effect persisted for an average of 7.5 months.

Validation of the Cumulative Illness Rating Scale in a geriatric residential population.

OBJECTIVE: To evaluate the validity of the Cumulative Illness Rating Scale (CIRS) in a geriatric institutional population by examining its associations with mortality, hospitalization, medication usage, laboratory findings and disability. DESIGN: A validation of the CIRS using self- and physician-report surveys, with archival data drawn from medical charts and facility records. SETTING: Long-term care facility with skilled nursing and congregate apartments. PARTICIPANTS: Four hundred thirty-nine facility residents selected on the basis of completeness of self-report data and physician ratings. PRIMARY MEASURES: Composite measures of illness severity and comorbidity, based on physicians' CIRS ratings; time to death or acute hospitalization after assessment; medication use, drawn from pharmacy records; medical chart data on laboratory tests; self-reported functional disability. RESULTS: CIRS illness severity and comorbidity indices, as well as individual CIRS items, were significantly associated with mortality, acute hospitalization, medication usage, laboratory test results, and functional disability. The CIRS showed good divergent validity vis a vis functional disability in predicting mortality and hospitalization. CONCLUSIONS: The CIRS appears to be a valid indicator of health status among frail older institution residents. The illness severity and comorbidity composites performed equally well in predicting longitudinal outcomes. Item-level analyses suggest that the CIRS may be useful in developing differential illness profiles associated with mortality, hospitalization, and disability.

Using biological indices to classify schizophrenia and other psychotic patients.

Although classification of mental disorders using more than clinical description would be desirable, there is scant evidence that available laboratory tests (i.e. biological indices) would provide more valid classifications than current diagnostic systems (e.g. DSM-IV). We used cluster analysis of four biological variables to classify 163 psychotic patients and 83 nonpsychiatric comparison subjects. Analyses revealed a three-cluster solution with the first cluster reflecting electrodermal deviance, the second cluster representing nondeviant biological function, and the third cluster reflecting increased nailfold plexus visibility and ocular motor dysfunction. To assess the construct validity of proband clusters we examined ocular motor performance in 156 first-degree relatives as a function of proband cluster membership. First-degree relatives of third cluster probands exhibited worse ocular motor performance than relatives of other cluster probands. Additionally, better classification sensitivity and specificity were obtained for the relatives when they were grouped by proband cluster than by proband DSM-IV diagnosis. When a single proband characteristic (i.e. eyetracking performance) was used to group relatives, classification sensitivity and specificity failed to significantly increase over grouping by proband DSM-IV diagnosis. Multivariate biologically defined clusters may offer an advantage over DSM-IV classification when examining nosology and etiology of psychotic disorders.

Prenatal viral infection causes alterations in nNOS expression in developing mouse brains.

Epidemiological evidence points to prenatal viral infection being responsible for some forms of schizophrenia and autism. We hypothesized that prenatal human influenza viral infection in day 9 pregnant mice may cause changes in the levels of neuronal nitric oxide synthase (nNOS), an important molecule involved in synaptogenesis and excitotoxicity, in neonatal brains. Brains from 35- and 56-day-old mice were prepared for SDS-gel electrophoresis and Western blotting using polyclonal anti nNOS antibody. Quantification of nNOS showed time and region-dependent changes in the levels of nNOS protein. Mean rostral brain area value from prenatally infected animals showed a significant (p=0.067) increase of 147% in nNOS levels at 35 days postnatally, with an eventual 29% decrease on day 56. Middle and caudal brain areas showed reductions in nNOS in experimental mice at 35 and 56 days, with a significant 27% decrease in nNOS in the middle segment of day 56 brains (p=0.016). Significant interactions were found between group membership and brain area (Wilks lambda=0.440, F(2.9)=5.72, p=0.025); there was also a significant interaction between brain area, group and age (Wilks lambda=0.437, F(2.9)=5.79, p=0.024). These results provide further support for the notion that prenatal viral infection affects brain development adversely via the pathological involvement of nNOS expression.

Somatic symptoms in anxious-depressed school refusers.

OBJECTIVE: To identify the most common physical complaints in a sample of adolescent school refusers with comorbid anxiety and depressive disorders. Whether somatic symptoms are more likely to be associated with high levels of anxiety or high levels of depression was also explored. METHOD: Forty-four adolescents in a treatment study were evaluated at baseline with structured psychiatric interviews and measures of anxiety, depression, and somatization. RESULTS: The most common somatic complaints were in the autonomic and gastrointestinal categories. In simple regression analyses, anxiety level as measured with the Revised Children's Manifest Anxiety Scale and depression level as measured with the Beck Depression Inventory each significantly predicted the severity of somatic symptoms. The correlation between percentage of days absent from school and severity of somatic symptoms approached significance (r = .27, p = .074). CONCLUSIONS: Knowledge that somatic complaints are commonly an expression of underlying anxiety and depression may facilitate more rapid referral for psychiatric assessment and treatment and thereby help avoid unnecessary medical workups and sequelae from school refusal.

Imipramine plus cognitive-behavioral therapy in the treatment of school refusal.

OBJECTIVE: To investigate the efficacy of 8 weeks of imipramine versus placebo in combination with cognitive-behavioral therapy (CBT) for the treatment of school-refusing adolescents with comorbid anxiety and major depressive disorders. METHOD: This was a randomized, double-blind trial with 63 subjects entering the study and 47 completing. Outcome measures were weekly school attendance rates based on percentage of hours attended and anxiety and depression rating scales. RESULTS: Over the course of treatment, school attendance improved significantly for the imipramine group (z = 4.36, p < .001) but not for the placebo group (z = 1.26, not significant). School attendance of the imipramine group improved at a significantly faster rate than did that of the placebo group (z = 2.39, p = .017). Over the 8 weeks of treatment, there was a significant difference between groups on attendance after controlling for baseline attendance; mean attendance rate in the final week was 70.1% +/- 30.6% for the imipramine group and 27.6% +/- 36.1% for the placebo group (p < .001). Defining remission as 75% school attendance, 54.2% of the imipramine group met this criterion after treatment compared with only 16.7% from the placebo group (p = .007). Anxiety and depression rating scales decreased significantly across treatment for both groups, with depression on the Children's Depression Rating Scale-Revised decreasing at a significantly faster rate in the imipramine group compared with the placebo group (z = 2.08, p = .037). CONCLUSIONS: Imipramine plus CBT is significantly more efficacious than placebo plus CBT in improving school attendance and decreasing symptoms of depression in school-refusing adolescents with comorbid anxiety and depression.

Differential expression of synaptosome-associated protein 25 kDa [SNAP-25] in hippocampi of neonatal mice following exposure to human influenza virus in utero.

We investigated the role of maternal exposure to human influenza virus [HI] in C57BL/6 mice on day 9 of pregnancy on the hippocampal expression of SNAP-25 in postnatal day 0 neonates, and compared them to sham-infected pups. The expression of SNAP-25 in infected neonates varied along the septotemporal axis of hippocampus and in various anatomic layers. Quantitative densitometric analysis of specific immunogold silver-enhanced SNAP-25 immunoreactivity [IR] showed increases of 40-347% over control in all septal-dorsal hippocampal layers except for the subplate layer. In mid septo-temporal hippocampus, SNAP-25 IR increased by 10-114% over control in all layers, except for the hippocampal plate, but the extent of this increase was smaller than in the dorsal-septal area. Finally,in temporal-ventral levels, SNAP-25 expression was reduced in all infected layers by 21-33% below control except for mild increases of 8.8 and 10% in subplate and hippocampal plate layers. Additionally, the infected SNAP-25 maximal density bin shifted to lower values dorsally and to higher values medially, with ventral maximal bins remaining unchanged when compared to controls. The differential expression of SNAP-25 in the hippocampi of infected neonates indicates a variable degree of vulnerability across the septo-temporal axis of hippocampus. It is surmised that while viral infection may induce excitotoxicity in the ventral hippocampus, it may cause reactive synapto-genesis in the medial and dorsal sectors of the developing brains of postnatal day 0 neonates.

Social control, health risk taking, and psychological distress among the elderly.

Most research on older adults' social networks has focused on the support-providing function of social relationships. Little gerontological research has addressed social control, or the role of social bonds in regulating deviant or risky behavior. Drawing on sociological theory, this study examined the hypothesis that social control discourages risky health practices while provoking psychological distress. Structured interviews conducted with 162 community-residing older adults assessed social control (direct attempts by other to influence participants' health practices and the existence of significant role obligations to others), health risk taking (medication misuse, alcohol consumption, cigarette smoking, and the overall level of unsound health practices), psychological functioning (depression, loneliness, and self-esteem), and interpersonal satisfaction (satisfaction with friends and family members). Analyses revealed little support for the hypothesis. Social control was only weakly related to participants' health practices and, contrary to expectation, was generally related to less psychological distress and to greater interpersonal satisfaction. Implications for social control theory and for further research are addressed.

Fluoxetine in treatment of adolescent patients with autism: a longitudinal open trial.

Retrospective chart reviews of seven adolescent and young adults with autistic disorder treated with fluoxetine alone or in combination with other medications were performed. Patient's ages varied from 9-20 years (M +/- SD, = 16 +/- 3.87). Fluoxetine doses ranged from 20-80 mg per day (M +/- SD of final doses 37.14 +/- 21). Duration of treatment ranged from 1.3-32 months (M 18.04 +/- 10.39). Patients' symptoms were monitored using the Aberrant Behavior Checklist (ABC) rating scale during every visit. Side effects included initial appetite suppression, vivid dreams, and hyperactivity. Improvement from baseline was seen in four subscales: irritability (21%), lethargy (37%), stereotype (27%), and inappropriate speech (21%). Lethargy subscales improved significantly during treatment (p < .029). Hyperactivity subscale increased by 14% but did not attain statistical significance. Fluoxetine appears to have important behavioral effects in treatment of clinic-referred autistic children. Future double-blind placebo controlled studies evaluating core and associated symptom response with fluoxetine are warranted.

Quantitative EEG findings associated with chronic stimulant and cannabis abuse and ADHD in an adult male substance use disorder population.

QEEG was studied in a population of chronic male PSUD/ADHD (psychoactive substance use disorder/attention deficit hyperactivity disorder) subjects vs. a matched sample of non-ADHD subjects with PSUD. Our first interest in conducting this study was to determine if the Thatcher University of Maryland database and complex demodulation method could replicate the specific QEEG findings reported for cocaine and cannabis using the John-NYU database and Fourier Transform method. The effects of cannabis and stimulants were also studied both separately and together to see if there were interactions and to see if the QEEG changes associated with chronic stimulant dependence were predicted by childhood ADHD status. Eyes-closed QEEGs were obtained and two independent artifacted 60 second samples were compared for reliability. The Thatcher database was used to analyze QEEG data from 56 subjects with mixed substance use disorder. Results showed that the Thatcher database replicates the John database for chronic stimulant dependence findings. Because of confounding variables of alcohol and polysubstance abuse, the findings related to cannabis and stimulant interaction were difficult to assess. Cannabis and stimulant dependence together produced more QEEG changes than either alone. More right temporal abnormalities were observed with stimulant dependence. In the absence of stimulant use, the QEEG effects of cannabis were relatively small; however, sample selection and methods used precluded comparison to previous studies. The persistent QEEG abnormalities associated with chronic stimulant dependence were independent of ADHD status in this sample using the methods of this study. Further research is needed to clarify the relationship of stimulant dependence with QEEG changes and ADHD status, and to clarify the interactions of chronic stimulant and cannabis abuse on QEEG.

Diagnostic stability of ADHD in a community sample of school-aged children screened for disruptive behavior.

A large school-based sample of children in Grades 1, 2, 3, and 4 were screened for disruptive behavior and subsequently assessed over a 5-year period for DSM-III-R symptoms of attention deficit hyperactivity disorder (ADHD) and other externalizing and internalizing behavior disorders. Parents completed structured diagnostic interviews in Years 1, 4, and 5, and teachers completed Behavioral Assessment for Children-Teacher Rating Scales behavioral ratings annually. For parent-derived diagnostic data, both inattention and hyperactivity/impulsivity symptom groups declined from Year 1 to Year 4, with hyperactivity showing more significant decline. For teacher-rated behavioral dimensions, the Attention Problems scale declined from Year 1 to Year 3 and stabilized thereafter. The Hyperactivity scale showed stability during the first 3 years before declining in Year 4. Of those children diagnosed with ADHD in Year 1, 69% still met criteria for ADHD in either Year 4 or 5. Persisters were more likely to exhibit coexisting conduct disorder in Year 1 and oppositional defiant disorder in Years 1, 4, and 5. Parents of persisters reported more psychosocial adversity on measures of parenting and marital satisfaction.

Family dimensions in anxious-depressed school refusers.

The Family Adaptability and Cohesion Evaluation Scale II (FACES II) was administered to 46 adolescents with comorbid anxiety and major depressive disorders and to their parents in a treatment study of school refusal. FACES II measures cohesion and adaptability dimensions, as well as family type (balanced to extreme). Generally, adolescents and parents reported low cohesion (i.e.. disengagement) and low adaptability (i.e.. rigidity) on FACES II. Adolescents and parents described their ideal families as significantly less disengaged and less rigid than their own families. Fifty percent of adolescents, 38% of fathers, and 24% of mothers classified their families as the extreme type. Adolescents in extreme families, when compared with adolescents in more balanced families, reported significantly higher scores on two of three depression instruments and on a measure of somatic symptoms. Family therapy to improve cohesion and adaptability and treatments focused on improving depression and somatic symptoms may improve family functioning and decrease the severity and course of school refusal.

Anxiety mediates the association between anxiety sensitivity and coping-related drinking motives in alcoholism treatment patients.

Anxiety sensitivity (AS), the tendency to interpret feelings of anxiety as dangerous, is a core dispositional trait in a well articulated and extensively studied cognitive model of proneness to anxiety disorder. In recent years, there has been an increasing body of findings that also links AS to the tendency to use alcohol in general and the tendency to use alcohol as a means of coping with negative affect in particular. We expand on this empirical base by proposing and testing a theoretical model in which anxiety symptoms mediate the association between AS and alcohol use. That is, we propose that AS promotes anxiety symptoms, which, in turn, promote alcohol use aimed at coping with anxiety and other negative affect states. Over a 1-year data collection period, we assessed 82 alcohol-dependent individuals shortly after they began an intensive alcoholism treatment program. Self-reported anxiety symptoms associated with distinct anxiety syndromes were obtained with reference to the month period preceding their entry into the treatment program. Other information, including the presence of withdrawal symptoms, was obtained via interview. We found that syndrome-related anxiety symptoms and Trait Anxiety, but not State Anxiety or withdrawal symptoms, mediated the significant association between AS and the self-reported tendency to use alcohol as a means of controlling anxiety symptoms. Demonstrating a similar pattern of findings, but much less robustly so, were tests of these mediator models using alcohol use aimed at coping with negative affect (vs. coping with anxiety per se) as an outcome. In discussing these findings, we attempt to further develop a coherent model that incorporates AS, anxiety symptoms, and drinking motives. Our findings suggest that these relationships may differ for negative affect not specifically related to anxiety. We also discuss the possible associations of AS to withdrawal symptoms implied by our findings.

Expectancies for alcohol to affect tension and anxiety as a function of time.

Alcohol outcome expectancies have been linked to drinking behavior on both empirical and theoretical grounds. Although typically measured as a static construct, we hypothesized that expectancies may be time-specific. Subjects rated their expectancies for a moderate amount of alcohol to increase, decrease, or not change their level of tension and anxiety. Ratings were repeated for when the intoxicating effects of the drinking would be: (1) "at their peak;" (2) "nearly worn off;" and (3) "completely worn off" (Time Epochs 1-3, respectively). As predicted, most subjects (72%) expected alcohol to reduce tension and anxiety at Time Epoch 1; however, significantly fewer subjects expected this effect at Time Epochs 2 and 3 (25% and 2%, respectively). Conversely, few subjects expected alcohol to worsen tension and anxiety at Time Epoch 1 (3.5%); however, significantly more subjects expected this effect at Time Epochs 2 and 3 (31% and 34%, respectively). Expectancies for Time Epoch 1 related most strongly to several measures of alcohol use, including drinking for the purpose of reducing tension (whole sample) and drinking frequency (men but not women). These findings show that tension-reduction expectancies are not stable over the course of a drinking episode and suggest the possibility of a treatment approach aimed at amplifying attention to expectancies for alcohol's more negative longer-term effects.

Attachment style classification and posttraumatic stress disorder in former prisoners of war.

Adult attachment style and post-traumatic stress disorder (PTSD) symptomatology were investigated in 107 former prisoner of war veterans. Those with secure attachment styles scored significantly lower on measures of PTSD than did those with insecure styles, and attachment style was a stronger predictor of PTSD symptom intensity than was trauma severity. The suggested association between attachment style and PTSD's development and persistence are discussed in relation to research and clinical practice.