ライフサイエンスコーパス: PTSD

1 PTSD arousal symptoms and tinnitus were directly depende

2 PTSD participants exhibited larger responses in locus co

3 PTSD patients had significantly higher highly sensitive-

4 PTSD risk was higher if fewer people reported being conn

5 PTSD symptoms were assessed at baseline and approximatel

6 PTSD symptoms were assessed in the emergency department

7 sing independent component analysis among 10 PTSD patients and 10 healthy survivors, who experienced

8 tudies covering seven types of trauma in 229 PTSD and 311 comparison individuals to synthesize the ex

9 IV-TR diagnostic criteria; the revised DSM-5 PTSD criteria have important implications for the assess

10 ng and clinical data from 1868 subjects (794 PTSD patients) contributed by 16 cohorts, representing t

11 2713 simulated agents was initialized with a PTSD prevalence of 4.38% (115751 cases) and distribution

12 ion for PTSD for individuals with high acute PTSD symptoms.

13 The Clinician-Administered PTSD Scale (CAPS) was administered at baseline (within 1

14 outcome of change in Clinician-Administered PTSD Scale total score.

15 h assessment with the Clinician-Administered PTSD Scale.

16 1 but no PTSD at either draw (n = 175), and PTSD that persisted beyond blood draw 1 (chronic PTSD; n

17 lence ratio [PR] 1.22, 95% CI 1.08-1.37) and PTSD (PR 1.35, 95% CI 1.07-1.71).

18 ciated with depression (1.37, 1.23-1.53) and PTSD (1.41, 1.15-1.74), as was working as a commercial f

19 evalence of depression (1.56, 1.37-1.78) and PTSD (2.25, 1.71-2.96).

20 effect of the intervention on depression and PTSD at 6 months post-transplant.

21 care leads to improvements in depression and PTSD symptoms at 6 months post-transplant.

22 ppeared to be associated with depression and PTSD, but after taking into account oil spill job experi

23 ad an increased prevalence of depression and PTSD.

24 urological symptoms, adverse life events and PTSD symptoms in 23 mixed-gender FND patients.

25 n overgeneralization of conditioned fear and PTSD derives largely from clinical observations, with li

26 inct cingulo-insular alterations for FND and PTSD symptoms and may advance our understanding of FND.

27 ular volumetric reductions, and that FND and PTSD symptoms would map onto distinct cingulo-insular ar

28 the highest amount of total hydrocarbons and PTSD remained (1.75, 1.11-2.76).

29 ween decreases in DNA methylation levels and PTSD symptoms at genomic regions in ZFP57, RNF39 and HIS

30 The FEP, MDD, and PTSD groups showed reductions in intranetwork connectivi

31 lacebo for the treatment of DD, AD, OCD, and PTSD in children and adolescents.

32 en levels contributes to fear regulation and PTSD risk in women.

33 on of the relation between combat trauma and PTSD symptoms by longitudinal changes in DNA methylation

34 stress-based psychiatric syndromes, such as PTSD.

35 entify the nature of the association between PTSD symptoms in the acute phase after trauma and the ch

36 nnectivity was analyzed and compared between PTSD and non-PTSD groups.

37 tudy is to determine the correlation between PTSD and intra-operative analgesia, intra-operative time

38 f PTSD, identify shared genetic risk between PTSD and other psychiatric disorders and highlight the i

39 evidence of overlapping genetic risk between PTSD and schizophrenia along with more modest evidence o

40 s to attend towards or away from threat, but PTSD patients showed greater attentional bias variabilit

41 h Questionnaire-8 and four-item Primary Care PTSD Screen to assess for probable depression and post-t

42 that persisted beyond blood draw 1 (chronic PTSD; n = 174).

43 associations of trauma exposure and chronic PTSD with biomarkers of inflammation (C-reactive protein

44 al function may be pathways by which chronic PTSD increases cardiovascular disease risk.

45 In addition, women with chronic PTSD had a greater increase in vascular cell adhesion mo

46 wn potential confounders, women with chronic PTSD had higher average C-reactive protein (B = 0.27, p

47 Overall, preclinical (and clinical) PTSD researchers are increasingly incorporating homologo

48 regulated in cases with symptoms of comorbid PTSD and depression and consistently in cases with anxie

49 1F, rs17759843, was associated with comorbid PTSD and depression and with PPM1F expression in both hu

50 found it to be lower in cases with comorbid PTSD and depression.

51 After multiple test correction, PTSD associated with methylation of CpG sites in the HDA

52 smaller hippocampi in subjects with current PTSD compared with trauma-exposed control subjects (Cohe

53 to the controls, patients who had developed PTSD showed enhanced mismatch negativity (MMN), increase

54 wn to predict posttraumatic stress disorder (PTSD) after subsequent traumas, it is unclear whether th

55 nces, such as posttraumatic stress disorder (PTSD) and depression, are not well understood.

56 gher rates of posttraumatic stress disorder (PTSD) and experience greater symptom severity and chroni

57 for probable posttraumatic stress disorder (PTSD) and probable depression.

58 omatology of post-traumatic stress disorder (PTSD) are alterations in arousal and reactivity which co

59 atients with post-traumatic stress disorder (PTSD) are at a significantly higher risk of developing h

60 er (OCD), and posttraumatic stress disorder (PTSD) are common mental disorders in children and adoles

61 Patients with posttraumatic stress disorder (PTSD) are hyperresponsive to unexpected or potentially t

62 high level of posttraumatic stress disorder (PTSD) arousal symptoms.

63 sms by which post-traumatic stress disorder (PTSD) at a young age contributes to an increased risk to

64 f developing post-traumatic stress disorder (PTSD) following a traumatic event.

65 erstanding of posttraumatic stress disorder (PTSD) has been partially attributed to the need for impr

66 mal models of posttraumatic stress disorder (PTSD) has required active collaboration between clinical

67 for treating posttraumatic stress disorder (PTSD) in many states of the union, yet its efficacy in t

68 that predict posttraumatic stress disorder (PTSD) in recent trauma survivors is important for early

69 evelopment of posttraumatic stress disorder (PTSD) indicate widespread immune dysregulation.

70 pression and post-traumatic stress disorder (PTSD) indicators.

71 Posttraumatic stress disorder (PTSD) is a common psychiatric disorder among service mem

72 Posttraumatic stress disorder (PTSD) is a common psychiatric illness, increasingly in t

73 Posttraumatic stress disorder (PTSD) is a debilitating psychiatric disorder with a life

74 Posttraumatic stress disorder (PTSD) is a prevalent and highly disabling disorder, but

75 Post-Traumatic Stress Disorder (PTSD) is a psychiatric disorder that develops in individ

76 ABSTRACT: Post-traumatic stress disorder (PTSD) is associated with increased cardiovascular (CV) r

77 Post-traumatic stress disorder (PTSD) is characterized by exaggerated fear expression an

78 Posttraumatic stress disorder (PTSD) may contribute to heightened cardiovascular diseas

79 reatments for posttraumatic stress disorder (PTSD) provide insufficient benefit for many patients.

80 ncer-related post-traumatic stress disorder (PTSD) symptoms and diagnoses.

81 ients' mood, post-traumatic stress disorder (PTSD) symptoms, and QOL 6 months post-transplant.

82 Post-traumatic stress disorder (PTSD) was measured with the Post-traumatic Stress Disord

83 ic target for posttraumatic stress disorder (PTSD), a mental illness characterized by the recurring a

84 atients with post-traumatic stress disorder (PTSD), and 122 healthy controls (HCs).

85 implicated in posttraumatic stress disorder (PTSD), and may partly reflect stress-induced glutamate e

86 la volumes in posttraumatic stress disorder (PTSD), but findings have not always been consistent.

87 treatment for posttraumatic stress disorder (PTSD), but many patients do not respond.

88 ons including posttraumatic stress disorder (PTSD), characterized by debilitating trauma-related intr

89 creening for post-traumatic stress disorder (PTSD), depression, anxiety, or alcohol misuse was effect

90 described in posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD), panic disorde

91 treatment for posttraumatic stress disorder (PTSD), has not been tested as an individual treatment am

92 xperience on post-traumatic stress disorder (PTSD), this study aims to explore the alteration of trip

93 ic stress on post-traumatic stress disorder (PTSD), this study examined longitudinal changes of genom

94 ociated with post-traumatic stress disorder (PTSD)-like symptoms.

95 available for posttraumatic stress disorder (PTSD).

96 e aspects of post-traumatic stress disorder (PTSD).

97 en of chronic posttraumatic stress disorder (PTSD).

98 ty to develop posttraumatic stress disorder (PTSD).

99 er (FND) and post-traumatic stress disorder (PTSD).

100 nic marker of posttraumatic stress disorder (PTSD).

101 s, including post-traumatic stress disorder (PTSD).

102 features of post-traumatic stress disorder (PTSD).

103 e syndrome of posttraumatic stress disorder (PTSD).

104 ty factor for posttraumatic stress disorder (PTSD); however, our understanding is limited by a paucit

105 a history of post-traumatic-stress-disorder (PTSD), and there exists a higher rate of PTSD amongst ve

106 s after trauma, fear circuitry and dysphoric PTSD symptoms appear to emerge as connected networks.

107 cal Manual of Mental Disorders, 4th Edition) PTSD due to that trauma was assessed.

108 ging Genetics through Meta-Analysis (ENIGMA) PTSD Working Group.

109 Young mice lacking the Fmn2 gene exhibit PTSD-like phenotypes and corresponding impairments of sy

110 dies for DD, 10 for AD, 8 for OCD, and 1 for PTSD.

111 l integration stressors (1.10, 1.05-1.16 for PTSD).

112 iness (odds ratio 1.17, 95% CI 1.05-1.28 for PTSD and 1.28, 1.16-1.41 for severe mental illness) and

113 tive of anesthesia type, when controlled for PTSD.

114 differences in prevalence between groups for PTSD (adjusted odds ratio 0.92, 95% CI 0.75-1.14), depre

115 n is a promising preventive intervention for PTSD for individuals with high acute PTSD symptoms.

116 key neuroscience "themes" most relevant for PTSD.

117 auma exposure reduced the susceptibility for PTSD-like symptoms.

118 re to combat trauma marks susceptibility for PTSD.

119 then extinction-based exposure therapies for PTSD.

120 gical and non-pharmacological treatments for PTSD are either ineffective or temporary with high relap

121 y after a civilian trauma can predict future PTSD symptoms.

122 ctivation soon after trauma predicted future PTSD symptom severity.

123 ns who served in Iraq or Afghanistan and had PTSD (N=26), subthreshold PTSD (N=19), or no PTSD (refer

124 individual CPT, approximately 50% still had PTSD and clinically significant symptoms.

125 The former also generally had higher PTSD symptoms.

126 ation and it is important to investigate how PTSD in the veteran population affects intra-operative a

127 uantify in vivo mGluR5 availability in human PTSD vs. healthy control (HCs) subjects.

128 animal models of PTSD, and review the human PTSD postmortem brain gene profiling studies performed t

129 was previously found to beneficially impact PTSD vulnerability factors, including neural fear respon

130 In PTSD patients, decreased connectivity was identified in

131 antly higher cortical mGluR5 availability in PTSD in vivo and positive correlations between mGluR5 av

132 the effects of cannabis and cannabinoids in PTSD and the preclinical and clinical literature on the

133 nism of adaptive psychotherapeutic change in PTSD.

134 nucleator Formin 2 (Fmn2) is deregulated in PTSD and in Alzheimer's disease (AD) patients.

135 n has led many to examine sex differences in PTSD risk factors.

136 Understanding individual differences in PTSD vulnerability will allow the development of improve

137 ue animal model of individual differences in PTSD-like behavior, allowing the study of genetic, devel

138 vide a broad view of immune dysregulation in PTSD and demonstrate inflammatory pathways of molecular

139 not previously been rigorously evaluated in PTSD patients.

140 pacity to benefit from prolonged exposure in PTSD is gated by the degree to which prefrontal resource

141 n indices of generalized conditioned fear in PTSD using systematic methods developed in animals known

142 nnection of SN with CEN and DMN was found in PTSD patients.

143 ating aberrant glucocorticoid functioning in PTSD.

144 ationship with mGluR5 and glucocorticoids in PTSD.

145 avioral and autonomic hyperresponsiveness in PTSD may arise from a hyperactive alerting/orienting sys

146 avioral and autonomic hyperresponsiveness in PTSD.

147 [SD] age, 33.2 [7.4] years), improvement in PTSD severity at posttreatment was greater when CPT was

148 treatment resulted in greater improvement in PTSD severity than group treatment.

149 ous explanation of increased inflammation in PTSD, GAD, PD, and phobias is via the activation of the

150 aggerated startle responses in daily life in PTSD participants (t >/= 4.39, whole-brain familywise er

151 positively correlated with right Glu/NAA in PTSD patients.

152 ce shared or distinct biological pathways in PTSD.

153 more general cognitive control processes in PTSD.

154 ing to increased cardiovascular (CV) risk in PTSD will pave the way for developing interventions to i

155 on may contribute to an increased CV risk in PTSD.

156 omic hyperresponsiveness to sudden sounds in PTSD is associated with locus coeruleus hyperresponsiven

157 Behaviourally, the alpha suppression in PTSD correlated with decreased spatial working memory pe

158 regulation across sex and modes of trauma in PTSD was also observed converging on common signaling ca

159 turbations across sex and modes of trauma in PTSD, including one wound-healing module downregulated i

160 clinically significant disease variation in PTSD.

161 rols, whereas wellbeing derived from yoga in PTSD is associated with lower time-variance of complexit

162 to emotional memory processes and increased PTSD risk, modulates the stress-induced shift from cogni

163 tial mechanisms that contribute to increased PTSD vulnerability in females.

164 rmed a combined analysis of five independent PTSD blood transcriptome studies covering seven types of

165 nergistic with blast exposure in influencing PTSD arousal symptoms.

166 the Post-traumatic Stress Disorder 8 items (PTSD-8) and severe mental illness was measured with the

167 to -0.19; P = .027], respectively) and lower PTSD symptoms (adjusted mean difference, -4.02; 95% CI,

168 to neural signatures of risk for maintaining PTSD symptoms after trauma exposure.

169 Thirteen male PTSD patients and trauma-exposed controls matched for ag

170 earning (SEFL) in rodents recapitulates many PTSD-associated behaviors, including stress-susceptible

171 ntral executive network relative to the MDD, PTSD, and HC groups (p<0.05 corrected); therefore, inter

172 Modeling PTSD is challenging, as it is a heterogeneous disorder w

173 6 months post-transplant, we assessed mood, PTSD symptoms, and QOL with the Hospital Anxiety and Dep

174 raw (n = 175), trauma at blood draw 1 but no PTSD at either draw (n = 175), and PTSD that persisted b

175 PTSD (N=26), subthreshold PTSD (N=19), or no PTSD (referred to as trauma control subjects) (N=17).

176 s analyzed and compared between PTSD and non-PTSD groups.

177 Application of PTSD diagnosis to patients with cancer has been critique

178 us research has demonstrated associations of PTSD with inflammatory and endothelial function biomarke

179 these studies reveal that the root causes of PTSD sex differences are complex, and partly represent i

180 nstrate that although the clinical course of PTSD symptoms shows heterogeneous patterns of developmen

181 The clinical course of PTSD varies between individuals, and patterns of symptom

182 n profiles in relation to the development of PTSD symptoms in two prospective military cohorts (one d

183 EFL model provides a tool for development of PTSD therapeutics that is compatible with the growing nu

184 ate genetic influences on the development of PTSD, identify shared genetic risk between PTSD and othe

185 military servicemen (n=93), the emergence of PTSD symptoms over a deployment period to a combat zone

186 Any contemporary neuroscience formulation of PTSD should include an understanding of fear conditionin

187 Patients without a history of PTSD were more likely to have received topical anesthesi

188 he best-available molecular genetic index of PTSD-for both European- and African-American individuals

189 ace time series model revealed indicators of PTSD almost immediately post-trauma, often many months p

190 erlying molecular and cellular mechanisms of PTSD are largely unknown.

191 erlying molecular and cellular mechanisms of PTSD remain unknown, recent studies indicate that PTSD i

192 ables refinement of current animal models of PTSD, and it supports the incorporation of homologous me

193 human peripheral blood and animal models of PTSD, and review the human PTSD postmortem brain gene pr

194 cal processes related to the pathogenesis of PTSD.

195 -releasing factor, in the pathophysiology of PTSD.

196 s by trauma type revealed a clear pattern of PTSD gene expression signatures distinguishing interpers

197 ent models to probe biological phenotypes of PTSD (e.g., sleep disturbances, hippocampal and fear-cir

198 years, the 2-year reduction in prevalence of PTSD among the full population, the 2-year reduction in

199 superior to UC in reducing the prevalence of PTSD in the full population: absolute benefit was clear

200 munity may be involved in the progression of PTSD, yet also identified candidate MRs driving the dise

201 n, the 2-year reduction in the proportion of PTSD cases among initial cases, and 10-year incremental

202 er (PTSD), and there exists a higher rate of PTSD amongst veterans than the general population.

203 ch other was associated with a lower risk of PTSD.

204 h no differences in remission or severity of PTSD at the 6-month follow-up.

205 Severity of PTSD symptoms across the three study groups was positive

206 Severity of PTSD was assessed at each assessment with the Clinician-

207 was positively associated with the slope of PTSD symptoms, such that decreases in ventral anterior c

208 presenting the largest neuroimaging study of PTSD to date.

209 reat presentations in a prospective study of PTSD.

210 in several pathways relevant for symptoms of PTSD.

211 the effects of trauma exposure from those of PTSD.

212 To determine the trajectories of PTSD symptoms among deployed military personnel with and

213 ent growth mixture modeling, trajectories of PTSD symptoms were determined in the total sample, as we

214 Overall, 4 trajectories of PTSD were characterized: resilient, pre-existing, new-on

215 r the genesis, maintenance, and treatment of PTSD.

216 of the glutamate system for the treatment of PTSD.

217 sm for cognitive dysfunction of this type of PTSD.

218 examine the neurobiological underpinnings of PTSD and the brain's response to trauma.

219 To determine the effects of CPT on PTSD and co-occurring symptoms and whether they differ w

220 large-scale neuroimaging consortium study on PTSD conducted by the Psychiatric Genomics Consortium (P

221 unction moderated the effect of treatment on PTSD symptoms.

222 SRIs or SNRIs in youths with DD, AD, OCD, or PTSD were included.

223 Relative to TENC participants, PTSD patients exhibited significantly lower NAA in right

224 ed life year avoided, and $0.80 to $1.61 per PTSD-free day.

225 to define the most optimal model to predict PTSD symptoms at 3 and 6 months among demographic, clini

226 terpersonal violence significantly predicted PTSD after subsequent random traumas (odds ratio (OR)=1.

227 itnessing atrocities significantly predicted PTSD after subsequent random traumas only among responde

228 or anxiety disorders significantly predicted PTSD in a multivariate model (OR=1.5-4.3) and that these

229 007]) with hippocampal activation predicting PTSD symptoms at 3 and 6 months.

230 D symptomatology, but its role in predicting PTSD is unknown.

231 ignificant predictor in the model predicting PTSD symptoms at 3 months (F11,22 = 4.33, p = .01) and 6

232 dministration early after trauma may prevent PTSD, because oxytocin administration was previously fou

233 om traumas only among respondents with prior PTSD (OR=5.6).

234 sion Scale and Patient Health Questionnaire, PTSD checklist, and Functional Assessment of Cancer Ther

235 participants with high acute clinician-rated PTSD symptom severity did show beneficial effects of oxy

236 ter trauma did not attenuate clinician-rated PTSD symptoms in all trauma-exposed participants with ac

237 y after trauma on subsequent clinician-rated PTSD symptoms.

238 ompared with nonuse, cannabis did not reduce PTSD symptoms.

239 Cancer-related PTSD has been documented in a minority of patients with

240 Existing literature on cancer-related PTSD has used DSM-IV-TR diagnostic criteria; the revised

241 he literature on treatment of cancer-related PTSD is sparse.

242 In this qualitative review of cancer-related PTSD literature, we highlight conceptual, methodological

243 Treatment of cancer-related PTSD should be approached with caution and be informed b

244 herwise healthy Veterans with combat-related PTSD were compared with 14 matched Controls without PTSD

245 Genetic factors are surprisingly relevant: PTSD has been shown to be highly heritable despite being

246 l studies with a control group that reported PTSD symptoms and adverse effects of plant-based cannabi

247 Additional phenotyping of male mice revealed PTSD-associated behaviors, including extinction-resistan

248 cal risk factors, which differentially shape PTSD vulnerability.

249 of triple network connectivity in a specific PTSD induced by a single prolonged trauma exposure.

250 ver, these studies suggest that sex-specific PTSD vulnerability is partly regulated by sex difference

251 Across all subjects, PTSD symptom severity was inversely associated with dors

252 Relative to trauma control subjects, PTSD patients showed stronger conditioned generalization

253 fghanistan and had PTSD (N=26), subthreshold PTSD (N=19), or no PTSD (referred to as trauma control s

254 w potential therapeutic approaches to target PTSD.

255 We tested the hypothesis that PTSD patients have augmented sympathetic nervous system

256 remain unknown, recent studies indicate that PTSD is associated with aberrant gene expression in brai

257 This represents the first report that PTSD is associated with MRS markers of hippocampus Glu e

258 These results taken together suggest that PTSD patients and trauma-exposed controls can be disting

259 Studies have suggested that PTSD patients have an overactive sympathetic nervous sys

260 (n = 6) but not with placebo (n = 7) on the PTSD Symptom Scale-Self-Report.

261 Follow-up measures were the PTSD Checklist-Civilian Version, Patient Health Question

262 er trauma was positively associated with the PTSD symptom intercept and predicted symptoms at 12 mont

263 constructs that are thought to be central to PTSD and exposure therapy effects, to identify the funct

264 vioral responses is thought to be central to PTSD symptomatology, but its role in predicting PTSD is

265 lation and expression that may contribute to PTSD in women.

266 king locus coeruleus system hyperactivity to PTSD hyperresponsiveness is sparse.

267 ted to cases where the earlier trauma led to PTSD.

268 overgeneralized fear conditioning related to PTSD.

269 s for research on pretrauma vulnerability to PTSD.

270 s indicates that bLRs are more vulnerable to PTSD-like behavior.

271 Thus, fear mechanisms represent a tractable PTSD biomarker in the study of sex differences in fear.

272 Trauma/PTSD status (based on structured diagnostic interviews)

273 d models, we examined associations of trauma/PTSD status with biomarkers measured twice, 10 to 16 yea

274 ations, is a promising approach for treating PTSD patients.

275 lant-based cannabis preparations in treating PTSD in adults.

276 s of the union, yet its efficacy in treating PTSD symptoms remains uncertain.

277 insight into molecular mechanisms underlying PTSD and suggest that mGluR5 may be a promising target f

278 Inclusion criteria were PTSD after military deployment and stable medication the

279 The primary outcomes were PTSD, depression or generalised anxiety disorder, and al

280 s to co-occur in linked individuals, whereas PTSD risk is increased with social fragmentation.

281 ance spectroscopy (MRS) to determine whether PTSD is associated with lower hippocampus levels of the

282 s of plant-based cannabis use in adults with PTSD.

283 on stressors were positively associated with PTSD and severe mental illness.

284 lead to a range of behaviors associated with PTSD.

285 n study suggest that SC for individuals with PTSD in the aftermath of a natural disaster is associate

286 METHOD: Individuals with PTSD underwent functional MRI (fMRI) at rest and while c

287 METHOD: Individuals with PTSD underwent functional MRI (fMRI) while completing th

288 This symptom predicts that individuals with PTSD will be biased to attend to potential dangers in th

289 Participants with PTSD (n = 28) showed more eye-blink reflexes and larger

290 ng outcomes of cannabis use in patients with PTSD are ongoing and are expected to be completed within

291 sensory change was altered in patients with PTSD relative to trauma-exposed matched controls who did

292 based cannabis preparations in patients with PTSD, but several ongoing studies may soon provide impor

293 ted polymorphic association to patients with PTSD.

294 d to see the tailored advice, but those with PTSD (83%) or anxiety or depression (84%) were more like

295 Here, we tested 28 combat Veterans with PTSD and 28 control Veterans on a dot probe task with ne

296 f blood pressure, we show that veterans with PTSD have augmented SNS and haemodynamic reactivity duri

297 RF1 receptor) antagonist in adult women with PTSD.

298 Women with trauma but without PTSD had higher average tumor necrosis factor alpha rece

299 re compared with 14 matched Controls without PTSD.

300 red with trauma-exposed participants without PTSD (n = 26).