ライフサイエンスコーパス: psychotic symptom

1 cipants with at-risk mental state attenuated psychotic symptoms).

2 (to a greater extent in those with isolated psychotic symptoms).

3 version for the subjects who developed fully psychotic symptoms.

4 , and 22 patients with major depression with psychotic symptoms.

5 sychotic relapse and control of breakthrough psychotic symptoms.

6 pulsive and aggressive behaviors rather than psychotic symptoms.

7 m, and might be linked to the development of psychotic symptoms.

8 28% of the participants reported attenuated psychotic symptoms.

9 youths: 53 typically developing and 53 with psychotic symptoms.

10 were compared with reductions in ratings of psychotic symptoms.

11 lthy controls, but not a greater increase in psychotic symptoms.

12 linking dysregulated dopamine function with psychotic symptoms.

13 than schizophrenia who do not have comorbid psychotic symptoms.

14 upted in patients with than in those without psychotic symptoms.

15 regulation may lead to aberrant salience and psychotic symptoms.

16 poral lobe associated with the occurrence of psychotic symptoms.

17 d Negative Syndrome Scale was used to assess psychotic symptoms.

18 of suicide attempts would be 56% to 75% for psychotic symptoms.

19 as a novel target for interventions to treat psychotic symptoms.

20 t updating of inferences and beliefs driving psychotic symptoms.

21 pairments are detectable before the onset of psychotic symptoms.

22 brain correlating with increased severity of psychotic symptoms.

23 en were asked about bullying experiences and psychotic symptoms.

24 arm is associated with children's reports of psychotic symptoms.

25 , which eventually developed into first-rank psychotic symptoms.

26 nstruct validity of children's self-reported psychotic symptoms.

27 ith an earlier age at onset of prodromal and psychotic symptoms.

28 in to modulate verbal learning and to induce psychotic symptoms.

29 irectly correlated with concurrently induced psychotic symptoms.

30 ssociated with an increased risk of onset of psychotic symptoms.

31 inetic movements has also been implicated in psychotic symptoms.

32 lay a role in the genesis and maintenance of psychotic symptoms.

33 tly related targets correlated with positive psychotic symptoms.

34 dual noise variance strongly correlated with psychotic symptoms.

35 ssed through increased paranoid ideation and psychotic symptoms.

36 ubstance use/abuse, depressive symptoms, and psychotic symptoms.

37 risk participants (n = 27) reported isolated psychotic symptoms.

38 h increased vulnerability for development of psychotic symptoms.

39 emiologically defined group of patients with psychotic symptoms.

40 sess the association with the development of psychotic symptoms.

41 nformation about the familial aggregation of psychotic symptoms.

42 in vivo in psychosis or related to positive psychotic symptoms.

43 t populations should routinely inquire about psychotic symptoms.

44 f nonpsychotic probands (34% versus 11%) had psychotic symptoms.

45 activity, which underlies the development of psychotic symptoms.

46 ce for impaired sensorimotor predictions and psychotic symptoms.

47 opamine projections to limbic regions causes psychotic symptoms.

48 ive (rho = .35, p = .13), negative, or total psychotic symptoms.

49 psychotic illness, but not patients without psychotic symptoms.

50 oculomotor CD abnormalities and more severe psychotic symptoms.

51 th an additional emphasis on severe positive psychotic symptoms.

52 action of antipsychotic drugs in alleviating psychotic symptoms.

53 the transition from anomalous experiences to psychotic symptoms.

54 sking threshold, which in turn was linked to psychotic symptoms.

55 or who had bipolar disorder or psychosis or psychotic symptoms.

56 ulation on the pathophysiologic mechanism of psychotic symptoms.

57 ion is likely necessary for the emergence of psychotic symptoms.

58 scent will experience persistent subclinical psychotic symptoms.

59 risk of developing subclinical and clinical psychotic symptoms.

60 e high doses of medication for their ongoing psychotic symptoms.

61 the latter contributing directly to positive psychotic symptoms.

62 s with baseline psychopathology who reported psychotic symptoms, 14% reported a suicide attempt by 3

63 09, and November 30, 2011, and 2321 endorsed psychotic symptoms: 1423 significant (psychosis spectrum

64 tional correlates of risk were predictive of psychotic symptoms 2 years later.

65 1) patients with DSM-IV PTSD with secondary psychotic symptoms, 2) patients with DSM-IV PTSD without

66 Approximately one-half of the patients with psychotic symptoms (47.6%) had taken a prescribed psycho

67 of them also experienced other non-clinical psychotic symptoms), 50 patients with a psychotic disord

68 About 50% of AD patients will develop psychotic symptoms (AD with Psychosis, or AD + P) and th

69 developed a highly specific configuration of psychotic symptoms (all of which could be convincingly t

70 rs' goals were to estimate the prevalence of psychotic symptoms among adults attending an urban gener

71 lobe regions, (ii) increased development of psychotic symptoms and (iii) decreased premorbid IQ.

72 ients with schizophrenia during remission of psychotic symptoms and 19 age- and sex-comparable contro

73 atterns between nondeleted participants with psychotic symptoms and 22q11DS suggest partially shared

74 atterns between nondeleted participants with psychotic symptoms and 22q11DS were similar but with imp

75 k phase characterised by attenuated or brief psychotic symptoms and a marked decline in functioning.

76 prodromal phase characterized by attenuated psychotic symptoms and a marked deterioration in psychos

77 between family income and the prevalence of psychotic symptoms and a positive association between pr

78 Both positive psychotic symptoms and anhedonia are associated with str

79 cebo in the short-term hospital treatment of psychotic symptoms and behavioral disturbances in nondep

80 vestigate the relationship between change in psychotic symptoms and change in metabolic parameters wi

81 n alters dopamine signalling events, causing psychotic symptoms and cognitive dysfunction.

82 This alteration is related to psychotic symptoms and could guide further therapies for

83 and to assess reports of anxiety, mood, and psychotic symptoms and disorders, other mental disorders

84 ted with reduced SNX7 expression-to positive psychotic symptoms and executive function deficits in bi

85 ater reductions in the mean severity of both psychotic symptoms and extrapyramidal side effects than

86 aining benefits was predicted by more severe psychotic symptoms and greater dysfunction and was follo

87 is use is associated with the development of psychotic symptoms and increased risk for schizophrenia.

88 alue of continuous measures (eg, duration of psychotic symptoms and intelligence quotient).

89 Delta9-Tetrahydrocannabinol increased psychotic symptoms and levels of anxiety, intoxication,

90 c drugs have equivocal efficacy in improving psychotic symptoms and may have side effects or risks th

91 Both psychotic symptoms and neurocognitive deficits appear to

92 Population-based studies evaluating psychotic symptoms and neurocognitive performance across

93 ctimisation increases the risk of individual psychotic symptoms and of a diagnosis of probable psycho

94 lationship between the duration of untreated psychotic symptoms and outcome; the superior responses o

95 Racial differences in psychotic symptoms and paranoid ideation persist even af

96 With logistic regression, psychotic symptoms and paranoid ideation were associated

97 ic drugs have been proven to alleviate acute psychotic symptoms and prevent their recurrence in schiz

98 herapy and autologous stem cell rescue, both psychotic symptoms and psychosocial functioning reverted

99 rmers experienced higher rates of concurrent psychotic symptoms and substance dependence.

100 ral circuitry for movement abnormalities and psychotic symptoms and suggest the potential value of in

101 Significant associations between psychotic symptoms and the CC genotype (p = 0.001 - p =

102 ficits that increase the risk for developing psychotic symptoms and the latter contributing directly

103 groups (those with mood fluctuations but no psychotic symptoms and those with no mood symptoms) was

104 he association between cerebellar volume and psychotic symptoms and, to a lesser extent, norm-violati

105 0 F20-29) or affective disorder (F30-39 with psychotic symptoms), and had enduring auditory verbal ha

106 mptoms, 2) patients with DSM-IV PTSD without psychotic symptoms, and 3) healthy matched comparison su

107 volumes and their relationship to cognition, psychotic symptoms, and age in probands with schizophren

108 nicians in the treatment of individuals with psychotic symptoms, and even if the association is not c

109 ng the study, individuals that had transient psychotic symptoms, and individuals that subsequently be

110 Global Assessment of Functioning (GAF), psychotic symptoms, and mood symptoms were rated at each

111 t for prediction of general psychopathology, psychotic symptoms, and norm-violating behavior.

112 hree dependent variables: paranoid ideation, psychotic symptoms, and psychotic symptoms/paranoid idea

113 rted frequency of marijuana use, subclinical psychotic symptoms, and several time-varying confounds (

114 increased risk for motor vehicle accidents, psychotic symptoms, and short-term cognitive impairment.

115 12 months for self-reported psychopathology, psychotic symptoms, and suicide attempts.

116 s and (b) interview-rated current-attenuated psychotic symptoms; and a comparison group (n = 20) who

117 Adolescents with psychopathology who report psychotic symptoms are at clinical high risk for suicide

118 It has been reported that childhood psychotic symptoms are common in the general population

119 Children's psychotic symptoms are familial and heritable and are as

120 Individuals who endorse psychotic symptoms are neurocognitively delayed across t

121 Psychotic symptoms are proposed to lie on a continuum, r

122 able evidence to support the hypothesis that psychotic symptoms are the result of abnormal salience a

123 els (eg, kinesia paradoxia) and that several psychotic symptoms are typical antipsychotic resistant a

124 s exhibited an increase in their subclinical psychotic symptoms as a function of their recent and/or

125 with PBD showed a stronger correlation with psychotic symptoms, as shown by the Positive and Negativ

126 has been tested for the improvement of acute psychotic symptoms, as well as for the improvement of co

127 Participants had at least 1 psychotic symptom assessed during administration of the

128 the authors assessed the risk of developing psychotic symptoms associated with maltreatment, bullyin

129 offer a novel approach for the treatment of psychotic symptoms associated with schizophrenia and Alz

130 95% CI=1.74-3.52) were more likely to report psychotic symptoms at age 12 than were children who did

131 Of the total sample, 7% reported psychotic symptoms at baseline.

132 ynthesis capacity predicted the worsening of psychotic symptoms at follow-up (r = 0.35; p < 0.05), bu

133 nalyses revealed that those individuals with psychotic symptoms at follow-up showed a reduced right h

134 orphometry analyses revealed that those with psychotic symptoms at follow-up showed significantly gre

135 ting criteria for brief limited intermittent psychotic symptoms at intake was associated with lower r

136 0 to 210; higher scores indicate more severe psychotic symptoms) at week 4.

137 More careful clinical assessment of psychotic symptoms (attenuated or frank) in mental healt

138 =11.1; P = .003) and control of breakthrough psychotic symptoms (beta = 0.2; t79 = 2.1; P = .04).

139 unmedicated individuals who experience early psychotic symptoms but fall below the threshold for a ca

140 importance of silliness and minimal positive psychotic symptoms) but expanded the syndrome to include

141 rotransmission contributes to the genesis of psychotic symptoms, but evidence also points to a widesp

142 th a role for dopamine in the development of psychotic symptoms, but is not strongly linked to hippoc

143 affect the association between bullying and psychotic symptoms, but reduced the significance of the

144 ch as prediction error signals, may underlie psychotic symptoms, but the mechanism by which such defi

145 ience of rewarding events, and contribute to psychotic symptoms by promoting aberrant perceptions and

146 ations, and it is thought that they suppress psychotic symptoms by serving as competitive antagonists

147 the findings indicate that children who have psychotic symptoms can be recruited for neuroscience res

148 he past month) further increased the odds of psychotic symptoms (cannabis: OR, 2.0 [95% CI, 1.1-3.5];

149 Bipolar disorder families in which psychotic symptoms cluster may carry susceptibility gene

150 bsequent worsening of sub-clinical total and psychotic symptoms, consistent with a role for dopamine

151 r significantly regarding psychotic relapse, psychotic symptom control, or hospitalization rates, and

152 Psychotic symptoms, defined as the occurrence of delusio

153 eviously demonstrated familial clustering of psychotic symptoms-defined as hallucinations and/or delu

154 Psychotic symptoms, delusions and hallucinations, occur

155 atients who continue to experience disabling psychotic symptoms despite optimal pharmacological treat

156 cal thickness in nondeleted individuals with psychotic symptoms differed from typically developing co

157 iod, and 16% of the participants experienced psychotic symptoms during 17% the follow-up period.

158 as well as for the consequent development of psychotic symptoms during adolescence.

159 We found that reliable assessments of psychotic symptoms during in-person or phone interviews

160 e was a 5-fold increase in the likelihood of psychotic symptoms during periods of methamphetamine use

161 dose-dependent increase in the occurrence of psychotic symptoms during periods of methamphetamine use

162 splaying violent behavior while experiencing psychotic symptoms during the 12-month period prior to i

163 nonadherence robustly predicted a return of psychotic symptoms during the early phase of schizophren

164 mptoms (e.g., apathy and avolition), but not psychotic symptoms (e.g., hallucinations and delusions),

165 duals and follow individuals as subthreshold psychotic symptoms emerge.

166 ents with first-episode psychosis experience psychotic symptoms for a mean of up to 2 years prior to

167 tic criteria for schizophrenia; however, the psychotic symptoms for schizophrenia, traditionally held

168 dolescents with psychopathology who reported psychotic symptoms had a nearly 70-fold increased odds o

169 renia", in whom an early stage with positive psychotic symptoms has progressed to a late stage charac

170 inical high risk (CHR) who progress to fully psychotic symptoms have been observed to show a steeper

171 e evidence that CHR patients with attenuated psychotic symptoms have glutamatergic abnormalities, alt

172 ificantly over time on substance dependence, psychotic symptoms, homelessness, and psychosocial outco

173 Psychotic symptoms, i.e., the presence of delusions and/

174 sessments at 6 months, was the difference in psychotic symptom improvement as measured with the PANSS

175 and enzyme activity and its association with psychotic symptoms in 22q11.2DS.

176 identified neuroimaging features that track psychotic symptoms in a dimension- or disorder-specific

177 blish methods for the reliable assessment of psychotic symptoms in a large, geographically dispersed

178 ely powered samples in which the presence of psychotic symptoms in AD has been well characterized.

179 For clinicians, the findings indicate that psychotic symptoms in childhood are often a marker of an

180 are clinically significant mood symptoms and psychotic symptoms in depressive episodes.

181 zophrenia to be used to treat depression and psychotic symptoms in HD.

182 NMDA-R antagonists elicit psychotic symptoms in humans and schizophrenia-relevant

183 and neurological disorders can contribute to psychotic symptoms in later life.

184 e of depressive symptoms in schizophrenia or psychotic symptoms in major depression, but earlier dise

185 ansition from well to non-mood disorder, and psychotic symptoms in mood episodes were significantly a

186 The occurrence of psychotic symptoms in patients with late-onset Alzheimer

187 s in the prevalence of paranoid ideation and psychotic symptoms in persons age >/=55 in an urban comm

188 Because reduction of psychotic symptoms in schizophrenia does not result in a

189 use is associated with an adverse course of psychotic symptoms in schizophrenia, and vice versa, eve

190 reatment for 2-8 weeks significantly reduced psychotic symptoms in schizophrenia.

191 aptive decision making and the generation of psychotic symptoms in schizophrenia.

192 ents and between baseline panic and positive psychotic symptoms in schizophrenia/schizoaffective diso

193 ers, these genes may result in clustering of psychotic symptoms in some bipolar disorder pedigrees.

194 how predictive processing models may explain psychotic symptoms in terms of alterations in prediction

195 dict, with cross-validation, the presence of psychotic symptoms in the context of mood fluctuation at

196 nt psychotic symptoms; or (2) modify risk of psychotic symptoms in the presence of neurodegeneration

197 SCs may either exacerbate previously stable psychotic symptoms (in vulnerable individuals) or trigge

198 frontal and limbic areas in the aetiology of psychotic symptoms, in subjects without the illness phen

199 Years before the onset of psychotic symptoms, individuals with schizophrenia, as a

200 ocuses on the latest (2010-2015) evidence of psychotic symptoms induced by ingestion of products cont

201 between SORT performance, fMRI activity, and psychotic symptoms is schizophrenia-specific.

202 ted glutamine, which was directly related to psychotic symptoms, is consistent with increased glutama

203 schizophrenia in individuals with prodromal psychotic symptoms, is predominantly localized in the as

204 ng is suggested to underlie the formation of psychotic symptoms, likely driven by elevated ventral st

205 t disturbances in this pathway may relate to psychotic symptom manifestation in patients.SIGNIFICANCE

206 sistent with animal models that propose that psychotic symptoms may be generated when hippocampal hyp

207 and preventing) the disorder on the basis of psychotic symptoms may be too narrow.

208 mptoms such as profound sleep disturbance or psychotic symptoms may dominate the clinical picture.

209 mplementary insights to a mechanism by which psychotic symptoms may emerge.

210 rs were not likely the result of interfering psychotic symptoms, medication, or medication side effec

211 ed ten (20.9%) patients reported one or more psychotic symptoms, most commonly auditory hallucination

212 Psychotic symptoms occur in ~40% of subjects with Alzhei

213 chotic drugs are effective for relieving the psychotic symptoms of first-episode psychosis (FEP), psy

214 induced psychosis recapitulates many of the psychotic symptoms of schizophrenia, the results from th

215 tween [(11)C]IMA107 BPND and the severity of psychotic symptoms or antipsychotic dosage.

216 ntial utility for clinical studies targeting psychotic symptoms or as a novel target for intervention

217 re strongly predict functional outcomes than psychotic symptoms or nonsocial cognitive deficits.

218 The high prevalence of psychotic symptoms or paranoid ideation among this aging

219 A significant difference in psychotic symptoms or paranoid ideation was found betwee

220 Blacks with psychotic symptoms or paranoid ideation, especially Cari

221 rare but severe complications such as mania, psychotic symptoms, or delirium need individual psychiat

222 rease susceptibility to an AD and subsequent psychotic symptoms; or (2) modify risk of psychotic symp

223 oups differed, regardless of the severity of psychotic symptoms other than AVHs.

224 cannabis use were associated with changes in psychotic symptoms over time even after gender, age, soc

225 were positively correlated with severity of psychotic symptoms (P = .02).

226 carriers were also more likely to experience psychotic symptoms (P = .03).

227 , the CBD group had lower levels of positive psychotic symptoms (PANSS: treatment difference=-1.4, 95

228 : paranoid ideation, psychotic symptoms, and psychotic symptoms/paranoid ideation.

229 Compared with patients without psychotic symptoms, patients with psychotic symptoms wer

230 tment on ketamine-induced schizophrenia-like psychotic symptoms, perceptual alterations, and subjecti

231 Psychotic symptoms, perceptual, and a number of subjecti

232 ular marijuana use on subsequent subclinical psychotic symptoms persisted even when adolescents stopp

233 at significant risk for continued attenuated psychotic symptoms, persistent or recurrent disorders, a

234 newly admitted to TFH facilities with active psychotic symptoms (positive and negative syndrome scale

235 Concurrent psychotic symptoms progressively increased with dementia

236 ty for psychosis in individuals experiencing psychotic symptoms (PSs) in the general population.

237 score (eta2partial = .055; P = .02) and the Psychotic Symptom Rating Scales delusion score (eta2part

238 ANSS positive syndrome and total scores, the Psychotic Symptom Rating Scales, the jumping to conclusi

239 delusions and hallucinations assessed by the Psychotic Symptoms Rating Scale (PSYRATS) at week 12.

240 rticipants were a score of at least 3 on the Psychotic Symptoms Rating Scale (PSYRATS) denoting a cur

241 at 12 weeks, measured by total score on the Psychotic Symptoms Rating Scales Auditory Hallucinations

242 poorer functioning and greater negative and psychotic symptom ratings predicted a subsequent shift t

243 se to assess suicides, suicide attempts, and psychotic symptom reduction in clinical trials of three

244 fying 16-year-olds with mood fluctuation and psychotic symptoms relative to the control groups (those

245 der remain based on the presence of specific psychotic symptoms, relative to affective and other symp

246 anisms that produce hallucinations and other psychotic symptoms remain unclear.

247 the mechanism by which such deficits produce psychotic symptoms remains to be established.

248 research should clarify the extent to which psychotic symptom reports among Hispanic patients are af

249 effects of C. sativa on verbal learning and psychotic symptoms, respectively.

250 puter scoring program to identify periods of psychotic symptom return.

251 eir expected level of subsequent subclinical psychotic symptoms rose by 21% and their expected odds o

252 r affective-spectrum psychotic disorder, and psychotic symptoms scoring at least 4 on at least one of

253 ontal WM volumes (F = 7.16, P < .001) and on psychotic symptom severity (F = 6.07, P = .003); the pat

254 These emerging patterns correlated with psychotic symptom severity and mirrored the neuromotor,

255 itive association between Kicer and positive psychotic symptom severity in individuals with bipolar d

256 ficantly positively correlated with positive psychotic symptom severity in the combined bipolar and s

257 pamine synthesis capacity is associated with psychotic symptom severity, irrespective of diagnostic c

258 trast, lower FAAH predicted greater positive psychotic symptom severity, with the strongest effect ob

259 s was significantly associated with lifetime psychotic symptom severity.

260 th the degree of disruption correlating with psychotic symptom severity.

261 ings show that individuals with non-clinical psychotic symptoms show a similar but less pronounced pa

262 urred in those at high risk who had isolated psychotic symptoms ('state' effects).

263 as >/=40% reduction in symptoms based on the psychotic symptom subscale of the Brief Psychiatric Rati

264 "Positive" psychotic symptoms, such as persecutory ideation, increa

265 minor and serious violence, while "negative" psychotic symptoms, such as social withdrawal, lowered t

266 ore, and were more likely to be experiencing psychotic symptoms than those who had not developed a ma

267 exhibit a systematic increase in subclinical psychotic symptoms that persists during periods of susta

268 ask; 27 high risk subjects reported isolated psychotic symptoms, the remaining high risk subjects and

269 DUP was defined as days from first psychotic symptom to first psychiatric hospitalization.

270 is the time from manifestation of the first psychotic symptom to initiation of adequate treatment.

271 rom healthy controls with regard to baseline psychotic symptoms (U=156.5, z=-0.70, P=.48).

272 The severity of psychotic symptoms was assessed using the Comprehensive

273 umatic stress disorder (PTSD) with secondary psychotic symptoms was associated with a familial vulner

274 In 18- to 21-year-olds, the presence of psychotic symptoms was associated with later hospitaliza

275 modeling indicated that the association with psychotic symptoms was bidirectional.

276 PTSD with secondary psychotic symptoms was not associated with an excess of

277 PTSD with secondary psychotic symptoms was not associated with familial psyc

278 The higher risk for psychotic symptoms was observed whether these events occ

279 tance use and ages at onset of prodromal and psychotic symptoms were determined by standardized metho

280 h bipolar I disorder (N=123) presenting with psychotic symptoms were followed over a 2-year period.

281 Moderate to severe psychotic symptoms were found in only 1.2%.

282 Psychotic symptoms were highly prevalent in this primary

283 Positive psychotic symptoms were more likely to result in assault

284 ports of social exclusion and an increase in psychotic symptoms were not associated with dopamine rel

285 Psychotic symptoms were prospectively rated on a frequen

286 In contrast, psychotic symptoms were rare.

287 the fact that significantly higher levels of psychotic symptoms were self-reported by Latinos (odds r

288 Psychotic symptoms were significantly correlated with in

289 ts without psychotic symptoms, patients with psychotic symptoms were significantly more likely to hav

290 Children's reports of psychotic symptoms were verified by clinicians.

291 Fifty-three patients with 22q11DS, 30 with psychotic symptoms, were compared with demographically m

292 schizophrenia with an acute exacerbation of psychotic symptoms, were randomly assigned to 6 weeks of

293 al networks, a phenomenon that could lead to psychotic symptoms when overly strong, could also underl

294 in patients that have major depression with psychotic symptoms, who typically have the most robust H

295 rst evidence that cannabidiol may ameliorate psychotic symptoms with a superior side-effect profile c

296 by the relative conformity of the patient's psychotic symptoms with her occupational practices and t

297 sociation between patients' IQ and affective psychotic symptoms with the local efficiency of the orbi

298 amphetamine use and the risk of experiencing psychotic symptoms within individuals over time.

299 everity as compared to the severity of other psychotic symptoms, working-memory capacity, and other c

300 bipolar disorder pedigrees most enriched for psychotic symptoms would show greater evidence of linkag