ライフサイエンスコーパス: psychotic symptom

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

2 regulation may lead to aberrant salience and psychotic symptoms.

3 poral lobe associated with the occurrence of psychotic symptoms.

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

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

6 t updating of inferences and beliefs driving psychotic symptoms.

7 pairments are detectable before the onset of psychotic symptoms.

8 brain correlating with increased severity of psychotic symptoms.

9 en were asked about bullying experiences and psychotic symptoms.

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

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

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

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

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

15 irectly correlated with concurrently induced psychotic symptoms.

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

17 inetic movements has also been implicated in psychotic symptoms.

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

19 tly related targets correlated with positive psychotic symptoms.

20 dual noise variance strongly correlated with psychotic symptoms.

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

22 ssed through increased paranoid ideation and psychotic symptoms.

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

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

25 h increased vulnerability for development of psychotic symptoms.

26 emiologically defined group of patients with psychotic symptoms.

27 nformation about the familial aggregation of psychotic symptoms.

28 t populations should routinely inquire about psychotic symptoms.

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

30 one relative who had affective disorder with psychotic symptoms.

31 ulation on the pathophysiologic mechanism of psychotic symptoms.

32 before interview, and current affective and psychotic symptoms.

33 with longer duration of untreated prodromal psychotic symptoms.

34 45 years of age or younger at onset of first psychotic symptoms.

35 alternatively, may be a by-product of severe psychotic symptoms.

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

37 declines would predict the presence of adult psychotic symptoms.

38 status and IQ at age 7 also predicted adult psychotic symptoms.

39 e brain dysgenesis, the earlier the onset of psychotic symptoms.

40 omosome 6p may be related to the severity of psychotic symptoms.

41 scent will experience persistent subclinical psychotic symptoms.

42 risk of developing subclinical and clinical psychotic symptoms.

43 action of antipsychotic drugs in alleviating psychotic symptoms.

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

45 the latter contributing directly to positive psychotic symptoms.

46 the transition from anomalous experiences to psychotic symptoms.

47 version for the subjects who developed fully psychotic symptoms.

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

49 sychotic relapse and control of breakthrough psychotic symptoms.

50 pulsive and aggressive behaviors rather than psychotic symptoms.

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

52 28% of the participants reported attenuated psychotic symptoms.

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

54 were compared with reductions in ratings of psychotic symptoms.

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

56 linking dysregulated dopamine function with psychotic symptoms.

57 than schizophrenia who do not have comorbid psychotic symptoms.

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

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

60 09, and November 30, 2011, and 2321 endorsed psychotic symptoms: 1423 significant (psychosis spectrum

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

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

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

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

65 owth hormone and homovanillic acid measures, psychotic symptom activation to methylphenidate, and mag

66 tain age at first odd behavior, age at first psychotic symptoms, age at first hospitalization, and ag

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

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

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

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

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

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

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

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

75 Both positive psychotic symptoms and anhedonia are associated with str

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

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

78 ormal cognitive processes that escalate into psychotic symptoms and contribute to addictive-drug-seek

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

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

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

82 Positive psychotic symptoms and extrapyramidal side effects at ba

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

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

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

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

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

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

89 Both psychotic symptoms and neurocognitive deficits appear to

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

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

92 Duration of untreated psychotic symptoms and of behavioral change was correlat

93 Duration of psychotic symptoms and of other symptoms marking a behav

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

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

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

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

98 yrus abnormalities contribute selectively to psychotic symptoms and that the extent of structural abn

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

100 narche, the later the ages at both the first psychotic symptoms and the first hospitalization.

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

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

103 0 F20-29) or affective disorder (F30-39 with psychotic symptoms), and had enduring auditory verbal ha

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

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

106 ffects of benztropine cotreatment, change in psychotic symptoms, and change in negative symptoms were

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

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

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

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

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

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

113 12 months for self-reported psychopathology, psychotic symptoms, and suicide attempts.

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

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

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

117 Psychotic symptoms are less common and show moderate per

118 Psychotic symptoms are more common in patients with Hunt

119 Individuals who endorse psychotic symptoms are neurocognitively delayed across t

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

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

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

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

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

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

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

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

128 95% CI=1.74-3.52) were more likely to report psychotic symptoms at age 12 than were children who did

129 ly the relationship of IQ at ages 4 and 7 to psychotic symptoms at age 23 in 547 offspring from a com

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

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

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

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

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

135 =11.1; P = .003) and control of breakthrough psychotic symptoms (beta = 0.2; t79 = 2.1; P = .04).

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

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

138 IQ decline is specific for psychotic symptoms, but follow-up assessment when the st

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

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

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

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

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

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

145 A change in one psychotic symptom, conceptual disorganization, was signi

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

147 sence of the "reality distortion" cluster of psychotic symptoms correlates with cerebral blood flow i

148 Psychotic symptoms, defined as the occurrence of delusio

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

150 Rates of psychotic symptoms-defined as hallucinations or delusion

151 Psychotic symptoms, delusions and hallucinations, occur

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

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

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

155 gnosed with schizophrenia, and only four had psychotic symptoms during a phase of their illness, all

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

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

158 bipolar I disorder and a negative history of psychotic symptoms during mood disorder episodes, 12 wer

159 bipolar I disorder and a positive history of psychotic symptoms during mood disorder episodes, and 12

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 ol (4, 8, and 16 mg/day) in the treatment of psychotic symptoms for 497 hospitalized patients with sc

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 that models normal cognitive development and psychotic symptom formation.

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

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

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

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

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

174 s with psychotic illness are associated with psychotic symptoms in AD but are clinically silent until

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

176 ere is an increased likelihood of developing psychotic symptoms in adulthood for a subgroup of indivi

177 ity in IQ during childhood was predictive of psychotic symptoms in adulthood.

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

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

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

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

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

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

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

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

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

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

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

189 ch as ketamine and phencyclidine precipitate psychotic symptoms in schizophrenic patients.

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

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

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

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

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

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

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

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

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

199 nifest sensory gating deficits without overt psychotic symptoms, it is likely that these deficits rep

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

201 Four of six adult patients had psychotic symptoms manifested as paranoid and grandiose

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

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

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

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

206 Patients with Huntington's disease and psychotic symptoms may have a familial predisposition to

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

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

209 ween the three treatment groups in levels of psychotic symptoms, motivation, and global functioning a

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

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

212 cannot be attributed to more severe positive psychotic symptoms or a greater duration of illness in t

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

214 nitudes of correlation between the levels of psychotic symptoms or disorganized symptoms and 2-year q

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

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

217 Blacks with psychotic symptoms or paranoid ideation, especially Cari

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

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

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

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

222 Only basal positive psychotic symptoms (P < .09) and plasma sodium (P < .18)

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

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

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

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

227 ctory bipolar disorder with active manic and psychotic symptoms participated in a 12-week open-label

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

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

230 Psychotic symptoms, perceptual, and a number of subjecti

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

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

233 isorder), premorbid functioning, duration of psychotic symptoms prior to study entry, baseline disorg

234 Concurrent psychotic symptoms progressively increased with dementia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

256 s was significantly associated with lifetime psychotic symptom severity.

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

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

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

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

261 Psychotic symptom subscores from the Brief Psychiatric R

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

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

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

265 severe emotional disturbances have transient psychotic symptoms that fall outside of current syndrome

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

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

268 sychosis, defined as the interval from first psychotic symptom to first psychiatric hospitalization,

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

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

271 The severity of psychotic symptoms was assessed using the Comprehensive

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

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

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

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

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

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

278 y have both been shown to be associated with psychotic symptoms, we carried out the first study of SP

279 es where clozapine was not clearly superior (psychotic symptoms, weight gain) were examined.

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

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

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

283 Psychotic symptoms were highly prevalent in this primary

284 Positive psychotic symptoms were more likely to result in assault

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

286 Psychotic symptoms were prospectively rated on a frequen

287 In contrast, psychotic symptoms were rare.

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

289 Psychotic symptoms were significantly correlated with in

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

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

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

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

294 Huntington's disease, 22 with and 22 without psychotic symptoms, were recruited from two university-a

295 ion to observe children and adolescents with psychotic symptoms while medication free.

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

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

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

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

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