ライフサイエンスコーパス: psychotic

1 xiety, low mood, combined and non-affective (psychotic).

2 ssants/benzodiazepines), and psychosis (anti-psychotics).

3 remained in a high-risk state or had become psychotic.

4 ions increased for NSAIDs (26%/28%) and anti-psychotics (0%/38%) and decreased for metformin (100%/75

5 moderate, 1.61-1.84; severe, 1.93-2.23; and psychotic, 2.73-3.07) were associated with more severe t

6 anti-depressants/benzodiazepines, 69%; anti-psychotics, 43%; NSAIDs, 28%; and metformin, 0.4%.

7 ted States with randomization of 335 acutely psychotic adults with schizophrenia.

8 Quality of life and psychotic and depressive symptom outcomes were found to

9 schizophrenia (Cohen d = 0.36, P < .001) and psychotic bipolar disorder (Cohen d = 0.33, P = .002) ha

10 izoaffective disorder, and 129 patients with psychotic bipolar disorder (mean [SD] age, 35.1 [12.0] y

11 and age in probands with schizophrenia (SZ), psychotic bipolar disorder (PBD), and schizoaffective di

12 a in 144 individuals with schizophrenia, 210 psychotic bipolar disorder probands, and 95 healthy indi

13 ects in frontotemporal and parietal regions; psychotic bipolar probands had small reductions, primari

14 neurocognitive functioning during the "near-psychotic," clinical high-risk (CHR) state of psychosis

15 A never-psychotic comparison group was also assessed.

16 A quarter of people with psychotic conditions experience persistent auditory verb

17 n, and with formation of false memories with psychotic content.

18 Maternal depression, a non-psychotic depressive episode of mild to major severity,

19 sensory and late cognitive processing across psychotic diagnostic groups.

20 ssment was lower in patients who developed a psychotic disorder (65.5 [12.0]) compared with those wit

21 (65.5 [12.0]) compared with those without a psychotic disorder (74.0 [14.0]).

22 ntly increased risk for the development of a psychotic disorder (odds ratio = 2.49; 95% CI, 1.24-5.00

23 infarction (one patient on eliglustat), and psychotic disorder (one patient on imiglucerase).

24 alth services among patients with a lifetime psychotic disorder and current chronic PTSD.

25 s between those who subsequently developed a psychotic disorder and those who did not was distinguish

26 ups: a schizophrenia group and those with no psychotic disorder at age >/=25 years.

27 092 individuals (0.95%) not diagnosed with a psychotic disorder at the time of examination were hospi

28 ata for age, sex, ethnicity, marital status, psychotic disorder diagnosis, subsequent hospital admiss

29 lator for the individualized prediction of a psychotic disorder in a 2-year period.

30 However, for adults with psychotic disorder or bipolar disorder, the additional c

31 ultra-high risk for psychosis do not develop psychotic disorder over the medium term.

32 Present classifications of psychotic disorder remain based on the presence of speci

33 cts of organic-induced and substance-induced psychotic disorder show that our diagnostic classificati

34 The risk of individuals having a psychotic disorder showed a roughly three-times increase

35 gnificantly mediated the association between psychotic disorder status and general cognition (beta =

36 amination were hospitalized for nonaffective psychotic disorder up to 9 years after the index examina

37 Presence of ICD-10 F10-33 psychotic disorder was confirmed using OPCRIT [operation

38 or bipolar disorder, schizophrenia, or other psychotic disorder was recorded on at least one inpatien

39 ded a sample of patients with a pre-existing psychotic disorder with a follow-up duration of at least

40 ed risk for hospitalization for nonaffective psychotic disorder within 14 days after examination (haz

41 als presenting with these features develop a psychotic disorder within 3 years.

42 , delusional disorder, or affective-spectrum psychotic disorder, and psychotic symptoms scoring at le

43 Diagnosis of a psychotic disorder, initial IQ, longitudinal IQ trajecto

44 cting later hospitalization for nonaffective psychotic disorder.

45 lly defined suspected PEs, definite PEs, and psychotic disorder.

46 subjects clinically at risk of developing a psychotic disorder.

47 ith later hospitalization for a nonaffective psychotic disorder.

48 In both cohorts, non-affective psychotic disorders (adjusted hazard ratio [HR] 1.25, 95

49 le participants were patients with diagnosed psychotic disorders (clinical group) and adults in the g

50 Patients with chronic psychotic disorders (CPD) exhibit deficient sensorimotor

51 efficiency was also significantly reduced in psychotic disorders (F3,587 = 4.01, P = .008) and positi

52 Patients diagnosed with psychotic disorders (for example, schizophrenia and bipo

53 of neighbourhood variations of non-affective psychotic disorders (NAPD) have focused mainly on incide

54 nia diagnosis from those who developed other psychotic disorders (R(2) = 9.2%, p = .002).

55 ven lower, even for severe disorders such as psychotic disorders and epilepsy.

56 s mortality; 2) mortality among persons with psychotic disorders and the extent to which cannabis use

57 ally examined the aetiological links between psychotic disorders and violence.

58 Psychotic disorders are characterized by attenuated acti

59 Psychotic disorders are currently grouped under broad ph

60 abis every day conferred the highest risk of psychotic disorders compared with no use of cannabis (ad

61 Individuals with psychotic disorders experience substantial health dispar

62 in an epidemiologically defined cohort with psychotic disorders followed for 20 years after first ho

63 y control participants and 375 patients with psychotic disorders from the Bipolar-Schizophrenia Netwo

64 All patients with psychotic disorders had significantly reduced CON local

65 Adults with psychotic disorders have dysconnectivity in critical bra

66 ng-term trajectories of social impairment in psychotic disorders have rarely been studied systematica

67 e calculated an overall relative risk of new psychotic disorders in daily smokers versus non-smokers

68 symptoms of patients later hospitalized for psychotic disorders in primary mental health outpatient

69 etes pharmacotherapy and drug management for psychotic disorders is essential, irrespective of whethe

70 The onset of psychotic disorders is preceded by a high-risk phase cha

71 he general cognitive deficit observed across psychotic disorders is similarly associated with functio

72 psychiatric disorders and that patients with psychotic disorders may develop dementia more often than

73 tion effect of cannabis use and diagnosis of psychotic disorders on mortality.

74 utoantibodies against glutamatergic NMDAR in psychotic disorders remains controversial, with detectio

75 ioning, but few studies have linked risk for psychotic disorders to a neural measure evoked during a

76 and those diagnosed with major depression or psychotic disorders were excluded.

77 represent candidates that may be causal for psychotic disorders when considered in the context of th

78 n a generalizability cohort of patients with psychotic disorders who were hospitalized for an acute p

79 served between cannabis use and diagnosis of psychotic disorders with regard to mortality.

80 is study of 304 adults at ultrahigh risk for psychotic disorders, 153 (50.3%) received omega-3 PUFAs

81 nding the basis for deficient PPI and MMN in psychotic disorders, as reduced NMDA activity is implica

82 nt dopamine antagonist that is used to treat psychotic disorders, but 50% of treated patients develop

83 s of violence are increased in patients with psychotic disorders, but the contribution of triggers fo

84 ound an excess mortality among subjects with psychotic disorders, but the level did not differ betwee

85 ates of smoking were reported in people with psychotic disorders, compared with controls.

86 nd feasible in patients with PTSD and severe psychotic disorders, including current symptoms.

87 Diabetes is highly prevalent in people with psychotic disorders, including schizophrenia and schizoa

88 uctural brain abnormalities are prominent in psychotic disorders, including schizophrenia.

89 urenic acid have been found in patients with psychotic disorders, including schizophrenia.

90 en reported in a proportion of patients with psychotic disorders, raising hopes for more appropriate

91 ences differed from that seen in adults with psychotic disorders, suggesting important differences be

92 tervention and the personalized treatment of psychotic disorders.

93 ted to the underlying familial diathesis for psychotic disorders.

94 le evidence that the thalamus is abnormal in psychotic disorders.

95 l categorization schemes for differentiating psychotic disorders.

96 al characteristic of schizophrenia and other psychotic disorders.

97 e that cannabis use can increase the risk of psychotic disorders.

98 nditions: post-traumatic stress disorder and psychotic disorders.

99 escence, is important in the pathogenesis of psychotic disorders.

100 ssessment and management in individuals with psychotic disorders.

101 on to baseline cannabis use and diagnosis of psychotic disorders.

102 e have increased prevalence in patients with psychotic disorders.

103 ce of persecutory delusions in patients with psychotic disorders.

104 psychophysiological alterations observed in psychotic disorders.

105 ups of disorders, the neurodevelopmental and psychotic disorders.

106 se, and type of cannabis used on the risk of psychotic disorders.

107 ffected the association between cannabis and psychotic disorders.

108 tanding of common mechanisms between FTD and psychotic disorders.

109 e of 5-HT2B receptors in the neurobiology of psychotic disorders.

110 e pathophysiology of schizophrenia and other psychotic disorders.

111 malities reported in adults with established psychotic disorders.

112 escence is associated with increased risk of psychotic disorders.

113 ture of schizophrenia and is common in other psychotic disorders.

114 ctive study of first-admission patients with psychotic disorders.

115 and Related Health Problems, Tenth Revision psychotic disorders.

116 eptor hypofunction in the pathophysiology of psychotic disorders.

117 mechanism underlies cognitive impairment in psychotic disorders.

118 experiences (PE; n=20) at increased risk for psychotic disorders; (b) people with extremely elevated

119 with bipolar disorder experiencing a current psychotic episode (n = 16, r = 0.60, P = .01), which rem

120 was defined as the occurrence of any mood or psychotic episode fulfilling DSM-IV-TR criteria.

121 schizophrenia sample experiencing a current psychotic episode, explaining 27% of the variance in sym

122 disorders who were hospitalized for an acute psychotic episode.

123 olar mood disorders (similar risk) and brief psychotic episodes (higher risk).

124 experiences (non-clinical group) and without psychotic experiences (controls).

125 ts in the general population with persistent psychotic experiences (non-clinical group) and without p

126 an association between schizophrenia PRS and psychotic experiences (OR per SD increase in PRS, 1.08;

127 noid, personalising interpretations of their psychotic experiences (p<0.008; p values are Sidak adjus

128 ing the RLT in three groups: (a) people with psychotic experiences (PE; n=20) at increased risk for p

129 Individuals in the general population with psychotic experiences (PEs) may show similar changes, su

130 ations between the schizophrenia PRS and (1) psychotic experiences (Psychosis-Like Symptom Interview

131 pulation that exhibit graded similarity with psychotic experiences (schizotypy).

132 Assessment of psychotic experiences among individuals with suicidal id

133 The appraisals of psychotic experiences among people in the non-clinical a

134 adolescents 13 to 16 years old who reported psychotic experiences and a matched sample of 28 adolesc

135 pts among individuals reporting ideation and psychotic experiences and meeting criteria for any psych

136 mnia is a causal factor in the occurrence of psychotic experiences and other mental health problems.

137 Psychotic experiences are also prevalent in adults, but

138 ION: We provide robust evidence that the way psychotic experiences are appraised differs between indi

139 The clinical group also appraised their psychotic experiences as being more negative, dangerous,

140 Twelve-month psychotic experiences assessed with the Composite Intern

141 appraisals might protect against persistent psychotic experiences becoming clinically relevant.

142 otic experiences, the 171 (9.7%) adults with psychotic experiences did not show a statistically signi

143 ofile of cognitive impairment in adults with psychotic experiences differed from that seen in adults

144 sample of 28 adolescents who did not report psychotic experiences drawn from a sample of 212 young p

145 Psychotic experiences in early life are associated with

146 first time that autistic traits and positive psychotic experiences interact with psychopathic tendenc

147 Psychotic experiences measured using the Psychosis Scree

148 ter focus on these phenotypes rather than on psychotic experiences might be required for prediction o

149 e symptoms and anxiety disorder but not with psychotic experiences or depression.

150 First-degree relatives of adults with psychotic experiences showed a small impairment on a mea

151 Only participants 50 years and older with psychotic experiences showed medium to large impairments

152 group participants, adolescents who reported psychotic experiences showed WM differences bilaterally

153 tion of psychopathic tendencies and positive psychotic experiences was associated with improved perfo

154 Psychotic experiences were assessed using a semistructur

155 Psychotic experiences were especially prevalent among in

156 spondents with suicidal ideation, those with psychotic experiences were likely to make an attempt dur

157 Respondents reporting psychotic experiences were more likely to report concurr

158 als by comparing individuals with persistent psychotic experiences without a need for care with patie

159 Compared with the group without psychotic experiences, the 171 (9.7%) adults with psycho

160 n to balance for sex, insomnia severity, and psychotic experiences, to receive either eight sessions

161 hopathology, indicating some specificity for psychotic experiences.

162 ed for care with patients and people without psychotic experiences.

163 e induced experiences into participants' own psychotic experiences.

164 over 12% of NSAID FDC sales and 53% of anti-psychotic FDC sales.

165 ID, anti-depressant/benzodiazepine, and anti-psychotic FDCs were marketed; sales volumes were high.

166 Psychotic features were relatively rare and did not dist

167 t (<1 y) onset patients with BPD Type I with psychotic features, and 70 recent onset patients with SZ

168 upted in patients with major depression with psychotic features.

169 met criteria for high risk or first-episode psychotic illness (FEP; together: psychosis true positiv

170 fective disorder, bipolar disorder, or other psychotic illness according to the Swedish version of th

171 Although the association between psychotic illness and cigarette smoking is well known, t

172 implications for understanding expression of psychotic illness and herald the importance of whole-gen

173 family members, including schizophrenia and psychotic illness and suicidal behavior.

174 of three available relatives affected with a psychotic illness and three available unaffected relativ

175 ferring vulnerability for the development of psychotic illness is still unknown.

176 The current definitions of psychotic illness lack biological validity, motivating a

177 ge range, 40-70 years; mean [SD] duration of psychotic illness, 24 [11] years), 26 were randomized to

178 In those who developed psychotic illness, this decline was significantly steepe

179 duals deemed to be potentially prodromal for psychotic illness.

180 might represent a key step in the pathway to psychotic illness.

181 NK3 locus in bipolar disorder, a major human psychotic illness.

182 of psychosis and an earlier age at onset of psychotic illness.

183 s associated with an earlier age at onset of psychotic illness.

184 at is distinct from that implicated in frank psychotic illness.

185 with, or at high risk of developing, a first psychotic illness.

186 l IQ trajectories and the risk of subsequent psychotic illness.

187 a connectome signature of familial risk for psychotic illness.

188 mptoms can be used to predict later onset of psychotic illness.

189 as a tool for identifying those at risk for psychotic illness.

190 irmed using OPCRIT [operational criteria for psychotic illness].

191 to reduce the overall burden associated with psychotic illnesses.

192 treating the biology of both depressive and psychotic illnesses.

193 esses and associated microglia activation in psychotic illnesses.

194 pathophysiology of the acute early phase of psychotic illnesses.

195 unctioning did not differ from that of never-psychotic individuals at 20 years, but the other groups

196 ulsivity, inattention, conduct problems, and psychotic-like experiences (eg, paranoid thoughts or cog

197 mpus/amygdala, when controlling for baseline psychotic-like experiences and cannabis use.

198 study investigated the neural correlates of psychotic-like experiences in youths during tasks involv

199 lative to control subjects, youths reporting psychotic-like experiences showed increased hippocampus/

200 rom London and Dublin sites were assessed on psychotic-like experiences, and those reporting signific

201 ith other hits, a risk factor for developing psychotic-like symptoms in adulthood.

202 Patients with major depression with psychotic major depression (PMD) and with nonpsychotic m

203 y was significantly reduced in patients with psychotic major depression.

204 Remission was defined as the absence of psychotic, manic, and severe depressive symptoms for at

205 hypofunction was described in patients with psychotic manifestations who exhibited autoantibodies bi

206 Finally, we show that anti-psychotic medications dose-dependently increase claudin-

207 ts with schizophrenia spectrum disorders and psychotic mood disorders, and associations of the empiri

208 We excluded actively psychotic or demented people, those with both suicidal i

209 a for alcohol dependence, with no concurrent psychotic or manic symptoms, no use of concurrent psycho

210 Altered states of consciousness, such as psychotic or pharmacologically-induced hallucinations, p

211 Associations between cannabis use and psychotic outcomes are consistently reported, but establ

212 We unveil that NMDAR-Ab from psychotic patients alter NMDAR synaptic transmission, su

213 resolution scanners, small sample sizes, and psychotic patients being on antipsychotics or not being

214 odies to D2R or NR1 were detected in 8 of 43 psychotic patients but not detected in any of 43 control

215 ate NMDA receptor (NMDAR-Ab) in about 20% of psychotic patients diagnosed with schizophrenia and very

216 rtical microcircuitry changes in brains from psychotic patients, and suggesting disinhibition.

217 e to antipsychotic drug treatment in acutely psychotic patients.

218 that bullying is associated with individual psychotic phenomena and with psychosis, and predicts the

219 e phospholipase-C inhibitor U73122, and anti-psychotic phenothiazines.

220 Other conditions represented were psychotic, posttraumatic stress or anxiety, somatoform,

221 Psychotic relapse and control of breakthrough psychotic

222 roups did not differ significantly regarding psychotic relapse, psychotic symptom control, or hospita

223 tive symptoms at moderate to severe, but not psychotic, severity levels.

224 ceptors may have preferential involvement in psychotic states produced by ketamine.

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

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

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

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

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

230 =11.1; P = .003) and control of breakthrough psychotic symptoms (beta = 0.2; t79 = 2.1; P = .04).

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

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

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

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

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

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

237 Both positive psychotic symptoms and anhedonia are associated with str

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

268 The severity of psychotic symptoms was assessed using the Comprehensive

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

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

271 0 F20-29) or affective disorder (F30-39 with psychotic symptoms), and had enduring auditory verbal ha

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

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

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

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

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

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

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

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

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

281 Psychotic symptoms, defined as the occurrence of delusio

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

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

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

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

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

287 ulation on the pathophysiologic mechanism of psychotic symptoms.

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

289 scent will experience persistent subclinical psychotic symptoms.

290 risk of developing subclinical and clinical psychotic symptoms.

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

292 the latter contributing directly to positive psychotic symptoms.

293 version for the subjects who developed fully psychotic symptoms.

294 action of antipsychotic drugs in alleviating psychotic symptoms.

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

296 the transition from anomalous experiences to psychotic symptoms.

297 sychotic relapse and control of breakthrough psychotic symptoms.

298 pulsive and aggressive behaviors rather than psychotic symptoms.

299 on depression, anxiety, substance abuse, and psychotic syndromes, with emphasis on the need to do fur

300 ee (19%) approved, 13 (81%) unapproved; anti-psychotics: ten formulations, three (30%) approved, seve