ライフサイエンスコーパス: psychotic

1 Examining the neurobiology of the psychotic-affective spectrum may greatly advance biologi

2 o Hecker, included more emphasis on positive psychotic and catatonic symptoms and severe dementia.

3 ment of core psychiatric symptoms, including psychotic and impulsivity symptoms, may be beneficial am

4 of psychotropic drug treatment each improved psychotic and mood symptoms in placebo-controlled trials

5 t antibiotics, two anti-epileptics, one anti-psychotic, and one anti-inflammatory medication.

6 middle temporal gyrus, and individuals with psychotic BD did not show significant differences from h

7 ith schizoaffective disorder (SAD), 132 with psychotic bipolar disorder (BD)), 315 of their nonpsycho

8 wed significantly lower activation than both psychotic bipolar disorder and healthy groups.

9 ches; 2) determine whether schizophrenia and psychotic bipolar disorder exhibit similar abnormalities

10 Both schizophrenia and psychotic bipolar disorder groups showed encoding- and m

11 is probands (Schizophrenia spectrum, n = 79; Psychotic Bipolar disorder, n = 61) and matched healthy

12 been well characterized in schizophrenia and psychotic bipolar disorder.

13 striatum differed between schizophrenia and psychotic bipolar disorder; individuals with schizophren

14 opamine synthesis in transdiagnoses of these psychotic conditions.

15 s-sectional sample of patients with remitted psychotic depression (n = 86) collected to date.

16 nts aged 18 years or older had an episode of psychotic depression acutely treated with sertraline plu

17 ral brain networks in patients with remitted psychotic depression and brain-behavior relationships we

18 elatively few studies on the neurobiology of psychotic depression have been pursued.

19 Neuroimaging studies investigating psychotic depression have provided evidence for distribu

20 ticipated in the Study of Pharmacotherapy of Psychotic Depression II randomized controlled trial.

21 Among patients with psychotic depression in remission, continuing sertraline

22 g antipsychotic medication for patients with psychotic depression in remission.

23 Psychotic depression is a severely disabling and potenti

24 were collected at the time of recurrence of psychotic depression or sustained remission.

25 We compared patients with remitted psychotic depression to healthy controls and found that

26 depressive disorder with psychotic features (psychotic depression) is a severe disorder.

27 1.28-2.27; p<0.0001), being diagnosed with a psychotic disorder (2.18, 1.95-2.44; p<0.0001) or bipola

28 associated with greater risk of developing a psychotic disorder (and other mental disorders), highlig

29 r = 0.35; p < 0.05), but not transition to a psychotic disorder (p = 0.22), and was not significantly

30 bis use with the strongest effect on odds of psychotic disorder across Europe and explore whether dif

31 o the striking variation in the incidence of psychotic disorder across the 11 studied sites.

32 en such patterns and the incidence rates for psychotic disorder across the study sites.

33 tive data were obtained on 240 patients with psychotic disorder and 178 healthy control participants

34 ychotic-naive patients with schizophrenia or psychotic disorder and 51 healthy control subjects under

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

36 n those with schizophrenia and those with no psychotic disorder at age >=25 years.

37 Prediction of current psychotic disorder at age 24 (N=47, 1.2%), by both self-

38 e is associated with increased risk of later psychotic disorder but whether it affects incidence of t

39 is use was associated with increased odds of psychotic disorder compared with never users (adjusted o

40 Both psychotic disorder diagnosis and dimensionally measured

41 S = 1.40, corrected p = 0.003) and the other psychotic disorder group (ES = 1.34, corrected p = 0.004

42 uals, including 210 diagnosed with a primary psychotic disorder or affective psychosis (bipolar disor

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

44 of 109 individuals (2.8%) met criteria for a psychotic disorder up to age 24, of whom 70% had sought

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

46 voluntary hospitalisation and diagnosis of a psychotic disorder were factors associated with the grea

47 The adjusted incident rates for psychotic disorder were positively correlated with the p

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

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

50 dorsal ACC are involved in schizophrenia and psychotic disorder, whereas increased glutamate levels i

51 n, bipolar disorder, schizophrenia, or other psychotic disorder.

52 nical risk for psychosis and 22 with a frank psychotic disorder.

53 Both carriers had a diagnosis of a psychotic disorder.

54 of cannabis use carried the highest odds for psychotic disorder.

55 017, on incidence of non-organic adult-onset psychotic disorder.

56 ults with and without a previously diagnosed psychotic disorder.

57 bute to variations in the incidence rates of psychotic disorder.

58 cting later hospitalization for nonaffective psychotic disorder.

59 ith later hospitalization for a nonaffective psychotic disorder.

60 eneral population and examined prediction of psychotic disorder.

61 0 [1.44-1.77]) than women, but not affective psychotic disorders (0.87 [0.75-1.00]).

62 c minorities were also at excess risk of all psychotic disorders (1.75 [1.53-2.00]), including non-af

63 otypes consortium included 326 probands with psychotic disorders (107 with schizophrenia (SZ), 87 wit

64 S for schizophrenia predicted progression to psychotic disorders (adjusted hazard ratio=1.10, 95% CI=

65 ed hazard ratio=5.02, 95% CI=3.53, 7.14) and psychotic disorders (adjusted hazard ratio=1.63, 95% CI=

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

67 Men were at higher risk of all psychotic disorders (incidence rate ratio 1.44 [1.27-1.6

68 Patients with recent-onset (<2 years) psychotic disorders (N=82) in early psychosis specialty

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

70 ility and progression to bipolar disorder or psychotic disorders among individuals diagnosed with uni

71 eripheral inflammatory marker alterations in psychotic disorders and establish clinical, neurocogniti

72 t differ significantly between patients with psychotic disorders and healthy control subjects (F(1,62

73 syndrome confers particularly high risk for psychotic disorders and is thus an important translation

74 Working memory (WM) is impaired in psychotic disorders and linked to functional outcome.

75 Patients with psychotic disorders are at high risk for type 2 diabetes

76 Schizophrenia and other psychotic disorders are highly debilitating psychiatric

77 We found marked variation in incidence of psychotic disorders by personal characteristics and plac

78 logy is complexity; core aspects of mood and psychotic disorders consistently coexist within individu

79 Individuals with psychotic disorders demonstrate evidence of accelerated

80 Brady Jr." from the "Psychotic Disorders Division, McLean Hospital, Harvard M

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

82 Neuroimaging studies of psychotic disorders have demonstrated abnormalities in s

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

84 These data indicate that DD, SZ, and other psychotic disorders have similar dysregulated mechanisms

85 during pregnancy increases offspring risk of psychotic disorders in adulthood, and that the magnitude

86 ancy is associated with an elevated risk for psychotic disorders in offspring and that the associatio

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

88 from brain imaging studies of patients with psychotic disorders indicates increased neural activity

89 The early course of illness in psychotic disorders is highly variable, and predictive b

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

91 ing hypothesis for schizophrenia and related psychotic disorders proposes that cortical brain disrupt

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

93 People with psychotic disorders show abnormalities in several organ

94 be transdiagnostic of the pathophysiology of psychotic disorders such as DD and SZ.

95 Compared with other psychotic disorders such as schizophrenia, relatively fe

96 subthreshold PSs and individuals with overt psychotic disorders support the notion of a psychosis co

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

98 nt knowledge linking schizophrenia and other psychotic disorders to epigenetics, based on PubMed and

99 The pooled incidence of all psychotic disorders was 26.6 per 100 000 person-years (9

100 ensive systematic review of the incidence of psychotic disorders was published in 2004.

101 risks of progression to bipolar disorder and psychotic disorders were 7.3% and 13.8%, respectively.

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

103 ssments to subjects with major depressive or psychotic disorders who had at least moderate depression

104 sed Whole Genome Sequencing of Affective and Psychotic Disorders" consortium.

105 st-episode psychosis (11 DD, 12 SZ, 12 other psychotic disorders) and 19 healthy controls.

106 th more severe mental illnesses (eg, primary psychotic disorders) having the largest effect sizes eve

107 raumatic stress disorder, schizophrenia, and psychotic disorders) not diagnosed during the 5-year per

108 tancy for up to 20-30 years in patients with psychotic disorders, and prognostic biomarkers are gener

109 apacity (DSC) of patients with SZ, DD, other psychotic disorders, and the DSC of healthy subjects.

110 their characterization across patients with psychotic disorders, and their potential alterations in

111 ugs (SGAs) are essential in the treatment of psychotic disorders, but are well-known for inducing sub

112 ons of whole-brain networks in patients with psychotic disorders, but not in their unaffected relativ

113 FPN exhibit evidence of accelerated aging in psychotic disorders, confirm associations between networ

114 even after accounting for family history of psychotic disorders, internalizing symptoms, and cogniti

115 ercular agent and key medicine used to treat psychotic disorders, is able to disrupt pH gradients acr

116 risk for progression to bipolar disorder or psychotic disorders, respectively, among individuals dia

117 hizophrenia-associated CNVs in patients with psychotic disorders, their unaffected relatives and cont

118 n early feature of schizophrenia and related psychotic disorders.

119 anisms of insulin signaling abnormalities in psychotic disorders.

120 nnish population, increasing risk broadly to psychotic disorders.

121 personality, affective or non-schizophrenia psychotic disorders.

122 WM and neuropsychological functioning across psychotic disorders.

123 an immune-based component to the etiology of psychotic disorders.

124 escence is associated with increased risk of psychotic disorders.

125 ween epigenetics and schizophrenia and other psychotic disorders.

126 re detectable in a subgroup of patients with psychotic disorders.

127 an unmet need for care in young people with psychotic disorders.

128 sample included 116 offspring with confirmed psychotic disorders.

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

130 clinical conditions including behavioral and psychotic disorders; hence its fast detection in clinica

131 Olanzapine is a second-generation anti-psychotic drug used to prevent neuroinflammation in pati

132 proportions in many countries and can induce psychotic episodes mimicking the clinical profile of sch

133 syndrome characterized by cerebellar ataxia, psychotic episodes, and obsessive behavior, as well as c

134 k was assessed by comparing the incidence of psychotic events 12 weeks before methylphenidate initiat

135 e incidence rate ratios (IRR) and 95% CIs of psychotic events after the initation of methylphenidate

136 birth, death, migration, medication use, and psychotic events for all eligible participants.

137 hylphenidate treatment increases the risk of psychotic events in adolescents and young adults, includ

138 The IRR of psychotic events in the 12-week period after initiation

139 ndividual design to compare the incidence of psychotic events in these individuals during the 12-week

140 We aimed to determine whether the risk of psychotic events increases immediately after initiation

141 disorder (ADHD), might increase the risk of psychotic events, particularly in young people with a hi

142 , 313 (8.1%, 95% CI=7.2, 9.0) had a definite psychotic experience since age 12.

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

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

145 els at age 12 among individuals who reported psychotic experiences (PEs) at age 18 (n = 64) were comp

146 The identification of early biomarkers of psychotic experiences (PEs) is of interest because early

147 Psychotic experiences affect more than 10% of children a

148 ratio=7.85, 95% CI=3.94, 15.63), but having psychotic experiences alone still marked a significantly

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

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

151 way in blood is associated with incidence of psychotic experiences and that these changes may reflect

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

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

154 elf-report and interviewer-rated measures of psychotic experiences at age 18 (PPVs, 2.9% and 10.0%, r

155 The authors investigated whether psychotic experiences at ages 11-12 predicted a psychiat

156 emographic and perinatal adversities and IQ, psychotic experiences at ages 11-12 predicted receiving

157 ever, longitudinal studies of the outcome of psychotic experiences based on unbiased information on m

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

159 he study results show a peak in incidence of psychotic experiences during late adolescence as well as

160 igated the incidence, course, and outcome of psychotic experiences from childhood through early adult

161 Psychotic experiences in childhood predict mental health

162 1,632 children ages 11-12 were assessed for psychotic experiences in face-to-face interviews.

163 study findings provide strong evidence that psychotic experiences in preadolescence index a transdia

164 The incidence rate of psychotic experiences increased between ages 13 and 24,

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

166 ealth settings) at baseline compared with no psychotic experiences or diagnosis at baseline (adjusted

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

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

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

170 Major depressive disorder with psychotic features (psychotic depression) is a severe di

171 a and 41 people with bipolar I disorder with psychotic features in order to: 1) characterize neural r

172 Psychotic features were relatively rare and did not dist

173 sis (schizophrenia and bipolar disorder with psychotic features) had an elevated masking threshold co

174 associated with emergence and persistence of psychotic features.

175 bjects and bipolar disorder patients without psychotic features.

176 CHR subjects who became psychotic had lower levels of ether phospholipids than C

177 mental disorders were schizophrenia or other psychotic illness (n=343 [65%]), bipolar disorder (n=115

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

179 Psychotic illness has consistently been associated with

180 Psychotic illness in 22q11DS was associated with more su

181 Psychotic illness in this highly penetrant deletion was

182 Psychotic illness is associated with cognitive control d

183 At 12 months, 17 (3%) deaths, one (<1%) psychotic illness, and one (<1%) case of bipolar disorde

184 re preferentially disrupted in patients with psychotic illness, but not patients without psychotic sy

185 as significantly greater in individuals with psychotic illness, regardless of the presence of the 22q

186 may peak at various points in the course of psychotic illness.

187 n the etiology and antipsychotic response in psychotic illness.

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

189 a connectome signature of familial risk for psychotic illness.

190 l microdeletion and a potent risk factor for psychotic illness.

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

192 es, which were affected by deletion size and psychotic illness.

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

194 Psychotic illnesses show variable responses to treatment

195 The presence of affective and psychotic illnesses was associated with graded disruptio

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

197 2 healthy control participants matched to 32 psychotic inpatients with SCZ-a state associated with co

198 acoustic startling reflex (PPI; a marker of psychotic-like behavior), memory, locomotor activity, an

199 had both (a) extreme levels of self-reported psychotic-like beliefs and experiences and (b) interview

200 20) who had average levels of self-reported psychotic-like beliefs and experiences.

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

202 Psychotic-like experiences (PLEs) during childhood are a

203 Psychotic-like experiences (PLEs) were assessed with the

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

205 In contrast, the Psychotic-like Experiences group had larger increases in

206 rum disorders-a Social Anhedonia group and a Psychotic-like Experiences group-and a control group, th

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

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

209 s impaired in healthy people who report more psychotic-like experiences.

210 = 75; 36 males, 39 females) with a range of psychotic-like experiences.

211 rning and inference are related to increased psychotic-like experiences.

212 ith anti-NMDAR encephalitis cause reversible psychotic-like features accompanied by changes (D1R decr

213 D1R) and dopamine 2 receptor (D2R) and cause psychotic-like features in mice.

214 The psychotic-like features, memory impairment, and changes

215 ta9-THC, individuals who developed transient psychotic-like symptoms (~70% of the sample) had signifi

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

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

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

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

220 sically unwell to attend clinic (bedridden), psychotic, or unable to give informed assent or consent.

221 ions is associated with an increased risk of psychotic outcomes, an effect on spatial working memory

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

223 pecific patient out of a group of unfamiliar psychotic patients.

224 ity of this circuit tracks the expression of psychotic phenomena across a broad spectrum of severity,

225 terature of patients with so-called isolated psychotic presentations (ie, with no, or minimal, neurol

226 Compared with healthy controls, psychotic probands showed decreased nodal efficiency mai

227 al dopamine autoregulation might precipitate psychotic relapse after antipsychotic discontinuation in

228 40% of the patients showed psychotic relapse after antipsychotic discontinuation.

229 Patients were monitored for psychotic relapse during 12 weeks after antipsychotic di

230 c symptoms of first-episode psychosis (FEP), psychotic relapse is common during the course of the ill

231 developing a strategy for the prevention of psychotic relapse related to antipsychotic discontinuati

232 whether this also holds for patients during psychotic remission.

233 ween network features and neurocognitive and psychotic scores was also assessed, revealing trends of

234 ansitions to schizophrenia usually came from psychotic-spectrum disorders.

235 ck in MAM rats, which may underlie the acute psychotic state often observed with switching to this tr

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

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

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

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

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

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

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

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

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

245 Both positive psychotic symptoms and anhedonia are associated with str

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

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

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

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

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

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

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

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

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

255 duals and follow individuals as subthreshold psychotic symptoms emerge.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

272 0 to 210; higher scores indicate more severe psychotic symptoms) at week 4.

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

274 0 F20-29) or affective disorder (F30-39 with psychotic symptoms), and had enduring auditory verbal ha

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

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

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

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

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

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

281 Psychotic symptoms, defined as the occurrence of delusio

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

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

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

285 sess the association with the development of psychotic symptoms.

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

287 activity, which underlies the development of psychotic symptoms.

288 ce for impaired sensorimotor predictions and psychotic symptoms.

289 th an additional emphasis on severe positive psychotic symptoms.

290 opamine projections to limbic regions causes psychotic symptoms.

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

292 psychotic illness, but not patients without psychotic symptoms.

293 oculomotor CD abnormalities and more severe psychotic symptoms.

294 action of antipsychotic drugs in alleviating psychotic symptoms.

295 the transition from anomalous experiences to psychotic symptoms.

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

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

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

299 t more frequent in subjects who later became psychotic than those who did not.

300 Recently, it has been proposed that psychotic traits may be linked to impaired predictive pr