ライフサイエンスコーパス: psychosis

1 viduals diagnosed with bipolar disorder with psychosis.

2 ntions and improve outcomes of first episode psychosis.

3 for 2 years from the onset of first-episode psychosis.

4 ond sample of 248 case subjects with chronic psychosis.

5 schizophrenia and subthreshold expression of psychosis.

6 rstood to play a part in the pathogenesis of psychosis.

7 uable window into mechanisms contributing to psychosis.

8 anization, are implicated in the etiology of psychosis.

9 ral connectivity predisposing individuals to psychosis.

10 consisted of suicidal or homicidal intent or psychosis.

11 luding three patients with hallucinations or psychosis.

12 overy therapy in patients with first-episode psychosis.

13 while holding constant the overall level of psychosis.

14 deficits are found prior to the onset of PD psychosis.

15 isk (UHR) for psychosis do not develop frank psychosis.

16 subcortex may be considered markers of early psychosis.

17 aturation processes associated with onset of psychosis.

18 are implicated in the disease progression of psychosis.

19 t for its association with schizophrenia and psychosis.

20 ehavior, and early, particularly attenuated, psychosis.

21 zation in children at familial high risk for psychosis.

22 l activation is not present in first-episode psychosis.

23 rmalities in white matter integrity in early psychosis.

24 help mitigate the harm from cannabis use in psychosis.

25 on cognitive impairment, mood disorders and psychosis.

26 most preventable risk factor for relapse of psychosis.

27 al correlates of thalamic dysconnectivity in psychosis.

28 ly susceptible to the effects of cannabis on psychosis.

29 s of metabolism may present after birth with psychosis.

30 line each contributed to individual risk for psychosis.

31 ntributions to the neurobiology of affective psychosis.

32 he onset of psychosis and risk of relapse of psychosis.

33 R 3.16; 95% CI 1.26-8.09) after the onset of psychosis.

34 wly hospitalized chronic patients with acute psychosis.

35 l target to improve outcome in patients with psychosis.

36 discontinued cannabis use after the onset of psychosis.

37 for those with shorter duration of untreated psychosis.

38 ce and insulin resistance, and first-episode psychosis.

39 o progressive dysregulation and the onset of psychosis.

40 eed for care, supporting cognitive models of psychosis.

41 ght to be at risk of psychosis or with early psychosis.

42 brain neurochemistry early in the course of psychosis.

43 or functional dysconnectivity in people with psychosis.

44 current 'predictive processing' theories of psychosis.

45 ene has been implicated in schizophrenia and psychosis.

46 derstanding of the developmental etiology of psychosis.

47 ays (SD 35 days) of a diagnosis of syndromal psychosis.

48 iated with dopaminergic dysfunction, such as psychosis.

49 and has been implicated in schizophrenia and psychosis.

50 pus of untreated patients with first-episode psychosis.

51 roximately 5% of patients with first-episode psychosis.

52 ch can lead to non-compliance and relapse of psychosis.

53 6 (3.6) years in 22 individuals with bipolar psychosis (13 male), 26.3 (4.4) years in 16 individuals

54 neteen untreated patients with first-episode psychosis (14 of them antipsychotic naive) and 20 health

55 s participated in the study (22 with bipolar psychosis [18 antipsychotic naive or free], 16 with schi

56 Among the persons with nonaffective psychosis, 184 (6.32%) had mothers with extremely inadeq

57 subjects were 46 patients with first-episode psychosis (20 with a schizophrenia spectrum disorder, 26

58 al and diagnostic criteria for first-episode psychosis (34.0 new cases per 100,000 person-years; 95%

59 is of first-episode non-organic or affective psychosis according to ICD-10 criteria, and were aged be

60 g 40 to 60% of individuals with AD (AD with psychosis (AD+P)).

61 In comparison with AD subjects without psychosis, AD+P subjects have more rapid cognitive decli

62 ed to treat schizophrenia, are used to treat psychosis, agitation and aggression in Alzheimer's disea

63 on receipt of such benefits in first-episode psychosis, along with the correlates and consequences of

64 abetic states in patients with first-episode psychosis alongside matched controls.

65 we enrolled 228 patients with first-episode psychosis and 105 healthy controls.

66 ger cohort of 63 first-episode patients with psychosis and 70 healthy matched controls to better unde

67 Seventy-six patients with a first episode of psychosis and 74 healthy controls were included.

68 ork connectivity as a distinctive feature of psychosis and aberrant intranetwork connectivity as a tr

69 omplished with a low risk of exacerbation of psychosis and adverse effects.

70 in two independent samples of patients with psychosis and argue against their progression in patient

71 lineated four factors (fear, anxious-misery, psychosis and behavioral symptoms) plus a general factor

72 analysis disclosed that status epilepticus, psychosis and cognitive dysfunction were statistically s

73 the pathogenic mechanism of 22q11DS-related psychosis and control its late onset.

74 Symptoms of psychosis and depression were established using question

75 information for the treatment of early-onset psychosis and highlights the importance of adverse event

76 apacity is elevated in bipolar disorder with psychosis and how this compares with schizophrenia and m

77 BF) in 52 individuals at ultra-high risk for psychosis and in 27 healthy volunteers.

78 hese have predictive value for conversion to psychosis and likelihood of violence in the future.

79 history of status epilepticus, diagnosis of psychosis and positron emission tomography or single-pho

80 She experienced ICU psychosis and postintensive care syndrome, but slowly re

81 and negative symptoms, periods of untreated psychosis and prodrome and premorbid adjustment.

82 t neuroinflammation is linked to the risk of psychosis and related disorders, as well as the expressi

83 en continued cannabis use after the onset of psychosis and risk of relapse of psychosis.

84 dopamine hyperstimulation is associated with psychosis and schizophrenia.

85 dopamine dysfunction in the pathoetiology of psychosis and suggest dopamine synthesis capacity as a p

86 dicating that they are at ultra high risk of psychosis and to determine whether microglial activity i

87 ted within the DLPFC with the development of psychosis and with functional outcome.

88 (988 Irish participants, including 798 with psychosis), and replication samples (528 UK patients wit

89 ludes effects of CBD on THC-induced anxiety, psychosis, and cognitive deficits.

90 ciated with cannabis use, such as addiction, psychosis, and cognitive impairment) than cannabis with

91 ted to our understanding of brain changes in psychosis, and could provide further insights into the n

92 eurocognitive tests to predict transition to psychosis, and determine if neurocognitive deficits are

93 d within 3.1 years after a substance-induced psychosis, and half the cases of conversion to bipolar d

94 the molecular architecture linking dopamine, psychosis, and psychosocial stress.

95 tive symptoms, side effects, exacerbation of psychosis, and responder rates were examined.

96 r evidence that 5alphaR mediates a number of psychosis- and mania-like complications of SD through im

97 p deprivation (SD) can trigger or exacerbate psychosis- and mania-related symptoms; the neurobiologic

98 omes and examine whether phases of untreated psychosis are linked with social network variables to de

99 t have been commonly reported in adults with psychosis are present early in life in youth with PS sym

100 tipsychotic treatment choices for paediatric psychosis are urgently needed because extrapolations fro

101 (in individuals with no previous history of psychosis) are reviewed.

102 gulate cortex of patients with first-episode psychosis as compared with healthy control subjects.

103 cribed amisulpride (25-75 mg daily) to treat psychosis as part of an open study (n = 28; 69-92 years;

104 (Gly) levels in patients with first-episode psychosis as well as age-matched healthy control subject

105 d bipolar disorder after a substance-induced psychosis, as well as risk factors for conversion.

106 d, we assessed 222 people with first-episode psychosis at entry into treatment using valid and reliab

107 is to screen all patients with first-episode psychosis at first presentation.

108 ho received a diagnosis of substance-induced psychosis between 1994 and 2014 (N=6,788); patients were

109 ts who presented with their first episode of psychosis between April 12, 2002, and July 26, 2013 had

110 Diminished social networks are common in psychosis but few studies have measured these comprehens

111 al surface area associated with a history of psychosis but no associations with mood state at the tim

112 compared to patients without early onset PD psychosis but no differences in cognitive, higher visual

113 earing voices) are typically associated with psychosis, but a minority of the general population also

114 ermediate phenotype with low effect size for psychosis, but GABA+/water measures do not fully support

115 nd Gly levels in patients with first-episode psychosis by means of echo time-averaged proton MRS at 4

116 METHOD: All new first-episode psychosis cases, 16-35 years old, presenting to early in

117 guing pattern of thalamic dysconnectivity in psychosis characterized by reduced prefrontal cortex (PF

118 sample of patients at clinical high risk for psychosis collected as part of the Early Detection, Inte

119 e impairment to seizures and, in rare cases, psychosis-collectively this is referred to as central ne

120 Psychosis commonly develops in adolescence or early adul

121 groups with very long duration of untreated psychosis confirm the need for earlier intervention or t

122 r tracts are recognized in people with early psychosis, consistent with dysconnectivity as a neuropat

123 scription can be optimized for first-episode psychosis, contributing to better outcomes with a lower

124 7-34.9) of patients with a substance-induced psychosis converted to either bipolar or schizophrenia-s

125 Patients had no history of drug abuse, psychosis, dementia/neurodegenerative diseases or medica

126 and expression data for 284 individuals with psychosis derived from a previously published randomised

127 rtion of individuals with a first episode of psychosis detected by ARMS services in secondary mental

128 olumes were significantly reduced across the psychosis dimension.

129 to further elucidate the progression of the psychosis disease state.

130 uals identified as ultra-high-risk (UHR) for psychosis do not develop frank psychosis.

131 of treatment, and long duration of untreated psychosis (DUP) is associated with poor clinical outcome

132 zation in patients at their first episode of psychosis, evaluating whether connectome-based descripti

133 Youths at clinical high risk (CHR) for psychosis exhibit similar, subtle symptoms to those with

134 Patients with first-episode psychosis experience psychotic symptoms for a mean of up

135 n comorbidities, functioning, cognition, and psychosis features across the full range of overall seve

136 Direct comparisons of psychosis features between 22q11DS and nondeleted (ND) i

137 ipsychotic-naive patients with first-episode psychosis (FEP) and 18 healthy control subjects complete

138 ns of GABA were analyzed in 41 first-episode psychosis (FEP) patients and 21 age- and sex-matched hea

139 In a clinical sample of first-episode psychosis (FEP) patients, we estimated the ability of PR

140 dysconnectivity in drug-naive first-episode psychosis (FEP).

141 ed 200 individuals at clinical high risk for psychosis for violent ideation and violent behavior usin

142 ject recruited first-admission patients with psychosis from all inpatient units of Suffolk County, Ne

143 35, p=0.012), an effect driven mainly by the psychosis groups.

144 91 (37%) of 245 patients with first-episode psychosis had a relapse over the 2 years of follow-up.

145 RPRETATION: Some patients with first-episode psychosis had antibodies against NMDAR that might be rel

146 Patients with first-episode psychosis had lower regional FA in multiple commissural,

147 s of cannabis who stopped after the onset of psychosis had the most favourable illness course with re

148 who were aged 16-35 years, had non-affective psychosis, had been clients of early intervention servic

149 though cannabis use after a first episode of psychosis has been associated with relapse, little is kn

150 bis use following the onset of first-episode psychosis has been linked to both increased risk of rela

151 Psychosis has been recognised as an abnormal state in ne

152 cial recovery in patients with first-episode psychosis; however, many individuals have continuing sev

153 r studies have estimated the heritability of psychosis in AD at 61%, but the underlying genetic sourc

154 c risk for schizophrenia and a lower risk of psychosis in AD.

155 data to inform antipsychotic prescribing for psychosis in Alzheimer's disease, the mechanisms underpi

156 receptor occupancy for optimal treatment of psychosis in Alzheimer's disease.

157 d outcome violent behavior and conversion to psychosis in at-risk individuals.

158 n ascertain the probability of conversion to psychosis in individual patients.

159 l health behaviour for people with suspected psychosis in Mid and North England.

160 ated with an increased risk for nonaffective psychosis in offspring (HR for BMI>/=17.0 and <18.5, 1.2

161 ated with an increased risk for nonaffective psychosis in offspring, consistent with historical studi

162 95% CI, 0.23-1.38) and risk for nonaffective psychosis in offspring.

163 e dopamine hyperfunction thought to underlie psychosis in patients.

164 postsynaptic factors in amphetamine-induced psychosis in SCH.

165 he detection of individuals who will develop psychosis in secondary mental health care is undetermine

166 The overall 6-year risk of psychosis in secondary mental health care was 3.02 (95%

167 g the need for transdiagnostic prediction of psychosis in secondary mental health care.

168 r tool for the transdiagnostic prediction of psychosis in secondary mental health care.

169 ulness for the transdiagnostic prediction of psychosis in secondary mental health care.

170 ation between antibody status and subsequent psychosis in the mothers.

171 vulnerable individuals) or trigger new-onset psychosis (in individuals with no previous history of ps

172 Pronounced variation in psychosis incidence, peaking before 20 years old, exists

173 Strategies for prevention of postpartum psychosis include lithium prophylaxis immediately postpa

174 present in both chronic and early stages of psychosis, includes reduced thalamic connectivity with t

175 ed with previous comprehensive first-episode psychosis interventions, NAVIGATE medication treatment i

176 Relapse, untreated psychosis, intolerable side effects and the lack of effe

177 nimal models suggest that the development of psychosis involves hyperactivity in the hippocampus that

178 uggests that dopamine abnormalities underlie psychosis, irrespective of diagnosis, implicating dopami

179 Psychosis is a common presenting feature in antibody-med

180 Schizophrenia-related psychosis is associated with disturbances in mesolimbic

181 nitive dysfunction in schizophrenia, whereas psychosis is associated with excessive dopamine release

182 e implicating neuropathology associated with psychosis is consistent with SZ being a circuit disorder

183 e outcomes in patients at ultrahigh risk for psychosis is dietary supplementation with long-chain ome

184 Substance-induced psychosis is strongly associated with the development of

185 link between cannabis use and development of psychosis is well established, less is known about the e

186 lopment of schizophrenia symptoms, including psychosis, later in life.

187 ices sites across England with first-episode psychosis, less than 6 weeks of treatment with antipsych

188 , particularly with reference to anxiety and psychosis-like symptoms.

189 alyses revealed thalamic hypoconnectivity in psychosis localized to dorsolateral PFC, medial PFC, and

190 (N = 12), methamphetamine dependence without psychosis (MA; N = 14) and healthy controls (N = 16).

191 Methamphetamine-associated psychosis (MAP) involves widespread neurocognitive and m

192 Genetic risk for psychosis may shape an individual's response to rewardin

193 ects of continued cannabis use on outcome in psychosis might be mediated through the effects of canna

194 nature of blood-brain barrier dysfunction in psychosis might be relevant to many aspects of disrupted

195 edications, age of illness onset, history of psychosis, mood state, age and sex differences on cortic

196 nly for a small proportion of transitions to psychosis (n = 52 of 1001; 5.19% in the derivation data

197 of 2876 AD subjects with (N=1761) or without psychosis (N=1115).

198 (n=40) and also those who developed clinical psychosis (n=12), compared with UHR subjects who remitte

199 of 2194 AD subjects with (N=734) or without psychosis (N=1460).

200 Postpartum psychosis offers an intriguing model to explore etiologi

201 Main Outcomes and Measures: Pretest risk of psychosis onset in individuals undergoing CHR assessment

202 mics of system change (eg, abrupt vs gradual psychosis onset), and determining the factors to which t

203 sk of relapse in the second year (Rt2) after psychosis onset.

204 05-0.46) but not in those with first-episode psychosis or chronic schizophrenia, whereas elevated Glx

205 ere followed up to the time of conversion to psychosis or last contact (up to 2 years).

206 olar disorder and/or a history of postpartum psychosis or mania according to DSM or ICD criteria or t

207 ely impaired, or who had bipolar disorder or psychosis or psychotic symptoms.

208 Patients with a history of psychosis or rapid-cycling bipolar disorder were exclude

209 t to which these alterations are specific to psychosis or represent a transdiagnostic feature of psyc

210 nificant transcriptome signatures related to psychosis or suicide.

211 alth state in those thought to be at risk of psychosis or with early psychosis.

212 arthritis increased the odds of subclinical psychosis (OR = 1.85; 95%CI = 1.72-1.99) and psychosis (

213 psychosis (OR = 1.85; 95%CI = 1.72-1.99) and psychosis (OR = 2.48; 95%CI = 2.05-3.01).

214 tional outcomes in people with first-episode psychosis, particularly in individuals not motivated to

215 e of maternal undernutrition in nonaffective psychosis pathogenesis.

216 re, we examined 16 drug-naive, first-episode psychosis patients and 16 healthy controls using PET and

217 Thirty-five first-episode psychosis patients, and 19 healthy controls, participate

218 connectivity in both chronic and early-stage psychosis patients.

219 l facial stimuli as a marker of the extended psychosis phenotype.

220 ain function and/or treatment in early-stage psychosis populations are needed.

221 esence of a suicidal plan, bipolar disorder, psychosis, posttraumatic stress disorder, substance depe

222 e (or decline) of psychopathology, including psychosis prediction, as well as to transdiagnostic emer

223 sity-based, outpatient programs studying the psychosis prodrome in North America.

224 y Detection, Intervention, and Prevention of Psychosis Program (EDIPPP).

225 Onset of psychosis proneness was similar among 22q11DS (mean: 11.

226 s in psychosis symptoms and age of onset for psychosis proneness; this continues to support the 22q11

227 Cognitive models of psychosis propose that appraisals (ie, the interpretatio

228 Parkinson's Disease (PD) psychosis refers to the spectrum of illusions, formed ha

229 e identified a network of schizophrenia- and psychosis-related genes, with more pronounced alteration

230 with six predictor variables in the NAPLS-2 psychosis risk calculator (unusual thoughts and suspicio

231 esents an external validation of the NAPLS-2 psychosis risk calculator using an independent sample of

232 sk patients converge to validate the NAPLS-2 psychosis risk calculator.

233 risk calculator was then used to generate a psychosis risk estimate for each case in the external va

234 maging and cerebrospinal fluid) and other PD psychosis risk factor data in patients who go on to deve

235 s most immediate uses will be in research on psychosis risk factors and in research-driven clinical (

236 ing against more rapid cognitive decline and psychosis risk in AD.

237 ive on the Structured Clinical Interview for Psychosis Risk Syndromes, which requires training to adm

238 bipolar disorder, N=50; schizophrenia, N=51; psychosis risk, N=39; and healthy control subjects, N=53

239 sed learning task specifically with elevated psychosis risk.

240 (22q11DS) is a promising model for studying psychosis risk.

241 behavior using the Structured Interview for Psychosis-Risk Syndromes (SIPS), and rated these accordi

242 ly significant association between increased psychosis RPS and reduced MID task performance (uncorrec

243 during follow-up, as well as a diagnosis of psychosis (RR=2.3 and 2.4, respectively; both p<0.001),

244 as performed in the setting of first-episode psychosis services in an inner-city area (London, Englan

245 years old, presenting to early intervention psychosis services in the East of England were identifie

246 in populations served by early intervention psychosis services.

247 since the introduction of early intervention psychosis services.

248 cipants; 1.57, 1.25-1.99, p=0.0001), greater psychosis severity (seven studies, 1494 participants; 1.

249 ficiently-wired connectome at first onset of psychosis show a better subsequent response to antipsych

250 nical high-risk individuals who converted to psychosis showed a steeper rate of cortical gray matter

251 iapine-ER versus aripiprazole in early-onset psychosis showed no significant group differences in sev

252 are present in association with less severe psychosis spectrum (PS) symptoms in youth.

253 Individuals on the psychosis spectrum (PS; n=19) and healthy young individu

254 morbid anxiety disorders were more likely in psychosis spectrum 22q11DS; substance-related disorders

255 Cognitive impairment occurs across the psychosis spectrum and is associated with functional out

256 on age and sex, stratifying for presence of psychosis spectrum disorder.

257 itis and mental health (depression spectrum, psychosis spectrum, anxiety, sleep disturbances and stre

258 eneral cognitive deficit observed across the psychosis spectrum.

259 in young healthy individuals and ones on the psychosis spectrum.

260 yperactivity disorder and conduct disorder), psychosis-spectrum symptoms, and fear (phobias).

261 The primary outcome was transition to psychosis status at 6 months.

262 ee relative with a history of schizophrenia, psychosis, suicide, depression, alcoholism, or autism (r

263 rarching similarities with ND individuals in psychosis symptoms and age of onset for psychosis pronen

264 Psychosis symptoms were related to reduced perfusion in

265 Accounting for higher overall psychosis symptoms, 22q11DS participants were still more

266 1, CI -4.74 to -1.21), duration of untreated psychosis (t=-0.86, p=0.031, CI -1.65 to -0.08) and prem

267 s users had a greater increase in relapse of psychosis than did both non-users (dCC-NC=0.36, 95% CI 0

268 ipsychotic naive patients with first-episode psychosis than in healthy matched controls.

269 specificity of white matter abnormalities in psychosis, their deviation from healthy aging, and the i

270 schizoaffective disorder worse than bipolar psychosis); this was not the case for biotypes.

271 , we further link claudin-5 suppression with psychosis through a distinct behavioural phenotype showi

272 Pooled analyses found first-episode psychosis to be related to insulin resistance (mean diff

273 s on persuading cannabis-using patients with psychosis to reduce use or shift to less potent forms of

274 for the conversion from a substance-induced psychosis to schizophrenia or bipolar disorder.

275 E, a comprehensive program for first-episode psychosis, to clinician-choice community care over 2 yea

276 course of blood-brain barrier alterations in psychosis, to determine whether blood-brain barrier dysf

277 children and adolescents with first-episode psychosis, to determine whether differences between the

278 lusions or as the initial phase of a unitary psychosis transitioning to mania and then dementia.

279 September 30, 2014, in 10 specialized early psychosis treatment services in Australia, Asia, and Eur

280 large cohort of patients with first-episode psychosis using classical cell-based assays in three lab

281 Individuals were evaluated for psychosis using the Structured Interview for Prodromal S

282 The 2-year probability of conversion to psychosis was 16%.

283 Cannabis use after onset of psychosis was assessed by self-reports in face-to-face f

284 A high risk for psychosis was associated with increased resting activity

285 e of psychosis within 2 years after onset of psychosis was defined as risk of subsequent admission to

286 is use over the first 2 years after onset of psychosis was investigated as a predictor variable for r

287 oved over time but the duration of untreated psychosis was not linked with the rate of improvement in

288 Self-harm after a substance-induced psychosis was significantly linked to a higher risk of c

289 se with no friends and duration of untreated psychosis was significantly longer for those with no fri

290 rientation dispersion and density imaging in psychosis, we found that processes compromising axonal f

291 eimer's disease and symptoms of agitation or psychosis were treated with risperidone for 16 weeks, af

292 th services and a diagnosis of non-affective psychosis, which are markers of severity of mental illne

293 r water increase during the first-episode of psychosis, which may be indicative of an acute neuroinfl

294 esent in individuals with a first episode of psychosis who have not been exposed to antipsychotic med

295 ured activity in patients with first-episode psychosis who received social recovery therapy plus earl

296 essing of ambiguous speech in people without psychosis who regularly hear voices.

297 dentify those patients at risk of developing psychosis who require an ARMS assessment and specialized

298 nversion rate was found for cannabis-induced psychosis, with 47.4% (95% CI=42.7-52.3) converting to e

299 th Revision diagnoses showed a lower risk of psychosis, with the exception of bipolar mood disorders

300 Relapse of psychosis within 2 years after onset of psychosis was de