コーパス検索結果 (１語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 lly defined suspected PEs, definite PEs, and psychotic disorder.
2 subjects clinically at risk of developing a psychotic disorder.
3 q11DS, 55 (13.4%) were diagnosed as having a psychotic disorder.
4 unded yet tenacious beliefs and a symptom of psychotic disorder.
5 spectively identify patients at high risk of psychotic disorder.
6 se who do and do not convert to a full-blown psychotic disorder.
7 Schizophrenia is currently classified as a psychotic disorder.
8 participants were known to have developed a psychotic disorder.
9 ted with a later diagnosis of a nonaffective psychotic disorder.
10 eneral population and examined prediction of psychotic disorder.
11 with at least two siblings suffering from a psychotic disorder.
12 n, bipolar disorder, schizophrenia, or other psychotic disorder.
13 nical risk for psychosis and 22 with a frank psychotic disorder.
14 Both carriers had a diagnosis of a psychotic disorder.
15 of cannabis use carried the highest odds for psychotic disorder.
16 017, on incidence of non-organic adult-onset psychotic disorder.
17 ults with and without a previously diagnosed psychotic disorder.
18 bute to variations in the incidence rates of psychotic disorder.
19 cting later hospitalization for nonaffective psychotic disorder.
20 ith later hospitalization for a nonaffective psychotic disorder.
21 an unmet need for care in young people with psychotic disorders.
22 ture of schizophrenia and is common in other psychotic disorders.
23 ctive study of first-admission patients with psychotic disorders.
24 and Related Health Problems, Tenth Revision psychotic disorders.
25 eptor hypofunction in the pathophysiology of psychotic disorders.
26 mechanism underlies cognitive impairment in psychotic disorders.
27 tervention and the personalized treatment of psychotic disorders.
28 ted to the underlying familial diathesis for psychotic disorders.
29 le evidence that the thalamus is abnormal in psychotic disorders.
30 l categorization schemes for differentiating psychotic disorders.
31 al characteristic of schizophrenia and other psychotic disorders.
32 e that cannabis use can increase the risk of psychotic disorders.
33 nditions: post-traumatic stress disorder and psychotic disorders.
34 escence, is important in the pathogenesis of psychotic disorders.
35 ssessment and management in individuals with psychotic disorders.
36 on to baseline cannabis use and diagnosis of psychotic disorders.
37 e have increased prevalence in patients with psychotic disorders.
38 ce of persecutory delusions in patients with psychotic disorders.
39 psychophysiological alterations observed in psychotic disorders.
40 ups of disorders, the neurodevelopmental and psychotic disorders.
41 se, and type of cannabis used on the risk of psychotic disorders.
42 ffected the association between cannabis and psychotic disorders.
43 tanding of common mechanisms between FTD and psychotic disorders.
44 e of 5-HT2B receptors in the neurobiology of psychotic disorders.
45 e pathophysiology of schizophrenia and other psychotic disorders.
46 malities reported in adults with established psychotic disorders.
47 ween epigenetics and schizophrenia and other psychotic disorders.
48 ls of neural noise have been demonstrated in psychotic disorders.
49 number of autoimmune diseases in people with psychotic disorders.
50 etting the stage for vulnerability for later psychotic disorders.
51 ajor psychiatric disorders, particularly for psychotic disorders.
52 tions in the hippocampus were evident across psychotic disorders.
53 e underlying mechanism and for prevention of psychotic disorders.
54 help elucidate etiological underpinnings of psychotic disorders.
55 but remain less well characterized in other psychotic disorders.
56 re detectable in a subgroup of patients with psychotic disorders.
57 ith the lack of friendships in patients with psychotic disorders.
58 pression, posttraumatic stress disorder, and psychotic disorders.
59 ball responses among patients with different psychotic disorders.
60 ciated with increased risk for affective and psychotic disorders.
61 ed to be a pathophysiological contributor to psychotic disorders.
62 ed dopamine synthesis capacity to particular psychotic disorders.
63 misdiagnosed in the United States as primary psychotic disorders.
64 delusions are a common symptom of a range of psychotic disorders.
65 es predisposing to schizophrenia and related psychotic disorders.
66 tially targeted by schizophrenia and related psychotic disorders.
67 sample included 116 offspring with confirmed psychotic disorders.
68 n early feature of schizophrenia and related psychotic disorders.
69 anisms of insulin signaling abnormalities in psychotic disorders.
70 nnish population, increasing risk broadly to psychotic disorders.
71 personality, affective or non-schizophrenia psychotic disorders.
72 WM and neuropsychological functioning across psychotic disorders.
73 an immune-based component to the etiology of psychotic disorders.
74 escence is associated with increased risk of psychotic disorders.
76 c minorities were also at excess risk of all psychotic disorders (1.75 [1.53-2.00]), including non-af
77 otypes consortium included 326 probands with psychotic disorders (107 with schizophrenia (SZ), 87 wit
78 is study of 304 adults at ultrahigh risk for psychotic disorders, 153 (50.3%) received omega-3 PUFAs
79 1.28-2.27; p<0.0001), being diagnosed with a psychotic disorder (2.18, 1.95-2.44; p<0.0001) or bipola
80 continuum model of cognitive dysfunction in psychotic disorders, 3) reports familiality of cognitive
81 ssment was lower in patients who developed a psychotic disorder (65.5 [12.0]) compared with those wit
83 bis use with the strongest effect on odds of psychotic disorder across Europe and explore whether dif
87 S for schizophrenia predicted progression to psychotic disorders (adjusted hazard ratio=1.10, 95% CI=
88 ed hazard ratio=5.02, 95% CI=3.53, 7.14) and psychotic disorders (adjusted hazard ratio=1.63, 95% CI=
89 n, and deprivation on risk of developing any psychotic disorder, all with qualitative patterns of int
90 en thought to be critical in the etiology of psychotic disorders, although the differential roles pla
91 dysfunction has often been reported in other psychotic disorders, although there are inconsistencies
92 ility and progression to bipolar disorder or psychotic disorders among individuals diagnosed with uni
93 ease in the risk of having a broadly defined psychotic disorder, an almost 8.5-fold increase in the r
94 tive data were obtained on 240 patients with psychotic disorder and 178 healthy control participants
95 ychotic-naive patients with schizophrenia or psychotic disorder and 51 healthy control subjects under
96 ical psychotic symptoms), 50 patients with a psychotic disorder and auditory verbal hallucinations, a
99 pocampal hypermetabolism leads to atrophy in psychotic disorder and suggest glutamate as a pathogenic
100 s between those who subsequently developed a psychotic disorder and those who did not was distinguish
101 e role of oxytocin in the pathophysiology of psychotic disorders and addictions and to extend clinica
104 eripheral inflammatory marker alterations in psychotic disorders and establish clinical, neurocogniti
105 plications for understanding the etiology of psychotic disorders and for informing social policy.
106 t differ significantly between patients with psychotic disorders and healthy control subjects (F(1,62
107 ing study in a large series of probands with psychotic disorders and healthy volunteers as part of th
108 Implications for treatment of parents with psychotic disorders and high-risk children are discussed
109 syndrome confers particularly high risk for psychotic disorders and is thus an important translation
111 are utilized extensively in the treatment of psychotic disorders and other psychiatric conditions, bu
112 s mortality; 2) mortality among persons with psychotic disorders and the extent to which cannabis use
113 ations for understanding the pathogenesis of psychotic disorders and the specific deficits that seem
115 road array of intermediate phenotypes across psychotic disorders and to test the hypothesis that inte
117 associated with greater risk of developing a psychotic disorder (and other mental disorders), highlig
120 , delusional disorder, or affective-spectrum psychotic disorder, and psychotic symptoms scoring at le
121 ith schizophrenia, 45 individuals with other psychotic disorders, and 33 healthy control subjects.
122 familiality of cognitive impairments across psychotic disorders, and 4) evaluates cognitive impairme
123 ble death, especially among individuals with psychotic disorders, and may also be common among noncli
124 tancy for up to 20-30 years in patients with psychotic disorders, and prognostic biomarkers are gener
125 apacity (DSC) of patients with SZ, DD, other psychotic disorders, and the DSC of healthy subjects.
126 their characterization across patients with psychotic disorders, and their potential alterations in
128 mic-pituitary-adrenal activity indicate that psychotic disorders are associated with elevated cortiso
137 nding the basis for deficient PPI and MMN in psychotic disorders, as reduced NMDA activity is implica
138 nd is thought to be dysregulated in mood and psychotic disorders, as well as in various phases of opi
143 092 individuals (0.95%) not diagnosed with a psychotic disorder at the time of examination were hospi
144 requency of experiences at age 12 predicting psychotic disorders at age 18 ranged from 5.5% to 22.8%.
146 experiences (PE; n=20) at increased risk for psychotic disorders; (b) people with extremely elevated
147 e is associated with increased risk of later psychotic disorder but whether it affects incidence of t
148 ourse, cognitive deficits are present in all psychotic disorders but are most severe and pervasive in
149 nt dopamine antagonist that is used to treat psychotic disorders, but 50% of treated patients develop
150 ugs (SGAs) are essential in the treatment of psychotic disorders, but are well-known for inducing sub
151 ons of whole-brain networks in patients with psychotic disorders, but not in their unaffected relativ
152 s of violence are increased in patients with psychotic disorders, but the contribution of triggers fo
153 ound an excess mortality among subjects with psychotic disorders, but the level did not differ betwee
154 pothesis that cannabis increases the risk of psychotic disorders by inducing the same dopaminergic al
155 We found marked variation in incidence of psychotic disorders by personal characteristics and plac
156 le participants were patients with diagnosed psychotic disorders (clinical group) and adults in the g
159 is use was associated with increased odds of psychotic disorder compared with never users (adjusted o
160 abis every day conferred the highest risk of psychotic disorders compared with no use of cannabis (ad
162 FPN exhibit evidence of accelerated aging in psychotic disorders, confirm associations between networ
163 logy is complexity; core aspects of mood and psychotic disorders consistently coexist within individu
168 ata for age, sex, ethnicity, marital status, psychotic disorder diagnosis, subsequent hospital admiss
172 efficiency was also significantly reduced in psychotic disorders (F3,587 = 4.01, P = .008) and positi
173 in an epidemiologically defined cohort with psychotic disorders followed for 20 years after first ho
177 y control participants and 375 patients with psychotic disorders from the Bipolar-Schizophrenia Netwo
178 S = 1.40, corrected p = 0.003) and the other psychotic disorder group (ES = 1.34, corrected p = 0.004
180 sorders, schizophrenia, and nonschizophrenic psychotic disorders) had substantially increased risks o
181 elevated dopamine synthesis capacity once a psychotic disorder has developed, little is known about
182 tent methamphetamine psychosis and a primary psychotic disorder has grown increasingly important.
187 general population, individuals with severe psychotic disorders have increased risks for smoking (od
188 ng-term trajectories of social impairment in psychotic disorders have rarely been studied systematica
189 These data indicate that DD, SZ, and other psychotic disorders have similar dysregulated mechanisms
190 th more severe mental illnesses (eg, primary psychotic disorders) having the largest effect sizes eve
191 clinical conditions including behavioral and psychotic disorders; hence its fast detection in clinica
194 the development of psychotic experiences and psychotic disorders in a large population-based sample o
195 during pregnancy increases offspring risk of psychotic disorders in adulthood, and that the magnitude
196 e calculated an overall relative risk of new psychotic disorders in daily smokers versus non-smokers
198 ancy is associated with an elevated risk for psychotic disorders in offspring and that the associatio
199 symptoms of patients later hospitalized for psychotic disorders in primary mental health outpatient
200 comorbidity between substance use and severe psychotic disorders in the Genomic Psychiatry Cohort.
205 Diabetes is highly prevalent in people with psychotic disorders, including schizophrenia and schizoa
208 from brain imaging studies of patients with psychotic disorders indicates increased neural activity
211 even after accounting for family history of psychotic disorders, internalizing symptoms, and cogniti
212 duals who may develop schizophrenia or other psychotic disorders is critical for predicting psychosis
213 etes pharmacotherapy and drug management for psychotic disorders is essential, irrespective of whethe
216 he general cognitive deficit observed across psychotic disorders is similarly associated with functio
217 th concern associated with schizophrenia and psychotic disorders is the long-term disability that inv
218 ercular agent and key medicine used to treat psychotic disorders, is able to disrupt pH gradients acr
219 ffective acute treatment for severe mood and psychotic disorders, it remains controversial because of
220 prevent the onset of schizophrenia and other psychotic disorders, longitudinal high-risk research on
221 psychiatric disorders and that patients with psychotic disorders may develop dementia more often than
222 t is unique to schizophrenia or is common to psychotic disorders more broadly, and its associations w
224 N=37), depressive psychosis (N=39), or other psychotic disorders (N=46) following index presentation,
226 (ASD) are at increased risk for nonaffective psychotic disorder (NAPD) or bipolar disorder (BD) is un
227 of neighbourhood variations of non-affective psychotic disorders (NAPD) have focused mainly on incide
228 raumatic stress disorder, schizophrenia, and psychotic disorders) not diagnosed during the 5-year per
229 eater than twofold increased likelihood of a psychotic disorder (odds ratio = 2.18 [95% confidence in
230 ntly increased risk for the development of a psychotic disorder (odds ratio = 2.49; 95% CI, 1.24-5.00
234 uals, including 210 diagnosed with a primary psychotic disorder or affective psychosis (bipolar disor
236 ued because of an adverse event (four due to psychotic disorder or hallucination within 10 days of st
237 erlie the propensity of stress to exacerbate psychotic disorders or predispose an individual to drug-
239 upport an overall change in the incidence of psychotic disorder over time, though diagnostic shifts (
241 r = 0.35; p < 0.05), but not transition to a psychotic disorder (p = 0.22), and was not significantly
242 eir patients with schizophrenia or a related psychotic disorder participated in a European multi-cent
245 e compared between 243 control subjects, 388 psychotic disorder probands, and 300 of their first-degr
246 ing hypothesis for schizophrenia and related psychotic disorders proposes that cortical brain disrupt
247 Of the remaining patients, nine developed a psychotic disorder (psychotic transition group) and 15 d
249 en reported in a proportion of patients with psychotic disorders, raising hopes for more appropriate
251 utoantibodies against glutamatergic NMDAR in psychotic disorders remains controversial, with detectio
252 risk for progression to bipolar disorder or psychotic disorders, respectively, among individuals dia
255 cts of organic-induced and substance-induced psychotic disorder show that our diagnostic classificati
258 gnificantly mediated the association between psychotic disorder status and general cognition (beta =
262 ences differed from that seen in adults with psychotic disorders, suggesting important differences be
263 subthreshold PSs and individuals with overt psychotic disorders support the notion of a psychosis co
264 to dissecting the genetic basis of mood and psychotic disorders that can inform future large-scale c
265 immune response in schizophrenia and related psychotic disorders that, we think, will be of interest
266 hizophrenia-associated CNVs in patients with psychotic disorders, their unaffected relatives and cont
267 previous diagnosis of schizophrenia or other psychotic disorder, those with glomerular disease, tubul
268 ioning, but few studies have linked risk for psychotic disorders to a neural measure evoked during a
269 nt knowledge linking schizophrenia and other psychotic disorders to epigenetics, based on PubMed and
270 ng clinical utility of antipsychotics beyond psychotic disorders to include depressive, bipolar, and
271 amination were hospitalized for nonaffective psychotic disorder up to 9 years after the index examina
272 of 109 individuals (2.8%) met criteria for a psychotic disorder up to age 24, of whom 70% had sought
273 D IMPLICATIONS OF KEY FINDINGS: Incidence of psychotic disorders varied markedly by age, sex, place a
275 or bipolar disorder, schizophrenia, or other psychotic disorder was recorded on at least one inpatien
277 Severity of cognitive impairments across psychotic disorders was consistent with a continuum mode
279 cohort of 470 first-admission patients with psychotic disorders was systematically assessed at basel
280 voluntary hospitalisation and diagnosis of a psychotic disorder were factors associated with the grea
281 replication; psychotic experiences (PEs) and psychotic disorder were measured by a semistructured int
283 risks of progression to bipolar disorder and psychotic disorders were 7.3% and 13.8%, respectively.
286 2, positive predictive values for predicting psychotic disorders were too low to offer real potential
287 represent candidates that may be causal for psychotic disorders when considered in the context of th
288 dorsal ACC are involved in schizophrenia and psychotic disorder, whereas increased glutamate levels i
289 tern of cortical thinning as patients with a psychotic disorder, which is suggestive of a similar, bu
290 ssments to subjects with major depressive or psychotic disorders who had at least moderate depression
291 n a generalizability cohort of patients with psychotic disorders who were hospitalized for an acute p
292 ded a sample of patients with a pre-existing psychotic disorder with a follow-up duration of at least
294 s not associated with an increased risk of a psychotic disorder, with lifetime cannabis use, or with
295 The UHR patients are at long-term risk for psychotic disorder, with the highest risk in the first 2
296 the hippocampal subfields were seen in all 3 psychotic disorders, with the most prominent differences
297 ed risk for hospitalization for nonaffective psychotic disorder within 14 days after examination (haz
299 ed on current clinical criteria convert to a psychotic disorder within a 2.5-year follow-up period.
300 en who had never been hospitalized, men with psychotic disorders without a personality disorder or a