Try a new search

Format these results:

Searched for:

person:qiw01

in-biosketch:true

Total Results:

16


Aberrant Resting-State Functional Connectivity of the Globus Pallidus Subregions in First-Episode Schizophrenia [Meeting Abstract]

Qi, W; Wen, Z; Chen, J; Wang, J; Milad, M; Goff, D C
Background: Functional abnormalities in the basal ganglia (BG) have been extensively reported in schizophrenia. Globus pallidus (GP), the output of BG, modulates excitatory and inhibitory pathways in the cortical-BG circuitry. We examined functional connectivity of GP subregions in first-episode schizophrenia (FES) in relation to psychotic symptoms and antipsychotic treatment response.
Method(s): Resting-state fMRI and clinical data were collected in 57 medication-naive FES participants and 63 healthy controls (HC) and repeated after 8 weeks in 28 FES and 35 HCs. We compared whole-brain connectivity of 8 subregions of the GP between groups after FDR-based multiple comparison correction and examined Spearman correlations between connectivity and symptoms before and after treatment.
Result(s): HCs displayed right anterior GPi (R-aGPi) negative connectivity that was absent in FES patients: differences between groups were significant in bilateral middle temporal gyrus, temporal pole, right inferior frontal gyrus, and left post-central gyrus. BPRS positive symptoms scores were positively correlated with R-aGPi connectivity with bilateral inferior temporal gyrus, temporal pole, right rostral anterior cingulate (rACC) and left orbital frontal gyrus. After antipsychotic treatment,R-aGPi connectivity decreased with right rACC, bilateral lateral occipital and cuneus cortex; these changes were associated with a decrease in BPRS positive symptoms.
Conclusion(s): Resting-state anticorrelated connectivity with R-aGPi might be necessary to maintain normal inhibition of the cortex. This function of the R-aGPi was impaired in FES patients, and the impairment was associated with positive symptoms. Restoring connectivity of the R-aGPi might be a mechanism to treat psychosis. Our findings provided important information for future applications of targeted treatment. Supported By: NIMH R01 MH084900 Keywords: First-episode Treatment-naive Schizophrenia, Globus Pallidus, Resting State Functional Connectivity, Treatment Mechanism
Copyright
EMBASE:2011560559
ISSN: 1873-2402
CID: 4857802

Association of Aripiprazole With Reduced Hippocampal Atrophy During Maintenance Treatment of First-Episode Schizophrenia

Wang, John; Hart, Kamber L; Qi, Wei; Ardekani, Babak A; Li, Chenxiang; Marx, Julia; Freudenreich, Oliver; Cather, Corinne; Holt, Daphne; Bello, Iruma; Diminich, Erica D; Tang, Yingying; Worthington, Michelle; Zeng, Botao; Wu, Renrong; Fan, Xiaoduo; Zhao, Jingping; Wang, Jijun; Goff, Donald C
PURPOSE/BACKGROUND/OBJECTIVE:Hippocampal volume loss in early schizophrenia has been linked with markers of inflammation and oxidative stress, and with less response of negative symptoms. Aripiprazole has been reported to preserve hippocampal volume and to reduce inflammation. METHODS/PROCEDURES/UNASSIGNED:Study 1 was a 12-month multicenter randomized placebo-controlled trial of citalopram added to clinician-determined second-generation antipsychotic medication in 95 patients with first-episode schizophrenia (FES), 19 of whom received aripiprazole. We compared participants taking aripiprazole with those on other antipsychotics to determine whether those on aripiprazole had less hippocampal volume loss. We also examined peripheral biomarker data from medication-naive patients with schizophrenia receiving 8 weeks of antipsychotic treatment (n = 24) to see whether markers of inflammation and oxidative stress that previously predicted hippocampal volume differed between aripiprazole (n = 9) and other antipsychotics (study 2). FINDINGS/RESULTS/UNASSIGNED:Aripiprazole was associated with a mean increase in hippocampal volume of 0.35% (SD, 0.80%) compared with a 0.53% decrease (SD, 1.2%) with other antipsychotics during the first year of maintenance treatment in patients with FES. This difference was significant after adjusting for age, sex, citalopram treatment, and baseline Brief Psychiatric Rating Scale score (B = 0.0079, P = 0.03). Aripiprazole was also associated with reduced concentrations of the inflammatory cytokines interleukin-8 and tumor necrosis factor (P < 0.01) during the first 8 weeks of treatment in medication-naive patients with FES. IMPLICATIONS/CONCLUSIONS/UNASSIGNED:These results suggest that aripiprazole may protect against hippocampal atrophy via an anti-inflammatory mechanism, but these results require replication in larger, randomized trials, and the clinical relevance of hippocampal volume loss is not established.
PMID: 33814546
ISSN: 1533-712x
CID: 4851232

Effect of citalopram on hippocampal volume in first-episode schizophrenia: Structural MRI results from the DECIFER trial

Qi, Wei; Blessing, Esther; Li, Chenxiang; Ardekani, Babak A; Hart, Kamber L; Marx, Julia; Freudenreich, Oliver; Cather, Corinne; Holt, Daphne; Bello, Iruma; Diminich, Erica D; Tang, Yingying; Worthington, Michelle; Zeng, Botao; Wu, Renrong; Fan, Xiaoduo; Troxel, Andrea; Zhao, Jingping; Wang, Jijun; Goff, Donald C
Hippocampal volume loss is prominent in first episode schizophrenia (FES) and has been associated with poor clinical outcomes and with BDNF genotype; antidepressants are believed to reverse hippocampal volume loss via release of BDNF. In a 12-month, placebo-controlled add-on trial of the antidepressant, citalopram, during the maintenance phase of FES, negative symptoms were improved with citalopram. We now report results of structural brain imaging at baseline and 6 months in 63 FES patients (34 in citalopram group) from the trial to assess whether protection against hippocampal volume loss contributed to improved negative symptoms with citalopram. Hippocampal volumetric integrity (HVI) did not change significantly in the citalopram or placebo group and did not differ between treatment groups, whereas citalopram was associated with greater volume loss of the right CA1 subfield. Change in cortical thickness was associated with SANS change in 4 regions (left rostral anterior cingulate, right frontal pole, right cuneus, and right transverse temporal) but none differed between treatment groups. Our findings suggest that minimal hippocampal volume loss occurs after stabilization on antipsychotic treatment and that citalopram's potential benefit for negative symptoms is unlikely to result from protection against hippocampal volume loss or cortical thinning.
PMID: 33857750
ISSN: 1872-7506
CID: 4851292

Correction to: Evaluating a screener to quantify PTSD risk using emergency care information: a proof of concept study

van der Mei, Willem F; Barbano, Anna C; Ratanatharathorn, Andrew; Bryant, Richard A; Delahanty, Douglas L; deRoon-Cassini, Terri A; Lai, Betty S; Lowe, Sarah R; Matsuoka, Yutaka J; Olff, Miranda; Qi, Wei; Schnyder, Ulrich; Seedat, Soraya; Kessler, Ronald C; Koenen, Karestan C; Shalev, Arieh Y
An amendment to this paper has been published and can be accessed via the original article.
PMID: 32600263
ISSN: 1471-227x
CID: 4514932

Evaluating a screener to quantify PTSD risk using emergency care information: a proof of concept study

van der Mei, Willem F; Barbano, Anna C; Ratanatharathorn, Andrew; Bryant, Richard A; Delahanty, Douglas L; deRoon-Cassini, Terri A; Lai, Betty S; Lowe, Sarah R; Matsuoka, Yutaka J; Olff, Miranda; Qi, Wei; Schnyder, Ulrich; Seedat, Soraya; Kessler, Ronald C; Koenen, Karestan C; Shalev, Arieh Y
BACKGROUND:Previous work has indicated that post-traumatic stress disorder (PTSD) symptoms, measured by the Clinician-Administered PTSD Scale (CAPS) within 60 days of trauma exposure, can reliably produce likelihood estimates of chronic PTSD among trauma survivors admitted to acute care centers. Administering the CAPS is burdensome, requires skilled professionals, and relies on symptoms that are not fully expressed upon acute care admission. Predicting chronic PTSD from peritraumatic responses, which are obtainable upon acute care admission, has yielded conflicting results, hence the rationale for a stepwise screening-and-prediction practice. This work explores the ability of peritraumatic responses to produce risk likelihood estimates of early CAPS-based PTSD symptoms indicative of chronic PTSD risk. It specifically evaluates the Peritraumatic Dissociative Experiences Questionnaire (PDEQ) as a risk-likelihood estimator. METHODS:We used individual participant data (IPD) from five acute care studies that used both the PDEQ and the CAPS (n = 647). Logistic regression calculated the probability of having CAPS scores ≥ 40 between 30 and 60 days after trauma exposure across the range of initial PDEQ scores, and evaluated the added contribution of age, sex, trauma type, and prior trauma exposure. Brier scores, area under the receiver-operating characteristic curve (AUC), and the mean slope of the calibration line evaluated the accuracy and precision of the predicted probabilities. RESULTS:Twenty percent of the sample had CAPS ≥ 40. PDEQ severity significantly predicted having CAPS ≥ 40 symptoms (p < 0.001). Incremental PDEQ scores produced a reliable estimator of CAPS ≥ 40 likelihood. An individual risk estimation tool incorporating PDEQ and other significant risk indicators is provided. CONCLUSION/CONCLUSIONS:Peritraumatic reactions, measured here by the PDEQ, can reliably quantify the likelihood of acute PTSD symptoms predictive of chronic PTSD and requiring clinical attention. Using them as a screener in a stepwise chronic PTSD prediction strategy may reduce the burden of later CAPS-based assessments. Other peritraumatic metrics may perform similarly and their use requires similar validation. TRIAL REGISTRATION/BACKGROUND:Jerusalem Trauma Outreach and Prevention Study (J-TOPS): NCT00146900.
PMID: 32122334
ISSN: 1471-227x
CID: 4340552

Effect of Citalopram on Hippocampal Atrophy in First-Episode Psychosis: Structural MRI Results From the DECIFER Trial [Meeting Abstract]

Qi, Wei; Li, Chenxiang; Blessing, Esther; Ardekani, Babak; Freudenreich, Oliver; Cather, Corinne; Holt, Daphne; Bello, Iruma; Diminich, Erica; Tang, Yingying; Worthington, Michelle; Zeng, Botao; Wu, Renrong; Fan, Xiaoduo; Wang, Jijun; Zhao, Jingping; Troxel, Andrea; Goff, Donald C.
ISI:000535308200399
ISSN: 0006-3223
CID: 4560802

A case of intractable psychosis following interferon therapy

Wu, Stephanie X; Qi, Wei; Liu, Albert; McGonigle, Daniel P
PMID: 31220917
ISSN: 1440-1614
CID: 3939362

Differentiating PTSD from anxiety and depression: Lessons from the ICD-11 PTSD diagnostic criteria

Barbano, Anna C; van der Mei, Willem F; deRoon-Cassini, Terri A; Grauer, Ettie; Lowe, Sarah Ryan; Matsuoka, Yutaka J; O'Donnell, Meaghan; Olff, Miranda; Qi, Wei; Ratanatharathorn, Andrew; Schnyder, Ulrich; Seedat, Soraya; Kessler, Ronald C; Koenen, Karestan C; Shalev, Arieh Y
OBJECTIVE:Posttraumatic stress disorder (PTSD) is frequently associated with depression and anxiety, but the nature of the relationship is unclear. By removing mood and anxiety diagnostic criteria, the 11th edition of the International Classification of Diseases (ICD-11) aims to delineate a distinct PTSD phenotype. We examined the effect of implementing ICD-11 criteria on rates of codiagnosed depression and anxiety in survivors with recent PTSD. METHOD/METHODS:Participants were 1,061 survivors of traumatic injury admitted to acute care centers in Israel. ICD-10 and ICD-11 diagnostic rules were applied to the Clinician-Administered PTSD Scale for DSM-IV. Co-occurring disorders were identified using the Structured Clinical Interview for DSM-IV (SCID). Depression severity was measured by the Beck Depression Inventory-II (BDI-II). Assessments were performed 0-60 ("wave 1") and 90-240 ("wave 2") days after trauma exposure. RESULTS:Participants identified by ICD-11 PTSD criteria were equally or more likely than those identified by the ICD-10 alone to meet depression or anxiety disorder diagnostic criteria (for wave 1: depressive disorders, OR [odds ratio] = 1.98, 95% CI [confidence interval] = [1.36, 2.87]; anxiety disorders, OR = 1.04, 95% CI = [0.67, 1.64]; for wave 2: depressive disorders, OR = 1.70, 95% CI = [1.00, 2.91]; anxiety disorders, OR = 1.04, 95% CI = [0.54, 2.01]). ICD-11 PTSD was associated with higher BDI scores (M = 23.15 vs. 17.93, P < 0.001 for wave 1; M = 23.93 vs. 17.94, P < 0.001 for wave 2). PTSD symptom severity accounted for the higher levels of depression in ICD-11 PTSD. CONCLUSIONS:Despite excluding depression and anxiety symptom criteria, the ICD-11 identified equal or higher proportion of depression and anxiety disorders, suggesting that those are inherently associated with PTSD.
PMID: 30681235
ISSN: 1520-6394
CID: 3610752

Clinical implications of the proposed ICD-11 PTSD diagnostic criteria

Barbano, Anna C; van der Mei, Willem F; Bryant, Richard A; Delahanty, Douglas L; deRoon-Cassini, Terri A; Matsuoka, Yutaka J; Olff, Miranda; Qi, Wei; Ratanatharathorn, Andrew; Schnyder, Ulrich; Seedat, Soraya; Kessler, Ronald C; Koenen, Karestan C; Shalev, Arieh Y
BACKGROUND:Projected changes to post-traumatic stress disorder (PTSD) diagnostic criteria in the upcoming International Classification of Diseases (ICD)-11 may affect the prevalence and severity of identified cases. This study examined differences in rates, severity, and overlap of diagnoses using ICD-10 and ICD-11 PTSD diagnostic criteria during consecutive assessments of recent survivors of traumatic events. METHODS:The study sample comprised 3863 survivors of traumatic events, evaluated in 11 longitudinal studies of PTSD. ICD-10 and ICD-11 diagnostic rules were applied to the Clinician-Administered PTSD Scale (CAPS) to derive ICD-10 and ICD-11 diagnoses at different time intervals between trauma occurrence and 15 months. RESULTS:The ICD-11 criteria identified fewer cases than the ICD-10 across assessment intervals (range -47.09% to -57.14%). Over 97% of ICD-11 PTSD cases met concurrent ICD-10 PTSD criteria. PTSD symptom severity of individuals identified by the ICD-11 criteria (CAPS total scores) was 31.38-36.49% higher than those identified by ICD-10 criteria alone. The latter, however, had CAPS scores indicative of moderate PTSD. ICD-11 was associated with similar or higher rates of comorbid mood and anxiety disorders. Individuals identified by either ICD-10 or ICD-11 shortly after traumatic events had similar longitudinal course. CONCLUSIONS:This study indicates that significantly fewer individuals would be diagnosed with PTSD using the proposed ICD-11 criteria. Though ICD-11 criteria identify more severe cases, those meeting ICD-10 but not ICD-11 criteria remain in the moderate range of PTSD symptoms. Use of ICD-11 criteria will have critical implications for case identification in clinical practice, national reporting, and research.
PMID: 29754591
ISSN: 1469-8978
CID: 3356992

Estimating the risk of PTSD in recent trauma survivors: results of the International Consortium to Predict PTSD (ICPP)

Shalev, Arieh Y; Gevonden, Martin; Ratanatharathorn, Andrew; Laska, Eugene; van der Mei, Willem F; Qi, Wei; Lowe, Sarah; Lai, Betty S; Bryant, Richard A; Delahanty, Douglas; Matsuoka, Yutaka J; Olff, Miranda; Schnyder, Ulrich; Seedat, Soraya; deRoon-Cassini, Terri A; Kessler, Ronald C; Koenen, Karestan C
A timely determination of the risk of post-traumatic stress disorder (PTSD) is a prerequisite for efficient service delivery and prevention. We provide a risk estimate tool allowing a calculation of individuals' PTSD likelihood from early predictors. Members of the International Consortium to Predict PTSD (ICPP) shared individual participants' item-level data from ten longitudinal studies of civilian trauma survivors admitted to acute care centers in six countries. Eligible participants (N=2,473) completed an initial clinical assessment within 60 days of trauma exposure, and at least one follow-up assessment 4-15 months later. The Clinician-Administered PTSD Scale for DSM-IV (CAPS) evaluated PTSD symptom severity and diagnostic status at each assessment. Participants' education, prior lifetime trauma exposure, marital status and socio-economic status were assessed and harmonized across studies. The study's main outcome was the likelihood of a follow-up PTSD given early predictors. The prevalence of follow-up PTSD was 11.8% (9.2% for male participants and 16.4% for females). A logistic model using early PTSD symptom severity (initial CAPS total score) as a predictor produced remarkably accurate estimates of follow-up PTSD (predicted vs. raw probabilities: r=0.976). Adding respondents' female gender, lower education, and exposure to prior interpersonal trauma to the model yielded higher PTSD likelihood estimates, with similar model accuracy (predicted vs. raw probabilities: r=0.941). The current model could be adjusted for other traumatic circumstances and accommodate risk factors not captured by the ICPP (e.g., biological, social). In line with their use in general medicine, risk estimate models can inform clinical choices in psychiatry. It is hoped that quantifying individuals' PTSD risk will be a first step towards systematic prevention of the disorder.
PMID: 30600620
ISSN: 1723-8617
CID: 3562822