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65 The Impact of PTSD and Mild Cognitive Impairment on Resting State Brain Functional Connectivity in World Trade Center Responders
- Sara L. Weisenbach, Sean A. P. Clouston, Jack R. Kaufman, Vincent Koppelmans, Scott A. Langenecker, Alison C. Pellecchia, Abigail J. Smith, Melissa A. Carr, Chuan Huang, Evelyn J. Bromet, Nikhil Palekar, Robert C. Welsh, Benjamin J. Luft
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- Journal:
- Journal of the International Neuropsychological Society / Volume 29 / Issue s1 / November 2023
- Published online by Cambridge University Press:
- 21 December 2023, pp. 849-850
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Objective:
Functional connectivity of the default mode network (DMN) during rest has been shown to be different among adults with Mild Cognitive Impairment (MCI) relative to aged-matched individuals without MCI and is predictive of transition to dementia. Post-traumatic stress disorder (PTSD) is also associated with aberrant connectivity of the DMN. Prior work from this group has demonstrated a higher rate of MCI and PTSD among World Trade Center (WTC) responders relative to the general population. The current study sought to investigate the main and interactive effects of MCI and PTSD on DMN functioning. Based on prior work, we hypothesized that MCI, but not PTSD, would predict aberrant connectivity in the DMN.
Participants and Methods:99 WTC responders aged 44–65 stratified by MCI status (yes/no) and PTSD status (yes/no) and matched for age in years, sex (male vs. female), race (white, black, and other), and educational attainment (high school or less, some college / technical school, and university degree), and occupation on September 11, 2001 (law enforcement vs. other) underwent fMRI using a 3T Siemens Biograph MR scanner. A single 10-minute continuous functional MR sequence was acquired while participants were at rest with their eyes open. Group-level analyses were conducted using SPM-12, with correction for multiple comparisons using AFNI's 3dClustSim. Based on this threshold, the number of comparisons in our imaging volume, and the smoothness of our imaging data as measured by 3dFWHMx-acf, a minimum cluster size of 1134 voxels was required to have a corrected p . .05 with 2-sided thresholding. Spherical 3 mm seeds were placed in the dorsal (4, -50, 26) and ventral (4, -60, 46) posterior cingulate cortex (PCC).
Results:Individuals with PTSD demonstrated significantly less connectivity of the dorsal posterior cingulate cortex (PCC) with medial insula (T = 5.21), subthalamic nucleus (T = 4.66), and postcentral gyrus (T = 3.81). There was no difference found in this study for connectivity between groups stratified by MCI status. There were no significant results for the ventral PCC seed.
Conclusions:Contrary to hypotheses that were driven by a study of cortical thickness in WTC responders, the impact of PTSD appears to outweigh the impact of MCI on dorsal DMN connectivity among WTC responders stratified by PTSD and MCI status. This study is limited by several issues, including low number of female and minority participants, relatively small group cell sizes (n = 23–27 per cell), a brief resting state sequence (10 minutes), and lack of a non-WTC control group. Importantly, responders are a unique population so generalizability to other populations may be limited. Individuals in the current study are now being followed longitudinally to relate baseline resting state functional connectivity with cognitive changes and changes in connectivity over a four-year period.
World Trade Center responders in their own words: predicting PTSD symptom trajectories with AI-based language analyses of interviews
- Youngseo Son, Sean A. P. Clouston, Roman Kotov, Johannes C. Eichstaedt, Evelyn J. Bromet, Benjamin J. Luft, H. Andrew Schwartz
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- Journal:
- Psychological Medicine / Volume 53 / Issue 3 / February 2023
- Published online by Cambridge University Press:
- 22 June 2021, pp. 918-926
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Background
Oral histories from 9/11 responders to the World Trade Center (WTC) attacks provide rich narratives about distress and resilience. Artificial Intelligence (AI) models promise to detect psychopathology in natural language, but they have been evaluated primarily in non-clinical settings using social media. This study sought to test the ability of AI-based language assessments to predict PTSD symptom trajectories among responders.
MethodsParticipants were 124 responders whose health was monitored at the Stony Brook WTC Health and Wellness Program who completed oral history interviews about their initial WTC experiences. PTSD symptom severity was measured longitudinally using the PTSD Checklist (PCL) for up to 7 years post-interview. AI-based indicators were computed for depression, anxiety, neuroticism, and extraversion along with dictionary-based measures of linguistic and interpersonal style. Linear regression and multilevel models estimated associations of AI indicators with concurrent and subsequent PTSD symptom severity (significance adjusted by false discovery rate).
ResultsCross-sectionally, greater depressive language (β = 0.32; p = 0.049) and first-person singular usage (β = 0.31; p = 0.049) were associated with increased symptom severity. Longitudinally, anxious language predicted future worsening in PCL scores (β = 0.30; p = 0.049), whereas first-person plural usage (β = −0.36; p = 0.014) and longer words usage (β = −0.35; p = 0.014) predicted improvement.
ConclusionsThis is the first study to demonstrate the value of AI in understanding PTSD in a vulnerable population. Future studies should extend this application to other trauma exposures and to other demographic groups, especially under-represented minorities.
Polygenic prediction of PTSD trajectories in 9/11 responders
- Monika A. Waszczuk, Anna R. Docherty, Andrey A. Shabalin, Jiaju Miao, Xiaohua Yang, Pei-Fen Kuan, Evelyn Bromet, Roman Kotov, Benjamin J. Luft
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- Journal:
- Psychological Medicine / Volume 52 / Issue 10 / July 2022
- Published online by Cambridge University Press:
- 23 October 2020, pp. 1981-1989
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Background
Genetics hold promise of predicting long-term post-traumatic stress disorder (PTSD) outcomes following trauma. The aim of the current study was to test whether six hypothesized polygenic risk scores (PRSs) developed to capture genetic vulnerability to psychiatric conditions prospectively predict PTSD onset, severity, and 18-year course after trauma exposure.
MethodsParticipants were 1490 responders to the World Trade Center (WTC) disaster (mean age at 9/11 = 38.81 years, s.d. = 8.20; 93.5% male; 23.8% lifetime WTC-related PTSD diagnosis). Prospective longitudinal data on WTC-related PTSD symptoms were obtained from electronic medical records and modelled as PTSD trajectories using growth mixture model analysis. Independent regression models tested whether six hypothesized psychiatric PRSs (PTSD-PRS, Re-experiencing-PRS, Generalized Anxiety-PRS, Schizophrenia-PRS, Depression-PRS, and Neuroticism-PRS) are predictive of WTC-PTSD outcomes: lifetime diagnoses, average symptom severity, and 18-year symptom trajectory. All analyses were adjusted for population stratification, 9/11 exposure severity, and multiple testing.
ResultsDepression-PRS predicted PTSD diagnostic status (OR 1.37, CI 1.17–1.61, adjusted p = 0.001). All PRSs, except PTSD-PRS, significantly predicted average PTSD symptoms (β = 0.06–0.10, adjusted p < 0.05). Re-experiencing-PRS, Generalized Anxiety-PRS and Schizophrenia-PRS predicted the high severity PTSD trajectory class (ORs 1.21–1.28, adjusted p < 0.05). Finally, PRSs prediction was independent of 9/11 exposure severity and jointly accounted for 3.7 times more variance in PTSD symptoms than the exposure severity.
ConclusionsPsychiatric PRSs prospectively predicted WTC-related PTSD lifetime diagnosis, average symptom severity, and 18-year trajectory in responders to 9/11 disaster. Jointly, PRSs were more predictive of subsequent PTSD than the exposure severity. In the future, PRSs may help identify at-risk responders who might benefit from targeted prevention approaches.
199 - Toxoplasma
- from Part XXIV - Specific organisms: parasites
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- By Roderick Go, SUNY School of Medicine at Stony Brook, Benjamin J. Luft, Stony Brook University Hospital
- Edited by David Schlossberg, Temple University, Philadelphia
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- Book:
- Clinical Infectious Disease
- Published online:
- 05 April 2015
- Print publication:
- 23 April 2015, pp 1279-1284
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Summary
Toxoplasmosis, caused by the obligate intracellular parasite Toxoplasma gondii, is responsible for significant morbidity and mortality throughout the world. Although it has long been recognized as a serious congenital disease, it is only with the advent of acquired immunodeficiency syndrome (AIDS) and the increased use of immunosuppressive therapy that toxoplasmosis has reached epidemic proportions.
Humans are incidental hosts in the life cycle of T. gondii. Acute infection occurs via ingestion of meats or water contaminated with tissue cysts or tachyzoites or by handling cats, the definitive host. Once the human host develops an adequate immune response, tissue cysts are formed and a chronic or latent infection ensues. Antibodies against T. gondii will be present in serum for life. When a chronically infected person becomes immunocompromised, particularly with defects in cell-mediated immunity, devastating reactivation of the latent infection may occur.
CLINICAL MANIFESTATIONS AND DIAGNOSIS
In the immunocompetent host, primary infection is often asymptomatic. Acute infection can mimic the symptoms of mononucleosis with a common manifestation of cervical or occipital lymphadenopathy. The lymph nodes usually are nontender, are nonsuppurative, and persist for less than 4 to 6 weeks. Infrequently, toxoplasmosis can lead to myocarditis, hepatitis, polymyositis, pneumonitis, and encephalitis.
Toxoplasmosis in the immunocompromised patient is most commonly manifested by toxoplasmic encephalitis (TE), usually alone but sometimes as part of a multiorgan infection. Isolated organ involvement without central ner- vous system (CNS) disease is uncommon. In the AIDS patient, TE usually develops when the CD4 lymphocyte count falls below 100/mm3, although the risk of developing overt infection begins when CD4 counts fall below 200/mm3.
197 - Toxoplasma
- from Part XXIV - Specific Organisms – Parasites
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- By Roderick Go, SUNY School of Medicine at Stony Brook, Benjamin J. Luft, SUNY School of Medicine at Stony Brook
- Edited by David Schlossberg
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- Book:
- Clinical Infectious Disease
- Published online:
- 05 March 2013
- Print publication:
- 12 May 2008, pp 1365-1370
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- Chapter
- Export citation
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Summary
Toxoplasmosis, caused by the obligate intracellular parasite Toxoplasma gondii, is responsible for significant morbidity and mortality throughout the world. Although it has long been recognized as a serious congenital disease, it is only with the advent of acquired immunodeficiency syndrome (AIDS) and the increased use of immunosuppressive therapy that toxoplasmosis has reached epidemic proportions.
Humans are incidental hosts in the life cycle of T. gondii. Acute infection occurs via ingestion of meats or beverages contaminated with tissue cysts or tachyzoites or by handling cats, the definitive host. Once the human host develops an adequate immune response, tissue cysts are formed and a chronic or latent infection ensues. Antibodies against T. gondii will be present in serum for life. When a chronically infected person becomes immunocompromised, particularly with defects in cell-mediated immunity, devastating reactivation of the latent infection may occur.
CLINICAL MANIFESTATIONS AND DIAGNOSIS
Toxoplasmosis in the AIDS patient is most commonly manifested by toxoplasmic encephalitis (TE), usually alone but sometimes as part of a multiorgan infection. Isolated organ involvement without central nervous system (CNS) disease is uncommon. In most cases, TE develops when the CD4 lymphocyte count falls below 100 mm3, although the risk of developing overt infection begins when CD4 counts fall below 200 mm3. The clinical manifestations of TE are protean, including signs and symptoms of focal or generalized neurologic dysfunction or more commonly both, depending on the number, size, and location of the lesions.