
Desmond J. Oathes
VerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 2003–2026
About
Desmond J. Oathes, PhD, is an Associate Professor of Psychiatry at the University of Pennsylvania's Perelman School of Medicine. He serves as the Associate Director of the Center for Neuromodulation in Depression and Stress and is a Co-Director of the Penn Brain Science, Translation, Innovation, and Modulation Center (brainSTIM). Additionally, he is a Staff Therapist at the Penn Center for the Treatment and Study of Anxiety and the Director of the Center for Brain Imaging and Stimulation. His research expertise includes functional MRI, transcranial magnetic stimulation, clinical psychology, psychophysiology, and cognitive neuroscience, with a focus on affective disorders such as depression, anxiety, PTSD, and MDD. His clinical expertise encompasses cognitive behavioral therapy, neuropsychological assessments, neurocognitive assessments, transcranial magnetic stimulation, and clinical supervision.
Research topics
- Artificial Intelligence
- Computer Science
- Data Mining
- Medicine
- Database
- Computer vision
- Psychology
- Physics
- Radiology
- Neuroscience
Selected publications
Spatial heterogeneity and subtypes of functional connectivity development in youth
Nature Communications · 2026-01-23
articleOpen accessBrain age prediction has been widely utilized to assess functional connectivity (FC) development, but conventional global brain age indices are limited in capturing spatial heterogeneity across the cortex. This study introduces a regional brain development index to characterize fine-grained FC maturation across cortical regions. We examined its spatial variability and stratified individuals into subtypes with distinct region-wise FC developmental patterns. Using data from the Philadelphia Neurodevelopmental Cohort (ages 8-23 years), we identified three distinct subtypes and found that individuals with advanced FC developmental pattern aligning with the sensorimotor-association axis exhibited superior cognitive performance. Robustness was confirmed through replication in the Human Connectome Project Development cohort. Further analyses revealed associations between FC development and gene expression linked to neural differentiation, synaptogenesis, and myelination. These findings suggest that spatial heterogeneity in FC development reflects cortical microstructure and hierarchical organization, underscoring its critical role in neurocognitive maturation during youth.
ASLPrep: A Robust Preprocessing Pipeline for ASL Data
Zenodo (CERN European Organization for Nuclear Research) · 2026-02-03
otherOpen accessArterial spin labeled (ASL) magnetic resonance imaging (MRI) is the primary method for noninvasively measuring regional brain perfusion in humans. We introduce ASLPrep, a suite of software pipelines that ensure the reproducible and generalizable processing of ASL MRI data.
Human orbitofrontal neural activity is linked to obsessive-compulsive behavioral dynamics
Cell · 2026-01-29 · 2 citations
articleOpen accessBiomarkers of obsessive-compulsive disorder (OCD) symptom dynamics and related behavior could advance personalized interventions. Aberrant activity in the orbitofrontal cortex (OFC) has been implicated in symptom exacerbation in OCD. We conducted an intracranial monitoring assay to identify high-resolution neurophysiologic correlates of OCD symptoms in the human OFC. We found that low-gamma power in the anteromedial OFC was consistently elevated during high symptom states in a symptom provocation task. Furthermore, electrical stimulation of the ventral basal ganglia that reduced OCD symptoms also reduced anteromedial OFC gamma power. These results link OFC gamma activity to moment-to-moment expression of OCD symptoms, providing mechanistic insights to guide therapeutic strategies such as deep brain stimulation.
Clinical Neurophysiology · 2026-04-26
articleOpen accessSenior authorOBJECTIVE: Major depressive disorder (MDD) may involve dysregulation of excitatory/inhibitory balance. Because sleep slow-waves facilitate homeostatic downscaling of excitatory synaptic strength, this study examined whether slow-wave disruption (SWD) could alter motor cortical excitability in individuals with and without MDD. METHODS: Thirty-seven adults (13 healthy controls [HC]; 24 with MDD) completed two overnight laboratory sessions (baseline and SWD, order counterbalanced). Slow-waves were reduced using auditory stimulation. Motor cortical excitability was assessed the following morning using transcranial magnetic stimulation (TMS)-generated single- and paired-pulse motor evoked potentials (MEPs). RESULTS: SWD increased MEPs during both single-pulse and paired-pulse TMS in individuals with MDD, whereas HC showed a pattern of decreased MEPs. At baseline, both groups exhibited reliable intracortical facilitation (ICF) and inhibition (ICI). Following SWD, facilitation patterns were preserved in both groups, while inhibitory effects were weakened in the HC but preserved in the MDD group. Relative values of ICF and ICI were unchanged following SWD in both groups. CONCLUSIONS: SWD increased motor cortical excitability in individuals with MDD, consistent with disruption of sleep-dependent synaptic downscaling. Because relative ICF and ICI remained unchanged despite shifts in raw MEP amplitude, these findings suggest that the heightened excitability may be driven by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-mediated mechanisms. SIGNIFICANCE: Slow-wave modulation may represent a non-pharmacologic approach to increasing motor cortical excitability and normalizing excitatory/inhibitory balance in MDD.
Journal of Affective Disorders · 2026-02-05
articleASLPrep: A Robust Preprocessing Pipeline for ASL Data
Zenodo (CERN European Organization for Nuclear Research) · 2026-03-16
otherOpen accessArterial spin labeled (ASL) magnetic resonance imaging (MRI) is the primary method for noninvasively measuring regional brain perfusion in humans. We introduce ASLPrep, a suite of software pipelines that ensure the reproducible and generalizable processing of ASL MRI data.
NIBS-BIDS: an extension to the brain imaging data structure for non-invasive brain stimulation
Zenodo (CERN European Organization for Nuclear Research) · 2026-03-29
preprintOpen accessThe Brain Imaging Data Structure (BIDS) is a community standard for organizing and sharing neuroimaging data. Here we present NIBS-BIDS (BEP037), an extension of BIDS for non-invasive brain stimulation (NIBS) data. This specification introduces a dedicated nibs/ datatype with a scalable framework for storing stimulation parameters, modality-specific device metadata, spatial targeting information, and event-level synchronization for transcranial magnetic stimulation (TMS), transcranial electrical stimulation (tES), and transcranial ultrasound stimulation (TUS). We describe the proposed data structure, its design rationale, and its intended role in facilitating reproducible NIBS research.
Causal connectivity maps derived from single-pulse interleaved TMS/fMRI
Scientific Reports · 2026-01-22 · 1 citations
articleOpen accessSenior authorUnderstanding causal interactions between cortical and subcortical brain regions is critical for mapping human functional connectivity. While non-invasive methods such as fMRI and diffusion imaging have provided valuable insights into brain connectivity, these approaches remain correlational and cannot establish causal circuit mechanisms. Here, we aimed to generate reliable causal connectivity maps using interleaved single-pulse transcranial magnetic stimulation with functional MRI (spTMS/fMRI). In over 80 participants, personalized connectivity-guided targets in the left hemisphere were selected to engage either the subgenual anterior cingulate cortex (sgACC) or basolateral amygdala (BLA). Voxelwise event-related BOLD maps quantified TMS-evoked responses, and group-level analyses controlled for head motion, pain, and somatosensory effects to isolate stimulation-specific activation. Stimulation of frontal regions targeting the sgACC induced responses in the sgACC and modulated distributed cortical and subcortical areas. Ventrolateral targets elicited negative BOLD responses in the amygdala and engaged widespread downstream regions. ROI-based analyses revealed no significant differences in evoked responses between sgACC- and BLA-targeted stimulations across participants. These results validate that image-guided TMS can causally engage distributed brain circuits, providing a robust framework for functional connectivity mapping. The publicly available causal connectivity maps offer a resource for future studies linking cortical stimulation sites with subcortical network responses.Clinical Trial Registration This study was registered on ClinicalTrials.gov under the identifier NCT04014959, and was open to enrollment from January 15, 2017 to October 1, 2020.
NIBS-BIDS: an extension to the brain imaging data structure for non-invasive brain stimulation
Zenodo (CERN European Organization for Nuclear Research) · 2026-03-29
preprintOpen accessThe Brain Imaging Data Structure (BIDS) is a community standard for organizing and sharing neuroimaging data. Here we present NIBS-BIDS (BEP037), an extension of BIDS for non-invasive brain stimulation (NIBS) data. This specification introduces a dedicated nibs/ datatype with a scalable framework for storing stimulation parameters, modality-specific device metadata, spatial targeting information, and event-level synchronization for transcranial magnetic stimulation (TMS), transcranial electrical stimulation (tES), and transcranial ultrasound stimulation (TUS). We describe the proposed data structure, its design rationale, and its intended role in facilitating reproducible NIBS research.
Whole-brain mapping of TMS-induced discomfort with large-scale concurrent TMS-fMRI
bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-02
articleOpen accessTranscranial magnetic stimulation (TMS) is a cornerstone tool for causal inference in human brain function and an increasingly used neuromodulation therapy, yet it induces well-recognized discomfort that may systematically bias measured outcomes. Despite its ubiquity, a critical gap remains in understanding how TMS-induced discomfort is represented across the brain and to what extent it contributes to TMS-evoked neural responses. Using concurrent TMS-fMRI across 11 cortical targets, we collected an unprecedented dataset (165 participants; 1,535 runs) spanning healthy participants and those with elevated affective symptoms. Cross-validated multivariate modeling revealed that TMS-induced discomfort engages distributed cortical and subcortical regions across sensorimotor, attentional, default mode, and limbic networks, with both shared and group-specific patterns. Discomfort-related activity accounted for approximately 12% and 25% of TMS-evoked responses in healthy and elevated-symptom groups, respectively, and varied systematically across stimulating sites. These findings identify TMS-induced discomfort as a substantial and previously under-characterized component of TMS-evoked neural responses, underscoring the need to explicitly measure and model it. By providing a whole-brain map of regional contributions associated with TMS-induced discomfort and an analytic framework to dissociate direct neuromodulatory effects from discomfort-related responses, this work improves the interpretability of TMS-evoked signals and supports more rigorous causal inference and therapeutic applications.
Recent grants
Network Control and Functional Context: Mechanisms for TMS Response
NIH · $2.8M · 2018–2023
Non-invasive neuromodulation mechanisms and dose/response metrics
NIH · $2.7M · 2016–2021
Individualized Closed Loop TMS for Working Memory Enhancement
NIH · $3.5M · 2019–2024
Frequent coauthors
- 149 shared
Amit Etkin
- 126 shared
Gregory A. Fonzo
Multidisciplinary Association for Psychedelic Studies
- 120 shared
Madeleine S. Goodkind
University of New Mexico
- 114 shared
Kathy Peng
Stanford University
- 111 shared
Meredith Harvey
- 111 shared
Steven E. Lindley
Stanford University
- 110 shared
Allison L. Thompson
Stanford University
- 110 shared
Sanno Zack
Stanford University
Education
- 2006
Ph.D.
The Pennsylvania State University
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