Center for Addiction Medicine

Joan A. Camprodon-Gimenez, MD, PhD

Joan Camprodon-Gimenez Square

Director, Division of Neuropsychiatry; Director, Transcranial Magnetic Stimulation (TMS) clinical service; Director, Laboratory for Neuropsychiatry & Neuromodulation at Massachusetts General Hospital. Assistant Professor of Psychiatry at Harvard Medical School

Contact:     (617) 724-5600


Dr. Camprodon is the director of the Division of Neuropsychiatry at Massachusetts General Hospital and an Assistant Professor of Psychiatry at Harvard Medical School. Clinically, he is the founding director of the MGH Transcranial Magnetic Stimulation (TMS) clinical service, a member of the Psychiatric Neurosurgery Committee and an attending physician in the departments of Psychiatry (Neuropsychiatry) and Neurology (Cognitive and Behavioral Neurology). He is board-certified in Psychiatry and Behavioral Neurology-Neuropsychiatry. Scientifically, he directs the Laboratory for Neuropsychiatry and Neuromodulation. His research uses multimodal combinations of neuroimaging and brain stimulation to investigate neural circuitry and plasticity in a translational manner. His laboratory works with a wide range of noninvasive and invasive neuromodulation techniques including transcranial direct current stimulation (tDCS), transcranial magnetic stimulation (TMS), electroconvulsive therapy (ECT) and deep brain stimulation (DBS) among others. He also uses functional and structural MRI, EEG and innovative simultaneous combinations of TMS and tDCS with neuroimaging. Dr. Camprodon is interested in understanding basic circuit properties of human neural networks and how maladaptive plastic changes lead to neuropsychiatric disorders. Critical efforts are geared towards applying the paradigms and methods of basic systems neuroscience to develop high-impact clinical tools, identify targets for therapeutic action and design individualized image-guided neuromodulation treatments.

Current Projects

Personalized target selection of TMS therapy using functional vs. structural connectivity MRI

NIH R21 MH113018-01.  Camprodon, Ning (PIs)   2017-19

This project aims to develop individualized image-guided strategies for therapeutic Transcranial Magnetic Stimulation (TMS) based on state-of-the art diffusion MRI (dMRI) tractography. We will retrospectively analyze both functional connectivity and diffusion tractography scans from 500 subjects in the Human Connectome Project database and 20 patients with depression treated with TMS in our center. Results will establish the comparative reliability of these imaging modalities to define therapeutic cortical targets in individual patients, in addition to estimating the clinical efficacy of dMRI-guided TMS and proposing its mechanisms of action based on white matter microstructural changes


A transdiagnostic assessment of electroconvulsive therapy modulation of anhedonia and reward circuitry: Targets, biomarkers and predictors of response

NIH R01 MH112737-01.  2017-22

This study will use Human Connectome Project neuroimaging protocols combined with dimensional behavioral measures to understand how ECT modulates reward brain circuits and dimensions in patients with unipolar and bipolar depression.


Modulating inhibitory control networks in gambling disorder with theta burst stimulation

NIH R21 DA042271-01 (Camprodon, Makris, Pallanti)  2017-19

In this project we will implement multimodal structural magnetic resonance imaging (MRI) and functional MRI methods of analysis in a population of pathological gamblers undergoing neuromodulation for motor inhibition control in order to further our understanding in this areas of inquiry.


Neuromodulation of memory and language networks in Alzheimer’s disease

NIH R21AG056958-01 (Camprodon, Dickerson, Eldaief) 2017-19

We will examine the selectivity of rTMS modulation using simultaneous functional MRI and FDG-PET, and will investigate the effects on memory and language task performance The ultimate goal of this research is to begin to determine how TMS changes brain network function in patients with diseased brains and whether this could potentially support benefits in cognitive function in typical and atypical clinical forms of AD.

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