Dr. Peter van Roessel, MD PhD, completed his MD at Stanford University and his residency training in psychiatry at Columbia University and the New York-Presbyterian Hospital in New York City, with additional training in psychodynamic psychotherapy (TFP) via the Columbia University Center for Psychoanalytic Training and Research. Prior to joining the clinical faculty at Stanford, he worked for several years as Associate Director of the general research unit of the New York State Psychiatric Institute, a premier state-funded research hospital affiliated with Columbia University.
At Stanford, Dr. van Roessel sees adult mood and anxiety disorders outpatients through the Assessment Clinics and participates in resident training and patient care as director of the resident Continuity Clinic and as a supervisor in psychodynamic psychotherapy. He additionally directs the third-year resident curriculum in psychopathology and psychopharmacology. As a member of the department's Rodriguez Translational Therapeutics Lab, he sees individuals with obsessive-compulsive spectrum disorders for evaluations and research-protocol driven clinical treatment and contributes to and leads clinical neuroscience studies pioneering rapid-acting interventions in OCD. Clinically motivated research interests include the nature and neural correlates of metacognitive ‘awareness’ (insight) in OCD and related disorders, and particularly the relationship of awareness to mechanisms of attentional control.
Dr. van Roessel pursued research training in basic neuroscience prior to his clinical training, completing an MPhil in Biology via the Open University, UK, for research performed at the Max Planck Institute for Developmental Biology in Tübingen Germany, and a PhD in molecular and developmental neurobiology at the University of Cambridge, UK. He has contributed to work in the lab of Dr Julia Kaltschmidt (Stanford) on studies of GABAergic/Glutamatergic interneuronal circuity in mouse. He received a 2018 NARSAD Young Investigator Award to pursue study of nitrous oxide as a rapid-acting treatment for OCD, he was a 2020-2022 Miller Foundation Fellow, and from 2020 to 2022 was a Advanced Fellow in Mental Illness Treatment and Research via the Sierra Pacific Mental Illness Research, Education, and Clinical Center of the Palo Alto VA. Dr. van Roessel is a Fellow of the American Psychiatric Association and a member of the American College of Psychiatrists.
Clinical Associate Professor, Psychiatry and Behavioral Sciences
PhD Training: University of Cambridge (2003) United Kingdom
Board Certification: American Board of Psychiatry and Neurology, Psychiatry (2011)
Residency: New York Presbyterian Hospital - Columbia University (2011) NY
Medical Education: Stanford University School of Medicine (2007) CA
Caloric Vestibular Stimulation for Modulation of Insight in Obsessive-Compulsive Spectrum Disorders
This study investigates whether caloric vestibular stimulation can modulate a measure of insight in obsessive-compulsive spectrum disorders.
Efficacy of Nitrous Oxide in OCD: Pilot Study
This study investigates whether the commonly used and well-tolerated inhaled anesthetic nitrous oxide can rapidly improve symptoms of OCD.
Study of Dextromethorphan in OCD and Related Disorders
The purpose of the study is to assess the tolerability and efficacy of dextromethorphan in combination with fluoxetine for symptom relief in OCD and related disorders.
Treatment-resistant OCD: Pharmacotherapies in adults.
2022; 120: 152352
Serotonin reuptake inhibitor (SRI) medications are well established as first-line pharmacotherapeutic treatment for Obsessive-Compulsive Disorder (OCD). However, despite the excellent safety profile and demonstrated efficacy of these medications, a substantial proportion of individuals with OCD fail to attain sufficient benefit from SRIs. In this narrative review, we discuss clinical features of OCD that have been associated with poorer response to SRIs, and we present pharmacotherapeutic interventions that have been explored as augmenting or alternative treatments for treatment-resistant OCD. We additionally highlight non-SRI interventions for OCD that are currently under investigation. Pharmacotherapeutic interventions were identified via expert consensus. To assess the evidence base for individual pharmacotherapies, targeted searches for relevant English-language publications were performed on standard biomedical research databases, including MEDLINE. Information relevant to ongoing registered clinical trials in OCD was obtained by search of ClinicalTrials.gov. Pharmacotherapies are grouped for review in accordance with the general principles of Neuroscience-based Nomenclature (NbN). Clinical features of OCD that may suggest poorer response to SRI treatment include early age of onset, severity of illness, duration of untreated illness, and the presence of symmetry/ordering or hoarding-related symptoms. Based on evolving pathophysiologic models of OCD, diverse agents engaging serotonin, dopamine, norepinephrine, glutamate, and anti-inflammatory pathways have been explored as alternative or adjunctive therapies for treatment-resistant OCD and have at least preliminary evidence of efficacy. Medications with dopamine antagonist activity remain the most robustly evidence-based of augmenting interventions, yet dopamine antagonists benefit only a minority of those who try them and carry elevated risks of adverse effects. Interventions targeting glutamatergic and anti-inflammatory pathways are less well evidenced, but may offer more favorable benefit to risk profiles. Ongoing research should explore whether specific interventions may benefit individuals with particular features of treatment-resistant OCD.
View details for DOI 10.1016/j.comppsych.2022.152352
View details for PubMedID 36368186
Valence processing alterations in SAPAP3 knockout mice and human OCD.
Journal of psychiatric research
2022; 151: 657-666
Abnormalities in valence processing - the processing of aversive or appetitive stimuli - may be an underrecognized component of obsessive-compulsive disorder (OCD). Preclinical rodent models have been critical in furthering pathophysiological understanding of OCD, yet there is a dearth of investigations examining whether rodent models of compulsive behavior show alterations in valence systems congruent with those seen in individuals with OCD. In this study, we sought to assess valence processing in a preclinical rodent model of compulsive behavior, the SAPAP3 knockout (KO) mouse model, and compare our preclinical findings to similar behavioral phenomena in OCD patients. In SAPAP3 KO mice, we used auditory fear conditioning and extinction to examine alterations in negative valence processing and reward-based operant conditioning to examine alterations in positive valence processing. We find that SAPAP3 KO mice show evidence of heightened negative valence processing through enhanced fear learning and impaired fear extinction. SAPAP3 KO mice also show deficits in reward acquisition and goal-directed behavior, suggesting impaired positive valence processing. In OCD patients, we used validated behavioral tests to assess explicit and implicit processing of fear-related facial expressions (negative valence) and socially-rewarding happy expressions (positive valence). We find similar trends towards enhanced negative and impaired positive valence processing in OCD patients. Overall, our results reveal valence processing abnormalities in a preclinical rodent model of compulsive behavior similar to those seen in OCD patients, with implications for valence processing alterations as novel therapeutic targets across a translational research spectrum.
View details for DOI 10.1016/j.jpsychires.2022.05.024
View details for PubMedID 35661523
Deconstructing Ketamine-Induced Changes in Cortisol and Dissociative and Affective States in a Controlled Mechanistic Study
ELSEVIER SCIENCE INC. 2022: S178-S179
View details for Web of Science ID 000789022200436
Acute Ketamine Modulates Cognitive Control Network Activity During Cognitive Inhibition: Evidence From a Mechanistic Trial
ELSEVIER SCIENCE INC. 2022: S225
View details for Web of Science ID 000789022200552
Accelerated Neuromodulation Therapy for Obsessive-Compulsive Disorder.
The open-label trial of Williams, Sudheimer, Cole, et al., suggests safety, feasibility, and high efficacy for treatment-refractory OCD of an accelerated, fMRI-guided, high-dose, cTBSmod protocol targeting the right frontal pole. Larger, randomized, controlled trials are needed to test the promising results of this pilot study. CLINICALTRIALS.GOV REGISTRY NUMBERS: NCT03404609.
View details for DOI 10.1016/j.brs.2021.02.013
View details for PubMedID 33631349
Examining subjective sleep quality in adults with hoarding disorder.
Journal of psychiatric research
Hoarding disorder (HD), characterized by difficulty parting with possessions and functionally impairing clutter, affects 2-6% of the population. Originally considered part of Obsessive-Compulsive Disorder (OCD), HD became a distinct diagnostic entity in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) in 2013. While sleep impacts OCD, little is known about sleep in HD. As HD patients often report poor sleep in clinical settings, understanding global subjective sleep quality and disturbances may lead to novel therapeutic targets. To address this gap, the authors used a sample of convenience: an existing data set designed to screen research study eligibility and explore the psychopathology and phenomenology of OCD and HD. The data set included information collected from individuals with HD (n=38), OCD (n=26), and healthy participants (n=22) about insomnia, sleep quality, and mood using interviews and structured instruments including the Insomnia Severity Index (ISI), Pittsburgh Sleep Quality Index (PSQI), and Depression Anxiety Stress Scales (DASS). In this data set, HD and OCD groups reported significantly greater insomnia symptoms and poorer sleep quality compared with healthy controls while controlling for depression, age, and gender. A sizable minority of HD and OCD individuals met criteria for comorbid sleep disorders. OCD and HD groups differed in delayed sleep phase prevalence. To our knowledge, this is the first study examining subjective sleep quality and insomnia in HD as compared to healthy individuals and those with OCD, while controlling for relevant clinical characteristics. Given that there are evidence-based treatments for insomnia and other sleep disorders, our study raises the possibility that treatment interventions targeting sleep may improve HD outcomes.
View details for DOI 10.1016/j.jpsychires.2020.10.044
View details for PubMedID 33309063
- Self-Reported Depressive Symptoms in Active and Retired Professional Hockey Players CANADIAN JOURNAL OF BEHAVIOURAL SCIENCE-REVUE CANADIENNE DES SCIENCES DU COMPORTEMENT 2020; 52 (2): 97–106
- Does Nitrous Oxide Help Veterans With Posttraumatic Stress Disorder? A Case Series. The Journal of clinical psychiatry 2020; 81 (4)
Neurocognitive Correlates of Insight in Hoarding Disorder
NATURE PUBLISHING GROUP. 2019: 159
View details for Web of Science ID 000509665600307
- Exploring Brain-Derived Neurotrophic Factor Val66Met Polymorphism and Extinction Learning-Based Treatment Outcome in Obsessive-Compulsive Disorder A Pilot Study JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY 2019; 39 (1): 91–93
Exploring Brain-Derived Neurotrophic Factor Val66Met Polymorphism and Extinction Learning-Based Treatment Outcome in Obsessive-Compulsive Disorder: A Pilot Study.
Journal of clinical psychopharmacology
View details for PubMedID 30531475
Clutter Blindness as an Insight Proxy in Hoarding Disorder: A Hypothesis-Generating Study
NATURE PUBLISHING GROUP. 2018: S387–S388
View details for Web of Science ID 000509546600710
Exploring BDNF Val66Met Polymorphism and Extinction Learning-Based Treatment Outcome in OCD: A Pilot Study
NATURE PUBLISHING GROUP. 2018: S387
View details for Web of Science ID 000509546600709
A Role for Dystonia-Associated Genes in Spinal GABAergic Interneuron Circuitry.
2017; 21 (3): 666–78
Spinal interneurons are critical modulators of motor circuit function. In the dorsal spinal cord, a set of interneurons called GABApre presynaptically inhibits proprioceptive sensory afferent terminals, thus negatively regulating sensory-motor signaling. Although deficits in presynaptic inhibition have been inferred in human motor diseases, including dystonia, it remains unclear whether GABApre circuit components are altered in these conditions. Here, we use developmental timing to show that GABApre neurons are a late Ptf1a-expressing subclass and localize to the intermediate spinal cord. Using a microarray screen to identify genes expressed in this intermediate population, we find the kelch-like family member Klhl14, implicated in dystonia through its direct binding with torsion-dystonia-related protein Tor1a. Furthermore, in Tor1a mutant mice in which Klhl14 and Tor1a binding is disrupted, formation of GABApre sensory afferent synapses is impaired. Our findings suggest a potential contribution of GABApre neurons to the deficits in presynaptic inhibition observed in dystonia.
View details for PubMedID 29045835
Sensory-Derived Glutamate Regulates Presynaptic Inhibitory Terminals in Mouse Spinal Cord
2016; 90 (6): 1189-1202
Circuit function in the CNS relies on the balanced interplay of excitatory and inhibitory synaptic signaling. How neuronal activity influences synaptic differentiation to maintain such balance remains unclear. In the mouse spinal cord, a population of GABAergic interneurons, GABApre, forms synapses with the terminals of proprioceptive sensory neurons and controls information transfer at sensory-motor connections through presynaptic inhibition. We show that reducing sensory glutamate release results in decreased expression of GABA-synthesizing enzymes GAD65 and GAD67 in GABApre terminals and decreased presynaptic inhibition. Glutamate directs GAD67 expression via the metabotropic glutamate receptor mGluR1β on GABApre terminals and regulates GAD65 expression via autocrine influence on sensory terminal BDNF. We demonstrate that dual retrograde signals from sensory terminals operate hierarchically to direct the molecular differentiation of GABApre terminals and the efficacy of presynaptic inhibition. These retrograde signals comprise a feedback mechanism by which excitatory sensory activity drives GABAergic inhibition to maintain circuit homeostasis.
View details for DOI 10.1016/j.neuron.2016.05.008
View details for PubMedID 27263971
Care within a Veterans Hospital - Earlier detection of colon cancer
SURGICAL ENDOSCOPY AND OTHER INTERVENTIONAL TECHNIQUES
2007; 21 (8): 1434-1440
In 1998 the Veterans Administration mandated an externally monitored targeted colon cancer screening rate that was expected to result in earlier cancer detection and improved patient survival. The effectiveness of the protocol was evaluated in a retrospective case series at a tertiary care Veterans Administration Hospital that included all patients with the diagnosis of colon cancer between 1991 and 2003.Tumor stage, tumor location, and patient survival data were recorded and compared to National Cancer Data Base (NCDB) benchmarks.The study facility had a greater percentage of early cancers and fewer later stage cancers than the NCDB benchmark. Overall survival was better for the VA cohort compared to NCDB (all-cause 5-year survival: VA, 0.72; NCDB, 0.47. p < or = .001).The VA facility had a significantly greater percentage of early cancers and fewer stage III or IV cancers compared to a national benchmark and significantly improved survival compared to the national benchmark.
View details for DOI 10.1007/s00464-006-9184-6
View details for PubMedID 17294311
Independent regulation of synaptic size and activity by the anaphase-promoting complex.
2004; 119 (5): 707–18
Neuronal plasticity relies on tightly regulated control of protein levels at synapses. One mechanism to control protein abundance is the ubiquitin-proteasome degradation system. Recent studies have implicated ubiquitin-mediated protein degradation in synaptic development, function, and plasticity, but little is known about the regulatory mechanisms controlling ubiquitylation in neurons. In contrast, ubiquitylation has long been studied as a central regulator of the eukaryotic cell cycle. A critical mediator of cell-cycle transitions, the anaphase-promoting complex/cyclosome (APC/C), is an E3 ubiquitin ligase. Although the APC/C has been detected in several differentiated cell types, a functional role for the complex in postmitotic cells has been elusive. We describe a novel postmitotic role for the APC/C at Drosophila neuromuscular synapses: independent regulation of synaptic growth and synaptic transmission. In neurons, the APC/C controls synaptic size via a downstream effector Liprin-alpha; in muscles, the APC/C regulates synaptic transmission, controlling the concentration of a postsynaptic glutamate receptor.
View details for PubMedID 15550251
Spreading silence with Sid.
2004; 5 (2): 208
RNA interference (RNAi) has been shown to spread from cell to cell in plants and in Caenorhabditis elegans, but it does not spread in other organisms, such as Drosophila. A recent report demonstrates that a membrane channel, encoded by the gene sid-1, is responsible for the spreading of RNAi between cells.
View details for PubMedID 14759251
Region-specific apoptosis limits neural stem cell proliferation.
2003; 37 (2): 185–87
Regulation of stem cell division is of particular interest, both for studies of development and for stem cell therapeutics. In this issue of Neuron, Bello et al. show that the number of divisions of Drosophila neural stem cells is limited, in a region-specific manner, by regulated apoptosis in response to a pulse of expression of the Hox gene abdominal-A (abdA).
View details for PubMedID 12546811
Imaging into the future: visualizing gene expression and protein interactions with fluorescent proteins.
Nature cell biology
2002; 4 (1): E15–20
Since its introduction into heterologous organisms as a marker of gene expression, the green fluorescent protein (GFP) has led a dramatic revolution in cell, developmental and neurobiology. By allowing breathtaking visualization of fluorescent fusion proteins as they move within and between cells, GFP has fundamentally transformed the spatial analysis of protein function. Now, new GFP technologies allow far more than simple observations of fusion protein localization. The growing family of fluorescent protein variants is enabling more sophisticated studies of protein function and illuminating wide-ranging processes from gene expression to second-messenger cascades and intercellular signalling. Together with advances in microscopy, new GFP-based experimental approaches are forging a second GFP revolution.
View details for PubMedID 11780139
Two-color GFP imaging demonstrates cell-autonomy of GAL4-driven RNA interference in Drosophila.
2002; 34 (1-2): 4
View details for DOI 10.1002/gene.10146
Activity of long-wavelength cones under scotopic conditions in the cyprinid fish Danio aequipinnatus.
Journal of comparative physiology. A, Sensory, neural, and behavioral physiology
1997; 181 (5): 493-500
In carp (Cyprinus) and goldfish (Carassius), long-wavelength cones are reported to be active under scotopic conditions. Using the electroretinogram (ERG), we tested another cyprinid fish, Danio aequipinnatus, which contains A1-based visual pigments and for which we had previously measured the spectral sensitivities of individual cones. Dark adaptation curves show a rod/cone break at about 45 min. When thoroughly dark-adapted, the spectral sensitivity function is broader than can be accounted for by self-screening of rhodopsin, but it can be modeled by an additive combination of rods and the 560-nm cones. Dim, red background light causes adaptation of rods and a broadening of the spectral sensitivity function, which can be simulated by increasing the proportion of cones in the model. Brighter red backgrounds adapt the 560-nm cones. Because of the effect of red adapting lights, the ERG evidence for the participation of long-wavelength cones close to visual threshold appears to be different in Danio than in the goldfish Carassius.
View details for PubMedID 9373956