Dr. Kratter is an adult psychiatrist and fellowship-trained neuropsychiatrist and clinical assistant professor in the Department of Psychiatry & Behavioral Sciences at Stanford University School of Medicine. He is also director of Invasive Technologies in the Stanford Brain Stimulation Laboratory.
His clinical interests include the psychiatric and cognitive aspects of movement disorders like Parkinson's and Tourette's as well as depression, obsessive-compulsive disorder, and non-invasive and invasive neuromodulation for neuropsychiatric illness.
His research interests focus on improving outcomes and understanding the mechanisms of neuromodulatory treatments. This includes both clinical and more mechanistic studies using techniques like repetitive transcranial magnetic stimulation (rTMS) and deep brain stimulation in combination with neuroimaging and electrophysiology. He is a co-investigator for such studies focusing on obsessive-compulsive disorder, major depressive disorder, and acute suidical ideation.
Dr. Kratter has published articles on topics such as deep brain stimulation for Parkinson’s disease and gene-targeting therapy for Huntington disease. His work has appeared in the Journal of Clinical Investigation, Proceedings of the National Academy of Science, and American Journal of Human Genetics. He also co-authored the chapter on major depression in the textbook Deep Brain Stimulation: Techniques and Practice.
Dr. Kratter has presented his work at the annual meetings of the American Neuropsychiatric Association, Hereditary Disease Foundation, and Society for Neuroscience. Topics include cognitive changes following deep brain stimulation for Parkinson’s disease, antipsychotic-induced thrombocytopenia, and mediators of pathology in Huntington’s disease.
For his scholarship and research achievements, Dr. Kratter has won multiple honors. They include the Miller Foundation Award for Psychiatric Research. He also won the Ruth L. Kirschstein National Research Service Award from the National Institute of Neurological Disorders and Stroke.
He is or has been a member of the American Neuropsychiatric Association, American Society of Clinical Psychopharmacology, American Association for Geriatric Psychiatry, Academy of Psychosomatic Medicine, and Society for Neuroscience.
Clinical Assistant Professor, Psychiatry and Behavioral Sciences
Honors & Awards
Molecular and Cell Biology Departmental I.L. Chaikoff Award, UC Berkeley (2005)
Fellowship, Medical Scientist Training Program (MSTP) , UCSF (2006)
Ruth L. Kirschstein National Research Service Award (F31), National Institute of Neurological Disorders and Stroke (NINDS). (2011)
National Residency Team Competitor, American Psychiatric Association MindGames (2017)
Honors Scholar, American Association for Geriatric Psychiatry (AAGP) (2018)
Best Poster Award for a Medical Trainee, University of Pittsburgh Department of Psychiatry Research Day (2019)
Miller Award for Psychiatric Research, Miller Foundation, Stanford University School of Medicine (2020 - 2021)
Board Certification: United Council for Neurologic Subspecialties, NeuroPsychiatry
Board Certification, United Council for Neurologic Subspecialties, Behavioral Neurology and Neuropsychiatry (2020)
Board Certification: American Board of Psychiatry and Neurology, Psychiatry (2019)
Fellowship: Stanford University Psychiatry and Behavioral Sciences (2020) CA
Residency: Western Psychiatric Institute and Clinic (2019) PA
Medical Education: University of California San Francisco Registrar Office (2015) CA
Accelerated Theta Burst in Treatment-Resistant Depression: A Dose Finding and Biomarker Study
This study evaluates the effectiveness of re-treatment using accelerated schedule of intermittent theta-burst stimulation for treatment-resistant depression. This is an open label study.
Neuroimaging Biomarkers for Predicting rTMS Response in OCD
This study evaluates an accelerated schedule of theta-burst stimulation using a Transcranial Magnetic Stimulation (TMS) device for treatment-resistant Obsessive Compulsive Disorder (OCD). In a randomized fashion, half the participants will receive accelerated theta-burst stimulation at the dorsomedial prefrontal cortex (DMPFC), while half will receive accelerated theta-burst stimulation at the right orbitofrontal (rOFC) site.
Bilateral Accelerated Theta Burst in Treatment-Resistant Bipolar Depression
This study evaluates an accelerated schedule of theta-burst stimulation using a transcranial magnetic stimulation device for treatment-resistant bipolar depression. In this open-label study, all participants will receive accelerated theta-burst stimulation.
Stanford is currently not accepting patients for this trial. For more information, please contact Nolan Williams, MD, 650-497-3933.
Depression history modulates effects of subthalamic nucleus topography on neuropsychological outcomes of deep brain stimulation for Parkinson's disease.
2022; 12 (1): 213
Patients with psychiatric symptoms, such as depression, anxiety, and visual hallucinations, may be at increased risk for adverse effects following deep brain stimulation of the subthalamic nucleus for Parkinson's disease, but there have been relatively few studies of associations between locations of chronic stimulation and neuropsychological outcomes. We sought to determine whether psychiatric history modulates associations between stimulation location within the subthalamic nucleus and postoperative affective and cognitive changes. We retrospectively identified 42 patients with Parkinson's disease who received bilateral subthalamic nucleus deep brain stimulation and who completed both pre- and postoperative neuropsychological testing. Active stimulation contacts were localized in MNI space using Lead-DBS software. Linear discriminant analysis identified vectors maximizing variance in postoperative neuropsychological changes, and Pearson's correlations were used to assess for linear relationships. Stimulation location was associated with postoperative change for only 3 of the 18 neuropsychological measures. Variation along the superioinferior (z) axis was most influential. Constraining the analysis to patients with a history of depression revealed 10 measures significantly associated with active contact location, primarily related to location along the anterioposterior (y) axis and with worse outcomes associated with more anterior stimulation. Analysis of patients with a history of anxiety revealed 5 measures with location-associated changes without a predominant axis. History of visual hallucinations was not associated with significant findings. Our results suggest that a history of depression may influence the relationship between active contact location and neuropsychological outcomes following subthalamic nucleus deep brain stimulation. These patients may be more sensitive to off-target (nonmotor) stimulation.
View details for DOI 10.1038/s41398-022-01978-y
View details for PubMedID 35624103
Lateralized Effect of Thalamic Deep Brain Stimulation Location on Verbal Abstraction.
Movement disorders : official journal of the Movement Disorder Society
BACKGROUND: Regionalized thalamic activity has been implicated in language function, and yet the effect of thalamic deep brain stimulation (DBS) on language-related clinical outcomes is underexplored.OBJECTIVE: The objective of this study was to determine if the location of stimulation within the thalamus correlates with changes in language-related neuropsychological outcomes following DBS for essential tremor.METHODS: Thirty patients with essential tremor underwent comprehensive neuropsychological evaluations before and after DBS surgery targeting the ventral intermediate nucleus of the thalamus. Changes in neuropsychological functions were evaluated. The relationships between language-related outcomes and stimulation location were assessed using both categorical and linear methods. Any significant results were further validated using linear discriminant analysis.RESULTS: Most neuropsychological functions remained unchanged at the group level. However, outcome on a measure of verbal abstraction was significantly dependent on stimulation location along the anterior-posterior axis within the left ventral lateral thalamus, with anterior stimulation associated with reduced verbal abstraction performance. This result was supported by linear discriminant analysis, which showed that stimulation locations with improved and reduced verbal abstraction function were best separated by a vector nearly parallel to the anterior-posterior axis. No stimulation location dependence was found for verbal abstraction outcome in the right thalamus or for outcomes of other language functions in either hemisphere.CONCLUSION: We demonstrate an effect of thalamic DBS on verbal abstraction as a function of left thalamic topography. This finding provides clinical evidence for the lateralization and regionalization of thalamic language function that may be relevant for understanding nonmotor effects of stimulation. © 2021 International Parkinson and Movement Disorder Society.
View details for DOI 10.1002/mds.28606
View details for PubMedID 33818819
- Can (or Should) We Treat Depression and Anxiety in Parkinson's Disease Algorithmically? The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry 2021
Association of Preoperative Visual Hallucinations With Cognitive Decline After Deep Brain Stimulation for Parkinson's Disease.
The Journal of neuropsychiatry and clinical neurosciences
OBJECTIVE: Deep brain stimulation (DBS) is effective for the motor symptoms of Parkinson's disease (PD). Although most patients benefit with minimal cognitive side effects, cognitive decline is a risk, and there is little available evidence to guide preoperative risk assessment. Visual illusions or visual hallucinations (VHs) and impulse-control behaviors (ICBs) are relatively common complications of PD and its treatment and may be a marker of more advanced disease, but their relationship with postoperative cognition has not been established. The authors aimed to determine whether any preoperative history of VHs or ICBs is associated with cognitive change after DBS.METHODS: Retrospective chart review identified 54 patients with PD who received DBS of the subthalamic nucleus or globus pallidus internus and who completed both pre- and postoperative neuropsychological testing. Linear regression models were used to assess whether any preoperative history of VHs or ICBs was associated with changes in attention, executive function, language, memory, or visuospatial cognitive domains while controlling for surgical target and duration between evaluations.RESULTS: The investigators found that a history of VHs was associated with declines in attention (b=-4.04, p=0.041) and executive function (b=-4.24, p=0.021). A history of ICBs was not associated with any significant changes.CONCLUSIONS: These results suggest that a history of VHs may increase risk of cognitive decline after DBS; thus, specific preoperative counseling and targeted remediation strategies for these patients may be indicated. In contrast, a history of ICBs does not appear to be associated with increased cognitive risk.
View details for DOI 10.1176/appi.neuropsych.20040077
View details for PubMedID 33203305
Anterior Sensorimotor Subthalamic Nucleus Stimulation Is Associated With Improved Voice Function.
BACKGROUND: Despite the impact of Parkinson disease (PD) on speech communication, there is no consensus regarding the effect of lead location on voice-related outcomes in subthalamic nucleus (STN) deep brain stimulation (DBS).OBJECTIVE: To determine the relationship of stimulation location to changes in cepstral analyses of voice following STN DBS.METHODS: Speech pathology evaluations were obtained from 14 PD subjects, before and after STN DBS, including audio-perceptual voice ratings (overall severity, loudness, hoarseness changes), measured indices of dysphonia (cepstral peak prominence and cepstral spectral index of dysphonia), and phonatory aerodynamics. The contact locations used for active stimulation at the time of postoperative voice evaluations were determined and assessed in relation to voice outcomes.RESULTS: Voice outcomes remained relatively unchanged on average. Stimulation locations in the anterior portion of the sensorimotor region of the left STN, however, were associated with improvements in voice severity scores, cepstral spectral index of dysphonia, shortness of breath, and phonatory airflow during connected speech. Posterior locations were associated with worsening of these outcomes. Variation in the medial-lateral or dorsal-ventral position on the left, and in any direction on the right, did not correlate with any voice outcome.CONCLUSION: Active contact placement within the anterior sensorimotor STN was associated with improved perceptual and acoustic-aerodynamic voice-related outcomes. These findings suggest an STN topography for improving airflow for speech, in turn improving how PD patients' voices sound.
View details for DOI 10.1093/neuros/nyaa024
View details for PubMedID 32199026
- DBS in major depression Deep Brain Stimulation: Techniques and Practice Thieme Medical Publishers. 2019
Serine 421 regulates mutant huntingtin toxicity and clearance in mice
JOURNAL OF CLINICAL INVESTIGATION
2016; 126 (9): 3585–97
Huntington's disease (HD) is a progressive, adult-onset neurodegenerative disease caused by a polyglutamine (polyQ) expansion in the N-terminal region of the protein huntingtin (HTT). There are no cures or disease-modifying therapies for HD. HTT has a highly conserved Akt phosphorylation site at serine 421, and prior work in HD models found that phosphorylation at S421 (S421-P) diminishes the toxicity of mutant HTT (mHTT) fragments in neuronal cultures. However, whether S421-P affects the toxicity of mHTT in vivo remains unknown. In this work, we used murine models to investigate the role of S421-P in HTT-induced neurodegeneration. Specifically, we mutated the human mHTT gene within a BAC to express either an aspartic acid or an alanine at position 421, mimicking tonic phosphorylation (mHTT-S421D mice) or preventing phosphorylation (mHTT-S421A mice), respectively. Mimicking HTT phosphorylation strongly ameliorated mHTT-induced behavioral dysfunction and striatal neurodegeneration, whereas neuronal dysfunction persisted when S421 phosphorylation was blocked. We found that S421 phosphorylation mitigates neurodegeneration by increasing proteasome-dependent turnover of mHTT and reducing the presence of a toxic mHTT conformer. These data indicate that S421 is a potent modifier of mHTT toxicity and offer in vivo validation for S421 as a therapeutic target in HD.
View details for DOI 10.1172/JCI80339
View details for Web of Science ID 000382513400036
View details for PubMedID 27525439
View details for PubMedCentralID PMC5004962
Sequence-Level Analysis of the Major European Huntington Disease Haplotype
AMERICAN JOURNAL OF HUMAN GENETICS
2015; 97 (3): 435–44
Huntington disease (HD) reflects the dominant consequences of a CAG-repeat expansion in HTT. Analysis of common SNP-based haplotypes has revealed that most European HD subjects have distinguishable HTT haplotypes on their normal and disease chromosomes and that ∼50% of the latter share the same major HD haplotype. We reasoned that sequence-level investigation of this founder haplotype could provide significant insights into the history of HD and valuable information for gene-targeting approaches. Consequently, we performed whole-genome sequencing of HD and control subjects from four independent families in whom the major European HD haplotype segregates with the disease. Analysis of the full-sequence-based HTT haplotype indicated that these four families share a common ancestor sufficiently distant to have permitted the accumulation of family-specific variants. Confirmation of new CAG-expansion mutations on this haplotype suggests that unlike most founders of human disease, the common ancestor of HD-affected families with the major haplotype most likely did not have HD. Further, availability of the full sequence data validated the use of SNP imputation to predict the optimal variants for capturing heterozygosity in personalized allele-specific gene-silencing approaches. As few as ten SNPs are capable of revealing heterozygosity in more than 97% of European HD subjects. Extension of allele-specific silencing strategies to the few remaining homozygous individuals is likely to be achievable through additional known SNPs and discovery of private variants by complete sequencing of HTT. These data suggest that the current development of gene-based targeting for HD could be extended to personalized allele-specific approaches in essentially all HD individuals of European ancestry.
View details for DOI 10.1016/j.ajhg.2015.07.017
View details for Web of Science ID 000361084700006
View details for PubMedID 26320893
View details for PubMedCentralID PMC4564985
Targeting H3K4 trimethylation in Huntington disease
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
2013; 110 (32): E3027–E3036
Transcriptional dysregulation is an early feature of Huntington disease (HD). We observed gene-specific changes in histone H3 lysine 4 trimethylation (H3K4me3) at transcriptionally repressed promoters in R6/2 mouse and human HD brain. Genome-wide analysis showed a chromatin signature for this mark. Reducing the levels of the H3K4 demethylase SMCX/Jarid1c in primary neurons reversed down-regulation of key neuronal genes caused by mutant Huntingtin expression. Finally, reduction of SMCX/Jarid1c in primary neurons from BACHD mice or the single Jarid1 in a Drosophila HD model was protective. Therefore, targeting this epigenetic signature may be an effective strategy to ameliorate the consequences of HD.
View details for DOI 10.1073/pnas.1311323110
View details for Web of Science ID 000322771100015
View details for PubMedID 23872847
View details for PubMedCentralID PMC3740882
PolyQ Disease: Too Many Qs, Too Much Function?
2010; 67 (6): 897–99
The nature of the gain-of-function toxicity found in polyglutamine (polyQ) diseases has been the subject of considerable debate. In this issue of Neuron, Duvick et al. and Nedelsky et al. show that, in two of these diseases, pathology is mediated by normal protein activity.
View details for DOI 10.1016/j.neuron.2010.09.012
View details for Web of Science ID 000282801100001
View details for PubMedID 20869586
View details for PubMedCentralID PMC3989162
Stereoselective macrocyclization through zirconocene-mediated coupling of achiral dialkynes
1,4-Bis[trimethylsilyl(ethynyl)]naphthalene () and 1,4-bis[trimethylsilyl(ethynyl)]anthracene () undergo diastereoselective coupling with Cp2Zr(py)(Me3SiC[triple bond, length as m-dash]CSiMe3) to give trimeric macrocycles in good yield.
View details for DOI 10.1039/b815750b
View details for Web of Science ID 000261960400026
View details for PubMedID 19099079