I received my BS dual degree in Biology and Psychology from the University of Georgia as part of the Honors Program. There I pursued undergraduate research under the mentorship of L. Stephen Miller Ph.D. on the neural substrates of emotional conflict processing and neuroimaging signatures of traumatic brain injury. After a brief hiatus from the academic world working as a veterinary technician, I enrolled in the San Diego State University/University of California-San Diego Joint Doctoral Program in Clinical Psychology. My primary research mentors were Murray B. Stein, M.D., M.P.H., and Martin P. Paulus, M.D. My graduate research focused on the functional neuroanatomy and developmental determinants of negative valence systems in anxiety and traumatic stress disorders. I also pursued a clinical specialization in the psychotherapeutic treatment of anxiety and traumatic stress disorders through practicum work at the VA San Diego Healthcare System Anxiety Disorders Clinic and PTSD Clinical Team. I received specialized training in Prolonged Exposure (PE) and Eye Movement Desensitization and Reprocessing (EMDR), and I am a certified Level 1 EMDR provider. I completed my clinical internship at the Memphis VA Medical Center and continued to pursue a clinical specialization in the treatment of traumatic stress disorders. There, I completed VA training and certification to deliver Cognitive Processing Therapy (CPT), an empirically-supported cognitive-behavioral treatment for PTSD. Seeking less humidity and greater sunshine, I returned to California in September 2013 to begin a T32 Biobehavioral Research Fellowship in the Department of Psychiatry and Behavioral Sciences at Stanford University School of Medicine under the mentorship of Dr. Amit Etkin. My postdoctoral research encompasses brain imaging approaches to characterizing heterogeneity in posttraumatic stress disorder, neural mechanisms underlying the therapeutic effects of prolonged exposure therapy, and investigation of novel computerized cognitive and affective training interventions for individuals with PTSD. My long-term career goal is to understand the neural mechanisms responsible for the emergence, expression, and resolution of trauma and stress-related symptomatology, and to leverage this knowledge towards the refinement of existing treatments and the development of novel treatments and preventative interventions.
Honors & Awards
T-32 Biobehavioral Research Fellowship, Department of Psychiatry, Stanford University School of Medicine (September 2013-August 2015)
Alan J. Jaworski Men in Science Award, University of Georgia (2005)
Member of Phi Beta Kappa Honors Soceity, Phi Beta Kappa (2004)
Cota-Robles Fellowship, University of California-San Diego (2007-2009)
Charter Scholarship, University of Georgia (2001-2005)
Vice Presidential Scholarship, University of Georgia (2001-2005)
James E. Casey Scholarship, National Merit Scholarship (2001-2005)
Presidential Scholar, University of Georgia (2001-2005)
Boards, Advisory Committees, Professional Organizations
Member, American Psychological Association (2011 - Present)
Member, Society for Neuroscience (2011 - 2012)
Member, Anxiety and Depression Association of America (2013 - Present)
Doctor of Philosophy, San Diego State University/University of California-San Diego Joint Doctoral Program, Clinical Psychology (2013)
Bachelor of Science, University of Georgia, Biology, Psychology (2005)
Community and International Work
San Francisco Center for Integrative Anxiety Solutions, 870 Market St, Ste 958, San Francisco, CA 94102
Anxiety disorders, post-traumatic stress disorder, mood disorders
San Francisco Bay Area
Opportunities for Student Involvement
Common and disorder-specific neural responses to emotional faces in generalised anxiety, social anxiety and panic disorders
BRITISH JOURNAL OF PSYCHIATRY
2015; 206 (3): 206-215
Background Although evidence exists for abnormal brain function across various anxiety disorders, direct comparison of neural function across diagnoses is needed to elicit abnormalities common across disorders and those distinct to a particular diagnosis. Aims To delineate common and distinct abnormalities within generalised anxiety (GAD), panic and social anxiety disorder (SAD) during affective processing. Method Fifty-nine adults (15 with GAD, 15 with panic disorder, 14 with SAD, and 15 healthy controls) underwent functional magnetic resonance imaging while completing a facial emotion matching task with fearful, angry and happy faces. Results Greater differential right amygdala activation to matching fearful v. happy facial expressions related to greater negative affectivity (i.e. trait anxiety) and was heightened across all anxiety disorder groups compared with controls. Collapsing across emotional face types, participants with panic disorder uniquely displayed greater posterior insula activation. Conclusions These preliminary results highlight a common neural basis for clinical anxiety in these diagnoses and also suggest the presence of disorder-specific dysfunction.
View details for DOI 10.1192/bjp.bp.114.149880
View details for Web of Science ID 000351478900006
View details for PubMedID 25573399
Greater preference consistency during the Willingness-to-Pay task is related to higher resting state connectivity between the ventromedial prefrontal cortex and the ventral striatum.
Brain imaging and behavior
The significance of why a similar set of brain regions are associated with the default mode network and value-related neural processes remains to be clarified. Here, we examined i) whether brain regions exhibiting willingness-to-pay (WTP) task-related activity are intrinsically connected when the brain is at rest, ii) whether these regions overlap spatially with the default mode network, and iii) whether individual differences in choice behavior during the WTP task are reflected in functional brain connectivity at rest. Blood-oxygen-level dependent (BOLD) signal was measured by functional magnetic resonance imaging while subjects performed the WTP task and at rest with eyes open. Brain regions that tracked the value of bids during the WTP task were used as seed regions in an analysis of functional connectivity in the resting state data. The seed in the ventromedial prefrontal cortex was functionally connected to core regions of the WTP task-related network. Brain regions within the WTP task-related network, namely the ventral precuneus, ventromedial prefrontal and posterior cingulate cortex overlapped spatially with publically available maps of the default mode network. Also, those individuals with higher functional connectivity during rest between the ventromedial prefrontal cortex and the ventral striatum showed greater preference consistency during the WTP task. Thus, WTP task-related regions are an intrinsic network of the brain that corresponds spatially with the default mode network, and individual differences in functional connectivity within the WTP network at rest may reveal a priori biases in choice behavior.
View details for DOI 10.1007/s11682-015-9435-z
View details for PubMedID 26271206
Early life stress and the anxious brain: evidence for a neural mechanism linking childhood emotional maltreatment to anxiety in adulthood.
Childhood emotional maltreatment (CEM) increases the likelihood of developing an anxiety disorder in adulthood, but the neural processes underlying conferment of this risk have not been established. Here, we test the potential for neuroimaging the adult brain to inform understanding of the mechanism linking CEM to adult anxiety symptoms.One hundred eighty-two adults (148 females, 34 males) with a normal-to-clinical range of anxiety symptoms underwent structural and functional magnetic resonance imaging while completing an emotion-processing paradigm with facial expressions of fear, anger, and happiness. Participants completed self-report measures of CEM and current anxiety symptoms. Voxelwise mediation analyses on gray-matter volumes and activation to each emotion condition were used to identify candidate brain mechanisms relating CEM to anxiety in adulthood.During processing of fear and anger faces, greater amygdala and less right dorsolateral prefrontal (dlPFC) activation partially mediated the positive relationship between CEM and anxiety symptoms. Greater right posterior insula activation to fear also partially mediated this relationship, as did greater ventral anterior cingulate (ACC) and less dorsal ACC activation to anger. Responses to happy faces in these regions did not mediate the CEM-anxiety relationship. Smaller right dlPFC gray-matter volumes also partially mediated the CEM-anxiety relationship.Activation patterns of the adult brain demonstrate the potential to inform mechanistic accounts of the CEM conferment of anxiety symptoms. Results support the hypothesis that exaggerated limbic activation to negative valence facial emotions links CEM to anxiety symptoms, which may be consequent to a breakdown of cortical regulatory processes.
View details for DOI 10.1017/S0033291715002603
View details for PubMedID 26670947
Cognitive-behavioral therapy for generalized anxiety disorder is associated with attenuation of limbic activation to threat-related facial emotions.
Journal of affective disorders
2014; 169: 76-85
The neural processes underlying the benefits of cognitive behavioral treatment (CBT) for generalized anxiety disorder (GAD) are not well understood.Twenty-one (n=21) adults with a principal diagnosis of GAD and eleven (n=11) non-anxious healthy controls (HC) underwent functional magnetic resonance imaging while completing a facial emotion processing task. Responses to threat-related emotionality (i.e., the contrast of fear and angry vs. happy faces) were assessed at pretreatment and again following 10 sessions of CBT in the GAD group and a comparable waiting period in the HC group.At pretreatment, GAD participants displayed blunted responses in the amygdala, insula, and anterior cingulate to the happy face-processing comparison condition, and greater amygdalo-insular connectivity. CBT was associated with attenuated amygdalar and subgenual anterior cingulate activation to fear/angry faces and heightened insular responses to the happy face comparison condition, but had no apparent effects on connectivity. Pre-treatment abnormalities and treatment-related changes were not associated with symptoms of worry.There was no active control condition (e.g., treatment waitlist) for comparison of treatment effects.Taken together, these results provide evidence for a dual-process psychotherapeutic model of neural systems changes in GAD in which cingulo-amygdalar reactivity to threat-cues is attenuated while insular responses to positive facial emotions are potentiated. Future work is needed to determine the clinical implications of these changes and their specificity to CBT.
View details for DOI 10.1016/j.jad.2014.07.031
View details for PubMedID 25171782
Neural functional and structural correlates of childhood, maltreatment in women with intimate-partner violence-related posttraumatic stress disorder
2013; 211 (2): 93-103
Childhood maltreatment (CM) is a strong risk factor for development of posttraumatic stress disorder (PTSD) upon adult exposure to extreme adverse events. However, the neural underpinnings of this relationship are not well understood. Here, we test the hypothesis that severity of CM history is positively correlated with emotion-processing limbic and prefrontal brain activation/connectivity and negatively correlated with prefrontal gray matter volumes in women with PTSD due to intimate-partner violence (IPV-PTSD). Thirty-three women with IPV-PTSD underwent structural and functional magnetic resonance imaging while completing a facial emotion processing task. Multivariate regressions examined the relationship of CM to patterns of activation, connectivity, and gray matter volumes. CM severity was: (a) positively correlated with ventral ACC activation while processing angry faces; (b) negatively correlated with dorsal ACC and insula activation while processing fear and angry faces, arising from positive correlations with the shape-matching baseline; (c) positively correlated with limbic-prefrontal connectivity while processing fear faces but negatively correlated with amygdalo-insular connectivity while processing fear and angry; and (d) negatively correlated with prefrontal gray matter volumes. These results suggest CM exposure may account for variability in limbic/prefrontal brain function and prefrontal structure in adulthood PTSD and offer one potential mechanism through which CM confers risk to future development of PTSD.
View details for DOI 10.1016/j.pscychresns.2012.08.006
View details for Web of Science ID 000316828400001
View details for PubMedID 23154098
Red Brain, Blue Brain: Evaluative Processes Differ in Democrats and Republicans
2013; 8 (2)
Liberals and conservatives exhibit different cognitive styles and converging lines of evidence suggest that biology influences differences in their political attitudes and beliefs. In particular, a recent study of young adults suggests that liberals and conservatives have significantly different brain structure, with liberals showing increased gray matter volume in the anterior cingulate cortex, and conservatives showing increased gray matter volume in the in the amygdala. Here, we explore differences in brain function in liberals and conservatives by matching publicly-available voter records to 82 subjects who performed a risk-taking task during functional imaging. Although the risk-taking behavior of Democrats (liberals) and Republicans (conservatives) did not differ, their brain activity did. Democrats showed significantly greater activity in the left insula, while Republicans showed significantly greater activity in the right amygdala. In fact, a two parameter model of partisanship based on amygdala and insula activations yields a better fitting model of partisanship than a well-established model based on parental socialization of party identification long thought to be one of the core findings of political science. These results suggest that liberals and conservatives engage different cognitive processes when they think about risk, and they support recent evidence that conservatives show greater sensitivity to threatening stimuli.
View details for DOI 10.1371/journal.pone.0052970
View details for Web of Science ID 000315970300009
View details for PubMedID 23418419
A meta-analysis of cognitive functioning in older adults with PTSD
JOURNAL OF ANXIETY DISORDERS
View details for DOI http://dx.doi.org/10.1016/j.janxdis.2013.01.001
Exaggerated and Disconnected Insular-Amygdalar Blood Oxygenation Level-Dependent Response to Threat-Related Emotional Faces in Women with Intimate-Partner Violence Posttraumatic Stress Disorder
2010; 68 (5): 433-441
Intimate-partner violence (IPV) is one of the most common causes of posttraumatic stress disorder (PTSD) among women. PTSD neuroimaging studies have identified functional differences in the amygdala and anterior cingulate cortex (ACC)/medial prefrontal cortex during emotion processing. Recent investigations of the limbic sensory system and its associated neural substrate, the insular cortex, have demonstrated its importance for emotional awareness. This study examined the hypothesis that women with IPV-PTSD show a dysregulation of this limbic sensory system while processing threat-related emotional faces.12 women with IPV-PTSD and 12 nontraumatized comparison women underwent blood oxygenation level-dependent functional magnetic resonance imaging while completing an emotional face-matching task.IPV-PTSD subjects relative to comparison subjects displayed increased activation of the anterior insula and amygdala and decreased connectivity among the anterior insula, amygdala, and ACC while matching to fearful versus happy target faces. A similar pattern of activation differences was also observed for angry versus happy target faces. IPV-PTSD subjects relative to comparison subjects also displayed increased dorsal ACC/medial prefrontal cortex activation and decreased ventral ACC activation when matching to a male versus a female target, and the extent of increased dorsal ACC activation correlated positively with hyperarousal symptoms.Women with IPV-PTSD display hyperactivity and disconnection among affective and limbic sensory systems while processing threat-related emotion. Furthermore, hyperactivity of cognitive-appraisal networks in IPV-PTSD may promote hypervigilant states of awareness through an exaggerated sensitivity to contextual cues, i.e., male gender, which relate to past trauma.
View details for DOI 10.1016/j.biopsych.2010.04.028
View details for Web of Science ID 000281126800006
View details for PubMedID 20573339
Transverse patterning dissociates human EEG theta power and hippocampal BOLD activation
2009; 46 (1): 153-162
View details for DOI 10.1111/j.1469-8986.2008.00719.x.