Mariana Schmajuk received her medical school education at Boston University School of Medicine in 2012. She completed her General Adult Psychiatry Residency program Mount Sinai School of Medicine in New York in 2016, serving as Chief Resident with a focus on the early transition from medical school to residency. She went on to complete her Consult-Liaison fellowship at New York-Presbyterian Hospital Columbia University Medical Center in 2017.
Dr. Schmajuk joined Stanford University CLP team in 2017. She is a primary member of the emergency medicine consultations, working collaboratively with a nurse practioner, social worker and residents. Clinically, Dr. Schmajuk focuses on treating patients with terminal neurological disorders and oncological processes. Dr. Schmajuk is the director of the Psychosomatic Continuity clinic where residents and fellows are able to assess and longitudinally treat patients with psychiatric sequela in the context of complex medical illness. She has a particular interest in brief psychotherapeutic interventions. She enjoys teaching medical students about CL psychiatry and interviewing skills. At present, Dr. Schmajuk is using techniques of applied improvisation to educate psychiatry residents and others about the building blocks of communication. She also is an active member of the bioethics committee.
- Consult-Liaison Psychiatry
Clinical Assistant Professor, Psychiatry and Behavioral Sciences
Medical Education: Boston University School of Medicine (2012) MA
Residency: Icahn School of Medicine at Mount Sinai (2016) NY
Board Certification: American Board of Psychiatry and Neurology, Psychosomatic Med/Consultation Liaison Psychiatry (2017)
Fellowship: New York Presbyterian Hospital - Columbia University NY
Board Certification: American Board of Psychiatry and Neurology, Psychiatry (2016)
- Psychotherapy in Transplant Patients Psychosocial Care of End-Stage Organ Disease and Transplant Patients 2019: 471–481
Face emotion labeling deficits in children with bipolar disorder and severe mood dysregulation
DEVELOPMENT AND PSYCHOPATHOLOGY
2008; 20 (2): 529–46
Children with narrow phenotype bipolar disorder (NP-BD; i.e., history of at least one hypomanic or manic episode with euphoric mood) are deficient when labeling face emotions. It is unknown if this deficit is specific to particular emotions, or if it extends to children with severe mood dysregulation (SMD; i.e., chronic irritability and hyperarousal without episodes of mania). Thirty-nine NP-BD, 31 SMD, and 36 control subjects completed the emotional expression multimorph task, which presents gradations of facial emotions from 100% neutrality to 100% emotional expression (happiness, surprise, fear, sadness, anger, and disgust). Groups were compared in terms of intensity of emotion required before identification occurred and accuracy. Both NP-BD and SMD youth required significantly more morphs than controls to label correctly disgusted, surprised, fearful, and happy faces. Impaired face labeling correlated with deficient social reciprocity skills in NP-BD youth and dysfunctional family relationships in SMD youth. Compared to controls, patients with NP-BD or SMD require significantly more intense facial emotion before they are able to label the emotion correctly. These deficits are associated with psychosocial impairments. Understanding the neural circuitry associated with face-labeling deficits has the potential to clarify the pathophysiology of these disorders.
View details for DOI 10.1017/S0954579408000266
View details for Web of Science ID 000255327500008
View details for PubMedID 18423093
View details for PubMedCentralID PMC2669935
Attention bias to threat faces in children with bipolar disorder and comorbid lifetime anxiety disorders
ELSEVIER SCIENCE INC. 2007: 819–21
Although comorbid anxiety disorders are common in children with bipolar disorder (BD), it is unclear how this comorbidity impacts the pathophysiology of the illness.Pediatric BD with lifetime anxiety (BD+ANX, n = 20), BD without lifetime anxiety (BD-ANX, n = 11), and controls (n = 14) were administered the visual-probe paradigm, which assesses attention bias to threat faces.Bipolar disorder +ANX demonstrated a stronger bias toward threat relative to BD-ANX and controls; the latter two did not differ from each other.Bipolar disorder +ANX showed a bias toward threat while, in two previous studies, anxious children showed a bias away from threat faces. Future studies should compare the pathophysiology of BD with and without a comorbid anxiety disorder and anxiety disorders presenting alone.
View details for DOI 10.1016/j.biopsych.2006.08.021
View details for Web of Science ID 000245002700013
View details for PubMedID 17338904
Different psychophysiological and behavioral responses elicited by frustration in pediatric bipolar disorder and severe mood dysregulation
AMERICAN JOURNAL OF PSYCHIATRY
2007; 164 (2): 309–17
Researchers disagree as to whether irritability is a diagnostic indicator for pediatric mania in bipolar disorder. The authors compared the behavioral and psychophysiological correlates of irritability among children with severe mood dysregulation (i.e., nonepisodic irritability and hyperarousal without episodes of euphoric mood) and narrow-phenotype bipolar disorder (i.e., a history of at least one manic or hypomanic episode with euphoric mood) as well as those with no diagnosis (i.e., healthy comparison children).Subjects with severe mood dysregulation (N=21) or narrow-phenotype bipolar disorder (N=35) and comparison subjects (N=26) completed the affective Posner task, an attentional task that manipulated emotional demands and induced frustration. Mood response, behavior (reaction time and accuracy), and brain activity (event-related potentials) were measured.The severe mood dysregulation and narrow-phenotype bipolar disorder groups both reported significantly more arousal than comparison subjects during frustration, but behavioral and psychophysiological performance differed between the patient groups. In the frustration condition, children with narrow-phenotype bipolar disorder had lower P3 amplitude than children with severe mood dysregulation or comparison subjects, reflecting impairments in executive attention. Regardless of emotional context, children with severe mood dysregulation had lower N1 event-related potential amplitude than comparison subjects or children with narrow-phenotype bipolar disorder, reflecting impairments in the initial stages of attention. Post hoc analyses demonstrated that the N1 deficit in children with severe mood dysregulation is associated with oppositional defiant disorder symptom severity.Results indicate that while irritability is an important feature of severe mood dysregulation and narrow-phenotype bipolar disorder, the pathophysiology of irritability may differ among the groups and is influenced by oppositional defiant disorder severity.
View details for DOI 10.1176/appi.ajp.164.2.309
View details for Web of Science ID 000243905700023
View details for PubMedID 17267795
Prevalence, clinical correlates, and longitudinal course of severe mood dysregulation in children
ELSEVIER SCIENCE INC. 2006: 991–97
Controversy concerning the diagnosis of pediatric bipolar disorder (BD) has focused attention on children with chronic irritability and hyperarousal. This syndrome has been called the "broad BD phenotype" or severe mood dysregulation (SMD). This study examines prevalence, concurrent Axis I diagnoses, and longitudinal outcome of SMD in an epidemiologic sample.Data were drawn from the Great Smoky Mountains Study, a longitudinal epidemiological study. Items from the Child and Adolescent Psychiatric Assessment were used to generate SMD criteria.Among 1420 children, the lifetime prevalence of SMD in children ages 9-19 was 3.3%. Most (67.7%) SMD youth had an Axis I diagnosis, most commonly attention-deficit/hyperactivity disorder (26.9%), conduct disorder (25.9%), and/or oppositional defiant disorder (24.5%). In young adulthood (mean age 18.3 +/- 2.1 years), youth who met criteria for SMD in the first wave (mean age 10.6 +/- 1.4 years) were significantly more likely to be diagnosed with a depressive disorder (odds ratio 7.2, confidence interval 1.3-38.8, p = .02) than youth who never met criteria for SMD.Severe mood dysregulation is relatively common in childhood and predicts risk for early adulthood depressive disorders. Research should continue to explore the course of illness in children with SMD.
View details for DOI 10.1016/j.biopsych.2006.08.042
View details for Web of Science ID 000241691600013
View details for PubMedID 17056393
Electrophysiological activity underlying inhibitory control processes in normal adults
2006; 44 (3): 384–95
In a recent ERP study of inhibitory control using the Stop-Signal Task [Pliszka, S., Liotti, M., Woldorff, M. (2000). Inhibitory control in children with attention-deficit/hyperactivity disorder: Event-related potentials identify the processing component and timing of an impaired right-frontal response-inhibition mechanism. Biological Psychiatry, 48, 238-246], we showed that in normal children (age 10-12 years) the Stop Signals elicited a robust, right-frontal-maximal N200 (latency approximately 200 ms) that was strongly reduced in children with ADHD. To further investigate the mechanisms of response inhibition, this paradigm was applied to 11 healthy young adults. To better distinguish response-inhibition-related activity from early attentional effects, a "Stop-Signal-Irrelevant" condition was added, in which subjects performed the task while ignoring the Stop Signals. In the Stop-Signal-Relevant condition, the right frontal N200 to the Stop Signals was larger for Successful inhibition (SI) than for Failed inhibition (FI) trials. The timing and distribution of this effect was strikingly similar to that of the right-frontal ADHD deficit reported in Pliszka et al. (2000), supporting this activity being related to successful normal inhibitory control processes. In contrast, a posterior N200 was larger for Stop-Relevant than for Stop-Irrelevant trials, likely reflecting enhanced early sensory attention to the Stop Signals when relevant. Two longer-latency failure-specific ERP effects were also observed: a greater frontopolar negative wave (370-450 ms) to Failed than Successful inhibitions, and a greater parietal positive slow wave (450-650 ms) for Failed inhibitions than ignore-stop trials, likely reflecting differential recruitment of error detection and correction mechanisms following Failed attempts to inhibit a response.
View details for DOI 10.1016/j.neuropsychologia.2005.06.005
View details for Web of Science ID 000235861600006
View details for PubMedID 16095637
The impact of reward, punishment, and frustration on attention in pediatric bipolar disorder
ELSEVIER SCIENCE INC. 2005: 532–39
Theories in affective neuroscience suggest that mood disorders involve perturbations in attention-emotion interactions. We tested the hypothesis that frustration adversely impacts attention and behavior in children with bipolar disorder (BPD).Thirty-five children with BPD and 26 normal control subjects completed: 1) a Posner attention task with feedback but no contingencies; 2) an affective Posner with contingencies; and 3) an affective Posner that used rigged feedback to induce frustration. Reaction time (RT) and event-related potential (ERP) data were collected.At baseline (task 1), there were no between-group differences in behavior or ERPs. Children with BPD exhibited reduced parietal P3 amplitude on task 3 only. On trials occurring after negative feedback, control subjects showed decreased RT when contingencies were introduced (task 2), whereas BPD subjects did not.The introduction of contingencies was associated with impaired performance of children with BPD, suggesting deficits in their ability to adapt to changing contingencies. In addition, frustration was associated with disrupted attention allocation in children with BPD. We hypothesize that children with BPD inappropriately deployed attention to their internal frustration rather than to the task, causing impaired performance.
View details for DOI 10.1016/j.biopsych.2005.01.006
View details for Web of Science ID 000232866300004
View details for PubMedID 15953589
Deficits in social cognition and response flexibility in pediatric bipolar disorder
AMERICAN JOURNAL OF PSYCHIATRY
2005; 162 (9): 1644–51
Little is known about neuropsychological and social-cognitive function in patients with pediatric bipolar disorder. Identification of specific deficits and strengths that characterize pediatric bipolar disorder would facilitate advances in diagnosis, treatment, and research on pathophysiology. The purpose of this study was to test the hypothesis that youths with bipolar disorder would perform more poorly than matched healthy comparison subjects on measures of social cognition, motor inhibition, and response flexibility.Forty outpatients with pediatric bipolar disorder and 22 comparison subjects (no differences in age, gender, and IQ) completed measures of social cognition (the pragmatic judgment subtest of the Comprehensive Assessment of Spoken Language, facial expression recognition subtests of the Diagnostic Analysis of Nonverbal Accuracy Scale, the oral expression subtest of the Test of Language Competence), inhibition and response flexibility (stop and stop-change tasks), and motor inhibition (continuous performance tasks).Pediatric bipolar disorder patients performed more poorly than comparison subjects on social-cognitive measures (pragmatic judgment of language, facial expression recognition) and on a task requiring response flexibility. These deficits were present in euthymic patients. Differences between patients and comparison subjects could not be attributed to comorbid attention deficit hyperactivity disorder.Findings of impaired social cognition and response flexibility in youths with pediatric bipolar disorder suggest continuity between pediatric bipolar disorder and adult bipolar disorder. These findings provide a foundation for neurocognitive research designed to identify the neural mechanisms underlying these deficits.
View details for DOI 10.1176/appi.ajp.162.9.1644
View details for Web of Science ID 000231559300011
View details for PubMedID 16135623