Sara Johansen’s work is focused on the intersection of mental health, technology, and design. As the Director of Clinical Innovation at Brainstorm: The Stanford Lab for Mental Health Innovation, she leads projects in research, education, and product development that aim to bridge the gap between clinicians and innovators in mental health technology. At Stanford, she created the Technology Innovation Pathway that provides clinical, research, and educational experiences in tech-based mental health care, and she is currently developing a tech-enabled clinic at Stanford that connects patients with smartphone apps to support their mental health care. Additionally, she is an advisor to early-stage startups and works as an industry consultant in mental health product design. Dr. Johansen earned her MD at the Stanford School of Medicine, and she is currently a resident psychiatrist in the Stanford Department of Psychiatry.
- Artificial Intelligence
Boards, Advisory Committees, Professional Organizations
Director of Clinical Innovation, Brainstorm: The Stanford Lab for Mental Health Innovation (2019 - Present)
Psychiatric Leadership and Entrepreneurship Caucus, American Psychiatric Association (2021 - Present)
Residency, Stanford University Adult Psychiatry Residency Program (2023)
MD, Stanford University School of Medicine (2019)
MS, University of Alaska Fairbanks (2014)
BS, University of Puget Sound (2011)
Past Psychiatric Conditions as Risk Factors for Postpartum Depression: A Nationwide Cohort Study.
The Journal of clinical psychiatry
2020; 81 (1)
OBJECTIVE: To compare risk for postpartum depression across prior psychiatric diagnoses.METHODS: The deidentified Optum© Clinformatics Data Mart of national commercial insurance claims was used to identify 1,166,577 women of reproductive age with first-observed incidence of pregnancy across all 50 United States from 2003 to 2016. Women with insurance coverage for at least 6 months prior to conception and following delivery were eligible (n = 336,522). Psychiatric diagnoses prior to pregnancy were identified by ICD-9-CM and ICD-10-CM codes, including depression, anxiety and panic disorders, bipolar disorder, obsessive-compulsive disorder, posttraumatic stress disorder, and eating disorders. Primary outcomes included postpartum depression diagnosis at 2 months and 1 year after delivery. Multiple variable logistic regression analysis assessed for independent associations between predictors and outcomes.RESULTS: Among 336,522 pregnancies, 9.4% of women were diagnosed with postpartum depression (n = 31,610). Five percent of women with no depression history developed postpartum depression, compared to 65% of women with depression prior to and during pregnancy. Among women with history of depression who were euthymic during pregnancy, 20% were diagnosed with postpartum depression. A major risk factor was a history of depression (OR = 2.7; 95% CI, 2.6-2.8; P < .001), and depression in pregnancy was a risk factor for continued depression in the postpartum period (OR = 13.1; 95% CI, 12.6-13.6; P < .001). All other psychiatric conditions, including anxiety and panic disorders, bipolar disorder, obsessive-compulsive disorder, posttraumatic stress disorder, and eating disorders, conferred risk for postpartum depression, independent of a comorbid depression history.CONCLUSIONS: We report that all psychiatric diagnoses investigated independently increase risk for postpartum depression and suggest that care providers inquire about psychiatric history to identify and closely monitor women at increased risk for postpartum depression.
View details for DOI 10.4088/JCP.19m12929
View details for PubMedID 31967747
- Management of perinatal depression with non-drug interventions BMJ-BRITISH MEDICAL JOURNAL 2019; 364
- Media-Related Education in Psychiatry Residency Programs ACADEMIC PSYCHIATRY 2018; 42 (5): 679–85
Contraceptive counseling in reproductive-aged women treated for breast cancer at a tertiary care institution: a retrospective analysis
2017; 96 (4): 248–53
The objective was to assess the frequency of documented contraceptive and fertility preservation counseling for women treated for breast cancer.We conducted a chart analysis of female breast cancer patients (n=211) ages 18-45 years receiving chemotherapy treatment at Stanford Comprehensive Cancer Center from 2010 to 2014. Primary outcomes of contraceptive counseling and fertility preservation counseling documentation were assessed for frequency. Secondary outcomes included pregnancy testing, contraception use and pregnancy during treatment.Among the total sample (n=211), sexual activity was documented in 24% of patients (n=51). Fifty-one percent (n=108) of patients received pregnancy testing prior to initiation of treatment. Past contraception use was documented in 74% of patients (n=156) and current contraception use in 25% (n=53). Twenty-six percent of patients received fertility preservation counseling alone (n=54), 10% received contraceptive counseling alone (n=22), and 12% received both types of counseling (n=25). Patients were three times more likely to receive contraceptive counseling if using contraception at diagnosis [odds ratio (OR) 3.1, confidence interval (CI) 1.1-9.1, p=.04], and older women were significantly less likely to receive counseling (OR 0.2, CI 0.1-1.0, p=.04). Two patients became pregnant and had an abortion during treatment (1%), and neither patient was using contraception nor received contraceptive or fertility preservation counseling.Documentation of fertility preservation counseling occurs more frequently than contraceptive counseling, but both occur suboptimally. Lack of documentation does not allow us to conclude that counseling did not occur, but it suggests the need to improve documentation and increase awareness of contraceptive needs and counseling.Women undergoing breast cancer treatment do not consistently receive counseling on contraception or fertility preservation as a part of their care. Efforts are needed to ensure that women treated for breast cancer routinely receive counseling about fertility preservation and contraceptive options.
View details for PubMedID 28645785
Isoflurane causes concentration-dependent inhibition of medullary raphe 5-HT neurons in situ
AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL
2015; 193: 51-56
Anesthetics have a profound influence on a myriad of autonomic processes. Mechanisms of general anesthesia, and how these mechanisms give rise to the multifaceted state of anesthesia, are largely unknown. The ascending and descending serotonin (5-HT) networks are key modulators of autonomic pathways, and are critically involved in homeostatic reflexes across the motor, somatosensory, limbic and autonomic systems. These 5-HT networks are thought to contribute to anesthetic effects, but how anesthetics affect 5-HT neuron function remains a pertinent question. We hypothesized that the volatile anesthetic isoflurane inhibits action potential discharge of medullary raphé 5-HT neurons.We conducted extracellular recordings on individual neurons in the medullary raphé region of the unanesthetized in situ perfused brainstem preparation to determine how exposure to isoflurane affects 5-HT neurons. We examined changes in 5-HT neuron baseline firing in response to treatment with either 1, 1.5, or 2% isoflurane. We measured isoflurane concentrations by gas chromatography-mass spectrometry (GC-MS) analysis.Exposure to isoflurane inhibited action potential discharge in raphé 5-HT neurons. We document a concentration-dependent inhibition over a range of concentrations approximating isoflurane MAC (minimum alveolar concentration required for surgical anesthesia). Delivered concentrations of isoflurane were confirmed using GC-MS analysis.These findings illustrate that halogenated anesthetics greatly affect 5-HT neuron firing and suggest 5-HT neuron contributions to mechanisms of general anesthesia.
View details for DOI 10.1016/j.autneu.2015.07.002
View details for Web of Science ID 000366077800008
View details for PubMedID 26213357
View details for PubMedCentralID PMC4658272
Isoflurane abolishes spontaneous firing of serotonin neurons and masks their pH/CO2 chemosensitivity
JOURNAL OF NEUROPHYSIOLOGY
2015; 113 (7): 2879-2888
Serotonin (5-hydroxytryptamine, 5-HT) neurons from the mouse and rat rostral medulla are stimulated by increased CO2 when studied in culture or brain slices. However, the response of 5-HT neurons has been variable when animals are exposed to hypercapnia in vivo. Here we examined whether halogenated inhalational anesthetics, which activate TWIK-related acid-sensitive K(+) (TASK) channels, could mask an effect of CO2 on 5-HT neurons. During in vivo plethysmography in mice, isoflurane (1%) markedly reduced the hypercapnic ventilatory response (HCVR) by 78-96% depending upon mouse strain and ambient temperature. In a perfused rat brain stem preparation, isoflurane (1%) reduced or silenced spontaneous firing of medullary 5-HT neurons in situ and abolished their responses to elevated perfusate Pco2. In dissociated cell cultures, isoflurane (1%) hyperpolarized 5-HT neurons by 6.52 ± 3.94 mV and inhibited spontaneous firing. A subsequent decrease in pH from 7.4 to 7.2 depolarized neurons by 4.07 ± 2.10 mV, but that was insufficient to reach threshold for firing. Depolarizing current restored baseline firing and the firing frequency response to acidosis, indicating that isoflurane did not block the underlying mechanisms mediating chemosensitivity. These results demonstrate that isoflurane masks 5-HT neuron chemosensitivity in vitro and in situ and markedly decreases the HCVR in vivo. The use of this class of anesthetic has a particularly potent inhibitory effect on chemosensitivity of 5-HT neurons.
View details for DOI 10.1152/jn.01073.2014
View details for Web of Science ID 000355000900083
View details for PubMedID 25695656
View details for PubMedCentralID PMC4416618
Isoflurane stimulates firing frequency and masks chemosensitivity of CO2-inhibited GABAergic neurons in situ
FEDERATION AMER SOC EXP BIOL. 2013
View details for Web of Science ID 000319883505141