Dr. Bajestan has received her PhD in Molecular and Cellular Neuroscience. She spent her training during her PhD and post-doctoral course in learning the molecular genetics and biology of neurological and psychiatric disorders. She later trained in Psychiatry at Stanford University and became a board certified General Psychiatrist by the American Board of Psychiatry and Neurology. Dr. Bajestan was the first neuropsychiatry fellow at Stanford University and established this fellowship with Dr. John Barry, her fellowship director. She is also board certified in Neuropsychiatry and Behavioral Neurology by the United Council of Neurological Subspecialties. She has undergone training in complex neuro-psychopharmacology, Interventional neuropsychiatry and different psychotherapy Orientations including Psychodynamic Psychotherapy, Cognitive and Behavioral Therapy (CBT), Psychodynamic Psychotherapy, Acceptance and Commitment Therapy (ACT), Hypnosis and Prolonged Exposure (PE).
Dr. Bajestan is the recipient of many national awards, such as American Psychiatric Association’s Leadership Award, American Association of Psychiatry Residency Director’s Brain Scholar Award, American College of Psychiatrists’ Laughlin Fellowship, American Neuropsychiatric Association’s Young Investigator’s Award, and Stanford University Psychiatry Department's Outstanding Resident Award. She is also the recipient of department of psychiatry's Chair’s Mission Award for Leadership and Professionalism.
Dr. Bajestan is currently the Neuropsychiatry Section Chief, the Associate Neuropsychiatry Fellowship Director and a Clinical Assistant Professor of Psychiatry and Behavioral Sciences at Stanford University.She is involved in clinical practice, research and training of the psychiatry residents and neuropsychiatry fellows. Dr. Bajestan is the neuropsychiatric consultant at Stanford University’s Inpatient Neurology Units, Epilepsy Monitoring Unit, and Outpatient Neurology Clinics. She also works in different psychiatry clinics in department of Psychiatry and Behavioral Sciences, providing consultations (mainly) and outpatient care (both medication management and psycho therapy). She takes joy in working closely with her patients, their family members, other health care providers, teaching/mentoring trainees and also attending to her research projects.
- Neuropsychiatry, Psychotherapy, Functional Neurological Symptom Disorders, Impulse Control Disorders (Both medication management and Psychotherapy), Anxiety Disorders
- For Clinical Issues, Call the Clinic at 650-723-8335, Please Do Not Use My Email ( HIPPA regulation)
Clinical Associate Professor, Psychiatry and Behavioral Sciences
Boards, Advisory Committees, Professional Organizations
Member, American Neuropsychiatric Association (2012 - Present)
Member, American Psychiatric Association (2009 - Present)
Resident Councilor, Northern California Psychiatric Association (2013 - 2014)
Fellowship: Stanford University Addiction Medicine Fellowship (2014) CA
Board Certification: NeuroPsychiatry, United Council for Neurologic Subspecialties
Board Certiffication, United Council of Neurological Subspecialties, Neuropsychiatry and Behavioral Neurology (2014)
Board Certification: Psychiatry, American Board of Psychiatry and Neurology (2013)
Neuropsychiatry Fellowship, Department of Psychiatry and Behavioral Sciences, Stanford University, Neuropsychiatry and Behavioral Neurology
Post-Doctoral Training, University of California, San Diego, Neuroscience
Residency: Department of Psychiatry, School of Medicine, Stanford University Hospital (2014)
PhD in Neuroscience, Kagoshima University, Graduate School of Medical and Dental Sciences, Japan University College London, England ( Visiting PhD Scholar), Neuroscience (2004)
Medical Education: Mashhad University of Medical Sciences (2001) Iran
Undergaduate, National Organization for Development of Exceptional Talents (NODET)
Current Research and Scholarly Interests
Treatment Outcome and Predictive Psychological Factors in Group Psychotherapy for Patients with Psychogenic Non-Epileptic Seizures and Psychogenic Movement Disorders ( groups are based on Psycho-dynamic Psychotherapy and Dialectical Behavioral Therapy) -recruiting. Contact Number: Dr. Ariela Karasov, MD. 650-723-8659
Psychiatric Presentations of C9orf72 Mutation: What Are the Diagnostic Implications for Clinicians?
journal of neuropsychiatry and clinical neurosciences
The C9orf72 mutation was identified as the most frequent genetic cause of frontotemporal dementia (FTD). In light of multiple reports of predominant psychiatric presentations of FTD secondary to C9orf72 mutation, the American Neuropsychiatric Association Committee on Research reviewed all studies on psychiatric aspects of this mutation to identify clinically relevant features for diagnosis. The most common psychiatric presentation is psychosis (21%-56%), with delusions, and/or multimodal hallucinations. Other presentations include late-onset mania and depression with cognitive impairment or catatonia. However, the frequency of C9orf72 mutations is low in typical schizophrenia or bipolar disorders (<0.1%). The authors provide clinical guidance on diagnosis and genetic testing.
View details for DOI 10.1176/appi.neuropsych.16090168
View details for PubMedID 28238272
Bedtime misalignment and progression of breast cancer.
2014; 31 (2): 214-221
Disruption of circadian rhythms, which frequently occurs during night shift work, may be associated with cancer progression. The effect of chronotype (preference for behaviors such as sleep, work, or exercise to occur at particular times of day, with an associated difference in circadian physiology) and alignment of bedtime (preferred vs. habitual), however, have not yet been studied in the context of cancer progression in women with breast cancer. Chronotype and alignment of actual bedtime with preferred chronotype were examined using the Morningness-Eveningness Scale (MEQ) and sleep-wake log among 85 women with metastatic breast cancer. Their association with disease-free interval (DFI) was retrospectively examined using the Cox proportional hazards model. Median DFI was 81.9 months for women with aligned bedtimes ("going to bed at preferred bedtime") (n = 72), and 46.9 months for women with misaligned bedtimes ("going to bed later or earlier than the preferred bedtime") (n = 13) (log rank p = 0.001). In a multivariate Cox proportional hazard model, after controlling for other significant predictors of DFI, including chronotype (morning type/longer DFI; HR = 0.539, 95% CI = 0.320-0.906, p = 0.021), estrogen receptor (ER) status at initial diagnosis (negative/shorter DFI; HR = 2.169, 95% CI = 1.124-4.187, p = 0.028) and level of natural-killer cell count (lower levels/shorter DFI; HR = 1.641, 95% CI = 1.000-2.695, p = 0.050), misaligned bedtimes was associated with shorter DFI, compared to aligned bedtimes (HR = 3.180, 95% CI = 1.327-7.616, p = 0.018). Our data indicate that a misalignment of bedtime on a daily basis, an indication of circadian disruption, is associated with more rapid breast cancer progression as measured by DFI. Considering the limitations of small sample size and study design, a prospective study with a larger sample is necessary to explore their causal relationship and underlying mechanisms.
View details for DOI 10.3109/07420528.2013.842575
View details for PubMedID 24156520
Association of AKT1 haplotype with the risk of schizophrenia in Iranian population
AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS
2006; 141B (4): 383-386
AKT-glycogen synthase kinase 3beta (GSK3beta) signaling is a target of lithium and has been implicated in the pathogenesis of mood disorders and schizophrenia. AKT1 protein level is decreased in the peripheral lymphocytes and brains of schizophrenic patients. The SNP2/3/4 TCG haplotype of AKT1 was associated with schizophrenia in patients with Northern European origin. In the present study, we genotyped five single nucleotide polymorphisms (SNP1-5) of AKT1 gene according to the original study in Iranians comprising of 321 schizophrenic patients and 383 controls, all residing in Mashhad city, Northeastern Iran. Haplotype analysis showed that the frequency of a five-SNP haplotype (AGCAG) was significantly higher in schizophrenic patients (0.068) than that of controls (0.034) (P = 0.03 after Bonferroni correction, OR = 2.04, CI = 1.2-3.4). In stratified analysis by schizophrenia subtypes, the frequency of the same haplotype was significantly higher in disorganized subtype (n = 78, frequency of haplotype=0.081) when compared with normal controls (P = 0.04 after Bonferroni correction, OR = 2.59, CI = 1.3-5.2). Our findings did not confirm the association of AKT1 SNP2/3/4 TCG haplotype with the risk of schizophrenia as reported in the original study but showed the evidence of association with a different haplotype, AKT1 five-SNP AGCAG haplotype, with the risk of schizophrenia in Iranian population.
View details for DOI 10.1002/ajmg.b.30291
View details for Web of Science ID 000238054200010
View details for PubMedID 16583435
Desert hedgehog-patched 2 expression in peripheral nerves during Wallerian degeneration and regeneration
JOURNAL OF NEUROBIOLOGY
2006; 66 (3): 243-255
Hedgehog proteins are important in the development of the nervous system. As Desert hedgehog (Dhh) is involved in the development of peripheral nerves and is expressed in adult nerves, it may play a role in the maintenance of adult nerves and degeneration and regeneration after injury. We firstly investigated the Dhh-receptors, which are expressed in mouse adult nerves. The Dhh receptor patched(ptc)2 was detected in adult sciatic nerves using RT-PCR, however, ptc1 was undetectable under the same experimental condition. Using RT-PCR in purified cultures of mouse Schwann cells and fibroblasts, we found ptc2 mRNA in Schwann cells, and at much lower levels, in fibroblasts. By immunohistochemistry, Ptc2 protein was seen on unmyelinated nerve fibers. Then we induced crush injury to the sciatic nerves of wild-type (WT) and dhh-null mice and the distal stumps of injured nerves were analyzed morphologically at different time points and expression of dhh and related receptors was also measured by RT-PCR in WT mice. In dhh-null mice, degeneration of myelinated fibers was more severe than in WT mice. Furthermore, in regenerated nerves of dhh-null mice, minifascicular formation was even more extensive than in dhh-null intact nerves. Both dhh and ptc2 mRNA levels were down-regulated during the degenerative phase postinjury in WT mice, while levels rose again during the phase of nerve regeneration. These results suggest that the Dhh-Ptc2 signaling pathway may be involved in the maintenance of adult nerves and may be one of the factors that directly or indirectly determines the response of peripheral nerves to injury.
View details for DOI 10.1002/neu.20216
View details for Web of Science ID 000235052600005
View details for PubMedID 16329124
Differences in viral and host genetic risk factors for development of human T-cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis between Iranian and Japanese HTLV-1-infected individuals
JOURNAL OF GENERAL VIROLOGY
2005; 86: 773-781
Human T-cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a neurological disease observed only in 1-2 % of infected individuals. HTLV-1 provirus load, certain HLA alleles and HTLV-1 tax subgroups are reported to be associated with different levels of risk for HAM/TSP in Kagoshima, Japan. Here, it was determined whether these risk factors were also valid for HTLV-1-infected individuals in Mashhad in northeastern Iran, another region of endemic HTLV-1 infection. In Iranian HTLV-1-infected individuals (n=132, 58 HAM/TSP patients and 74 seropositive asymptomatic carriers), although HLA-DRB1*0101 was associated with disease susceptibility in the absence of HLA-A*02 (P=0.038; odds ratio=2.71) as observed in Kagoshima, HLA-A*02 and HLA-Cw*08 had no effect on either the risk of developing HAM/TSP or HTLV-1 provirus load. All Iranian subjects possessed tax subgroup A sequences, and the protective effects of HLA-A*02 were observed only in Kagoshima subjects with tax subgroup B but not in those with tax subgroup A. Both the prevalence of HTLV-1 subgroups and the host genetic background may explain the different risks levels for HAM/TSP development in these two populations.
View details for DOI 10.1099/vir.0.80509-0
View details for Web of Science ID 000227367500029
View details for PubMedID 15722539
High seroprotection rate induced by intradermal administration of a recombinant hepatitis B vaccine in young healthy adults: Comparison with standard intramuscular vaccination
EUROPEAN JOURNAL OF EPIDEMIOLOGY
2004; 19 (9): 871-875
Intradermal (ID) vaccination has been proposed as a cost-saving alternative for administration of Hepatitis B (HB) vaccine to implement of mass vaccination of high-risk groups, particularly in developing countries. Therefore, the effectiveness of ID vaccination needs to be evaluated and verified in different ethnic backgrounds. The present study is a randomized trail using a recombinant vaccine (Heberbiovac) to compare immunogenecity and safety of an intradermal low-dose (4 microg) with standard dose (20 microg) of intramuscular (IM) vaccination in healthy Iranian population. Participants were 143 healthy Iranian medical and nursing students randomly allocated to ID or IM vaccination group. The vaccine was inoculated at 0, 1 and 6 months intervals. Serum samples were collected 1 month after the last vaccination and the anti-HBs response was determined using ELISA. The overall seroprotection rate (anti-HBs level > or = 10 IU/L) was 97.3% for ID vaccination group, which was not different from that of IM vaccination group (98.55%) (p = 0.99). Similarly, geometric mean titers (GMT) of anti-HBs were not significantly different between ID (1164.1 IU/L) and IM (1071.8 IU/L) vaccination groups (p = 0.4). There was no significant difference in seroprotection rate and GMT of anti-HBs between sexes. Although induration and hyperpigmentation at the site of injection were more frequently observed in ID vaccination group, no other clinically adverse effects were observed in both vaccination groups. We conclude that the ID route, which would require one-fifth of the standard dose, would be suitable for use in certain groups such as high-risk adults when the cost of vaccine is the inhibiting factor for mass vaccination.
View details for Web of Science ID 000223739100007
View details for PubMedID 15499897