CAP Profiles

Bio

Bio

Emmanuel During, M.D. is a neurologist and psychiatrist specialized in sleep medicine. He completed psychiatry residency in Paris, France, after which he relocated to the US to conduct neuroimaging research at N.Y.U., New York, with Drs. Osorio and De Leon. He then completed neurology residency at Cedars-Sinai Medical Center, Los Angeles, followed by a sleep medicine fellowship at Stanford University, where he joined the faculty as assistant professor with a dual appointment in Neurology and Sleep Medicine.
He directs the Stanford Parasomnia Clinic and founded the Sleep-related Movement Disorders Clinic. Additionally, he evaluates patients with a wide range of sleep and neurological complaints. Given his unique training and expertise, he has been receiving an increasing number of referrals for the evaluation of patients with complex neuropsychiatric and sleep disorders. He is particularly committed to teaching trainees at bedside and is actively involved in the core sleep fellowship and neurology residency curriculae.
Aside from his clinical work, he conducts several research studies as P.I. or co-investigator in clinical trials using new drugs to treat refractory REM sleep Behavior Disorder (RBD), characterizing the natural history of RBD, the role of our gut microbiome in Restless Legs Syndrome (RLS) and its relation with iron metabolism, or the effect of an immunomodulating drug used to treat atopic dermatitis on sleep architecture and quality. His most recent interest pertains to home devices that enhance slow wave sleep (SWS) via auditory closed-loop stimulation. He is particularly interested in studying the effect of SWS enhancement on sleep quality, cognition and biological markers related to Alzheimer's pathology.

Clinical Focus

  • Neuropsychiatry
  • Sleep Medicine

Academic Appointments

Honors & Awards

  • Resident Best Teaching Award, Cedars-Sinai Medical Center, CA (2015)
  • Medal Award for best Doctoral Thesis defense, Paris 7 University, France (2008)
  • Psychiatry Resident of the Year Award, Paris 7 University, France (2008)

Boards, Advisory Committees, Professional Organizations

  • Member, American Academy of Sleep Medicine (AASM) REM sleep Behavior Disorder (RBD) Task Force (2018 - Present)
  • Member, International RBD Study Group (IRBDSG) (2018 - Present)
  • Member, American Academy of Sleep Medicine (2016 - Present)
  • Member, American Academy of Neurology (2015 - Present)
  • Member, Conseil National de l'Ordre des Medecins - France (2008 - Present)

Professional Education

  • Board Certification: Sleep Medicine, American Board of Psychiatry and Neurology (2017)
  • Fellowship, Stanford University, Sleep Medicine (2016)
  • Board Certification: Neurology, American Board of Psychiatry and Neurology (2015)
  • Residency, Cedars-Sinai Medical Center, CA, Neurology (2015)
  • Internship, Banner Good Samaritan Hospital, AZ, Internal Medicine (2012)
  • Board Certification, Psychiatry, Paris Diderot University, France (2008)
  • MD, Louis Pasteur University, Medical School, France (2003)

Contact

  • Stanford Sleep Medicine Center 450 Broadway St Pavilion B MC 5704 Redwood City, CA 94063
    • Tel: (650) 723-6601
    Fax: (650) 721-3448

Links

Research & Scholarship

Current Research and Scholarly Interests

REM sleep behavior disorder: an early symptom of neurodegeneration

Clinical Trials

  • Natural History Study of Synucleinopathies Recruiting

    Synucleinopathies are a group of rare diseases associated with worsening neurological deficits and the abnormal accumulation of the protein α-synuclein in the nervous system. Onset is usually in late adulthood at age 50 or older. Usually, synucleinopathies present clinically with slowness of movement, coordination difficulties or mild cognitive impairment. Development of these features indicates that abnormal alpha-synuclein deposits have destroyed key areas of the brain involved in the control of movement or cognition. Patients with synucleinopathies and signs of CNS-deficits are frequently diagnosed with Parkinson disease (PD), dementia with Lewy bodies (DLB) or multiple system atrophy (MSA). However, accumulation of alpha-synuclein and death of nerve cells can also begin outside the brain in the autonomic nerves. In such cases, syncucleinopathies present first with symptoms of autonomic impairment (unexplained constipation, urinary difficulties, and sexual dysfunction). In rare cases, hypotension on standing (a disorder known as orthostatic hypotension) may be the only clinical finding. This "pre-motor" autonomic stage suggests that the disease process may not yet have spread to the brain. After a variable period of time, but usually within 5-years, most patients with abnormally low blood pressure on standing develop cognitive or motor abnormalities. This stepwise evolution indicates that the disease spreads from the body to the brain. Another indication of this spread is that acting out dreams (i.e., REM sleep behavior disorder, RBD) a problem that occurs when the lower part of the brain is affected, may also be the first noticeable sign of Parkinson disease. The purpose of this study is to document the clinical features and biological markers of patients with synucleinopathies and better understand how these disorders evolve over time. The study will involve following patients diagnosed with a synucleinopathy (PD/DLB and MSA) and those believed to be in the "pre-motor" stage (with isolated autonomic impairment and/or RBD). Through a careful series of follow-up visits to participating Centers, we will focus on finding biological clues that predict which patients will develop motor/cognitive problems and which ones have the resilience to keep the disease at bay preventing spread to the brain. We will also define the natural history of MSA - the most aggressive of the synucleinopathies.

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  • Sodium Oxybate for Treatment of Excessive Daytime Sleepiness and Cataplexy in Narcolepsy Recruiting

    The purpose of this study is to determine whether FT218 is safe and effective for the treatment of excessive daytime sleepiness and cataplexy in subjects with narcolepsy.

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Publications

All Publications

  • Sustained quality-of-life improvements over 10 years after deep brain stimulation for dystonia Movement Disorders Hogg, E., During, E., Tan, E., Athreya, K., Eskenazi, J., Wetheimer, J., Mamelak, A., Alterman, R., Tagliati, M. 2018; 33 (7): 1160-1167
  • A Case of Narcolepsy Type 2 and Postural Tachycardia Syndrome Secondary to Lesions of the Thalamus and Amygdala JOURNAL OF CLINICAL SLEEP MEDICINE Kim, P., During, E., Miglis, M. 2018; 14 (3): 479–81

    Abstract

    Although there are reports of narcolepsy type 1 caused by lesions of the central nervous system, there are far fewer reports of narcolepsy type 2 (NT2) caused by discrete brain lesions. We report a case of a patient in whom NT2 was diagnosed after a viral illness, and inflammatory lesions in the right thalamus and amygdala were found. In addition, symptoms of autonomic impairment developed and postural tachycardia syndrome was subsequently diagnosed in this patient. To our knowledge this is the first reported case of NT2 resulting from central nervous system lesions in these discrete locations, as well as the first reported case of postural tachycardia syndrome associated with narcolepsy.

    View details for DOI 10.5664/jcsm.7006

    View details for Web of Science ID 000427477700023

    View details for PubMedID 29458703

    View details for PubMedCentralID PMC5837851

  • A case series of REM sleep behavior disorder in pure autonomic failure Clin Auton Res Miglis, M., Muppidi, S., During, E., Jaradeh, J. 2017; 27 (1)

    View details for DOI 10.1007/s10286-016-0386-2

  • The Epidemic of Sleep Deprivation: A Modern Curse Huffington Post During, E. 2017
  • Hypersomnia: Etiologies Encyclopedia of Sleep During, E., Dimitriu, A., Guilleminault, C. 2017; 2nd
  • Sleep and Movement Disorders Sleep and Neurologic Disease Ashbrook, L., During, E. Elsevier. 2017; 1st
  • The Functions of Sleep Sleep and Neurologic Disease During, E., Kawai, M. Elsevier. 2017; 1st
  • Central Disorders of Hypersomnolence Review of Sleep Medicine During, E., Sullivan, S., Mignot, E. 2017; 4th
  • Parasomnias Sleepy or Sleepless: A Clinical Approach to the Sleep Patient During, E., Avidan, A. Springer . 2015; 1st
  • The interaction between sleep-disordered breathing and apolipoprotein E genotype on cerebrospinal fluid biomarkers for Alzheimer's disease in cognitively normal elderly individuals NEUROBIOLOGY OF AGING Osorio, R. S., Ayappa, I., Mantua, J., Gumb, T., Varga, A., Mooney, A. M., Burschtin, O. E., Taxin, Z., During, E., Spector, N., Biagioni, M., Pirraglia, E., Lau, H., Zetterberg, H., Blennow, K., Lu, S., Mosconi, L., Glodzik, L., Rapoport, D. M., de Leon, M. J. 2014; 35 (6): 1318-1324

    Abstract

    Previous studies have suggested a link between sleep disordered breathing (SDB) and dementia risk. In the present study, we analyzed the relationship between SDB severity, cerebrospinal fluid (CSF) Alzheimer's disease-biomarkers, and the ApoE alleles. A total of 95 cognitively normal elderly participants were analyzed for SDB severity, CSF measures of phosphorylated-tau (p-tau), total-tau (t-tau), and amyloid beta 42 (Aβ-42), as well as ApoE allele status. In ApoE3+ subjects, significant differences were found between sleep groups for p-tau (F[df2] = 4.3, p = 0.017), and t-tau (F[df2] = 3.3, p = 0.043). Additionally, among ApoE3+ subjects, the apnea and/or hypopnea with 4% O2-desaturation index was positively correlated with p-tau (r = 0.30, p = 0.023), t-tau (r = 0.31, p = 0.021), and Aβ-42 (r = 0.31, p = 0.021). In ApoE2+ subjects, the apnea and/or hypopnea with 4% O2-desaturation index was correlated with lower levels of CSF Aβ-42 (r = -0.71, p = 0.004), similarly to ApoE4+ subjects where there was also a trend toward lower CSF Aβ-42 levels. Our observations suggest that there is an association between SDB and CSF Alzheimer's disease-biomarkers in cognitively normal elderly individuals. Existing therapies for SDB such as continuous positive airway pressure could delay the onset to mild cognitive impairment or dementia in normal elderly individuals.

    View details for DOI 10.1016/j.neurobiolaging.2013.12.030

    View details for Web of Science ID 000333970800012

    View details for PubMedID 24439479

  • The concept of FDG-PET endophenotype in Alzheimer's disease NEUROLOGICAL SCIENCES During, E. H., Osorio, R. S., Elahi, F. M., Mosconi, L., de Leon, M. J. 2011; 32 (4): 559-569

    Abstract

    Often viewed as a potential tool for preclinical diagnosis in early asymptomatic stages of Alzheimer's disease (AD), the term "endophenotype" has acquired a recent popularity in the field. In this review, we analyze the construct of endophenotype-originally designed to discover genes, and examine the literature on potential endophenotypes for the late-onset form of AD (LOAD). We focus on the [18F]-fluoro-2-deoxyglucose (FDG) PET technique, which shows a characteristic pattern of hypometabolism in AD-related regions in asymptomatic carriers of the ApoE E4 allele and in children of AD mothers. We discuss the pathophysiological significance and the positive predictive accuracy of an FDG-endophenotype for LOAD in asymptomatic subjects, and discuss several applications of this endophenotype in the identification of both promoting and protective factors. Finally, we suggest that the term "endophenotype" should be reserved to the study of risk factors, and not to the preclinical diagnosis of LOAD.

    View details for DOI 10.1007/s10072-011-0633-1

    View details for Web of Science ID 000292706900004

    View details for PubMedID 21630036

  • A Critical Review of Dissociative Trance and Possession Disorders: Etiological, Diagnostic, Therapeutic, and Nosological Issues CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE During, E. H., Elahi, F. M., Taieb, O., Moro, M., Baubet, T. 2011; 56 (4): 235-242

    Abstract

    Although the Diagnostic and Statistical Manual of Mental Disorders (DSM), Fourth Edition, acknowledges the existence of dissociative trance and possession disorders, simply named dissociative trance disorder (DTD), it asks for further studies to assess its clinical utility in the DSM-5. To answer this question, we conducted the first review of the medical literature.The MEDLINE, CINAHL, and PsycINFO databases were searched from 1988 to 2010, seeking case reports of DTD according to the DSM or the International Classification of Diseases definitions. For each article, we collected epidemiologic and clinical data, explanatory models used by authors, treatments, and information on the outcome.We found 28 articles reporting 402 cases of patients with DTD worldwide. The data show an equal proportion of female and male patients, and a predominance of possession (69%), compared with trance (31%). Amnesia is reported by 20% of patients. Conversely, hallucinatory symptoms during possession episodes were found in 56% of patients and thus should feature as an important criterion. Somatic complaints are found in 34% of patients. Multiple explanatory models are simultaneously held and appear to be complementary.Data strongly suggest the inclusion of DTD in the DSM-5, provided certain adjustments are implemented. DTD is a widespread disorder that can be understood as a global idiom of distress, probably underdiagnosed in Western countries owing to cultural biases, whose incidence could increase given the rising flow of migration. Accurate diagnosis and appropriate management should result from a comprehensive evaluation both of sociocultural and of idiosyncratic issues, among which acculturation difficulties should systematically be considered, especially in cross-cultural settings.

    View details for Web of Science ID 000290063000007

    View details for PubMedID 21507280

  • GREATER RISK OF ALZHEIMER'S DISEASE IN OLDER ADULTS WITH INSOMNIA JOURNAL OF THE AMERICAN GERIATRICS SOCIETY Osorio, R. S., Pirraglia, E., Agueera-Ortiz, L. F., During, E. H., Sacks, H., Ayappa, I., Walsleben, J., Mooney, A., Hussain, A., Glodzik, L., Frangione, B., Martinez-Martin, P., de Leon, M. J. 2011; 59 (3): 559-562

    View details for DOI 10.1111/j.1532-5415.2010.03288.x

    View details for Web of Science ID 000288215600031

    View details for PubMedID 21391952