Bio


Dr. Miglis received his B.S. in Biology from the University of North Florida and his MD from the University of Florida. After serving as a medical intern at Washington Hospital Center/Georgetown University, he completed his neurology residency at Bellevue and NYU Hospital in New York City. He then completed two fellowships, the first in Autonomic Disorders at the Beth Israel Deaconess Medical Center of Harvard Medical school, and the second in Sleep Medicine at the Stanford Sleep Medicine Center. Dr Miglis is board certified in neurology and sleep medicine by the American Board of Psychiatry and Neurology. Dr. Miglis treats a wide variety of neurological diseases and has a special interest in Autonomic Disorders, Sleep Disorders, and the interaction between these conditions.

Clinical Focus


  • Neurology
  • Autonomic Disorders
  • Sleep Medicine

Academic Appointments


Boards, Advisory Committees, Professional Organizations


  • Member, American Academy of Neurology Sleep Medicine Educational Committee (2018 - Present)
  • Member, International REM Sleep Behavior Study Group (2018 - Present)

Professional Education


  • Fellowship:Stanford University Sleep Medicine Fellowship (2013) CA
  • Board Certification: Sleep Medicine, American Board of Sleep Medicine (2013)
  • Board Certification: Neurology, American Board of Psychiatry and Neurology (2011)
  • Fellowship, Stanford University Medical Center, Sleep Medicine (2013)
  • Fellowship, Beth Israel Deaconess Medical Center/Harvard Medical School, Autonomic Disorders and Clinical Neurophysiology (2012)
  • Residency, New York University, Neurology (2011)
  • Internship, Washington Hospital Center/Georgetown University (2008)
  • Medical Education:University of Florida College of Medicine (2007) FL

Current Research and Scholarly Interests


Sleep disorders in patients with Ehlers Danlos Syndrome

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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All Publications


  • The microbiome in autonomic medicine and other updates in recent autonomic research. Clinical autonomic research : official journal of the Clinical Autonomic Research Society Miglis, M. G., Muppidi, S. 2019

    View details for DOI 10.1007/s10286-019-00621-z

    View details for PubMedID 31363881

  • Autonomic impairment as a potential biomarker in idiopathic REM-sleep-behavior disorder. Autonomic neuroscience : basic & clinical Zitser, J., During, E. H., Chiaro, G., Miglis, M. G. 2019; 220: 102553

    Abstract

    Autonomic dysfunction is common in REM-sleep behavior disorder (RBD). Several studies have demonstrated abnormalities in heart rate variability, cardiac scintigraphy, and cardiovascular autonomic reflex testing. In addition, the type and severity of these abnormalities may correlate with rate of phenoconversion from idiopathic RBD (iRBD) to manifest neurodegenerative disease. This article summarizes the current literature on autonomic impairment in iRBD, with specific focus on the role of autonomic impairment as a potential biomarker of disease progression. REM sleep physiology and relevant anatomy is also discussed in relation to the central autonomic network and autonomic neurodegeneration.

    View details for DOI 10.1016/j.autneu.2019.05.005

    View details for PubMedID 31219036

  • Do astronauts get postural tachycardia syndrome? And other updates on recent autonomic research. Clinical autonomic research : official journal of the Clinical Autonomic Research Society Miglis, M. G., Muppidi, S. 2019

    View details for DOI 10.1007/s10286-019-00613-z

    View details for PubMedID 31089931

  • Autonomic Symptom Burden in Idiopathic Hypersomnia Kim, P., Cheung, J., Schneider, L., Trotti, L., Miglis, M. LIPPINCOTT WILLIAMS & WILKINS. 2019
  • Dopamine transporter imaging versus myocardial MIBG scintigraphy for the diagnosis of prodromal synucleinopathies-and other updates on autonomic research. Clinical autonomic research : official journal of the Clinical Autonomic Research Society Miglis, M. G., Muppidi, S. 2019

    View details for DOI 10.1007/s10286-019-00600-4

    View details for PubMedID 30904961

  • Ion channels PIEZOs identified as the long-sought baroreceptor mechanosensors for blood pressure control, and other updates on autonomic research. Clinical autonomic research : official journal of the Clinical Autonomic Research Society Miglis, M. G., Muppidi, S. 2019

    View details for DOI 10.1007/s10286-018-00588-3

    View details for PubMedID 30604163

  • A novel autosomal recessive orthostatic hypotension syndrome: and other updates on recent autonomic research. Clinical autonomic research : official journal of the Clinical Autonomic Research Society Miglis, M. G., Muppidi, S. 2018

    View details for DOI 10.1007/s10286-018-0578-z

    View details for PubMedID 30415401

  • Orthostatic Hypotension JACC State-of-the-Art Review JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY Freeman, R., Abuzinadah, A. R., Gibbons, C., Jones, P., Miglis, M. G., Sinn, D. 2018; 72 (11): 1294–1309

    Abstract

    Neurogenic orthostatic hypotension is a highly prevalent and disabling feature of autonomic failure due to both peripheral and central neurodegenerative diseases. Community-based epidemiological studies have demonstrated a high morbidity and mortality associated with neurogenic orthostatic hypotension. It is due to impairment of baroreflex-mediated vasoconstriction of the skeletal muscle and splanchnic circulation and is caused by damage or dysfunction at central and/or peripheral sites in the baroreflex efferent pathway. Nonpharmacological and pharmacological interventions may be implemented to ameliorate the symptoms of orthostatic intolerance and improve quality of life. Many patients will be adequately treated by education, counseling, removal of hypotensive medications, and other nonpharmacological interventions, whereas more severely afflicted patients require pharmacological interventions. The first stage of pharmacological treatment involves repletion of central blood volume. If unsuccessful, this should be followed by treatment with sympathomimetic agents.

    View details for PubMedID 30190008

  • Autonomic dysfunction in multiple sclerosis and other updates on recent autonomic research. Clinical autonomic research : official journal of the Clinical Autonomic Research Society Miglis, M. G., Muppidi, S. 2018

    View details for DOI 10.1007/s10286-018-0548-5

    View details for PubMedID 30014341

  • Reply to "Syncope is associated with electroencephalography changes" and to "Video-EEG during tilt-table testing is an invaluable aid for understanding syncope". Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology Muppidi, S., Miglis, M. G., Razavi, B. 2018; 129 (7): 1500–1501

    View details for DOI 10.1016/j.clinph.2018.04.601

    View details for PubMedID 29729888

  • Orthostatic hypotension: does the heart rate matter? And other updates on recent autonomic research. Clinical autonomic research : official journal of the Clinical Autonomic Research Society Miglis, M. G., Muppidi, S. 2018

    View details for DOI 10.1007/s10286-018-0532-0

    View details for PubMedID 29779066

  • Sleep disorders in patients with postural tachycardia syndrome: A review of the literature and guide for clinicians. Autonomic neuroscience : basic & clinical Miglis, M. G., Barwick, F. 2018

    Abstract

    Fatigue is common in POTS, and patients often report unrefreshing sleep. These symptoms are directly correlated with a reduced quality of life, however the treatment of sleep disorders in this population remains a challenge. This article will review the current literature on the prevalence of sleep disorders in POTS, their association with the underlying pathophysiology of POTS, and current treatment paradigms.

    View details for PubMedID 29773483

  • Postural Orthostatic Tachycardia: The Stanford experience Jaradeh, S., Muppidi, S., Miglis, M., Sinn, D., Krugomova, I., Prieto, T. LIPPINCOTT WILLIAMS & WILKINS. 2018
  • Myasthenia Symptom Burden, Sleep and Fatigue: Are they related? Yang, S., Miglis, M., Jaradeh, S., Muppidi, S. LIPPINCOTT WILLIAMS & WILKINS. 2018
  • The clinical utility of qualitative electroencephalography during tilt table testing - A retrospective study CLINICAL NEUROPHYSIOLOGY Muppidi, S., Razavi, B., Miglis, M. G., Jaradeh, S. 2018; 129 (4): 783–86

    Abstract

    To assess electroencephalography (EEG) changes during tilt table testing in syncope and other orthostatic syndromes.We retrospectively reviewed consecutive tilt table studies with simultaneous EEG from April 2014 to May 2016 at our center. All patients had video EEG during tilt table. All patients had at least 10 min of head up tilt unless they had syncope or did not tolerate the study. Video EEG was interpreted by epileptologists.Eighty-seven patients met the inclusion criteria. Mean age was 45 years, and 55 were women. Seven patients (∼8%) had syncope during tilt table, 11 patients (∼12%) had significant neurogenic orthostatic hypotension and a separate group of 11 patients (∼12%) had significant orthostatic tachycardia. Valsalva responses were abnormal in 7 of the 11 patients with orthostatic hypotension, suggesting an underlying neurogenic orthostatic hypotension. Visually discernable EEG changes were seen in only 3 patients (∼43%) who had syncope and in 1 patient (∼9%) with orthostatic tachycardia.Qualitative EEG analysis based on visual inspection during tilt table study revealed abnormalities in less than half the patients with syncope and a very small fraction with orthostatic tachycardia.Routine qualitative EEG recording might not be clinically useful during tilt table studies.

    View details for DOI 10.1016/j.clinph.2018.01.058

    View details for Web of Science ID 000427485900010

    View details for PubMedID 29448152

  • Is your autonomic function good enough to be an Olympian? And other updates on recent autonomic research CLINICAL AUTONOMIC RESEARCH Miglis, M. G., Muppidi, S. 2018; 28 (2): 177–79

    View details for DOI 10.1007/s10286-018-0521-3

    View details for Web of Science ID 000427880500006

    View details for PubMedID 29541877

  • Migraine and Autonomic Dysfunction: Which Is the Horse and Which Is the Jockey? CURRENT PAIN AND HEADACHE REPORTS Miglis, M. G. 2018; 22 (3): 19

    Abstract

    Symptoms of autonomic dysfunction are common in patients with migraine, both during and between migraine attacks. Studies evaluating objective autonomic testing in patients have found significant, though somewhat conflicting results. The purposes of this review are to summarize and interpret the key findings of these studies, including those evaluating heart rate variability, autonomic reflex testing, and functional imaging in patients with migraine. The neuroanatomy of the central autonomic network as it relates to migraine is also reviewed.Several studies have evaluated autonomic balance in migraineurs, with conflicting results on the magnitude of sympathetic versus parasympathetic dysfunction. Most studies demonstrate sympathetic impairment, with a lesser degree of parasympathetic impairment. Three trends have emerged: (1) migraine with aura tends to produce more significant autonomic dysfunction than migraine without aura, (2) sympathetic impairment is more common than parasympathetic impairment, and (3) sympathetic impairment is common in the interictal period, with increased sympathetic responsiveness during the ictal period, suggesting adrenoreceptor hypersensitivity.

    View details for PubMedID 29476276

  • Autonomic dysfunction predicts poor outcome in stroke: Updates on recent autonomic research CLINICAL AUTONOMIC RESEARCH Miglis, M. G., Muppidi, S. 2018; 28 (1): 9–11

    View details for DOI 10.1007/s10286-017-0498-3

    View details for Web of Science ID 000424641400004

    View details for PubMedID 29305815

  • 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 PubMedID 29458703

    View details for PubMedCentralID PMC5837851

  • Postural tachycardia in hypermobile Ehlers-Danlos syndrome: A distinct subtype? AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL Miglis, M. G., Schultz, B., Muppidi, S. 2017; 208: 146–49

    Abstract

    It is not clear if patients with postural tachycardia syndrome (POTS) and Ehlers-Danlos syndrome (hEDS) differ from patients with POTS due to other etiologies. We compared the results of autonomic testing and healthcare utilization in POTS patients with and without hEDS.Patients with POTS+hEDS (n=20) and POTS controls without hypermobility (n=20) were included in the study. All patients underwent autonomic testing, and the electronic medical records were reviewed to determine the number and types of medications patients were taking, as well as the number of outpatient, emergency department, and inpatient visits over the prior year.Patients with hEDS had twice as many outpatient visits (21 v. 10, p=0.012), were taking more prescription medications (8 vs. 5.5, p=0.030), and were more likely to see a pain physician (70% vs 25%, p=0.005). Autonomic testing demonstrated a slight reduction in heart rate variability and slightly lower blood pressures on tilt table testing in hEDS patients, however for most patients these variables remained within the range of normal. Orthostatic tachycardia on tilt table testing was greater in POTS controls (46bpm vs 39bpm, p=0.018). Abnormal QSweat responses were common in both groups (38% of POTS+hEDS and 36% of POTS controls).While autonomic testing results were not significantly different between groups, patients with POTS+hEDS took more medications and had greater markers of healthcare utilization, with chronic pain likely playing a prominent role.

    View details for PubMedID 28986003

  • SLEEP AND AUTONOMIC IMPAIRMENT IN EHLERS-DANLOS SYNDROME: A CASE SERIES Schultz, B. J., Miglis, M. G., Guilleminault, C. ELSEVIER SCIENCE BV. 2017: E296–E297
  • Is the answer just beneath the surface? And other updates on recent autonomic research CLINICAL AUTONOMIC RESEARCH Miglis, M. G., Muppidi, S. 2017; 27 (6): 357–59

    View details for DOI 10.1007/s10286-017-0475-x

    View details for Web of Science ID 000415130600002

    View details for PubMedID 28983689

  • Let's not forget about the vagus and other updates on recent autonomic research CLINICAL AUTONOMIC RESEARCH Muppidi, S., Miglis, M. G. 2017; 27 (4): 219–21

    View details for DOI 10.1007/s10286-017-0451-5

    View details for Web of Science ID 000406639200005

    View details for PubMedID 28725943

  • Is postural tachycardia syndrome in the head or in the heart? And other updates on recent autonomic research CLINICAL AUTONOMIC RESEARCH Miglis, M. G., Muppidi, S. 2017; 27 (3): 145–47

    View details for DOI 10.1007/s10286-017-0423-9

    View details for Web of Science ID 000401920400005

    View details for PubMedID 28502022

  • Is pure autonomic failure an early marker for Parkinson disease, dementia with Lewy bodies, and multiple system atrophy? And other updates on recent autonomic research CLINICAL AUTONOMIC RESEARCH Muppidi, S., Miglis, M. G. 2017; 27 (2): 71-73

    View details for DOI 10.1007/s10286-017-0408-8

    View details for Web of Science ID 000399093100003

    View details for PubMedID 28255741

  • A case series of REM sleep behavior disorder in pure autonomic failure CLINICAL AUTONOMIC RESEARCH Miglis, M. G., Muppidi, S., During, E., Jaradeh, S. 2017; 27 (1): 41-44

    Abstract

    Data on the prevalence of RBD in patients with PAF are limited, with discrepancies in the literature regarding prevalence. We aimed to provide further data on this association with a series of eight patients with PAF.We reviewed the electronic medical records of all patients seen at the Stanford neurology clinics from 2012 to 2016 who were given a provisional diagnosis of PAF (343 patients), and further screened by procedure codes to identify those patients who underwent both attended video-polysomonography and autonomic testing (18 patients), and met strict exclusionary criteria (8 patients).The mean age of our patients was 69 years, and 63 % were women. The mean duration of autonomic symptoms was 11.2 years, and the mean duration of dream enactment was 3.75 years. All patients demonstrated evidence of adrenergic failure on autonomic testing. Five out of 8 (63 %) met diagnostic criteria for RBD, confirmed on vPSG.Our series supports the concept that RBD in PAF may be more common than previously reported, and that the presence of RBD suggests brainstem involvement in some cases of PAF. In addition, the timing of RBD symptoms relative to the emergence of autonomic symptoms may be useful to help distinguish these conditions.

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

    View details for Web of Science ID 000394183100007

  • The sacral parasympathetic system is actually sympathetic-and other updates on recent autonomic research CLINICAL AUTONOMIC RESEARCH Miglis, M. G., Muppidi, S. 2017; 27 (1): 5–6

    View details for DOI 10.1007/s10286-017-0396-8

    View details for Web of Science ID 000394183100002

    View details for PubMedID 28108826

  • Sleep and the Autonomic Nervous System SLEEP AND NEUROLOGIC DISEASE Miglis, M. G., Miglis, M. G. 2017: 227–44
  • SLEEP AND NEUROLOGIC DISEASE Preface SLEEP AND NEUROLOGIC DISEASE Miglis, M. G., Miglis, M. G. 2017: XIII
  • A case series of REM sleep behavior disorder in pure autonomic failure. Clinical autonomic research Miglis, M. G., Muppidi, S., During, E., Jaradeh, S. 2016: -?

    Abstract

    Data on the prevalence of RBD in patients with PAF are limited, with discrepancies in the literature regarding prevalence. We aimed to provide further data on this association with a series of eight patients with PAF.We reviewed the electronic medical records of all patients seen at the Stanford neurology clinics from 2012 to 2016 who were given a provisional diagnosis of PAF (343 patients), and further screened by procedure codes to identify those patients who underwent both attended video-polysomonography and autonomic testing (18 patients), and met strict exclusionary criteria (8 patients).The mean age of our patients was 69 years, and 63 % were women. The mean duration of autonomic symptoms was 11.2 years, and the mean duration of dream enactment was 3.75 years. All patients demonstrated evidence of adrenergic failure on autonomic testing. Five out of 8 (63 %) met diagnostic criteria for RBD, confirmed on vPSG.Our series supports the concept that RBD in PAF may be more common than previously reported, and that the presence of RBD suggests brainstem involvement in some cases of PAF. In addition, the timing of RBD symptoms relative to the emergence of autonomic symptoms may be useful to help distinguish these conditions.

    View details for PubMedID 27757562

  • Kleine-Levin Syndrome CURRENT NEUROLOGY AND NEUROSCIENCE REPORTS Miglis, M. G., Guilleminault, C. 2016; 16 (6)

    Abstract

    Kleine-Levin syndrome is a rare recurrent hypersomnia associated with symptoms of behavioral and cognitive impairment. This article reviews common presenting symptoms, differential diagnosis, diagnostic workup, and potential treatment options. Current updates on functional imaging studies and long-term neuropsychological studies are reviewed.

    View details for DOI 10.1007/s11910-016-0653-6

    View details for PubMedID 27137943

  • Autonomic dysfunction in primary sleep disorders SLEEP MEDICINE Miglis, M. G. 2016; 19: 40-49

    Abstract

    The autonomic nervous system plays an important role in the coordination of many important physiologic functions during sleep. Many patients with untreated sleep disorders will describe symptoms of autonomic impairment, and a majority of patients with autonomic impairment have some form of sleep disorder. This article will explore possible explanations for this connection, as well as review the current literature on autonomic impairment in common primary sleep disorders including obstructive sleep apnea, insomnia, restless legs syndrome, periodic limb movement disorder, narcolepsy, and rapid eye movement sleep behavior disorder.

    View details for DOI 10.1016/j.sleep.2015.10.001

    View details for Web of Science ID 000376518600008

    View details for PubMedID 27198946

  • Sleep disorders in patients with postural tachycardia syndrome. Clinical autonomic research Miglis, M. G., Muppidi, S., Feakins, C., Fong, L., Prieto, T., Jaradeh, S. 2016; 26 (1): 67-73

    Abstract

    Patients with postural tachycardia syndrome (POTS) often describe symptoms of fatigue, sleepiness, and lack of refreshing sleep. We aimed to provide further objective measures of sleep in patients with POTS.POTS patients (n = 18) were selected based on autonomic testing and evaluation at our center. Controls (n = 16) of similar age, gender, and BMI were selected from new patients referred to the Stanford Sleep Disorders Clinic for any sleep-related complaint. All patients underwent polysomnography and completed several sleep questionnaires and a 2-week sleep diary.POTS patients and control subjects were of similar age (27 ± 10.2 vs. 29 ± 5.4 years, p = 0.92) and Body Mass Index (21 ± 3.8 vs. 24 ± 4.1, p = 0.14). The majority of subjects in both groups were females (72 % POTS vs. 81 % controls). POTS patients scored higher on subjective fatigue scales but not sleepiness scales. POTS patients scored in the normal range on the BDI and the "evening" category on the MEQ. Their sleep diaries were not different from controls. With the exception of mild OSA, slightly reduced %REM and prolonged REM latency, their PSG data were normal and no different from controls.It is unlikely that the sleep-related complaints of POTS patients are the result of a primary sleep disorder unique to POTS. We propose that a combination of factors such as body fatigue, chronic pain, and other somatic symptoms common in POTS patients might be the underlying reason for sleep-related symptoms in POTS.

    View details for DOI 10.1007/s10286-015-0331-9

    View details for PubMedID 26695400

  • Autonomic dysfunction in primary sleep disorders Sleep Medicine Miglis, M. G. 2016; 19
  • Emerging Subspecialties in Neurology: Autonomic disorders. Neurology Palma, J., Cook, G. A., Miglis, M. G., Loavenbruck, A. 2015; 84 (10): e73-5

    View details for DOI 10.1212/WNL.0000000000001337

    View details for PubMedID 25754808

    View details for PubMedCentralID PMC4352100

  • Prevalence of REM sleep behavior disorder in multiple system atrophy: a multicenter study and meta-analysis CLINICAL AUTONOMIC RESEARCH Palma, J., Fernandez-Cordon, C., Coon, E. A., Low, P. A., Miglis, M. G., Jaradeh, S., Bhaumik, A. K., Dayalu, P., Urrestarazu, E., Iriarte, J., Biaggioni, I., Kaufmann, H. 2015; 25 (1): 69-75

    Abstract

    Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia frequently affecting patients with synucleinopathies, but its exact prevalence in multiple system atrophy (MSA) is unclear. Whether questionnaires alone are sufficient to diagnose RBD is also unknown.We performed a cross-sectional study of patients with probable MSA from six academic centers in the US and Europe. RBD was ascertained clinically and with polysomnography; we also performed a meta-analysis according to PRISMA guidelines for studies published before September 2014 that reported the prevalence of RBD in MSA. A random-effects model was constructed using weighted prevalence proportions. Only articles in English were included. Studies were classified into those that ascertained the presence of RBD in MSA clinically and with polysomnography. Case reports or case series (≤5 patients) were not included.Forty-two patients completed questionnaires and underwent polysomnography. Of those, 32 (76.1 %) had clinically suspected RBD and 34 (81 %) had polysomnography-confirmed RBD. Two patients reported no symptoms of RBD but had polysomnography-confirmed RBD. The primary search strategy yielded 374 articles of which 12 met the inclusion criteria. The summary prevalence of clinically suspected RBD was 73 % (95 % CI, 62-84 %) in a combined sample of 324 MSA patients. The summary prevalence of polysomnography-confirmed RBD was 88 % (95 % CI, 79-94 %) in a combined sample of 217 MSA patients.Polysomnography-confirmed RBD is present in up to 88 % of patients with MSA. RBD was present in some patients that reported no symptoms. More than half of MSA patients report symptoms of RBD before the onset of motor deficits.

    View details for DOI 10.1007/s10286-015-0279-9

    View details for Web of Science ID 000353286500009

    View details for PubMedID 25739474

  • Daytime Sleepiness SLEEP MEDICINE CLINICS Miglis, M. G., Kushida, C. A. 2014; 9 (4): 491-+
  • Kleine-Levin syndrome: a review. Nature and science of sleep Miglis, M. G., Guilleminault, C. 2014; 6: 19-26

    Abstract

    Kleine-Levin syndrome is a recurrent hypersomnia associated with symptoms of hyperphagia, hypersexuality, and cognitive impairment. This article reviews the current available research and describes common clinical symptoms, differential diagnosis, and acceptable workup and treatment. Although deficits have traditionally been thought to resolve between episodes, functional imaging studies and long-term neuropsychological testing in select patients have recently challenged this notion. This may suggest that Kleine-Levin syndrome is not as benign as previously considered.

    View details for DOI 10.2147/NSS.S44750

    View details for PubMedID 24470783

  • Sleep Disorders in Patients with Postural Tachycardia Syndrome Miglis, M., Gibbons, C., Freeman, R. LIPPINCOTT WILLIAMS & WILKINS. 2013
  • Right sided headache Case Based Neurology Miglis, M., Graber, J. Demo. 2013; 1: 261–5
  • Seropositive myasthenia and autoimmune autonomic ganglionopathy: Cross reactivity or subclinical disease? AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL Miglis, M. G., Racela, R., Kaufmann, H. 2011; 164 (1-2): 87-88

    Abstract

    Autoimmune autonomic ganglionopathy (AAG) and myasthenia gravis (MG) are both autoimmune channelopathies mediated by antibodies directed against nicotinic acetylcholine receptors. While both diseases target acetylcholine receptors, skeletal muscle and ganglionic receptor subtypes have key immunologic and genetic distinctions, and reports of patients with both AAG and MG are rare. We report a patient with antibody-confirmed AAG and elevated levels of ACh binding antibodies that did not meet clinical or electrodiagnostic criteria for MG. We presume that his skeletal muscle nAChR seropositivity was a false positive, perhaps due to the cross reactivity of the patient's ganglionic nAChR antibodies with skeletal nAChR subtypes.

    View details for DOI 10.1016/j.autneu.2011.06.005

    View details for Web of Science ID 000295346500013

    View details for PubMedID 21745762

  • Intracranial Venous Thrombosis After Placement of a Lumbar Drain NEUROCRITICAL CARE Miglis, M. G., Levine, D. N. 2010; 12 (1): 83-87

    Abstract

    Lumbar drains are frequently used in clinical neuroscience and are often managed in the neurointensive care unit. Complications are generally rare, and intracranial venous thrombosis (IVT) and infarction has not been reported.We report the case of a 45-year-old woman who developed a cerebrospinal fluid (CSF) leak after spinal surgery. Fifteen hours after placement of a lumbar drain she developed pure alexia and color agnosia caused by left lateral sinus thrombosis with hemorrhagic infarction in the posterior inferior left temporal lobe. We review the literature on the association of IVT with injury to the spinal dura, and we propose a mechanism whereby the lumbar drain may facilitate its development.We found 29 cases in which spinal dural injury was followed by IVT. The association is not coincidental, because nearly all cases were associated with post-dural puncture headache, which occurs in only a minority of cases of dural puncture. Injury to the spinal dura alters the distribution of craniospinal elasticity causing profound intracranial CSF hypotension on assuming the erect posture. This causes acute dilation of cerebral veins resulting in both orthostatic headache and venous stasis. We propose that placement of the lumbar drain and elevation of the head of the bed aggravated intracranial CSF hypotension and facilitated IVT.When a lumbar drain is placed for treatment of a spinal CSF leak, the patient should remain flat in bed. Any patient with post-dural injury headache that intensifies after an initial plateau, persists for longer than a week, or loses its orthostatic character should be evaluated for intracranial sinus or venous thrombosis.

    View details for DOI 10.1007/s12028-009-9278-9

    View details for Web of Science ID 000275742800015

    View details for PubMedID 19834826

  • A piece of my mind. Annie. JAMA Miglis, M. 2009; 306 (18): 1960-1.
  • Effect of taurine on platelets and the plasma coagulation system PLATELETS Miglis, M., Wilder, D., Reid, T., Bakaltcheva, I. 2002; 13 (1): 5-10

    Abstract

    It is not yet clear what exact mechanisms are at work in hibernating animals that prevent clot formation and maintain tissue perfusion under conditions of very slow blood flow and increased blood viscosity brought about by the low temperatures. It has been shown that the total amino acid pool increases more then two fold in hibernating animals with taurine accounting for about 50% of this increase [Storey et al., Proc Natl Acad Sci USA 1988; 85(21): 8350-4]. This work investigates the effect of taurine on platelets and the plasma coagulation system. Taurine was added at different concentrations in the range between 5 and 25 mM to donor plasma. Using STA/STA Compact coagulation analyzer the following tests were performed: prothrombin time (PT), activated partial thromboplastin time (APTT), and thrombin time (TT). At the highest concentration tested (25 mM) taurine prolonged TT by 9%. The prolongation was statistically significant but not clinically significant retaining TT within normal limits (16.7-20.7 s). PT and APTT remained unchanged by taurine. The effect of taurine on platelets was assessed by platelet aggregation by thrombin, extent of platelet shape change (ESC) induced by ADP, and thrombelastography. Taurine at 5 mM final concentration inhibited platelet aggregation by 10%. Increasing taurine concentration to 25 mM did not result in a further augmentation of the inhibitory effect. ESC was unaffected by taurine. Clot strength determined by thrombelastography also remained unchanged by taurine.

    View details for Web of Science ID 000173601100001

    View details for PubMedID 11918831