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

Professional Education

  • 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

Research & Scholarship

Current Research and Scholarly Interests

Sleep disorders in patients with Ehlers Danlos Syndrome


All Publications

  • 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
  • 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: -?


    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)


    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 Web of Science ID 000376282500003

    View details for PubMedID 27137943

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


    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


    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

  • 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


    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

  • Kleine-Levin syndrome: a review. Nature and science of sleep Miglis, M. G., Guilleminault, C. 2014; 6: 19-26


    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

  • 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


    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


    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


    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