Clinical Focus


  • Clinical Neurophysiology

Academic Appointments


Administrative Appointments


  • Director, Muscle and Nerve Laboratory, Medical College of Wisconsin, Milwaukee, Wisconsin (1992 - 2011)
  • Director, Autonomic Laboratory, Medical College of Wisconsin, Milwaukee, Wisconsin (1993 - 2011)
  • Director, Neuromuscular Division, Medical College of Wisconsin, Milwaukee, Wisconsin (1996 - 2011)
  • Director, Neurophysiology Fellowship, Medical College of Wisconsin, Milwaukee, Wisconsin (1997 - 2002)
  • Neurology Service Chief, Froedtert Hospital, Milwaukee, Wisconsin (1997 - 2010)
  • Autonomic Society Strategic Committee for Consensus Statement, American Autonomic Society (1997 - Present)
  • Professor and Chair, Department of Neurology, Medical College of Wisconsin, Milwaukee, Wisconsin (2000 - 2011)
  • Professor and Director, Autonomic Disorders Program, Stanford University, Stanford, California (2011 - Present)

Honors & Awards


  • Research Travel Award, Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania (1981)
  • Muscular Dystrophy Association Award, Department of Neurology (1990, 1993, 1994)
  • Health Advancement Award Nomination, Combined Health Appeal of Wisconsin (1994)
  • Teacher of the Year Award, Department of Neurology, Medical College of Wisconsin, Milwaukee, Wisconsin (1991, 1992, 1996, 1999)
  • Editorial Board, Neurology Section, Wisconsin Medical Journal (1996-2001)
  • Editorial Board, Journal of Clinical Neuromuscular Disease (2000-2005)
  • Top Doctors, in the United States (2000-2011)
  • Fellowship Award, American Academy of Neurology (2000)
  • Fellowship Award, Americal College of Physicians and the American Academy of Internal Medicine (2005)
  • Fellowship Award, American Neurological Association (2007)

Professional Education


  • Board Certification: United Council for Neurologic Subspecialties, Autonomic Disorders (2011)
  • Board Certification: American Board of Electrodiagnostic Medicine, Electrodiagnostic Medicine (1990)
  • Fellowship: Mayo Clinic Rochester (1988) MN
  • Board Certification: American Board of Psychiatry and Neurology, Clinical Neurophysiology (1996)
  • Residency: University of Michigan Hospital (1989) MI
  • Board Certification: American Board of Psychiatry and Neurology, Neurology (1988)
  • Residency: University of Cincinnati (1987) OH
  • Residency: Universite Paris VI - Pierre et Marie Curie Hospitals (1984)
  • Internship: Mouassat University Hospital (1979)
  • Medical Education: Faculty of Medicine (1979)
  • Board Certification, Clinical Neurophysiology, American Board of Psychiatry and Neurology (2006)
  • Board Certification, Clinical Neurophysiology, American Board of Electrodiagnostic Medicine (1989)
  • Board Certification, Neurology, American Board of Psychiatry and Neurology (1988)
  • Board Certification, Neurology, French Board of Psychiatry and Neurology (1984)
  • Fellowship, Mayo Clinic, Rochester, Minnesota USA (1987)
  • Fellowship, Departments of Neurology and Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, Michigan USA (1987)
  • Residency, University of Cincinnati Medical Center, Ohio USA (1987)
  • Residency, La Pitie-salpetriere and Bicetre Hospitals, Universite de Pierre et Marie Curie, Paris, France (1984)
  • M.D., Faculty of Medicine, University of Damascus, Syria (1979)
  • BSc., French Laic School, Damascus, Syria (1973)

Current Research and Scholarly Interests


Clinical interests include autonomic disorders, small fiber neuropathies and the development of effective methods of testing and treating these disorders. Prior work has focused on small fiber painful and autonomic neuropathies; syndromes of orthostatic intolerance and syncope; gastrointestinal motility dysfunction; cyclic vomiting; protacted Gastroesophageal Reflux; non-allergic rhinitis syndromes; and the relationship between the autonomic nervous system and normal or abnormal sleep. Additional areas of interest include the neurology of phonation and swallowing disorders, and peripheral nerve injury and repair.

2023-24 Courses


All Publications


  • Children With PANS May Manifest POTS. Frontiers in neurology Chan, A., Gao, J., Houston, M., Willett, T., Farhadian, B., Silverman, M., Tran, P., Jaradeh, S., Thienemann, M., Frankovich, J. 2022; 13: 819636

    Abstract

    Pediatric acute-onset neuropsychiatric syndrome (PANS) is characterized by an abrupt-onset of severe psychiatric symptoms including OCD, anxiety, cognitive difficulties, and sleep issues which is thought to be a post-infection brain inflammatory disorder. We observed postural orthostatic tachycardia syndrome (POTS) which resolved with immunomodulation in a patient with Pediatric acute-onset neuropsychiatric syndrome (PANS). Here, we aim to present a case of POTS and to examine the prevalence of (POTS) in our PANS cohort, and compare the clinical characteristics of patients with and without POTS.We conducted this cohort study of patients meeting PANS criteria who had at least three clinic visits during the study period. We included data from prospectively collected questionnaires and medical record review. We present a case followed by statistical comparisons within our cohort and a Kaplan-Meier analysis to determine the time-dependent risk of a POTS diagnosis.Our study included 204 patients: mean age of PANS onset was 8.6 years, male sex (60%), non-Hispanic White (78%). Evidence of POTS was observed in 19/204 patients (9%) with 5/19 having persistent POTS defined as persistent abnormal orthostatic vitals, persistent POTS symptoms, and/or continued need for pharmacotherapy for POTS symptoms for at least 6 months). In this PANS cohort, patients with POTS were more likely to have comorbid joint hypermobility (63 vs 37%, p = 0.04), chronic fatigue (42 vs 18%, p = 0.03), and a family history of chronic fatigue, POTS, palpitations and syncope. An unadjusted logistic regression model showed that a PANS flare (abrupt neuropsychiatric deterioration) was significantly associated with an exacerbation of POTS symptoms (OR 3.3, 95% CI 1.4-7.6, p < 0.01).Our study describes a high prevalence of POTS in patients with PANS (compared to the general population) and supports an association between POTS presentation and PANS flare within our cohort.

    View details for DOI 10.3389/fneur.2022.819636

    View details for PubMedID 35557616

    View details for PubMedCentralID PMC9086964

  • Epileptic Seizure Induced by Head-Up Tilt: A Case Series Study. Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society Toprani, S., Jaradeh, S., Falco-Walter, J. J. 2022

    Abstract

    Epilepsy and syncope can be difficult to distinguish, with misdiagnosis resulting in unnecessary or incorrect treatment and disability. Combined tilt-table and video EEG (vEEG) testing (tilt-vEEG) is infrequently used to parse these entities even at large centers. Because of the discovery of a rare case of epileptic seizure induced by head-up tilt (HUT) (no prior cases have been published), the authors sought to verify the rarity of this phenomenon.An observational, retrospective case series study of all combined tilt-vEEG studies performed at Stanford Health Care over a 2-year period was performed. Studies were grouped into categories: (1) abnormal tilt and normal vEEG; (2) abnormal vEEG and normal tilt; (3) abnormal vEEG and abnormal tilt; (4) normal tilt and normal vEEG, with neurologic symptoms; and (5) normal tilt and normal vEEG without neurologic symptoms.Sixty-eight percent of patients had an abnormal study (categories A-C), with only 3% having both an abnormal tilt and an abnormal EEG (category C). Of these, one patient had a focal epileptic seizure induced by HUT. With HUT positioning, the patient stopped answering questions and vEEG showed a left temporal seizure; systolic blood pressure abruptly dropped to 89 mm Hg (64 mm Hg below baseline); heart rate did not change, but pacemaker showed increased firing (threshold: <60 bpm).Combined tilt-table and vEEG evaluation was able to identify a previously unreported scenario-head-up tilt provocation of an epileptic seizure-and improve treatment. Combined tilt and vEEG testing should be considered for episodes that persist despite treatment to confirm proper diagnosis.

    View details for DOI 10.1097/WNP.0000000000000926

    View details for PubMedID 35394972

  • ANA Investigates Dysautonomia. Annals of neurology Richie, M., Goss, A., Jaradeh, S. 2021

    View details for DOI 10.1002/ana.26273

    View details for PubMedID 34787333

  • Cutaneous Alpha-Synuclein is Correlated with Autonomic Impairment in Isolated REM Sleep Behavior Disorder. Sleep Miglis, M. G., Zitser, J., Schneider, L., During, E., Jaradeh, S., Freeman, R., Gibbons, C. H. 2021

    Abstract

    STUDY OBJECTIVES: To define the clinical implications of cutaneous phosphorylated alpha-synuclein (p-syn) and its association with subjective and objective measures of autonomic impairment and clinical features including antidepressant use in isolated REM sleep behavior disorder (iRBD).METHODS: Twenty-five iRBD patients had quantified neurological and cognitive examinations, olfactory testing, questionnaires, autonomic function testing, and 3 punch skin biopsies (distal thigh, proximal thigh, neck). Skin biopsies were stained for the pan-axonal marker PGP 9.5 and co-stained with p-syn, and results were compared to 28 patients with Parkinson's disease (PD) and 18 healthy controls. Equal numbers of iRBD patients on and off antidepressants were recruited. The composite autonomic severity scale (CASS) was calculated for all patients.RESULTS: P-syn was detected in 16/25 (64%) of iRBD patients, compared to 27/28 (96%) of PD and 0/18 controls. The presence of p-syn at any biopsy site was correlated with both sympathetic (CASS adrenergic r = 0.6, p < 0.05) and total autonomic impairment (CASS total r = 0.6, p < 0.05) on autonomic reflex testing in iRBD patients. These results were independent of the density of p-syn at each site. There was no correlation between p-syn and antidepressant use.CONCLUSIONS: In patients with iRBD, the presence of cutaneous p-syn was detected in most patients and was associated with greater autonomic dysfunction on testing. Longitudinal follow-up will aid in defining the predictive role of both skin biopsy and autonomic testing in determining phenoconversion rates and future disease status.

    View details for DOI 10.1093/sleep/zsab172

    View details for PubMedID 34244806

  • Cutaneous Alpha-Synuclein is Correlated with Autonomic Impairment in Isolated REM Sleep Behavior Disorder Miglis, M., Zitser-Koren, J., Rajan, S., During, E., Schneider, L., Jaradeh, S., Freeman, R., Gibbons, C. LIPPINCOTT WILLIAMS & WILKINS. 2021
  • Orthostatic intolerance with Klippel-Trenaunay syndrome. Clinical autonomic research : official journal of the Clinical Autonomic Research Society Sinn, D. I., Shaik, R., Miglis, M. G., Muppidi, S., Jaradeh, S. 2021

    View details for DOI 10.1007/s10286-021-00791-9

    View details for PubMedID 33655381

  • Myasthenia Symptom Burden, Fatigue, and Sleep: Are They Related? Journal of clinical neuromuscular disease Yang, S., Miglis, M. G., Jaradeh, S., Muppidi, S. 2021; 22 (3): 123–28

    Abstract

    OBJECTIVE: Our aim is to explore the relationship between myasthenia gravis (MG)-related symptom burden, sleep quality, and fatigue in a diverse group of self-identified MG patients.METHODS: Patients provided relevant myasthenia disease data and completed the MG QOL-15, Epworth sleepiness scale, Pittsburgh Sleep Quality Index, and fatigue severity score (FSS) online. MG activities of daily living scale (MG-ADL) was completed on a follow-up telephone interview.RESULTS: One hundred ninety-six patients completed the online survey and 99 provided MG-ADL data. The mean age was 52 ± 15.34 years, 88 were acetylcholine receptor antibody positive, and 21 were muscle specific kinase positive. The mean MG-ADL was 6.81, indicating a moderate MG disease burden. Forty-seven (24%) reported high Epworth sleepiness scale scores, 152 (77%) reported high Pittsburgh Sleep Quality Index scores, and 162 (82%) reported high FSS scores. Correlation analysis correcting for body mass index and sleep apnea revealed a moderate positive correlation between MGQOL-15, MG-ADL, and FSS.CONCLUSIONS: There is a moderate positive correlation between various MG-specific outcome measures and fatigue severity.

    View details for DOI 10.1097/CND.0000000000000321

    View details for PubMedID 33595995

  • Autonomic function test during the COVID-19 pandemic: the Stanford experience. Clinical autonomic research : official journal of the Clinical Autonomic Research Society Sinn, D. I., Muppidi, S. n., Miglis, M. G., Jaradeh, S. n. 2021

    View details for DOI 10.1007/s10286-020-00752-8

    View details for PubMedID 33387099

  • A case report of postural tachycardia syndrome after COVID-19. Clinical autonomic research : official journal of the Clinical Autonomic Research Society Miglis, M. G., Prieto, T., Shaik, R., Muppidi, S., Sinn, D., Jaradeh, S. 2020

    View details for DOI 10.1007/s10286-020-00727-9

    View details for PubMedID 32880754

  • Association of GAD-65 Antibodies with Autonomic Dysfunction in non-Type I diabetic patients Bozinov, N., Kipp, L., Nguyen, L., Jaradeh, S. LIPPINCOTT WILLIAMS & WILKINS. 2020
  • Management of cyclic vomiting syndrome in adults: Evidence review. Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society Sharaf, R. N., Venkatesan, T., Shah, R., Levinthal, D. J., Tarbell, S. E., Jaradeh, S. S., Hasler, W. L., Issenman, R. M., Adams, K. A., Sarosiek, I., Stave, C. D., Li, B. U., Sultan, S. 2019; 31 Suppl 2: e13605

    Abstract

    BACKGROUND: This evidence review was conducted to inform the accompanying clinical practice guideline on the management of cyclic vomiting syndrome (CVS) in adults.METHODS: We followed the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) framework and focused on interventions aimed at prophylactic management and abortive treatment of adults with CVS. Specifically, this evidence review addresses the following clinical questions: (a) Should the following pharmacologic agents be used for prophylaxis of CVS: amitriptyline, topiramate, aprepitant, zonisamide/levetiracetam, or mitochondrial supplements? (b) Should the following pharmacologic agents be used for abortive treatment: triptans or aprepitant?RESULTS: We found very low-quality evidence to support the use of the following agents for prophylactic and abortive treatment of CVS: amitriptyline, topiramate, aprepitant, zonisamide/levetiracetam, and mitochondrial supplements. We have moderate certainty of evidence for the use of triptans as abortive therapy. We found limited evidence to support the use of ondansetron and the treatment of co-morbid conditions and complementary therapies.CONCLUSIONS: This evidence review helps inform the accompanying guideline for the management of adults with CVS which is aimed at helping clinicians, patients, and policymakers, and should improve patient outcomes.

    View details for DOI 10.1111/nmo.13605

    View details for PubMedID 31241818

  • Guidelines on management of cyclic vomiting syndrome in adults by the American Neurogastroenterology and Motility Society and the Cyclic Vomiting Syndrome Association. Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society Venkatesan, T., Levinthal, D. J., Tarbell, S. E., Jaradeh, S. S., Hasler, W. L., Issenman, R. M., Adams, K. A., Sarosiek, I., Stave, C. D., Sharaf, R. N., Sultan, S., Li, B. U. 2019; 31 Suppl 2: e13604

    Abstract

    The increasing recognition of cyclic vomiting syndrome (CVS) in adults prompted the development of these evidence-based guidelines on the management of CVS in adults, which was sponsored by the American Neurogastroenterology and Motility Society (ANMS) and the Cyclic Vomiting Syndrome Association (CVSA). GRADE (Grading of Recommendations, Assessment, Development, and Evaluation) framework was used and a professional librarian performed the literature search. The expert committee included the President of the CVSA who brought a patient perspective into the deliberations. The committee makes recommendations for the prophylaxis of CVS, treatment of acute attacks, diagnosis, and overall management of CVS. The committee strongly recommends that adults with moderate-to-severe CVS receive a tricyclic antidepressant (TCA), such as amitriptyline, as a first-line prophylactic medication and receive topiramate or aprepitant as alternate prophylactic medications. Zonisamide or levetiracetam and mitochondrial supplements (Coenzyme Q10, L-carnitine, and riboflavin) are conditionally recommended as alternate prophylactic medications, either alone or concurrently with other prophylactic medications. For acute attacks, the committee conditionally recommends using serotonin antagonists, such as ondansetron, and/or triptans, such as sumatriptan or aprepitant to abort symptoms. Emergency department treatment is best achieved with the use of an individualized treatment protocol and shared with the care team (example provided). The committee recommended screening and treatment for comorbid conditions such as anxiety, depression, migraine headache, autonomic dysfunction, sleep disorders, and substance use with referral to appropriate allied health services as indicated. Techniques like meditation, relaxation, and biofeedback may be offered as complementary therapy to improve overall well-being and patient care outcomes.

    View details for DOI 10.1111/nmo.13604

    View details for PubMedID 31241819

  • Role of chronic cannabis use: Cyclic vomiting syndrome vs cannabinoid hyperemesis syndrome. Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society Venkatesan, T., Levinthal, D. J., Li, B. U., Tarbell, S. E., Adams, K. A., Issenman, R. M., Sarosiek, I., Jaradeh, S. S., Sharaf, R. N., Sultan, S., Stave, C. D., Monte, A. A., Hasler, W. L. 2019; 31 Suppl 2: e13606

    Abstract

    Cannabis is commonly used in cyclic vomiting syndrome (CVS) due to its antiemetic and anxiolytic properties. Paradoxically, chronic cannabis use in the context of cyclic vomiting has led to the recognition of a putative new disorder called cannabinoid hyperemesis syndrome (CHS). Since its first description in 2004, numerous case series and case reports have emerged describing this phenomenon. Although not pathognomonic, a patient behavior called "compulsive hot water bathing" has been associated with CHS. There is considerable controversy about how CHS is defined. Most of the data remain heterogenous with limited follow-up, making it difficult to ascertain whether chronic cannabis use is causal, merely a clinical association with CVS, or unmasks or triggers symptoms in patients inherently predisposed to develop CVS. This article will discuss the role of cannabis in the regulation of nausea and vomiting, specifically focusing on both CVS and CHS, in order to address controversies in this context. To this objective, we have collated and analyzed published case series and case reports on CHS in order to determine the number of reported cases that meet current Rome IV criteria for CHS. We have also identified limitations in the existing diagnostic framework and propose revised criteria to diagnose CHS. Future research in this area should improve our understanding of the role of cannabis use in cyclic vomiting and help us better understand and manage this disorder.

    View details for DOI 10.1111/nmo.13606

    View details for PubMedID 31241817

  • Cyclic vomiting syndrome: Pathophysiology, comorbidities, and future research directions. Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society Hasler, W. L., Levinthal, D. J., Tarbell, S. E., Adams, K. A., Li, B. U., Issenman, R. M., Sarosiek, I., Jaradeh, S. S., Sharaf, R. N., Sultan, S., Venkatesan, T. 2019; 31 Suppl 2: e13607

    Abstract

    Cyclic vomiting syndrome (CVS) is characterized by severe episodic emesis in adults and children. Cannabinoid hyperemesis syndrome is an increasingly recognized CVS-like illness that has been associated with chronic cannabis use. There are significant gaps in our understanding of the pathophysiology, clinical features, comorbidities, and effective management options of CVS. Recommendations for treating CVS are based on limited clinical data, as no placebo-controlled, randomized trials have yet been conducted. Diseases associated with CVS, including migraine, mitochondrial disorders, autonomic dysfunction, and psychiatric comorbidities, provide clues about pathophysiologic mechanisms and suggest potential therapies. We review our current understanding of CVS and propose future research directions with the aim of developing effective therapy. Establishing a multicenter, standardized registry of CVS patients could drive research on multiple fronts including developing CVS-specific outcome measures to broaden our understanding of clinical profiles, to serve as treatment end points in clinical trials, and to provide a platform for patient recruitment for randomized clinical trials. Such a robust database would also facilitate conduct of research that aims to determine the underlying pathophysiological mechanisms and genetic basis for CVS, as well as identifying potential biomarkers for the disorder. Soliciting government and industry support is crucial to establishing the necessary infrastructure and achieving these goals. Patient advocacy groups such as the Cyclic Vomiting Syndrome Association (CVSA), which partner with clinicians and researchers to disseminate new information, to promote ongoing interactions between patients, their families, clinicians, investigators, to support ongoing CVS research and education, must be an integral part of this endeavor.

    View details for DOI 10.1111/nmo.13607

    View details for PubMedID 31241816

  • Author response: Video NeuroImages: Paraneoplastic spinal myoclonus associated with Caspr2 antibodies. Neurology Hines, H., Murray, N. M., Ahmad, S., Jaradeh, S., Gold, C. A. 2019; 92 (6): 303

    View details for DOI 10.1212/WNL.0000000000006871

    View details for PubMedID 30718327

  • Wired for Threat: Clinical Features of Nervous System Dysregulation in 80 Children. Pediatric neurology Elbers, J., Jaradeh, S., Yeh, A. M., Golianu, B. 2018

    Abstract

    BACKGROUND: The negative effect of perceived stress on health has become a cultural epidemic. Despite many health implications, the clinical impact of stress on the nervous system is not well understood. This case series describes the symptom profiles of 80 children with nervous system dysregulation attributed to maladaptive neuroendocrine responses to stress.METHODS: We reviewed of 80 children with nervous system dysregulation identified from a single, tertiary care pediatric neurology clinic. Included patients were between five and 17 years of age, with unexplained medical symptoms lasting three months or longer affecting at least four of six neurological domains: (1) somatization, (2) executive function, (3) autonomic function, (4) digestion, (5) sleep, and (6) emotional regulation. Medical symptoms, diagnoses, and detailed social histories were collected.RESULTS: Of 80 children, 57 were female (71%), 57 were Caucasian (71%), with median age of 14 years. Symptoms had a mean duration of 32 months, and included: 100% somatic symptoms, 100% emotional dysregulation, 92.5% disrupted sleep, 82.5% autonomic dysregulation, 75% executive dysfunction, and 66% digestive problems. Overall, 94% reported chronic or traumatic stressors; adverse childhood experiences were present in 65%.CONCLUSIONS: Perceived stress impacts many functions of the neuroendocrine system through experience-dependent plasticity, resulting in a constellation of symptoms and functional impairments we describe as nervous system dysregulation. The pathophysiology of these symptoms involves dysregulation of subcortical, hormonal, and autonomic circuits, which remain largely untested. Recognition and understanding of maladaptive neurophysiology in stress-related symptoms has important implications for diagnosis, treatment, and advances in health research.

    View details for PubMedID 30343833

  • 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
  • Video NeuroImages: Paraneoplastic spinal myoclonus associated with Caspr2 antibodies. Neurology Hines, H., Murray, N. M., Ahmad, S., Jaradeh, S., Gold, C. A. 2018; 90 (14): 660–61

    View details for PubMedID 29610228

  • 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

  • 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

  • Pediatric Anti-ganglionic Antibody Positive Autonomic Neuropathy: Clinical Presentation and Response to Treatment PEDIATRIC NEUROLOGY Tiongson, E., Pimentel, N., Ramos-Platt, L., Jaradeh, S. 2016; 64: 72-76

    Abstract

    Autoimmune autonomic neuropathy is rare in children. There are few pediatric reports documenting anti-ganglionic antibodies.We present two children with anti-ganglionic antibody positive autonomic neuropathy, including their presentation, results of testing, and treatment course.Both children had delayed diagnoses because of the presence of vague autonomic symptoms. Treatment with multiple immunotherapies appears to bring at least a partial response and can be monitored with anti-ganglionic antibody titers.Our findings contribute to the sparse literature in pediatric autoimmune autonomic neuropathy and highlight the need for additional studies to create diagnostic criteria and define optimal treatment regimens.

    View details for DOI 10.1016/j.pediatrneurol.2016.06.007

    View details for Web of Science ID 000389169300013

    View details for PubMedID 27569256

  • 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

  • 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

  • Cumulative Brain Injury from Motor Vehicle-Induced Whole-Body Vibration and Prevention by Human Apolipoprotein A-I Molecule Mimetic (4F) Peptide (an Apo A-I Mimetic) JOURNAL OF STROKE & CEREBROVASCULAR DISEASES Yan, J., Zhang, L., Agresti, M., Yan, Y., LoGiudice, J., Sanger, J. R., Matloub, H. S., Pritchard, K. A., Jaradeh, S. S., Havlik, R. 2015; 24 (12): 2759-2773

    Abstract

    Insidious cumulative brain injury from motor vehicle-induced whole-body vibration (MV-WBV) has not yet been studied. The objective of the present study is to validate whether whole-body vibration for long periods causes cumulative brain injury and impairment of the cerebral function. We also explored a preventive method for MV-WBV injury.A study simulating whole-body vibration was conducted in 72 male Sprague-Dawley rats divided into 9 groups (N = 8): (1) 2-week normal control; (2) 2-week sham control (in the tube without vibration); (3) 2-week vibration (exposed to whole-body vibration at 30 Hz and .5 G acceleration for 4 hours/day, 5 days/week for 2 weeks; vibration parameters in the present study are similar to the most common driving conditions); (4) 4-week sham control; (5) 4-week vibration; (6) 4-week vibration with human apolipoprotein A-I molecule mimetic (4F)-preconditioning; (7) 8-week sham control; (8) 8-week vibration; and (9) 8-week 4F-preconditioning group. All the rats were evaluated by behavioral, physiological, and histological studies of the brain.Brain injury from vibration is a cumulative process starting with cerebral vasoconstriction, squeezing of the endothelial cells, increased free radicals, decreased nitric oxide, insufficient blood supply to the brain, and repeated reperfusion injury to brain neurons. In the 8-week vibration group, which indicated chronic brain edema, shrunken neuron numbers increased and whole neurons atrophied, which strongly correlated with neural functional impairment. There was no prominent brain neuronal injury in the 4F groups.The present study demonstrated cumulative brain injury from MV-WBV and validated the preventive effects of 4F preconditioning.

    View details for DOI 10.1016/j.jstrokecerebrovasdis.2015.08.007

    View details for Web of Science ID 000367388800016

    View details for PubMedCentralID PMC5664147

  • Cumulative Brain Injury from Motor Vehicle-Induced Whole-Body Vibration and Prevention by Human Apolipoprotein A-I Molecule Mimetic (4F) Peptide (an Apo A-I Mimetic). Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association Yan, J. G., Zhang, L. L., Agresti, M., Yan, Y., LoGiudice, J., Sanger, J. R., Matloub, H. S., Pritchard, K. A., Jaradeh, S. S., Havlik, R. 2015; 24 (12): 2759-73

    Abstract

    Insidious cumulative brain injury from motor vehicle-induced whole-body vibration (MV-WBV) has not yet been studied. The objective of the present study is to validate whether whole-body vibration for long periods causes cumulative brain injury and impairment of the cerebral function. We also explored a preventive method for MV-WBV injury.A study simulating whole-body vibration was conducted in 72 male Sprague-Dawley rats divided into 9 groups (N = 8): (1) 2-week normal control; (2) 2-week sham control (in the tube without vibration); (3) 2-week vibration (exposed to whole-body vibration at 30 Hz and .5 G acceleration for 4 hours/day, 5 days/week for 2 weeks; vibration parameters in the present study are similar to the most common driving conditions); (4) 4-week sham control; (5) 4-week vibration; (6) 4-week vibration with human apolipoprotein A-I molecule mimetic (4F)-preconditioning; (7) 8-week sham control; (8) 8-week vibration; and (9) 8-week 4F-preconditioning group. All the rats were evaluated by behavioral, physiological, and histological studies of the brain.Brain injury from vibration is a cumulative process starting with cerebral vasoconstriction, squeezing of the endothelial cells, increased free radicals, decreased nitric oxide, insufficient blood supply to the brain, and repeated reperfusion injury to brain neurons. In the 8-week vibration group, which indicated chronic brain edema, shrunken neuron numbers increased and whole neurons atrophied, which strongly correlated with neural functional impairment. There was no prominent brain neuronal injury in the 4F groups.The present study demonstrated cumulative brain injury from MV-WBV and validated the preventive effects of 4F preconditioning.

    View details for DOI 10.1016/j.jstrokecerebrovasdis.2015.08.007

    View details for PubMedID 26433438

    View details for PubMedCentralID PMC5664147

  • 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

  • Surface-evoked laryngeal sensory action potential evaluation in neurogenic chronic cough. Journal of voice Bock, J. M., Koszewski, I. J., Blumin, J. H., Toohill, R. J., Merati, A. L., Prieto, T. E., Jaradeh, S. S. 2014; 28 (5): 624-630

    Abstract

    Neurogenic chronic cough is currently a diagnosis of exclusion. We hypothesized that surface-evoked laryngeal sensory action potential (SELSAP) testing could be used to help establish a diagnosis of laryngeal sensory neuropathy as a cause of chronic cough, based on altered SELSAP waveform morphology.Retrospective cohort study.Laryngeal electromyographic (EMG) data including SELSAP waveform testing from patients with chronic cough were directly compared with a control population without significant laryngeal symptoms, and statistical analysis of unilateral and bilateral neuropathy injury subgroups was performed.Thirty patients with a chief complaint of chronic cough underwent laryngeal EMG testing since January 2000 with needle EMG and surface nerve conduction studies. SELSAP waveform analysis of unilateral and bilateral laryngeal neuropathy demonstrated significantly lowered median SELSAP peak amplitude compared with controls (P < 0.01).Patients with suspected neurogenic chronic cough demonstrate statistically significant alterations in SELSAP waveform that can support a diagnosis of laryngeal sensory neuropathy.

    View details for DOI 10.1016/j.jvoice.2014.02.009

    View details for PubMedID 24880673

  • The Correlation between Calcium Intensity and Histopathological Changes in Brachial Plexus Nerve Injuries JOURNAL OF RECONSTRUCTIVE MICROSURGERY Davis, J., O'Connor, E., Zhang, L., Agresti, M., Matloub, H. S., Sanger, J., Jaradeh, S. S., Yan, J. 2013; 29 (7)

    Abstract

    Background After nerve injury, an influx of calcium exceeds the homeostatic capacity, which damages peripheral nerves. Previous studies identified that following nerve crush, function improves as calcium levels normalize.Methods Electrophysiological analysis was performed to measure the compound muscle action potential of 15 patients' damaged nerves. These samples were evaluated for calcium level and also stained with a Luxol fast blue and neurofilament antibodies to evaluate the myelin sheath and neurofilaments of the nerves. Based on the Sunderland scale, we identified three exclusive types of peripheral nerve injury groups.Results There was a correlation between histopathological damage and calcium levels of 0.81 (p < 0.005). The average relative fluorescence units (RFUs) was 235.28 ± 19, which corresponds to 5.3 × 10-7 M of calcium, five times the normal value.Conclusion Our study shows promising clinical implications via faster pathology results by the RFU technique. This approach of calcium staining, though still in clinical trials, offers significant clinical application, allowing physicians to get the clinically diagnostic nerve injury degree faster and will also facilitate better strategies for further treatment or future surgeries.

    View details for DOI 10.1055/s-0033-1345436

    View details for Web of Science ID 000323110900009

    View details for PubMedID 23661333

  • Fatigue Prevalence and Correlates in a Cohort of Patients with Autonomic Dysfunction Barboi, A., Jaradeh, S., Ouyang, B., Yellick, M., Prieto, T. LIPPINCOTT WILLIAMS & WILKINS. 2013
  • A new noninvasive method for determination of laryngeal sensory function. Laryngoscope Bock JM, Blumin JH, Toohill RJ, Merati AL, Prieto TE, Jaradeh SS. 2011; 121 (1): 158-163
  • Helicoid end-to side and oblique attachment technique in repair of the musculocutaneous nerve injury with the phrenic nerve as a donor: an experimental study in rats. Microsurgery Yan YH, Yan JG, Matloub HS, Zhang LL, Hettinger P, Sanger J, Jaradeh SS. 2011; 31 (2): 122-129
  • Autonomic nerve function in adults with cyclic vomiting syndrome: a prospective study. Neurogastroenterol Motility Venkatesan T, Prieto T, Barboi A, Li B, Schroeder A, Hogan W, Ananthakrishnan A, Jaradeh S. 2010; 22 (12) (e339): 1303-1307
  • Performing and Processing FNA of Anterior Fat Pad for Amyloid. Journal of Visualized Experiments Shidham VB, Hunt B, Jaradeh SS, Barboi AC, Devata S, Hari P. 2010; (44): 1747
  • Impact of Autonomic Dysfunction on Inflammatory Bowel Disease. J Clin Gastroenterol Ananthakrishnan AN, Issa M, Barboi A, Jaradeh S, Zadvornova Y. Skaros S, Johnson K, Otterson MF, Binion DG. 2010; 44 (4): 272-279
  • Neuromuscular manifestations in a patient with Ehlers-Danlos type IV. J Clinical Neuromuscular Disease Barboi A, Dennis C, Timins M, Peltier W, Klotz C, Jaradeh S. 2009; 11 (2): 81-87
  • Cortical brain mapping of peripheral nerves using functional magnetic resonance imaging in a rodent model. Journal of Reconstructive Microsurgery Cho YR, Johns SR, Pawela CP, Li R, Kao DS, Shulte ML, Runquist ML, Yan JG, Hudetz AG, Jaradeh SS, Hyde JS, Matloub HS. 2008; 24 (8): 551-558