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Dr. Miglis is a Clinical Associate Professor in the departments of Neurology and Neurological Sciences and Psychiatry and Behavioral Sciences. He received his MD from the University of Florida. After serving as a medical intern at Washington Hospital Center/Georgetown University, he completed his neurology residency New York University. 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. He is director of the Stanford Multiple System Atrophy Center of Excellence and the Stanford Parasomnia Sleep Disorders Clinic, and is extensively involved in the multidisciplinary Stanford Post-Acute COVID Syndrome (PACS) clinic. 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. His research efforts are currently focused on mechanisms of autonomic dysfunction in Long-COVID/PASC and the central nervous system hypersomnias, in particular Idiopathic Hypersomnia. He is also site principle investigator of the North American Prodromal Synucleinopathy Study and has several ongoing studies evaluating skin biopsy and autonomic testing as markers of disease progression in isolated REM sleep behavior disorder.
Prodromal markers of neurodegeneration in REM sleep behavior disorderAutonomic dysfunction in Long-COVIDPostural tachycardia syndrome
A Novel Noninvasive Thermoregulatory Device for Postural Tachycardia Syndrome
The investigators hope to learn the feasibility and preliminary efficacy of the Embr device
for improving thermal comfort in individuals with POTS and impaired thermoregulation.
Feasibility will be assessed via usage of the Embr device and participant feedback.
Preliminary efficacy measures will include temperature-related symptoms and temperature-
related quality of life in individuals with POTS and impaired thermoregulation.
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Natural History Study of Synucleinopathies
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