Neurology / 14.01.2025
Long Wait Times To See A Neurologist, Especially for MS, Epilepsy and Parkinson’s Patients
MedicalResearch.com Interview with:
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Dr. Callaghan[/caption]
Brian C. Callaghan, MD, Ph.D, FAAN,
Chair of the American Academy of Neurology’s Health Services Research Subcommittee
University of Michigan Health in Ann Arbor, Michigan
MedicalResearch.com: What is the background for this study?
Response: Access to neurologists can be a challenge, but few studies have attempted to quantify wait times to see neurologists and the factors that affect how long a patient must wait.
MedicalResearch.com: What are the main findings?
Response: Patients on Medicare wait an average of 34 days to see a neurologist after being referred by another physician with almost one in five waiting more than 90 days.
Dr. Callaghan[/caption]
Brian C. Callaghan, MD, Ph.D, FAAN,
Chair of the American Academy of Neurology’s Health Services Research Subcommittee
University of Michigan Health in Ann Arbor, Michigan
MedicalResearch.com: What is the background for this study?
Response: Access to neurologists can be a challenge, but few studies have attempted to quantify wait times to see neurologists and the factors that affect how long a patient must wait.
MedicalResearch.com: What are the main findings?
Response: Patients on Medicare wait an average of 34 days to see a neurologist after being referred by another physician with almost one in five waiting more than 90 days.
Dr. Factor[/caption]
Stewart A. Factor, D.O.
Professor of Neurology
Director of the Movement Disorders Program
Vance Lanier Chair of Neurology
Emory University School of Medicine
MedicalResearch.com: What is the background for this study? Would you briefly explain what is meant by OFF episodes.
Response: Parkinson’s disease (PD) is a chronic, progressive neurodegenerative disease characterized by motor symptoms, including tremor at rest, rigidity and impaired movement, as well as significant non-motor symptoms, such as cognitive impairment, psychiatric symptoms and autonomic symptoms (i.e. urinary issues, constipation, low blood pressure). It is the second-most common neurodegenerative disease after Alzheimer’s disease and it is predicted that the prevalence of Parkinson’s disease will double by the year 2040. The symptoms of PD are in substantial part, due to loss of dopamine nerve cells in the brain. The current standard of care for PD includes replacing the dopamine loss by the use of oral carbidopa/levodopa. Levodopa is a precursor of dopamine, converted in the brain.
OFF episodes have been a significant unmet need in Parkinson’s disease since the emergence of levodopa. Initially, levodopa controls PD symptoms in a continuous fashion throughout the day. With time the response becomes less predictable and patients experience a re-emergence or worsening of PD symptoms. These episodes are what we mean by OFF episodes. OFF episodes can be characterized, in part, by re-emergence of motor symptoms including tremor, stiffness or slowed movement that can happen at any point during the day. OFF episodes typically begin within the first five years of treatment and occur at the end of a dose. This is referred to as end of dose failure or wearing off. Within the first four to six years after diagnosis, regardless of disease severity, up to 60 percent of people with PD experience OFF episodes. With time these episodes become longer, more severe and disabling, more frequent and less predictable as PD progresses. They can take up more than half the day
OFF episodes may alter a persons’ ability to perform everyday activities by slowing or even precluding their completion. The result is significant burden and distress for people living with Parkinson’s disease (PD) and their care partners.
CTH-300 was a Phase 3, 12-week, randomized, double-blind, placebo-controlled, parallel group, study examining the efficacy, safety and tolerability of apomorphine hydrochloride sublingual film (KYNMOBI) in people with levodopa-responsive PD complicated by OFF episodes. The primary endpoint was a mean change in the score from pre-dose in the Movement Disorder Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS) Part III Motor Examination at 30 minutes after dosing at the 12-week visit of the maintenance treatment phase. The key secondary endpoint was the percentage of people with PD with a patient-rated full ON (or best) response within 30 minutes at the 12-week visit of the maintenance treatment phase.
Dr. Hänggi[/caption]
MedicalResearch.com: What is the background for this study?
Response: Anti-MAG neuropathy is a rare form of acquired demyelinating neuropathy. The disease onset normally presents after the age of 50 years and is 2.7 times more frequent in men than in women, with a prevalence of about 1 in 100,000. It is caused by the production of monoclonal anti-MAG IgM antibodies that recognize the HNK-1 epitope. The myelin-associated glycoprotein MAG is a mediator for the formation and maintenance of the myelin sheaths. There is strong evidence that the binding and deposition of anti-MAG IgM autoantibodies on myelin sheath is responsible for the demyelination, which clinically manifests itself as a peripheral neuropathy affecting primarily sensory nerves. However, the causes and the exact mechanisms behind the expansion of anti-MAG IgM producing B-cell and plasma cell clones are not fully understood.
Most off-label treatments aim to reduce pathogenic autoantibody titers by depleting autoantibody-producing B cell clones which interfere with antibody-effector mechanisms, or physically remove autoantibodies from the circulation. Most frequently, the anti-CD20 monoclonal antibody rituximab is used to treat anti-MAG neuropathy patients. However, all of these treatment options often lack of selectivity, efficiency, or can induce severe adverse effects in some patients.
Polyneuron has designed PN-1007 to highly selectively target the IgM autoantibodies that cause anti-MAG neuropathy. PN-1007 is a glycopolymer that mimics the natural HNK-1 carbohydrate epitope found on myelin of peripheral nerves and binds to the circulating disease-causing antibodies. By eliminating these pathogenic antibodies, PN-1007 may protect the integrity of the neuronal myelin sheaths of anti-MAG neuropathy patients.
Dr. Mishra[/caption]
Santosh K. Mishra M.Tech., PhD
Assistant Professor of Neuroscience
Department of Molecular Biomedical Sciences
NC State Veterinary Medicine
Raleigh, NC 2760
MedicalResearch.com: What is the background for this study? Would you briefly explain what is meant by atopic dermatitis?
Response: Chronic allergic itch is a worldwide problem that leads to substantial health expenses,but what causes this universal urge to scratch remains elusive in chronic allergic itch. Atopic dermatitis is a common allergic skin disease that often associated with extremely itchy and inflamed skin.
In our study, we showed, for the first time, a molecular pathway that is involved in chronic allergic itch as we identified an endogenous mediator (periostin) and a new role for its sensory neuron receptor, the integrin αVβ3, which drives the excitability and transmission of itch signal to the spinal cord.

