Bruce Hughes, MD: When we were looking at the different therapies, I was looking at all of the high-efficacy therapies out there and the data on [the impact of] brain volume loss. It is striking how, when you look at it, it kind of boils down to 3 areas, and that is anti-CD20, S1P receptor modulators, and natalizumab with regard to best data on impacting the decrease in cerebral brain volume loss. That ties in with our high-efficacy [therapy], and utilizing that information, you can then, [in]s your discussionwith patients, come up with the best therapy that we think is optimal for them. I always bring up that we dont necessarily knock it out of the park with our first attempt, but what well do, the promise is not that well have an optimal outcome, but that well monitor and, if were not headed toward optimal outcome, well make a switch and well make an adjustment. Just based on that mantra of efficacy, tolerability, safety triad that needs to come together. Are there any other thingsthat we havent touched on that would be beneficial with regard to health care providers who are managing patients with multiple sclerosis?

Robert Naismith, MD: Just to recap, what weve been discussing is that you really need to shut down the acute inflammation as early as possible. You need to stop that process because, although its not perfectly correlated to chronic inflammation and neurodegeneration, there is definitely an input from acute inflammation of those processes. So stopping that acute inflammatory component is going to benefit the patient long term because nowadays we talk about expanding lesions and microglial activation, but what if we can prevent that in the first place? I feel like using these highly effective therapies to shut down the inflammatory reaction, the bloodstream break down early is going to benefit patients. Now, unfortunately, we probably dont catch patients at the very start of their disease. Were lucky with MS compared to other degenerative disorders that we do catch them quite early in the whole process, but they may have had MS for years before you even see them the first time. If you think maybe Epstein-Barr virus [EBV] is the spark that lights the fuse and they get EBV in their teens, like at the age of 17 [or] 18, there may be processes taking place with MS pathogenesis and the susceptible patient for many years before they present in their 20s, 30s, and 40s. We cant go back and reverse that, but what we can do is try to stop that inflammation and to slow down the processes that will take place from then on out.

We cant go back and stop the processes that have already taken place because we know that they already have the cognitive issues when they present. They already have changes in brain volume when they present with RIS [radiologically isolated syndrome] or their first episode. So you cant go back to the very, very beginning, but were still able to catch most patients quite early and get them on therapies. And I monitor them to make sure that were doing our best to stop the inflammation, stop new MRI lesions, and to do our best to stabilize the disease process and their symptoms.

Bruce Hughes, MD: Yes, I think that is right. Capturing the disease process before the horse is out of the barn. We talk a lot about this need for being able to impact the disease process centrally in the brain and spinal cord vs peripherally with our agents that shut down inflammation, so extremely well. But could you obviate the need for essentially acting if you treat the disease process early enough and effectively enough? To your point, we know this, right? Clinically isolated syndrome [CIS], the cognitive testing, just that theres the program, and I completely agree with that, is that you do neurocognitive testing on patients with CIS and theyre decidedly more defective than the general age-matched population. Likewise, and Ive always found this very interesting when were looking at this data for brain volume loss, we again have learned, whereas previously we thought that was a later manifestation of multiple sclerosis, that actually the brain volume loss, the speed with which the loss occurs, is most rapid in the first few years of diagnosis, not when its decades old. So I think that does encapsulate very well the importance. I think we tied in high-efficacy therapy, brain volume loss, cognitive functioning, and some tools to monitor and to help manage that in our MS patients.

Id like to thank you for sharing your expertise, Dr Naismith. Thank you for watching this Neurology Live Peers & Perspectives. If you enjoyed the content, please subscribe for our e-newsletters to receive upcoming Peers & Perspectives and other great content right in your inbox.

Transcript is AI-generated and edited for clarity and readability.

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WEDNESDAY, Nov. 15, 2023 (HealthDay News) -- Cardiac 18F-dopamine positron emission tomography (PET) can identify at-risk individuals who are subsequently diagnosed with a central Lewy body disease (LBD), according to a study published online Oct. 26 in the Journal of Clinical Investigation.

David S. Goldstein, M.D., Ph.D., from the National Institutes of Health in Bethesda, Maryland, and colleagues assessed the predictive value of low versus normal cardiac 18F-dopamine PET in at-risk individuals. Thirty-four participants with three or more confirmed risk factors underwent serial cardiac 18F-dopamine PET at intervals of 1.5 years for 7.5 years or until diagnosis of Parkinson disease.

Nine and 25 patients had low and normal initial myocardial 18F-dopamine-derived radioactivity, respectively. The researchers found that eight of nine with low initial radioactivity and one of 11 with normal radioactivity were diagnosed with a central LBD (LBD+) at seven years of follow-up. All nine LBD+ participants had low 18F-dopamine-derived radioactivity before or at the time of diagnosis of a central LBD, while only one of the 25 participants without a central LBD had persistently low radioactivity.

"We think that in many cases of Parkinson and dementia with Lewy bodies the disease processes don't actually begin in the brain. Through autonomic abnormalities the processes eventually make their way to the brain," Goldstein said in a statement. "The loss of norepinephrine in the heart predicts and precedes the loss of dopamine in the brain in Lewy body diseases."

Abstract/Full Text

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Cardiac 18F-Dopamine PET: A Promising Predictor of Lewy Body ... - HealthDay

A. Gordon Smith, MD, FAAN

According to a new survey on neurologists in the United States, patients with generalized myasthenia gravis (gMG) who faced social determinants of health (SODH) challenges experienced health care access inequities when initiating and continuing treatment for their condition. These findings suggest the need to mitigate treatment-related disparities in gMG by assisting patients with treatment costs, transportation, and in-home infusions, as well as increasing awareness and patient advocacy.1

Among 150 neurologists who completed the survey in October 2022, respondents estimated that 33% of their patients with gMG faced care inequities and 74.7% (n = 112) reported it is more difficult for these patients to afford prescribed gMG therapies. Notably, 67.3% (n = 101) of respondents reported these patients experienced a greater difficulty in continuing gMG treatment and 60.0% (n = 90) noted these patients had a greater likelihood of experiencing exacerbation or crisis-related hospitalization.

These findings were presented at the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM) meeting, held November 1-4, in Phoenix, Arizona, by senior author A. Gordon Smith, MD, FAAN, professor and chair of neurology, and Kenneth and Dianne Wright Distinguished Chair in clinical and translational research at Virginia Commonwealth University, and colleagues. Investigators conducted a 42-item online survey on healthcare access which was deployed to neurologists using email. The questions centered around demographics, diagnosis, treatment, and continuity of care in patients with gMG that were considered to be facing SDOH challenges. These challenges could pertain to any racial/ethnic minority or financial limitations.

READ MORE: Subcutaneous Efgartigimod PH20 Demonstrates Efficacy for Generalized Myasthenia Gravis in Open Label ADAPT-SC+ Trial

In comparison with other patients with gMG, respondents viewed patients who faced inequities as less receptive to infusion therapies and thymectomy and were less likely to be presented with newer therapies. In addition, these patients were reportedly less likely to receive payor approval for antibody-based biologics, IVIg, and plasmapheresis, and were more likely to have trouble traveling to infusion centers. The respondents also identified the cost of treatment/insurance and transportation issues as the biggest contributors to the difficulties in obtaining and continuing treatment for gMG.

In an additional analysis presented at AANEM 2023 by the same authors, neurologists reported that patients with gMG who faced SDOH challenges were also more likely to experience healthcare inequities when receiving diagnosis. Flexible scheduling, improved transportation options, and increased primary care education were noted as ways to address these health disparities. Approximately 84% (n = 126) of the respondents were board certified in neurology and the remainder were in neuromuscular or electrodiagnostic medicine, roughly half were university affiliated.2

About 55% of respondents (n = 82) indicated the patients who faced health inequalities also experienced longer duration between symptom onset and gMG diagnosis and 56% had a higher likelihood of diagnosis in an inpatient setting (n = 84). Similarly, 55.3% (n = 83) reported these patients had more difficulty scheduling appointments and 76.7% (n = 115) reported these patients had more difficulty attending appointments. Additionally, 72.7% (n = 109) reported these patients missed more appointments. The neurologists from the survey suggested that these disparities were because of treatment cost, challenges with appointments, transportation difficulties, being less likely to seek care, and more likely to visit an emergency room as the disease progressed.

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This study was the first structured survey of neurophobia among Chinese medical students and resident trainees, comprising 351 respondents from a tertiary teaching hospital in Beijing, China. Our results showed high difficulty and low confidence scores for neurology. This is in line with the results of prior studies in different parts of the world, including the United States, United Kingdom, Canada, South America, and Asian and African countries, revealing that neurophobia is a global issue across diverse educational systems [4,5,6,7,8, 12,13,14,15] (Table 3).

In this study, both medical students and residents agreed that neurology was the most difficult medical discipline, and they felt the least confident in dealing with patients with neurological problems, in contrast to the six other specialties in primary care settings. Two-thirds of the medical students and more than half of the resident trainees had neurophobia. This prevalence is higher than previous estimates by Jozefowcz [3] and a survey conducted in Singapore [7], indicating that neurophobia should be taken seriously in China. Over the past 30years, neurology perception has remained unchanged in contrast to the rapidly changing requirements for neurological care in an aging population. Medical education authorities and neurology educators should pay particular attention to these issues.

Consistent with previous studies [4, 6, 8], neuroanatomy was the main reason for difficulty in neurology. In the digital era, neuroanatomy education can be improved from conventional sectional images by employing innovative strategies, such as computer-based instructional 3-dimensional models, web-based neuroscience and neurology teaching videos, blended and flipped strategies, and problem-based effective teaching in neuroanatomy.

The poor integration of preclinical and clinical neurological teaching is another major complaint. Almost 80% of the medical students stated that a combination of neuroanatomy, neuroscience, and clinical neurology would be the best approach. Fragmentation in the learning of basic neuroscience with clinical neurology should be tackled by integrating basic neuroscience learning with early, effective, and multiple clinical exposures more efficiently under a neuro-mentorship program. Furthermore, introducing preclinical revision courses in areas such as neuroscience and neuroanatomy through case-based learning when students enter clinical training could be another useful approach.

In Peking Union Medical College, medical students are required to be involved in a total of 8weeks neurology attachment in the clerkship year (6th year) and internship year (7th year). The internal medicine residency training program included a 4-week rotation in the Department of Neurology at PUMCH. Some respondents suggested that the lack of rotation time and restricted exposure to neurological patients led them to consider neurology a difficult subject, which should be addressed urgently. In such a limited rotation time, multiple novel educational interventions would help students organize, re-engage, and manage their learning approaches for a deeper understanding through selfdirected, problem-based, and team-based learning.

In our study, a high proportion of the residents expected more online self-directed learning resources. Utilization of online resources in neurology teaching and its distinct success over other teaching approaches has been signified in prior studies [18,19,20,21]. Online teaching has been revealed to enhance neurology knowledge at the final clinical attachment and residency rotation stages compared to textbooks. The incorporation of video tutorials as part of the online educational approach could offer a reasonable addition to increasing patient exposure and bedside teaching for residents.

It is noteworthy that neurology is regarded as a difficult and challenging subject, but this did not reduce students interest in or enthusiasm for neurology, and a substantial number of medical students tended to pursue neurology in their future careers. However, once resident trainees begin clinical practice, they may become less neurophobic. Although there was a relatively wide range of neurophobias among medical students and young residents, a trend toward gradual improvement was observed. We speculate that ongoing neurological education and clinical exposure to overcome neurophobia will initially target medical students and then seamlessly continue via postgraduate education.

Owing to the unique, difficult, and complex nature of neurology, neurophobia has long existed worldwide, and our research reached the same conclusions. The presence of neurophobia in various medical communities around the globe raises concerns about its adverse effects on the quality of patient care and management. Researchers have presented several evidence-based recommendations for overcoming neurophobia. Neurology education curriculum reforms, a paradigm shift from a traditional knowledge-based curriculum to a student-centered, and competency-driven education [22], neuro-mentorship programs, evidence-based effective educational interventions, and problem-based and integrated learning, would be the way forward to removing neurophobia.

As China continues to grow, the need for physicians to adequately address the health needs of its population has become increasingly important. In the future, the government should provide more political support and financial investments to improve the overall capability of global cooperation and communication in neurology education, reinforce partnerships and cultures, identify differences between China and the rest of the world, propose targeted improvement measures to solve neurophobia, and ultimately provide excellent talent reserves for brain science in the twenty-first century.

This study had several limitations. This study was conducted in a single medical institution. PUMCH is a tertiary comprehensive teaching hospital in China and a national referral center offering diagnostic and therapeutic care for complex and rare disorders. Therefore, it may be difficult to generalize our findings to other Chinese medical schools and hospitals. Therefore, multi-center studies are required to confirm these conclusions. Investigations are also warranted to estimate whether intervention measures such as increased patient exposure, more online resources, and enhanced integration of neuroanatomy, neuroscience, and clinical neurology may result in better performance in neurology education.

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Receiving a clot-busting drug in an ambulance-based mobile stroke unit (MSU) increases the likelihood of averting strokes and complete recovery compared with standard hospital emergency care, according to researchers at Weill Cornell Medicine,NewYork-Presbyterian, UTHealthHouston,Memorial Hermann-Texas Medical Center andfiveothermedical centers across the United States.

Thestudy, published online in the Annals of Neurology on Oct. 6, determined that MSU care was associated withboth increased odds of averting stroke compared with hospital emergency medical service (EMS) 18% versus 11%, respectively and a higher percentage of patients 31% versus 21% had early symptom resolution, within 24 hours after a stroke.

Patients in this study were treated with tissue plasminogen activator (t-PA), a mainstay medication delivered intravenously (IV) in stroke cases. The drug dissolves the clot in an artery that is blocking blood flow to the brain, making treatment time critical. While this is known to improve patient outcomes, how many patients fully recover afterward wasn't clear from prior research, said lead authorDr. Babak Benjamin Navi,associate professor, vice chair for hospital neurology services and chief of stroke and hospital neurology, in the neurology department at Weill Cornell Medicine. He is alsoacting medical director of theMSU, operated by NewYork-Presbyterian, in collaboration with Weill Cornell Medicine, Columbia University Irving Medical Center and the Fire Department of New York.

On average, the faster you treat someone, the more likely you are to have a good functional outcome because youre able to preserve more brain tissue, said Navi, who is alsoassociate professor of neuroscience at theFeil Family Brain and Mind Research Instituteat Weill Cornelland the medical director of the stroke center at NewYork-Presbyterian/Weill Cornell Medical Center. The brain can only sustain reduced blood flow for so long before permanent injury develops.

Using multicenter trial data from 2014 to 2020, the researchers evaluated 1,009 patients: 644 received t-PA in an MSU, and 365 received EMS care. Overall, patients received t-PA at a median interval of 87 minutes after the onset of stroke symptoms. The study found that with t-PA treatment in this time frame, about one in four patients who had a suspected stroke recovered within 24 hours and one in six averted a stroke with no demonstrable trace of brain injury on an MRI.

The outcome improved for patients treated by an MSU since the time from symptom onset to treatment was 37 minutes faster than for EMS care, meaning many more patients received vital t-PA within the crucial first hour. MSU care further increased the odds of averting a stroke with nearly one-third of patients recovering to normal within 24 hours. In addition, the researchers found other factors that contributed to better patient outcome: treatment within the first 45 minutes, younger age, being female, history of high cholesterol, lower blood pressure, lower stroke severity and no blockage of large blood vessels.

Every 40 seconds, someone in the United States has a stroke, according to the American Heart Association. This study highlights the need for optimizing stroke systems of care, Navi said. Further expediting the delivery of t-PA through MSUs should be a priority to increase the proportion of averted strokes.

Navi is also hoping that Medicare will assign MSU services a billing code in the near future so that it can be embedded within stroke systems of care and become a financially viable model.

Currently, he is working with researchers from UTHealth Houston on a study to evaluate the cost effectiveness of MSUs, which should be published next year. Such studies will hopefully lead to a shift in regulations and reimbursements, and how MSUs are led, managed and integrated within emergency medical services, he said.

Co-principal investigators for the BEST-MSU trial, which produced the data for this analysis, were Dr. James C. Grotta, director of stroke research at the Clinical Innovation and Research Institute at Memorial Hermann - Texas Medical Center and director of the Mobile Stroke Unit Consortium; and Dr. Jose-Miguel Yamal, departmentof biostatistics at UTHealth Houston School of Public Health.

Also contributing to this effort wasDr. John Volpi, director of the Eddy Scurlock Stroke CenterHouston MethodistStanley H. Appel Department of Neurology and associate professor of clinical neurology in neurology at Weill Cornell Medicine.

This study was funded by grant R-1511-33024 from the Patient-Centered Outcomes Research Institute.

Many Weill Cornell Medicine physicians and scientists maintain relationships and collaborate with external organizations to foster scientific innovation and provide expert guidance. The institution makes these disclosures public to ensure transparency. For this information, see the profiles for Dr. Babak Benjamin Navi.

Heather Lindsey is a freelance writer for Weill Cornell Medicine.

Link:
Mobile units increase odds of averting stroke | Cornell Chronicle - Cornell Chronicle

New data from the phase 3 PROPEL study (NCT04138277) showed that treatment with cipaglucosidase alfa (Pombiliti)/miglustat (Opfolda), a recently approved 2-component agent, was effective in patients with late-onset pompe disease (LOPD) for up to 104 weeks. These data, presented at the 2023 American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) annual meeting, held November 1-4, in Phoenix, Arizona, highlight the longterm sustained impact of this combination approach.1

Led by Tahseen Mozaffar, MD, director of the division of neuromuscular diseases in the department of neurology at the School of Medicine at UC Irvine, 119 patients from the original double-blind trial entered the open-label extension (OLE), 91 of which were enzyme-replacement therapy (ERT)-experienced and 28 who were ERT-nave. At 104 weeks, the mean change in percentage predicted 6-minute walk distance (6MWD) change was +3.1 (SD, 8.07) for ERT-experienced patients who continued on with cipaglucosidase alfa/miglustat (cipa/mig; n = 82) vs 0.5 (SD, 7.76) for those who switched from alglucosidase alfa/placebo (alg/pbo; n = 37).

Over the same time, investigators observed changes of +8.6 (SD, 8.57) and 8.9 (SD, 11.65) for ERT-nave patients in the cipa/mig and alg/pbo groups, respectively. Forced vital capacity (FVC), a measure of lung function, was improved through treatment. At the conclusion of the analysis, mean change in percentage predicted FVC was 0.6 (SD, 7.50) for the cipa/mig group and 3.8 (SD, 6.23) for the switch group in ERT-experienced patients, and 4.8 (SD, 6.48) and 3.1 (SD, 6.66) in ERT-nave patients, respectively.

The 2-component therapy, marketed by Amicus Therapeutics, also improved biomarker levels of creative kinase and hexose tetrasaccharide over the 104-week stretch. During that time, treatment with the combination medication did not result in any new safety signals, with 3 noted patients discontinuing treatment because of infusion-associated reactions of urticaria, urticaria and hypotension, and anaphylaxis.

WATCH NOW: The Role of Biomarkers in Myasthenia Gravis Diagnosis and Treatment: Hong Sun, MD, PhD

The 52-week analysis of the study, published in Neurology in 2022, showed a mean improvement in 6MWD of 14 m with cipa/mig vs approved ERT therapy but did not reach statistical superiority (P = .072). The 2-component therapy achieved a nominally statistically significant and clinically meaningful 3% mean improvement in percentage predicted FVC for superiorirt over approved therapy (P = .023). Outcomes consistently favored cipa/mig in all subgroups for the overall and ERT-experienced populations, regardless of baseline 6MWD and percentage predicted FVC.2

Earlier this year, at the 2023 American Academy of Neurology annual meeting, Mozaffar presented data from an open-label phase 1/2 study (NCT02675465) assessing the combination agent in patients with LOPD. Also known as study ATB200-02, pooled analyses of the ERT-experienced cohorts showed improvements in 6MWD from baseline of 3.1 m (standard deviation [SD], 44.75; n = 16), 33.5 m (SD, 49.62; n = 16), 25.2 m (SD, 63.30; n = 13), and 9.8 m (SD, 85.98; n = 12), 20.7 m (SD, 101.84; n = 9), respectively, across months 6, 12, 24, and 48 of treatment. Comparatively, the ERT-nave cohort reported improvements of 36.7 m (SD, 29.08; n = 6) at 6 months, 57.0 m (29.96; n = 6) at 12 months, 54.4 m (SD, 36.18; n = 6) at 24 months, and 43.5 m (45.19; n = 5) at 36 months; and 52.2 m (SD, 46.59; n = 4) at 48 months.3

The trial enrolled 3 cohorts of adult ambulatory patients based on ERT experience: those with 2 to 6 years (n = 11; aged 18-65 years) or with 7 or more years (n = 6; aged 18-75 years) were both administered 20 mg/kg alglucosidase alfa biweekly, while those who were ERT-nave (n = 6; aged 18-65 years) were given doses of 20 mg/kg IV cipaglucosidase alfa/260 mg miglustat orally biweekly.

All told, findings showed that percent predicted sitting FVC was generally stable or improved in the ERT-experienced cohorts, with a mean change from baseline of 0.9% (SD, 8.69; n = 16), 1.2% (SD, 5.95; n = 16), 1.0% (SD, 7.65; n = 13), 0.3% (SD, 6.69; n = 10), and 1.0 (SD, 6.42, n = 6) at 6, 12, 24, 36, and 48 months, respectively. In the ERT-nave cohort, pFVC improved by 4.2% (SD, 5.04; n = 6), 3.2% (SD, 8.42; n = 6), 4.7% (SD, 5.09; n = 6), 6.2% (SD, 3.35; n = 5), and 8.3% (SD, 4.50, n = 4) at the same respective time points.

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Bruce Hughes, MD: Hello, and thank you for joining this Neurology Live Peers & Perspectives presentation titled, Disability Progression and Maintenance of Cognitive Function in Multiple Sclerosis. Im your host, Dr Bruce Hughes. I am the medical director of the Ruan Multiple Sclerosis and Research Center in Des Moines, Iowa. Joining me today is Dr Robert Naismith, whos an MS [multiple sclerosis] specialist and researcher at Washington University in St. Louis, [Missouri]. Today, we will be talking about how patients with multiple sclerosis acquire disability and the concept of progression independent of relapse activity or PIRRA. We will discuss current understanding of cognitive decline in multiple sclerosis and share data on how various disease modifying therapies impact PIRRA and cognitive health in multiple sclerosis. Thank you for being here today.

I think well start with how our understanding of acquiring disability has changed over the years and maybe you can make some comments on raw relapse-associated worsening vs PIRRA.

Robert Naismith, MD:Absolutely, as a neurologist and a scientist, you always try to think back to whats happening in the disease and how to translate that to the patient experience. So whenever I think about multiple sclerosis, you have these different components that are taking place and to some degree alongside each other. So, you have acute inflammation, chronic inflammation and neurodegeneration. So, like with the last iteration of the criteria, what we do in our assessments and practice is we say whether patients have a subtype of MS with or without activity, or with or without progression. And we try to relate that back to the pathogenesis of whats happening with the disease. And activity is synonymous with new MRI lesions or relapses and those represent blood-brain barrier breakdowns. We have a new lesion that forms over the course of some short period of time. It may have neurologic dysfunction that occurs with it. And then theres some resolution of that maybe due to reduction of edema, decreased inflammation in that region, and maybe even some remyelination. If you talk about with activity, then that means you have a new lesion. You may or may not have a relapse associated with that. Whereas with progression, that may be due either to chronic inflammation because we know that these acute lesions turn into these chronic lesions and those can cause damage, and then you have neurodegeneration, and thats what we refer to as progression. And neurodegeneration is the dropout of neurons and axons over time because theyre in this hostile environment thats proinflammatory, and theyre working very hard to maintain their function. So there are these big metabolic demands that are put on them.

So the patient just knows that theyre doing worse. They come in and say, Im not as good as I was last time. And as a neurologist, we have to figure out what the reason is. The patient only knows that theyre doing worse. And we have to figure out, are they having relapse activity? Are they having a pseudo exacerbation? Are they having paroxysmal symptoms? Or are they having neurodegeneration or progression? Because a lot of patients just say, I must be progressing. So we need to sort that all out.

When you think about the ways people worsen, theres RAW, [which is] relapse-associated worsening. And that refers to worsening due to acute inflammation with a new lesion within the central nervous system with the referable symptom that the patients experiencing. Whereas PIRRA is without that acute inflammation. So it could either be from the chronic inflammatory state that these lesions undergo and is actually present throughout the central nervous system or maybe because of the dropout of neurons just over time. These things are interrelated, but they dont correlate perfectly. So we know that the acute inflammation is early in the disease and this acute inflammation leads to this neurodegeneration, but its not a 1:1 correlation. A lot of our treatments are aimed to address that acute inflammation to prevent the chronic inflammation and prevent the neurodegeneration. So RAW is relapse with activity and then PIRRA is worsening of disability without that relapse or that new MRI lesion.

Transcript is AI-generated and edited for clarity and readability.

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The most precious resource that we have in the world is the pediatric brain, says Christopher Giza, MD, professor of pediatrics and neurosurgery and pediatric neurology division chief, UCLAs Mattel Childrens Hospital.

They represent the future of both the individuals they inhabit and the society they will influence, he fervently believes.

This is our worlds future. No matter your specialty, your goal at the end of the day is for your patient to have the healthiest, most developed brain that is possible given their circumstance.

However, brain injuries during childhood present a huge challenge. The top cause of severe traumatic brain injury (TBI) in infants is abusive head trauma (formerly called shaken baby syndrome).

Dr. Giza says he also regularly sees children injured via car/bicycle/skateboard accidents, falls, sports and recreation and other circumstances.

Children arent just little adults, says Dr. Giza. Because their brains are smaller doesnt mean their problems are smaller. Traumatic brain injury in a developing brain is the most complex injury, to the most complex organ, at the most complex time. The leading cause of acquired death and disability for people under 40 isnt cancer or hemorrhage or stroke; its TBI.

Dr. Giza has been at UCLA for 30 years. He graduated from Dartmouth College, received his medical degree from West Virginia University, interned at the University of Pennsylvania and trained in adult and pediatric neurology at UCLA.

Then he took a two-year detour: He joined the Yosemite Search and Rescue (YOSAR) team. I was mediocre among the world-class climbers in Yosemite, but I was the only physician on the team, he says.

He stayed connected to UCLA via involvement with a research project cataloging patients whod undergone pediatric epilepsy brain surgery, while also providing care to climbers whod fallen and suffered brain and spinal cord injuries.

In 1998, Dr. Giza left Yosemites ruggedness to return to UCLA. I was given the opportunity to work as a postdoctoral fellow for three years to undertake basic laboratory research in TBI, he explains.

In 2001, he joined the faculty. In 2011, he traveled to Afghanistan as a civilian advisor to the Department of Defense, and in 2012, he founded UCLA BrainSPORT, a comprehensive sports concussion/mild TBI program for safety, performance, outreach, research and treatment. In 2014, UCLA BrainSPORT was invited to President Obamas Healthy Kids and Safe Sports Concussion Summit, where President Obama announced the UCLA program.

The idea is not to make people stop playing sports but to understand risks and benefits in regard to brain development and to prevent brain injuries, says Dr. Giza.

Having served on the CDC Pediatric Mild TBI Committee, NCAA Concussion Task Force and the California Athletic Commission, he now serves on the Major League Soccer Concussion Program Committee, the National Basketball Association Concussion Committee, advises the U.S. Soccer Federation and directs the NFL Neurological Care Program at UCLA.

Once called the silent epidemic, TBI is more widely recognized today because of issues publicized by sports and the military.

Yet it is still invisible in many ways, says Dr. Giza. A cancer or stroke survivor can be an inspiring spokesperson for their condition. But for people with TBIs, its harder. Those with severe injuries may find it difficult to be spokespeople because of their injuries. And those who get better often dont want the stigma of being identified as someone with a brain injury.

Dr. Giza says he uses his vision of the supreme importance of developing brains as an anchor for education around pediatric brain injuries. His division, comprised of 14 faculty and 15 fellows, plus nurses, dietitians, occupational therapists and research assistants, offers a concussion champions TBI course, which trains 50 primary care providers in each session.

Weve never turned down an opportunity to speak about it, he says. If a small school wants us to talk to fourth graders about head injuries, well send someone. We recently did an education program for physicians, NPs and PAs in the Los Angeles Unified School District to prepare for fall sports.

Dr. Giza recently returned from the University of Tasmania in Australia, where he participated in a massive online course on head injuries. We have had tens of thousands of people viewing it, he says, noting he then went to the Queensland Childrens Hospital and provided input on new concussion guidelines for Australia and New Zealand.

Thats one way to reach a lot of people, Dr. Giza adds. But another way is right here, with daily clinics. We started with one half-day pediatric head injury clinic per week, and now we have five. Pediatric neurology clinics happen every day of the week, and cover other diagnoses like epilepsy, headaches, neurodevelopment, autism, cerebral palsy, genetics and much more.

He stresses how essential it is to teach future, as well as current, care providers about pediatric head injuries and TBI. UCLA has a pediatric neurology residency program, a pediatric epilepsy fellowship program and a sports neurology and neuropsychology fellowship program affiliated with BrainSPORT.

In addition, we train occupational therapists, general pediatricians, sports medicine doctors, etc. Then each takes what weve taught them into their own practices and spreads understanding exponentially, he says. Were aiming for all the impact we can get, because ensuring childrens brains develop to their fullest potential is the single most important thing we can do. Ive dedicated my life to it.

Biomarkers may hold key to better brain injury treatments

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Kallol Ray Chaudhuri talks to Marika Davies about facing racial discrimination during his career and putting patients at the heart of research

After a long and arduous clinic, Kallol Ray Chaudhuri likes to take his team to the pub. I strongly believe that work should also be pleasurable and fun, he says.

Ray Chaudhuri, professor of neurology and director of the Parkinson Foundation Centre of Excellence at Kings College Hospital and Kings College London, was born in India to a medical family. His interest in neurology was sparked at a young age, sitting in on his fathers medical clinics on the ground floor of their home. I used to find it fascinating, he recalls. That concept of being in medicine and seeing patients was ingrained into me at a very early stage.

In 1984 Ray Chaudhuri graduated from Calcutta Medical College and moved to the UK to continue his training. Despite pressure to return to India to work in his fathers practice, he decided to pursue a career as a clinical academic in London, becoming a consultant neurologist in 1995 and research director at Kings College Hospital in 2018.

Ray Chaudhuri is proud of the work at the Parkinson Centre and of the feedback they get from patients. We have a plan to develop care for people based not only on medicine but on overall wellness, he explains. This has become incredibly popular and is being adopted in many different countries. Patient feedback is proof that what we do is relevant and has a tangible impact on the people we serve.

As a clinical academic Ray Chaudhuri says his research is very patient orientated. People think research is where you go to the laboratory and do cell culture stuff, but theyve forgotten about the real beauty of clinical research, he says. I love seeing patients and trying to bring innovation to the clinic by mixing education and research.

Ray Chaudhuri says that throughout his career he has encountered racial discrimination. Some consultants would refuse to talk to me directly or make derogatory comments about colleagues whose English wasnt that good. I learnt pretty early that if I was going to make a mark Id have to work really hardone of my bosses once told me I had to be twice as good as a local person to get a job, he recalls. Even after I became established and formed my own research group there was a lot of focus on trying to find errors in my work; the scrutiny was extremely high compared with colleagues who were doing the same sort of work.

Outside of work Ray Chaudhuri enjoys playing in a folk rock band and writing music. He is currently composing songs about the lived experiences of patients with Parkinsons disease. He is also active in rhinoceros conservation in South Africa, where he travels twice a year to raise money and awareness.

Ray Chaudhuri encourages his juniors to travel abroad to meetings wherever they can and to choose a career path that they enjoy. Enjoyment in work is absolutely crucial so its important that you get job satisfactionthat will often give you joy and help your work-life balance, he says.

He also tells his juniors not to be daunted by challenges that come their way. From my own experience, if I let those things into my head I wouldnt be where I am, he says. Sometimes if you have to be better than the others to be where you are, so be it.

Ray has made exceptional contributions to the field of medicine and his dedication to nurturing the next generation remains unmatched. Despite being snowed under with work and other commitments he still gives his team the attention and help they need to succeed.

He has worked to get Kings College Hospitals centre recognised as a Parkinsons Centre of Excellence, one of only two in the UK. He created the UKs first Parkinsons patient group to review all studies before we take them on, emphasising the need to have patients at the heart of our research and care. Ray sits on the equality, diversity, and inclusivity panel at our trust, working to improve representation of our communities in research.

Our career plans and projections have been shaped by Ray, and we will be forever grateful to his guidance, help, and kindness.

Mubasher A Qamar, Lucia Batzu, Silvia Rota, Valentina Leta, and Aleksandra Podlewska are fellows at the Parkinson Foundation Centre of Excellence at Kings College Hospital.

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Caring for the whole person: the consultant neurologist - The BMJ

Northwestern Medicine investigators have identified a novel therapeutic agent that is effective in treating metastatic breast cancer and brain metastases with minimal side effects, according to a recent study published in the Journal of Clinical Investigation.

The study, led by Maciej Lesniak, MD, chair and the Michael J. Marchese Professor of Neurosurgery, found that metixene, a central nervous system small-molecule inhibitor drug, induced cancer cell death in mouse models of different metastatic breast cancer subtypes and extended survival in mice with brain metastases.

The significance of this project lies in its potential to address a pressing clinical challenge: the treatment of brain metastases, particularly in the context of breast cancer. It offers hope for improving the quality of life and survival outcomes for a substantial number of patients affected by brain metastases, a common and serious complication of cancer. The identification of a novel therapeutic agent, metixene, and its mechanistic insights add a promising dimension to the field of cancer research and treatment, said Jawad Fares, MD, MSc, a neurosurgery resident at Northwestern Medicine and a postdoctoral fellow in the Lesniak laboratory who was lead author of the study.

Breast cancer is one of the major causes of brain metastases and is also the most common cause of cancer-related death in women worldwide, according to the World Health Organization. A lack of clinical trials and new therapeutic options has also slowed progress in treating patients with breast cancer brain metastases.

In the current study, the investigators screened more than 320 FDA-approved drugs known to cross the blood-brain barrier, which prevents foreign substances, including most drugs, from entering the brain. Among the drugs tested, metixene an antiparkinsonian drug was identified as a top candidate for killing cancer cells in various subtypes of metastatic breast cancer and brain metastases.

In a series of in vivo experiments, metixene not only decreased the size of breast tumors in mice, but also increased the lifespan of mice with multi-organ site metastases, intracranial solitary metastasis, and multiple brain metastases.

Subsequent functional analysis further showed that metixene induced incomplete autophagy when waste accumulates inside a cell and fails to be recycled and reused in cancer cells by activating the NDRG1 protein, which caused the cancer cells to trigger their own death.

Using CRISPR-Cas9 gene editing to knockout NDRG1 in breast cancer cell lines also led to autophagy completion and the reversal of metixene-induced apoptosis, or programmed cell death, in the cancer cells, according to the authors.

The study highlights the potential clinical significance of metixene as a promising therapeutic agent for the treatment of metastatic cancer and brain metastases. The drug was noted for having minimal reported side effects in humans, which makes it a strong candidate for consideration in clinical translation, i.e., further investigation and potential use in human clinical trials, Fares said.

Co-authors include Crismita Dmello, PhD, research assistant professor of Neurological Surgery, Peng Zhang, PhD, assistant professor of Neurological Surgery, Atique Ahmed, PhD, the Allen Buckner Kanavel Professor of Neurosurgery, Jason Miska, PhD, assistant professor of Neurological Surgery, Irina Balyasnikova, PhD, professor of Neurological Surgery, C. David James, PhD, Professor Emeritus of Neurological Surgery, Adam Sonabend, MD, associate professor of Neurological Surgery, and Amy Heimberger, MD, PhD, the Jean Malnati Miller Professor of Brain Tumor Research.

Lesniak, Dmello, Zhang, Ahmed, Miska, Balyasnikova, James, Sonabend and Heimberger are members of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.

This work was supported by National Institutes of Health grants P50CA221747, R35CA197725, R01NS87990 and R01NS093903.

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Novel Therapy Extends Survival in Metastatic Cancer - News Center - Feinberg News Center

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Newswise MINNEAPOLIS People who live in neighborhoods with lower socioeconomic status are less likely to receive clot-busting medications or undergo clot-removing procedures after they have a stroke than people who live in neighborhoods with higher socioeconomic status, according to a study published in the November 1, 2023, online issue of Neurology, the medical journal of the American Academy of Neurology.

These treatments can greatly reduce death and disability from stroke, but previous studies have shown that few people actually receive the treatments, said study author Amy Ying Xin Yu, MD, of the University of Toronto in Canada. We wanted to see how socioeconomic disparities play a role, especially in an area where everyone has access to universal health care.

The study looked at all people living in Ontario, Canada, who had an ischemic stroke during a five-year period, for a total of 57,704 people. Ischemic stroke is caused by a blockage of blood flow to the brain and is the most common type of stroke.

The study looked to see how many of those people were treated with clot-busting drugs or surgery to remove blood clots.

Researchers also looked at participants neighborhoods and divided them into five groups based on their neighborhoods socioeconomic status, which was determined by factors such as the percentage of adults without a high school diploma, unemployment rate and income level.

A total of 17% of those living in the neighborhoods with the lowest socioeconomic status were treated, compared to 20% of those living in the neighborhoods with the highest socioeconomic status.

When researchers took into account other factors that could affect treatment, such as age, high blood pressure and diabetes, they found that people in the neighborhoods with the lowest socioeconomic status were 24% less likely to be treated than people in the neighborhoods with the highest socioeconomic status. There was no difference in treatment between the neighborhood with the lowest status and the middle three neighborhoods.

Our study underscores the need for tailored interventions to address socioeconomic disparities in access to acute stroke treatments, including educational and outreach programs to increase awareness about the signs and symptoms of stroke in various languages and efforts to distribute resources more equitably across neighborhoods, Yu said. Further research is needed to examine the specific causes of these disparities, so we can find ways to address the larger systemic issues that need to be improved to better serve people from under-resourced neighborhoods.

A limitation of the study was that researchers did not have information on other factors that could affect stroke treatment, such as the time symptoms started or how severe the stroke was.

The study was supported by ICES, a health research institute in Ontario; the Heart and Stroke Foundation of Canada; PSI Foundation; and Ontario Health Data Platform.

Learn more about stroke at BrainandLife.org, home of the American Academy of Neurologys free patient and caregiver magazine focused on the intersection of neurologic disease and brain health. Follow Brain & Life on Facebook, Twitter and Instagram.

When posting to social media channels about this research, we encourage you to use the hashtags #Neurology and #AANscience.

The American Academy of Neurology is the worlds largest association of neurologists and neuroscience professionals, with over 40,000 members. The AAN is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimers disease, stroke, migraine, multiple sclerosis, concussion, Parkinsons disease and epilepsy.

For more information about the American Academy of Neurology, visit AAN.com or find us on Facebook, Twitter, Instagram, LinkedIn and YouTube.

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Does Your Neighborhood Affect Your Care After a Stroke? - Newswise

The NFL Players Association's investigation into why Tua Tagovailoa was allowed to return in Week 3 after appearing to suffer a head injury took a drastic turn Saturday afternoon.

The union fired the independent neurotrauma doctor who was "involved" in the situation at the game between the Miami Dolphins and the Buffalo Bills, according to Pro Football Talk. Tagovailoa suffered what the team announced was a "head injury" after being knocked to the ground, standing up and stumbling before leaving the game. The hit appeared to end Tagovailoa's day, but he ended up returning to the game for the second half to lead the Dolphins to a 21-19 win.

That decision raised a lot of eyebrows and prompted the NFLPA to officially open up an investigation into the incident.

Tagovailoa was reportedly checked for a concussion all week and passed all the necessary tests leading to the Dolphins' Week 4 game against the Cincinnati Bengals just four days later. Tagovailoa suffered another scary-looking injury Thursday night, though, after being slammed to the ground before he was stretchered off the field and taken to a hospital. He was discharged that night and flew home with the team.

The investigation is still ongoing, but the independent doctor and the Dolphins team physician were reportedly interviewed on Friday as part of the investigation, according to NFL Network's Tom Pelissero. The NFLPA reportedly found that the doctor made "several mistakes" during the game.

Tua Tagovailoa is at the center of a major NLFPA investigation. (Photo by Megan Briggs/Getty Images)

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NFLPA reportedly fires independent neurologist who was at Week 3 game where Tua Tagovailoa returned after head injury - Yahoo Sports

To find out if the brain development of a newborn baby is normal, doctors usually look at among other things a small reflex action, triggered by exerting a tiny amount of pressure on the palm of the hand or the sole of the foot. This little movement in the first months of life provides invaluable information.

Llus Barraquer Roviralta considered the father of neurology in Spain first utilized this technique over a century ago at Sant Pau Hospital in Barcelona. A full 140 years of scientific advances (and three generations of Barraquers) have now passed in the neurology clinics of Sant Pau. Today, specialized services in this area of medicine have taken giant leaps, thanks to the development of imaging technology.

This is the decade of neurology, proclaims Albert Lle, the current director of the department that Barraquer created. The 50-year-old neurologist recently received a lot of media attention after his team successfully treated the 92-year-old former premier of Catalonia, Jordi Pujol, after he suffered a stroke. Pujol was released from hospital last weekend.

This interview has been translated and edited for clarity and brevity.

Question. How has the field of neurology changed in 140 years?

Answer. Neurological disorders are becoming more frequent. Many of these are age-related diseases this is to be expected, given that people are living longer. Its projected that the prevalence of degenerative diseases could triple within the next 30 years.

Q. How has the prognosis of these diseases evolved?

A. Thirty years ago, there were very few diseases that had effective treatment. In most cases, the causes and mechanisms were not well understood. For strokes, there were only antiaggregants, such as aspirin. Practically nothing was known about degenerative diseases. As for neuromuscular diseases, only cortisone or very broad-acting immunosuppressants were available. What has happened in recent years is that more knowledge about the causes has resulted in more effective treatments.

Q. It used to be said that neurologists know all about the diseases, but they cant cure any of them

A. This belief is totally obsolete. There are effective treatments for cerebral vascular diseases, for stopping blood clots from growing or causing problems there are very effective treatments for migraines, theres gene therapy treatment being carried out for spinal muscular atrophy. Perhaps the most difficult diseases to treat are Alzheimers and Parkinsons.

Q. These are good times for neurology, then?

A. We are in a fantastic era, because of the therapeutic tools we have access to. But the rise of neurological diseases is also, in turn, a time bomb, because it can squeeze health services. We have aging populations, a greater prevalence of chronic diseases all of this comes at a very high cost, the treatments arent cheap. This is why its very important to have adequate plans for Alzheimers, for example, or for other neurodegenerative diseases, to prioritize where were going to put the money do we put it into long-term care homes or do we put it in research?

Q. Last week, former Catalan premier Jordi Pujol was proof that strokes can be reversible, even at an advanced age.

A. Today, more and more work is being done on biological age rather than on chronological age. That is, you can be 60 years old, but have the brain of an 80-year-old, because youve had an unhealthy lifestyle.

The rise of neurological diseases is a time bomb, because it can squeeze health services

Q. Mar Castellanos, the head of neurology at A Corua Hospital, said in an interview with EL PAS that strokes dont just take place among the elderly more and more often, they are affecting the working age population. Why is this happening?

A. A stroke is highly influenced by lifestyle: smoking, diabetes, high cholesterol, a sedentary lifestyle, high stress levels age is not the only factor.

Q. Speaking of lifestyle even though were living longer, are we living worse? Are we harming our brain with our habits?

A. I think there is still a lack of awareness regarding the prevention and early detection of neurological diseases. In the case of a stroke, for example, there are people who still think that its not necessary to go to the emergency room, that you can wait and see if it goes away. We see this every day. And why is this happening? Because cardiovascular or cancer prevention campaigns began in the 1970s, but in neurology, they started much later weve been repeating this message for less time. In the case of a stroke, time is brain: the longer it takes to get to the hospital, the more brain damage there will be. Neurological diseases have been largely neglected from the point of view of awareness campaigns and funding.

Q. Theres a kind of knowledge black hole when it comes to neurodegenerative diseases, which still have no treatment. Why?

A. Alzheimers, Parkinsons these are very difficult diseases to study and treat. Sometimes, many years may pass before a person notices the first symptoms. By the time they begin to notice and seek help, there is already significant brain damage. When someone has a tumor, oncologists do a biopsy of the tissue, analyze it and look for viable treatment options. But you cant do a biopsy in the brain: we depend on imaging techniques, which dont have microscopic resolution. We arent able to examine these diseases in detail in the early stages not knowing whats happening during these critical years makes it difficult to find treatments.

In Alzheimers, there are more than 50 genes involved its very difficult to know what the sequence of events is. Even so, I would say that much progress has been made. And its also very clear that the greatest advances have been made in the degenerative diseases that have received the most funding, like Alzheimers and MS. The common thread of all chronic diseases except for strokes is to understand the immune system in our brain, about which very little is known. This will be essential research over the coming decades.

Q. How can the healthcare system remain sustainable?

A. Its necessary to carry out a cost-effectiveness analysis. If we manage to reduce or postpone the onset of Alzheimers for five years with effective treatments, we can reduce the number of total cases and, most importantly, improve peoples quality of life. This has a very high cost, but maybe it will buy patients a few extra years of life outside of long-term care.

Originally posted here:
Time is brain: The longer you take to go to the hospital after a stroke, the worse the damage - EL PAS USA

Over the last decade, research at Michigan Medicine has shown how exposure to toxins in the environment, such as pesticides and carcinogenic PCBs, affect the risk of developing and dying from amyotrophic lateral sclerosis.

Now, investigators have developed anenvironmental risk score that assesses a persons risk for developing ALS, as well as for survival after diagnosis, using a blood sample.

The results are published in theJournal of Neurology, Neurosurgery and Psychiatry.

For the first time, we have a means collecting a tube of blood and looking at a persons risk for ALS based on being exposed to scores of toxins in the environment, said first authorStephen Goutman, M.D., M.S., director of the Pranger ALS Clinic and associate director of the ALS Center of Excellence at University of Michigan.

Researchers obtained over 250 blood samples from participants in Michigan both with and without ALS. They calculated individual risk and survival models using 36 persistent organic pollutants.

Several individual pollutants were significantly associated with ALS risk. However, the risk for developing the disease was most strongly represented by a mixture of pesticides in the blood.

When considering the mixture of these pollutants, a person who was in the highest group of exposure had twice the risk of developing ALS compared to someone in the lowest group of exposure.

Our results emphasize the importance of understanding the breadth of environmental pollution and its effects on ALS and other diseases, said senior authorEva Feldman, M.D., Ph.D., James W. Albers Distinguished Professor at U-M, the Russell N. DeJong Professor of Neurology at U-M Medical School and director of the NeuroNetwork for Emerging Therapies at Michigan Medicine.

The research teams first understanding of the environments impact on ALS came in 2016 when investigators foundelevated levels of pesticides in the blood of patients with the disease.

They later uncovered thatexposure to organic pollutants advances ALS progression and contributes to worse outcomes.

When we can assess environmental pollutants using available blood samples, that moves us toward a future where we can assess disease risk and shape prevention strategies, Feldman said.

Environmental risk scores have been robustly associated with other diseases, including cancers, especially when coupled with genetic risk. This is a burgeoning application that should be further studied as we deal with the consequences of pollutants being detected throughout the globe.

Additional authors include Jonathan Boss, Dae-Gyu Jang, Ph.D., Bhramar Mukherjee, Ph.D., Rudy J. Richardson, Ph.D., and Stuart Batterman, Ph.D., all of University of Michigan.

This research was supported by the National ALS Registry/Agency for Toxic Substances and Disease Registry at the CDC (grants 1R01TS000289, CDC/ATSDR 200-2013-56856).

This research was also supported by theNational Institute of Diabetes and Digestive and Kidney Diseases, the National Institute of Environmental Health Sciences and the National Center for Advancing Translational Sciences at the National Institutes (grants K23ES027221, R01ES030049, R01NS127188, UL1TR002240). Additional support from the NeuroNetwork for Emerging Therapies, the NeuroNetwork Therapeutic Discovery Fund, the Peter R. Clark Fund for ALS Research, the Sinai Medical Staff Foundation, and Scott L. Pranger, University of Michigan.

Paper cited: Environmental risk scores of persistent organic pollutants associate with higher ALS risk and shorter survival in a new Michigan case/control cohort, Journal of Neurology, Neurosurgery and Psychiatry. DOI:10.1136/jnnp-2023-332121

Journal of Neurology Neurosurgery & Psychiatry

Data/statistical analysis

People

Environmental risk scores of persistent organic pollutants associate with higher ALS risk and shorter survival in a new Michigan case/control cohort,

27-Sep-2023

This research was supported by the National ALS Registry/Agency for Toxic Substances and Disease Registry at the CDC (grants 1R01TS000289, CDC/ATSDR 200-2013-56856). This research was also supported by the National Institute of Diabetes and Digestive and Kidney Diseases, the National Institute of Environmental Health Sciences and the National Center for Advancing Translational Sciences at the National Institutes (grants K23ES027221, R01ES030049, R01NS127188, UL1TR002240). Additional support from the NeuroNetwork for Emerging Therapies, the NeuroNetwork Therapeutic Discovery Fund, the Peter R. Clark Fund for ALS Research, the Sinai Medical Staff Foundation, and Scott L. Pranger, University of Michigan.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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Drawing a tube of blood could assess ALS risk from environmental ... - EurekAlert

Background

Medical comorbidities and neurological manifestations are commonly associated with COVID-19, though specific relationships remain unclear.

The aim of this study is to investigate the relationship between medical comorbidities and neurological manifestations in patients with COVID-19.

We reviewed medical comorbidities and COVID-19-related central nervous system (CNS) and peripheral nervous system (PNS) manifestations in 484 consecutive patients with COVID-19.

Neurological manifestations were seen in 345 (71%) of 484 COVID-19 patients. CNS manifestations included headaches (22%), altered mental status (19%), dizziness (8%), gait imbalance (5%), strokes (four patients, <1%), and seizures (two patients, <1%). PNS manifestations included myalgia (31%), hypogeusia (8%), hyposmia (6%), critical illness myopathy (nine patients, 2%), visual disturbance (six patients, 1%), rhabdomyolysis (four patients, <1%), and nerve pain (one patient, <1%). There were 153 (32%) patients with CNS manifestations, 98 (20%) patients with PNS manifestations, and 94 (19%) patients with combined CNS and PNS manifestations. Comorbidities such as cardiac disease (22%), dementia (17%), hypertension (16%), and chronic obstructive pulmonary disease (COPD; 13%) were significantly associated with CNS manifestations. No comorbidities were associated with PNS manifestations.

Neurological manifestations were common in our sample of 484 COVID-19 patients, with headache and altered mental status being the most common CNS manifestations and myalgia being the most common PNS manifestation. Cardiac disease, dementia, hypertension, and COPD were more common in patients with CNS manifestations. Providers should be vigilant about the possible emergence of CNS manifestations in COVID-19 patients with these comorbid conditions.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the disease it causes, coronavirus disease 2019 (COVID-19), can present with a range of manifestations such as fever, cough, shortness of breath, fatigue, nausea, vomiting, and diarrhea. Multiple medical comorbidities have been linked to severe disease and mortality, including cardiovascular diseases, cancer, chronic kidney disease, chronic lung diseases, dementia, diabetes mellitus, and obesity. Research has also documented a diverse constellation of central nervous system (CNS) and peripheral nervous system (PNS) manifestations including altered mental status, dizziness, gait imbalance, headache, hyposmia, hypogeusia, seizure, and stroke [1-3]. These neurological signs and symptoms have been reported in more than half of hospitalized patients with COVID-19 and are associated with an increased risk of mortality [1,4,5]. Interestingly, involvement of the CNS and PNS is independent of the severity of the respiratory disease, presenting a challenge for treating neurologists.

While medical comorbidities and neurological manifestations have well-documented associations with COVID-19, there remains much to learn about the specific nature of these relationships. As such, it is important to understand which medical comorbidities increase the risk of neurological manifestations in patients with COVID-19 and whether specific comorbidities increase the risk for CNS or PNS manifestations. This study investigates the association between medical comorbidities and CNS and PNS manifestations in patients with COVID-19 to further elucidate the nature of these relationships.

Data were collected through a clinical chart review of 484 consecutive patients with SARS-CoV-2 infection seen in outpatient clinics and the hospital between February 20, 2020, and July 4, 2020, at EvergreenHealth Medical Center in Kirkland, WA, the first hospital with reported cases in the United States. All patients had SARS-CoV-2 infection confirmed by polymerase chain reaction testing of a nasopharyngeal sample. The study was approved by Western Institutional Review Board, which is our institutional review board and ethics committee.

Data included demographic characteristics, medical history, and presenting manifestations. Only new-onset neurological manifestations were analyzed. Chart notes were independently reviewed by a neurologist and neuropsychologist, and data were cross-referenced for accuracy. Presenting signs and symptoms were reported by patients, family members, care partners, nursing staff, emergency responders, and physicians.

Descriptive statistics (mean [M], standard deviation [SD], percentage) were computed for relevant variables. Categorical variables were presented as absolute values along with percentages and compared using the Pearson 2 test. All tests were two-sided, with a p-value less than 0.05 considered statistically significant. All 345 patients displaying neurological signs and symptoms were divided into three groups: (1) patients with only CNS manifestations, (2) patients with only PNS manifestations, and (3) patients with both CNS and PNS manifestations. Chi-square tests were carried out using Excel functions and null hypothesis. The critical 2 value for comparison of three groups was calculated using two degrees of freedom with a p-value of 0.05. The problem 2 was calculated for each comorbid condition by summing the values calculated using the formula (O-E)2/E for each CNS, PNS, and CNS/PNS groups, where O = observed frequency of CNS, PNS, or CNS/PNS group, and E = expected frequency of the comorbid condition of each of the CNS, PNS, or CNS/PNS group. If the problem 2 value for the comorbid condition is greater than the calculated 2 value of the comorbid condition group, the null hypothesis was rejected, indicating that the difference between observed frequencies and expected frequencies is large enough to be considered statistically significant.

Clinical characteristics and preadmission comorbidities of patients with nervous system involvement are presented in Table 1. Neurological manifestations were seen in 345 (71%) of 484 COVID-19 patients. The average age of patients with neurological manifestations was 59 years (M = 58.8, SD = 20.6). The majority were Caucasian/white (79.4%), with slightly more females (51%). In our sample of 484 COVID-19 patients, there were 153 (32%) patients with CNS manifestations, 98 (20%) patients with PNS manifestations, and 94 (19%) patients with combined CNS and PNS manifestations. CNS manifestations included headaches (107 patients, 22%), altered mental status (92 patients, 19%), dizziness (40 patients, 8%), gait imbalance (23 patients, 5%), strokes (four patients, <1%), and seizures (two patients, <1%). PNS manifestations included myalgia (151 patients, 31%), hypogeusia (38 patients, 8%), hyposmia (27 patients, 6%), critical illness myopathy (nine patients, 2%), visual disturbance (six patients, 1%), rhabdomyolysis (four patients, <1%), and nerve pain (one patient, <1%). The most common comorbid condition associated with CNS manifestations was cardiac disease. Comorbidities such as cardiac disease (108 patients, 22%), dementia (83 patients, 17%), hypertension (76 patients, 16%), and COPD (61 patients, 13%) were significantly associated with CNS manifestations. No comorbidities were associated with PNS manifestations.

In our review of 484 patients with COVID-19 presenting to outpatient clinics and the emergency department, 345 (71%) had neurological manifestations. Of the 345 patients with neurological manifestations, 153 (32%) had CNS manifestations, 98 (20%) had PNS manifestations, and 94 (19%) had both CNS and PNS manifestations. Several comorbid conditions were associated with CNS manifestations (cardiac disease, dementia, hypertension, and COPD), though no comorbidities were associated with PNS manifestations. Our results are largely consistent with those of prior studies and suggest that neurological signs and symptoms are common presenting features of COVID-19 [6-8].

The pathophysiology of neurological manifestations in COVID-19 is mechanistically diverse and includes direct neuroinvasion, immune dysregulation and systemic inflammation, hypoxic-ischemic processes, endothelial damage and microvascular injury, maladaptation of the angiotensin-converting enzyme (ACE2) pathway, and the unique psychosocial impacts of this infection and related pandemic [5,9]. Several studies have reported the presence of SARS-CoV-2 in the cerebral spinal fluid and postmortem brain tissue of COVID-19 patients with encephalitis [10,11]. Early reports suggested that SARS-CoV-2 may gain access through nasal epithelial cells, infiltrating the bloodstream and lymph to reach other tissues [12-15]. However, while the neurotrophic properties of the virus represent one potential route to neurological dysfunction, research indicates that neurological complications are more commonly the result of severe systemic inflammation rather than direct neuroinvasion [16]. Immune-mediated mechanisms influence function of macrophages, microglia, and astrocytes, and are closely related to the development of a systemic inflammatory response. The neurovirulence of COVID-19 correlates with its ability to induce proinflammatory cytokine signals from astrocytes and microglia. SARS-CoV-2 can promote a proinflammatory state by activating glial cells [17]. Virus proliferation in lung tissue may precipitate cerebral hypoxia and anaerobic metabolism, leading to manifestations such as altered mental status, dizziness, gait imbalance, and stroke. This is particularly true for vulnerable individuals such as those with cardiac disease, hypertension, dementia, and COPD [4]. Strokes have been documented extensively in COVID-19 patients, though less than 1% of our patients experienced stroke.

Early research demonstrated that SARS-CoV-2 attaches to ACE2 receptors in the capillary endothelium [18,19], which, in turn, may cause abnormally elevated blood pressure, acute cerebral infarction or hemorrhage, and/or cerebral sinus venous thrombosis. ACE2 is expressed in various organs including the brain, lung, and blood vessels, and plays a role in regulation of a potent vasoactive peptide hormone, angiotensin II. ACE2 also acts as anti-inflammatory, and inhibition of ACE2 results in overactivation of inflammatory pathways. Additionally, psychosocial stressors caused by COVID-19 may also contribute to autonomic dysfunction. Autonomic dysfunction is characterized by elevated sympathetic activity and withdrawal of parasympathetic activity and is a common pathophysiological condition in patients with heart disease, hypertension, and diabetes [20].

Hyposmia is a well-known neurological manifestation of COVID-19. However, hyposmia occurred in only 27 (6%) of our patients, likely due to the older age and high rate of dementia in our sample. Hyposmia may be due to infection of olfactory epithelium and trigeminal nerves by SARS-CoV-2 [21,22]. Altered mental status is another commonly documented CNS manifestation of COVID-19 and occurred in 92 (19%) of our patients. Prior research suggests that altered mental status is a particularly lethal manifestation of COVID-19, specifically in older adults presenting to the emergency department, in most cases causing acute on chronic neurocognitive dysfunction strongly influenced by systemic inflammation and hypoxic-ischemic mechanisms [5].

Our study identified myalgia and headache as the most common neurological manifestations. Limited information exists regarding the mechanisms and timing of headache in patients with COVID-19. Direct viral invasion of the nervous system as well as the cytokine release syndrome can cause headache. Headache may be due to infection of nasal cavity trigeminal nerve endings and/or endothelial cells in the trigeminovascular system, and/or irritation of trigeminal nerve endings due to increased proinflammatory cytokines [23].

The association of comorbid conditions with neurological manifestations has been reported previously; however, the specific association of comorbid conditions with CNS manifestations, PNS manifestations, and combined CNS/PNS manifestations was unclear. Our study finds that several comorbid conditions were associated with CNS manifestations, though no comorbidities were associated with PNS manifestations. It is unclear whether cardiac disease, hypertension, dementia, and/or COPD made these patients more prone to CNS manifestations or whether systemic inflammation and/or other mechanisms led to CNS involvement.

There are limitations of our study that are worth mentioning. As a retrospective study focused on acute neurological manifestations, we lack information regarding persisting problems and outcomes. Furthermore, we lack data on the results of diagnostic studies that could enhance the results of our findings such as results of serology, electroencephalography, and neuroimaging. We also lack data on patient medications, which could also influence treatment options for COVID-19 manifestations.

Medical comorbidities and neurological manifestations are common in COVID-19 patients. The most common CNS manifestations in our sample were headache and altered mental status. The most common PNS manifestation was myalgia. Comorbid conditions such as cardiac disease, dementia, hypertension, and COPD were more prevalent in patients with CNS manifestations. Future research may further investigate CNS and PNS manifestations and their relationships with laboratory studies, electroencephalography, neuroimaging, medications, and patient outcomes.

Our study provides further evidence of neurological involvement in COVID-19. To our knowledge, there are few studies specifically analyzing the association between medical comorbidities and CNS or PNS manifestations in COVID-19. Providers should be vigilant about the possible emergence of CNS manifestations in COVID-19 patients with cardiac disease, hypertension, dementia, and COPD. Proper management of comorbid disease conditions in patients with COVID-19 may minimize CNS manifestations leading to improved outcomes.

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A Study on the Correlations Between Comorbid Disease Conditions and Central and Peripheral Neurological Manifestations of COVID-19 - Cureus

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Nathan Carberry, M.D., has joined the University of Miami Health System's Neuromuscular Division as an assistant professor of clinical neurology.

Dr. Carberry studied bioengineering at the University of Pennsylvania and earned his medical degree at New York Medical College, with AOA honors society distinction. He completed his medical internship, neurology residency, and fellowship in clinical neurophysiology (EMG/Neuromuscular Medicine) at Columbia University College of Physicians and Surgeons. Dr. Carberry's clinical and research interests are electrodiagnostic medicine, motor neuron disease, and neuropathy.

Name:Nathan Carberry, M.D.

Title:Assistant Professor of Clinical Neurology, Neuromuscular Division

Clinical Specialties:Neuromuscular medicine (motor neuron disease and neuropathy) and general neurology

Research Interests: Electrodiagnostic medicine, motor neuron disease, and neuropathy

Education:

Certifications:

Languages Spoken:English

Practice Locations:

1150 NW 14th Street- Suite 609

Appointments: 305-243-3100

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Dr. Nathan Carberry Joins the Department of Neurology - InventUM | University of Miami Miller School of Medicine

Lourdes Hospital is the only mission hospital that performs Deep Brain Stimulation: Dr. Sreeram Prasad, HOD,..  ETHealthWorld

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Lourdes Hospital is the only mission hospital that performs Deep Brain Stimulation: Dr. Sreeram Prasad, HOD,.. - ETHealthWorld

RWJBarnabas Health Medical Group provides comprehensive neurological care for patients with a full spectrum of conditions affecting the brain, spine or central nervous system. Our neurology team is led by a group of distinguished, board-certified physicians who treat complex conditions in both children and adults. Our goal is to improve our patients quality of life with compassionate expertise through expert medical management by utilizing the most advanced neuro diagnostic technologies available.

Some of the neurological conditions we treat include:

If youve been experiencing unexplained symptoms such as chronic headaches, memory loss, poor balance, or numbness and pain, it could indicate you have a problem related to your brain and/or nervous system. Seeing a neurologist for an exam is important if youve noticed any memory or concentration problems, muscle weakness or tremors, numbness, loss of coordination, or communication deficits.

Neurologists are physicians who specialize in treating diseases that affect the brain, spine, and nervous system, and a thorough neurological exam can help your doctor determine the cause of your symptoms.

During your neurological exam, your neurologist will conduct several evaluations. This may include cognitive testing, as well as checking your balance, sensory function, gait, language comprehension, eye control, motor strength and control, and many other skills. These detailed physical examinations are noninvasive and painless, and the exams are adapted for younger patients or other people with diminished consciousness or cognitive abilities.

Backed by a multidisciplinary team of medical experts, your neurologist can also connect you with one of our world-class neurosurgeons if surgery on your back, spine or brain becomes medically necessary.

To make an appointment with one of our RWJBarnabas Health Medical Group neurologists, please visit ourPhysician Locator to find a provider near you. You can make an appointment online, call the office or visithealthconnect.rwjbh.org/hcweb to book directly.

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New Jersey Neurology | RWJBarnabas Health Medical Group

What is neurology?

Neurology is the branch of medicine that is concerned with the study and treatment of disorders of the nervous system.

Thehealthcare providerwho specializes in neurology is called a neurologist. After completing medical school, healthcare providers specializing in adult neurology complete 1 year of residency in internal medicine and 3 years of neurology residency.

Neurologists treat disorders of the brain, spinal cord, and nerves, including, but not limited to, the following:

Muscle disorders and pain

Headache

Epilepsy

Neuritis and neuropathy

Brain and spinal cord tumors

Multiple sclerosis

Parkinson disease

Stroke

Myasthenia gravis

Muscular dystrophy

Alzheimer disease and other forms of memory problems

As a specialist, the neurologist sees patients with a wide range of problems and may act as a patient's principal or consulting healthcare provider, while the family healthcare provider, or primary care provider, is generally in charge of a patient's total health care.

Read this article:
Neurology | Johns Hopkins Medicine

A neurologist is a medical doctor who specializes in treating diseases of the nervous system. The nervous system is made of two parts: the central and peripheral nervous system. It includes the brain and spinal cord.

Illnesses, disorders, and injuries that involve the nervous system often require a neurologists management and treatment.

Before they can practice, neurologists must:

Neurologists manage and treat neurological conditions, or problems with the nervous system. Symptoms that commonly require a neurologist include:

People who are having problems with their senses, such as touch, vision, or smell, may also need to see a neurologist. Problems with senses are sometimes caused by nervous system disorders.

Neurologists also see patients with:

Because the nervous system is complex, a neurologist may specialize in a specific area. Theyll do a fellowship in that area after residency training. Subspecialties have evolved to narrow a doctors focus.

There are many subspecialties. Some examples include:

During your first appointment with a neurologist, theyll likely perform a physical exam and a neurological exam. A neurological exam will test muscle strength, reflexes, and coordination.

Since different disorders can have similar symptoms, your neurologist may need more testing to make a diagnosis.

Neurologists may recommend a variety of procedures to help diagnose or treat a condition. These procedures may include:

Your neurologist may use a lumbar puncture to test your spinal fluid. They may recommend the procedure if they believe your symptoms are caused by a problem in your nervous system that can be detected in your spinal fluid.

The procedure involves inserting a needle into the spine after numbing it and taking a sample of spinal fluid.

This procedure can help your neurologist diagnose myasthenia gravis. In this test, your doctor injects you with a medicine called Tensilon. Then they observe how it affects your muscle movements.

An EMG measures electrical activity between your brain or spinal cord to a peripheral nerve. This nerve is found in your arms and legs, and is responsible for muscle control during times of movement and rest.

EMGs can help your neurologist diagnose spinal cord disease as well as general muscle or nerve dysfunction.

During this test, your neurologist-technician inserts small electrodes into your muscles to help measure activity during periods of movement and rest. Such activity is recorded by a machine attached to the electrodes with a series of wires, which may be somewhat uncomfortable.

Oftentimes, a neurologist will order a nerve conduction velocity (NCV) study in conjunction with an EMG. While an EMG measures muscle activity, an NCV assesses the ability of your nerves to send the necessary signals that control these muscles. If your neurologist recommends both tests, youll likely do the EMG first.

During an NCV test, electrodes are taped over the same muscles that you had EMG electrodes in previously. Two sets of electrodes are used here one sends small pulses in an effort to stimulate your nerves, while the other set measures the results.

In all, the average EMG/NCV combination test may take about an hour or longer to complete. Youll want to avoid any stimulants, such as caffeine and nicotine, several hours before your test, or else these substances may alter your results.

Your neurologist may also ask that you dont take any blood-thinning medications or nonsteroidal anti-inflammatory drugs (NSAIDs) for 24 hours ahead of the EMG.

With electrodes applied to your scalp, an EEG measures electrical activity in the brain. Its used to help diagnose conditions of the brain, including inflammation, tumors, and injuries, as well as seizures and psychiatric disorders.

Unlike an EMG, an EEG doesnt usually cause any discomfort. Before the test, a technician places electrodes around the scalp that look like small cups. As small charges in the brain are measured through the electrodes, the technician will create changes in the environment to measure brain signals, such as different lighting or noises.

Like an EMG, youll need to avoid stimulants the day prior to the test. You can also expect the EEG to take an hour. Sometimes the test is done while youre sleeping.

Neurologists may use other types of tests, as well. Although they may not perform the test, they may order it, review it, and interpret the results.

To make a diagnosis, a neurologist may use imaging tests such as:

Other diagnostic procedures include sleep studies and angiography. Angiography determines blockages in the blood vessels going to the brain.

Your neurologist may help you manage your symptoms and neurological disorder alone, or with your primary care physician and other specialists. You can book an appointment with a neurologist in your area using our Healthline FindCare tool.

Read more from the original source:
Neurologist: Definition, Treatments, Areas, and More - Healthline