Newswise A new study involving University of Portsmouth researchers has uncovered key molecular defects underlying a rare developmental brain condition in children.

The research team, led by Dr Reza Maroofian, Dr Rauan Kaiyrzhanov and Professor Henry Houlden at University College London Queen Square Institute of Neurology, investigated the role of a specific regulatory protein in the brain known as acyl-CoA-binding domain-containing protein 6, or ACBD6. Up until now, the implication of defects in this protein have been unknown.

This study, published in the journal Brain, uncovered the role of malfunctioning ACBD6 in an ultra-rare condition in children, known as Autosomal Recessive ACBD6-related disorder. This is characterised by delays in the development of cognitive and motor skills, and is associated with dystonia and parkinsonism.

Co-lead author Dr Rauan Kaiyrzhanov said:The direct and immediate impact of this study is by introducing these genetic disorders to the medical community will help to diagnose the families affected by this condition worldwide. However, the long-term and wider effect of this study is that this ultra-rare condition can help us better understand the biology of these conditions in humans and advance our knowledge of biological mechanisms linked to much more common neurodegenerative movement disorders, like Parkinsons disease and dystonia.

This discovery was made possible through the use of advanced genomic technologies and extensive global data sharing, with 89 clinicians and scientists from 72 institutes involved worldwide.

Co-author Professor Matt Guile, Professor of Developmental Genetics at the University of Portsmouth said:We are delighted to contribute to this important piece of new research which will help improve the lives of patients and their families. This is part of our wider work to discover how Xenopus tadpoles can be used to support the diagnosis of rare genetic diseases.

The understanding of this rare disorder began with the study of a complex neurological disorder affecting three siblings from a single family, who had mutations in the ACBD6 gene. Thanks to extensive international collaboration over the following years, more affected families with similar genetic disorders were identified, and gradually a resemblance began to emerge among the distinct clinical and radiological features of those affected.

The researchers investigated 45 affected individuals from 28 unrelated families and extended their study to include animal models. This multifaceted approach uncovered evidence highlighting the essential role of ACBD6 in maintaining a healthy nervous system.

Co-lead author Dr Reza Maroofian said:This study underscores the untapped power of systematically investigating a relatively large number of well-defined individuals affected by ultra-rare disorders and highlights how much we can learn about human biology and pathology from these studies which are currently severely neglected and under-funded.

This international endeavour stands as a testament to the relentless dedication and collective expertise of the global scientific community and highlights the critical importance of not marginalising ultra-rare conditions.

Go here to read the rest:
New study reveals molecular causes of rare neurological condition ... - Newswise

News from NYU Langone Health

Today Is National Clean Out Your Fridge Day FOX 5 New York November 15 -Rabia A. De Latour, MD, assistant professor, Department of Medicine, Division of Gastroenterology and Hepatology

NYU Langone Streamlines Spine Radiosurgery Treatment to One Day Beckers Hospital Review November 15 -Alec Kimmelman, MD, PhD, the Anita Steckler and Joseph Steckler Chair, and professor, Department of Radiation Oncology, Perlmutter Cancer Center -Thomas B. Daniels, MD, clinical associate professor, Department of Radiation Oncology

Brave Soap Opera Star John York, 64, Readies Himself for Long Transplant Journey to Treat Blood and Bone Marrow Cancers SurvivorNet November 14 -Jun H. Choi, MD, clinical assistant professor, Department of Medicine, Division of Hematology and Medical Oncology, Perlmutter Cancer Center

Clinical Challenges: Atopic Dermatitis in Infants (Free log-in required.) Medpage Today November 15 -Vikash S. Oza, MD, associate professor, the Ronald O. Perelman Department of Dermatology, Department of Pediatrics

Artificial Intelligence and Machine Learning Could Enhance MS Diagnosis and Management NeurologyToday November 16 -Rachel Kenney, PhD, assistant professor, Departments of Neurology, and Population Health

New Training Recommendations for the Transition from Pediatric to Adult Neurology NeurologyToday November 16 -Aaron Nelson, MD, associate professor, Department of Neurology

Scientists Identify Potential Mechanism for Sudden Unexplained Death in Epilepsy NeurologyToday November 16 -Orrin Devinsky, MD, professor, Departments of Neurology, Neurosurgery, and Psychiatry, Comprehensive Epilepsy Center

Highlights of the 2023 International Mesothelioma Symposium Asbestos November 13 -Daniel H. Sterman, MD, the Thomas and Suzanne Murphy Professor of Pulmonary and Critical Care Medicine, Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, professor, Department of Cardiothoracic Surgery, Perlmutter Cancer Center

NYU Langone Health Performs Worlds First Whole-Eye & Partial-Face Transplant Eye News November 15 -Eduardo D. Rodriguez, MD, DDS, the Helen L. Kimmel Professor of Reconstructive Plastic Surgery, chair, the Hansjrg Wyss Department of Plastic Surgery -Vaidehi S. Dedania, MD, associate professor, Department of Ophthalmology -Samer Al-Homsi, MD, clinical professor, Department of Medicine, Division of Hematology and Medical Oncology, Perlmutter Cancer Center -Bruce E. Gelb, MD, associate professor, vice chair of quality, Department of Surgery, Division of Transplant Surgery

First Whole Eye Transplant Science-Based Medicine November 15 -Eduardo D. Rodriguez, MD, DDS, the Helen L. Kimmel Professor of Reconstructive Plastic Surgery, chair, the Hansjrg Wyss Department of Plastic Surgery

Cautious Hope Over Landmark Eye Transplant Optician November 16 -Eduardo D. Rodriguez, MD, DDS, the Helen L. Kimmel Professor of Reconstructive Plastic Surgery, chair, the Hansjrg Wyss Department of Plastic Surgery

Heres What a Polygenic Test Canand CantTell You About Your Health SELF November 15 -Jeffrey S. Berger, MD, associate professor, Department of Medicine, the Leon H. Charney Division of Cardiology, Center for the Prevention of Cardiovascular Disease

Is Manifesting Real? Heres the Science TheSkimm November 15 -Thea Gallagher, PsyD, clinical assistant professor, Department of Psychiatry

Spending Just ONE Night in the Emergency Room Before Being Admitted to the Hospital Can Increase Your Risk of Death, Study Suggests Daily Mail November 15 -Marc K. Siegel, MD, clinical professor, Department of Medicine, Division of General Internal Medicine

An AI Doctor in a Box Coming to a Mall Near You Forbes November 15 -Arthur L. Caplan, PhD, the Drs. William F. and Virginia Connolly Mitty Professor, Department of Population Health, Division of Medical Ethics

Whats The Worst That Could Happen? A Toothless FDA Health Affairs November 13 -Arthur L. Caplan, PhD, the Drs. William F. and Virginia Connolly Mitty Professor, Department of Population Health, Division of Medical Ethics -Lisa Kearns, senior research associate, Department of Medicine, Division of Medical Ethics

A Reduction in the Hippocampus in the Brain Linked to Cognitive Decline Risk Medical News Today November 15 -Shae Datta, MD, clinical assistant professor, Department of Neurology, NYU Langone HospitalLong Island, Concussion Center

VIDEO: Surgeon Physiologic Stress May Increase with Patient BMI During THA Healio November 15 -Joshua C. Rozell, MD, assistant professor, Department of Orthopedic Surgery, NYU Langone HospitalBrooklyn

Can You Fly While Pregnant? Health-Reporter November 15 -Meleen Chuang, MD, clinical associate professor, Department of Obstetrics and Gynecology, Family Health Centers

Go here to see the original:
NYU Langone Health in the NewsThursday, November 16, 2023 - NYU Langone Health

WATCH TIME: 5 minutes

"Our study indicates that CPAP treatment in patients with MS and sleep apnea is associated with a reduction in fatigue and an improvement in physical quality of life, offering potential benefits for long-term symptom management. Clinicians should consider exploring sleep apnea as a factor contributing to fatigue and poor sleep quality in patients with MS, as adequate treatment may lead to noticeable symptom improvement."

Fatigue, a prevalent symptom in multiple sclerosis (MS), is frequently associated with underrecognized sleep disturbances, which significantly contributes to the symptoms impact.1 In a new post-randomized controlled trial observational study, long-term continuous positive airway pressure (CPAP) use was associated with significant improvements in fatigue and physical quality of life in patients with MS and obstructive sleep apneahypopnea.2 Senior author Daria Trojan, MD, MSc, associate professor in the department of neurology and neurosurgery at McGill University, presented the findings in a scientific session at MSMilan 2023, the 9th Joint ECTRIMS-ACTRIMS meeting, held October 1113, in Milan, Italy.

In the analysis, investigators observed significant improvements in CPAP-treated patients (n = 16) compared with nonCPAP-treated patients (n = 12) for the Fatigue Severity Scale (P = .03) and MS Quality of Life-54 physical component score (P = .02). In addition, morning fatigue improved significantly (P = .048) in CPAP-treated patients compared with nonCPAP-treated patients. Also, investigators observed no significant improvements in the other outcome measures with CPAP treatment. Notably, measures of better CPAP adherence were associated with improvement on the Pittsburgh Sleep Quality Index (P = .039) and MS Quality of Life-54 physical component score (P = .049).

At the meeting, Trojan spoke an interview with NeurologyLive to discuss how CPAP treatment can impact fatigue, sleep quality, and overall well-being in patients with MS, as well as shared the key considerations for long-term adherence. She also talked about the measures that clinicians can take to address the challenges of CPAP adherence in patients with MS, and the alternative sleep apnea treatments that should be explored. In addition, Trojan spoke about the lack of data on other treatments for sleep apnea in MS, an area she suggests should be studied further in the future as well as CPAP therapy in this patient population.

See the original post here:
Effects of Long-term CPAP Therapy in Multiple Sclerosis: Daria ... - Neurology Live

Parkinson disease (PD), once thought of solely as a movement disorder, is now recognized as a complex heterogeneous condition with a wide range of symptoms. These symptoms encompass both motor and non-motor aspects, such as bradykinesia, sleep disturbances, and cognitive impairment. Despite being the second-most common neurodegenerative disease in the US, many patients remain undiagnosed or misdiagnosed due to the variability of the disease.

Recently, an extensive study published in npj PD showed that in 2019 only 40% of PD Medicare beneficiaries visited a neurologist in the calendar year, with only 9% of patients seeing a movement disorders specialist. The study revealed that a majority of PD patients failed to take advantage of recommended therapy services, like mental health or physical therapy, partly attributable to the lack of specialty care access and accurate diagnosis. These disheartening results highlight several glaring barriers within the PD care ecosystem.

To ensure favorable patient outcomes, the healthcare community must prioritize early and accurate diagnosis of PD and expand virtual care options. By doing so, individuals can receive timely access to the therapies they need, leading to improved quality of life and better disease management.

PD is challenging to diagnose because many initial symptoms are vague. Patients may complain about trouble sleeping during the early stages of PD, so their primary care physician (PCP) will suggest melatonin or refer them to a sleep medicine specialist. Similarly, other early symptoms such as constipation and loss of smell are often dismissed or misdiagnosed by PCPs.

Cognitive problems may also be present, but many patients will disregard them, chalking up their forgetfulness or problems thinking to old age. Patients may also experience increased mood disorders but are often referred to a psychiatrist.

If a patient shows movement symptoms, like frozen shoulder, less dexterity, or toe rigidity, they will typically get bounced to a physical therapist or orthopedic or podiatry doctor. In these cases, these specialists may misdiagnose the patient, who will eventually undergo surgery to fix their issues rather than being treated for PD. If a tremor is present, a patients family physician may diagnose them with essential tremor, a more common condition than PD.

Since PD affects many different systems in the body, PCPs often cannot diagnose PD in patients correctly. When referred to a specialist, it is rarely a neurologist or a movement disorders specialist. Ultimately, the patient continually gets bounced around the healthcare system, never being correctly diagnosed with PD or receiving the suitable therapies to alleviate their symptoms.

Patients over 60 who present with these early symptoms of PD will first typically visit their primary care facility. In many cases, their symptoms are, in fact, attributable to conditions other than PD.

However, because PD is one of the leading neurological disorders, we need to help PCPs employ a standardized protocol for the elderly population. Suppose a patient is complaining about sleep disorders, anosmia, constipation, or changes in gait (which we know are all PD-associated symptoms). In that case, PCPs should flag patients as potentially having PD and push them in the right direction for care.

Two procedures we can incorporate today into this PD standardized protocol are objective diagnostics testing and telemedicine in the field of neurology.

If patients are not able to visit a neurologist or movement disorders specialist due to demographics, then the first thing we can offer patients to improve care is an objective diagnostic test.

Surprisingly, a skin biopsy is one of the most reliable diagnostics for PD, able to detect abnormal deposits of alpha-synuclein, a hallmark of PD. Compared to dopamine transporter (DAT) scans, this method can diagnose PD ten years sooner, meaning patients can undergo the appropriate treatment strategy earlier in the disease. Fortunately, a skin biopsy is a straightforward outpatient procedure done in a medical office without the need for patients to stop other medications. If we can push this forward and accurately diagnose patients early, we can ensure patients get the care they deserve.

Next, we can offer patients telemedicine options and have trained specialists to assist in diagnosing PD. We can break down borders by offering patients access to certified neurologists through online software or mobile apps to evaluate if an individuals symptoms are attributable to PD or another condition. Rather than having to wait months for an in-office visit with a neurologist, patients can get care faster and from the comfort of their own homes. Since many health organizations already utilize telemedicine for dermatology and psychiatry, we can dramatically improve patient outcomes if we bring telemedicine to neurology and the movement disorders arena.

In the US, it has been reported that over one million individuals are living with PD. In all likelihood, this is a gross underestimate of the number of PD patients in the nation due to misdiagnosis and lack of care access. To limit the barriers to care, we need to take drastic measures in pouring resources into standardizing protocols, specifically by providing objective diagnostics and virtual care options. By doing so, we can alleviate the suffering of many patients nationwide and, at the same time, significantly reduce the socioeconomic burden on our healthcare systems.

StrivePD is a free iOS disease management application FDA-cleared on the Apple Watch that passively collects tremor and dyskinesia data via Apples Movement Disorder API. People with Parkinsons (PwPD) can download the app and explore interactive charts to track their symptoms over time and understand how medications and physical activity impact them. Users will gain insights to guide their care journey and have the ability to share their data with clinical specialists for a personalized strategy. PwPD or caregivers can download the app on theApple App Store today. For neurologists and movement disorder specialists, reach out tosupport@runelabs.ioto understand your patients disease progression and gain insights into their quality of life beyond the clinic.

View original post here:
Improving Access to care in Parkinson Disease: Expanding ... - Neurology Live

THURSDAY, Nov. 16, 2023 (HealthDay News) -- Pronounced neuroaxonal damage precedes disability worsening events with or without preceding clinical relapses in people with multiple sclerosis (MS), according to a study published online Nov. 6 inJAMA Neurology.

Ahmed Abdelhak, M.D., from University of California at San Francisco, and colleagues assessed whether and when neurofilament light chain (NfL) levels are elevated in the context of confirmed disability worsening (CDW) with MS. The analysis included data from two observational cohorts seen at tertiary MS centers (609 and 1,290 participants).

The researchers found that NfL z scores were 0.71 units higher in the first cohort and 0.32 higher in the second cohort for CDW associated with clinical relapse versus stable MS. Higher NfL was detected preceding CDW independent of clinical relapse for two visits preceding the event and for the visit directly preceding the event. Findings were similar for the subset of individuals with relapsing-remitting MS.

"This cohort study documents the occurrence of NfL elevation in advance of clinical worsening and may hint to a potential window of ongoing dynamic central nervous system pathology that precedes the diagnosis of CDW," the authors write.

Several authors disclosed ties to industry.

Abstract/Full Text(subscription or payment may be required)

Continue reading here:
Neurofilament Light Chain Levels Show Precedence in Multiple ... - HealthDay

Neuropsychiatric symptoms of Long COVID, including brain fog, inability to concentrate, and headache, have puzzled researchers and clinicians, who are hunting for those symptoms causes. A new study found that neuroinflammation and blood-brain-barrier dysfunction are not likely drivers of the symptoms, giving researchers more clues in their quest to uncover what actually may be the culprit.

Scientists have proposed many potential causes of the neuropsychiatric symptomsincluding damage of the blood vessels in the brain, ongoing brain inflammation, and lingering viral infection. This study is the first time researchers have tested a large cohort of people living with Long COVID for spinal fluid markers of brain inflammation and blood-brain-barrier dysfunction. The researchers published their findings in JAMA Network Open on November 10, and the outcome is significant even with the negative finding.

Our study suggests that interventions that are aimed at quieting brain inflammation likely wont help people with Long COVID, says Shelli Farhadian, MD, PhD, assistant professor of medicine (infectious diseases) at Yale School of Medicine (YSM) and first author of the study.

For many years, Farhadian and Serena Spudich, MD, Gilbert H. Glaser Professor of Neurology and senior author, have been studying neurological abnormalities caused by human immunodeficiency virus (HIV) infection. An important way to assess this is through cerebrospinal fluid (CSF), which offers a window into the brains of living people. Its the only part of the central nervous system thats easily accessible, says Farhadian. It can and has already told us a lot about the brain and people living with other infections and inflammatory diseases like multiple sclerosis, HIV, and Parkinsons disease. Researchers can look at proteins and cells in the spinal fluid to see if there is any neurological dysfunction, including abnormal immune activity or blood-brain-barrier impairment.

Beginning in late 2020, the team began enrolling participants with self-reported neurological or psychiatric Long COVID symptoms. Many of the patients were enrolled in the YSM Department of Neurologys neuroCOVID clinic. The researchers had to rely on the self-reporting of symptoms because there are no established diagnostic criteria for Long COVID.

As a control, researchers were able to use CSF and blood samples that predated COVID-19. Its increasingly difficult to find people who have never had COVID-19, says Farhadian. The CDC estimates that over 90 percent of people by this point have been infected. But fortunately, over the past decade, Farhadian and Spudich were already enrolling healthy people from the New Haven community as volunteers to donate blood samples and CSF as research volunteers. Their team was able to use these samples collected before the pandemic as a control.

Our study suggests that interventions that are aimed at quieting brain inflammation likely wont help people with Long COVID.

All participants in the experimental cohort consented to give blood samples and underwent a lumbar puncture to collect CSF. Using these samples, researchers measured levels of inflammatory proteins called cytokines, immune cells, and neopterin, another marker of inflammation. They also evaluated the CSF-to-blood albumin ratio, which indicates blood-brain-barrier integrity. We chose these markers because theyve previously been found to be elevated in other neuroinflammatory conditions, says Farhadian.

The researchers did not find any significant differences between the experimental and control groups, suggesting that neuroinflammation and blood-brain-barrier dysfunction are unlikely to be the causes of neuropsychiatric symptoms associated with Long COVID. Now, the team can turn its attention to other potential causes of Long COVID and eventually home in on those that are supported by scientific evidence. Its been two years since the pandemic, and its time to reassess what we know and dont know about Long COVID so that we can focus our efforts on finding a solution, says Farhadian. We were really lucky that our participants were generous in agreeing to enroll in our study.

Farhadian and Spudich now plan to focus on other hypotheses that may reveal the biological underpinnings of neuropsychiatric symptoms of Long COVID. They will do this by leading translational research conducted through the COVID Mind Study at Yale, Specifically, the team will study whether lingering viral infection of the central nervous system plays a role in symptoms.

Other research led by Lindsay McAlpine, MD, instructor in the division of neurological infections and global neurology and co-author of the neuroinflammation and blood-brain-barrier study, is assessing structural and vascular brain abnormalities. We still dont understand whats causing neurological Long COVID, says Farhadian. But our hope is that with more studies, we can start to eliminate some of the possibilities and zero in on some of the others.

Go here to see the original:
Brain Fog: New Study Examines Causes of This Long COVID ... - Yale School of Medicine

WATCH TIME: 3 minutes

"You see a lot of lectures in terms of clinical experience, real-world evidence, but also highlighting a lot of the new data on many of the novel treatments that have emerged in the past few years."

Migraine headache has long been recognized as one of the most burdensome and prevalent diseases worldwide. There are several types of migraine, including abdominal migraine, basilar-type migraine, hemiplegic migraine, menstrual-related migraine, retinal migraine, and migraine without headache. In recent years, there have been significance advances in the treatment of these disorders, including the introduction of calcitonin gene-related peptide (CGRP)-targeting agents, which have proven to be effective and safe options.

In addition to its traditional meeting, the American Headache Society (AHS) is hosting its annual Headache Symposium, taking place November 15-19th in Scottsdale, Arizona. The 4-day event is designed for not just neurologists and headache specialists, but for a wide range of medical professionals including general practitioners, psychiatrists, physician assistants, nurses, dentists, and much more. Throughout the meeting, attending clinicians can learn more about the advances in headache migraine disorders, including ways to enhance patients experience, complementary medicine, and headache in children, among other topics.

Prior to the meeting, NeurologyLive sat down with Emad Estemalik, MD, director of the headache section at Cleveland Clinics Neurological Institute, to discuss the excitement around the event fueled by some of the recent advances in the field. Estemalik, who serves as an assistant professor of neurology at the Lerner School of Medicine, also provided context on some of the current unmet needs in the field, such as why certain patients and genders experience a worse condition. While he recognizes the significant strides made, Estemalik believes there is room for continued growth.

See more here:
Excitement Behind the 2023 American Headache Society ... - Neurology Live

November 15, (THEWILL) The lead consultant of Neurology at the University Of Calabar Teaching Hospital, Professor Ekanem Ephraim, has so far spent about 116 days in kidnappers den in Cross River State.

Professor Ephraim was kidnapped about four months ago on July 13, 2023, around the Atimbo Axis of Calabar Municipality, by unknown gunmen and taken into captivity.

Her abduction reportedly took place at her residence in Calabar by kidnappers, who posed as relations to a patient in dire need of medical attention.

The incident shook the medical community in the state and the state branch of the Nigeria Medical Association embarked in an industrial action to protest against the rising spate of doctor targeted kidnappings in the state.

The industrial action lasted for about forty days and occasioned a major and unquantified crisis in the states healthcare sector.

The strike action was later called off by the State NMA in the wake of the deteriorating health sector in the state and the need to give government a chance to arrest the situation.

In suspending the industrial action, the state Chairman of the Nigeria Medical Association disclosed that Following a letter of appeal from Gov. Otu, advice of the national president of the association and for the sake of many of the citizens who are suffering, we have suspended the strike to give government time to rescue our member.

This action has been carried out despite the fact that our member has not been released; however, if any of our member is kidnapped again, we will go back to strike.

We are appealing to security agents to step up and maintain the momentum that has been established in the last few weeks, which has reduced cases of kidnapping in the state, Archibong had stated then.

However, following her prolonged stay in captivity, Dr Felix Archibong has bemoaned her colleagues prolonged captivity.

Dr Archibong said that it was regrettable that security agencies and the state government have not been able secure her release after several promises made to that effect.

While noting that the state have become inhabitable due to the activities of kidnappers, said several others, including medical personnel, have suffered same fate as Prof. Ephraim.

This is the situation in the state and it is regrettable that our colleague is still in captivity after 115 days.

We are trying so hard not to make industrial action another alternative to getting the government and security agencies to keep to their promises, he stated.

Originally posted here:
Insecurity: UCTH's Neurology Professor Remains In Kidnappers ... - thewill news media

Hackensack Meridians Neuroscience Institute is proud to announce the recertification of its Center for Multiple Sclerosis and Related disease at Hackensack University Medical Center as aCenter for Comprehensive Multiple Sclerosis Care through the National Multiple Sclerosis Societys Partners in MS Care program. The renewal of the national certification also recognizes HUMC neurologists also practice out of JFK University Medical Center, making similar services available in Edison.

The Hackensack Meridian Neuroscience Institute at Jersey Shore University Medical Centers Center for Multiple Sclerosis is also nationally recognized by the National MS Society as a Comprehensive MS Center, renewing its certification earlier this year.

While the search for a cure formultiple sclerosis (MS) continues, effective strategies can help modify or slow the diseases progression, treat relapses (also called attacks or exacerbations), improve symptoms and function, and address emotional health.

As a Comprehensive MS Center, the Hackensack Meridian Neuroscience Institute, isnt just treating one aspect of a persons MS diagnosis, but working collaboratively across disciplines to treat the whole patient, saidFlorian Thomas, M.D., Ph.D.,Chair of Neuroscience Institute & Department of Neurology atHackensack University Medical Center and Founding Chair and Professor of Neurology and Associate Dean for Faculty Advancement at Hackensack Meridian School of Medicine.MS impacts many aspects of a patients life. By working with colleagues across our network, our MS Centers offer convenient and complete care for all aspects of our patients MS diagnosis.

An accurate diagnosis of MS is the first step and clinicians at Centers across our network are skilled in ruling out conditions that mimic MS and confirming the disease. Once a diagnosis is confirmed, symptom management is important. By offering care for symptoms such as bladder, bowel and sexual dysfunction, botox injections and intrathecal baclofen therapy pump for spasticity, rehabilitative assessments and care for physical or cognitive impairment, headache management, infusion therapy, pain management, specialty sleep services, speech therapy, swallow therapy and vision services.

TheCenter for Multiple Sclerosis and Related Diseases at Hackensack University Medical Center has been treating patients with this collaborative model for seven years. This recertification further recognizes the success of this model saidKrupa Pandey, M.D., Associate Professor of Neurology at Hackensack Meridian School of Medicine, and Director of the MS Center at Hackensack University Medical Center and Clinical Research for Neurosciences at Hackensack University Medical Center. MS is a complex disease, and symptoms are not the same patient to patient. Since the inception of the Center, we have continued to expand the research division and addition of clinicians such as psychologists trained in adjustment to the diagnosis, neuro-ophthalmologists to recognize the impact of MS on the eyes and neuro-rehabilitative care to improve or maintain day to day functioning.

In January, the MS Center at Jersey Shore University Medical Center was certified as a Center for Comprehensive MS Care through the National Multiple Sclerosis Societys Partners in MS Care program.

Im so incredibly proud of our centers team and the care we provide our patients, saidDavid Duncan, M.D. FAAN MSCS, Program Director of the MS Center at Jersey Shore University Medical Center.In three short years we have expanded into a dynamic comprehensive Multiple Sclerosis Program which focuses on all the aspects of treating and managing multiple sclerosis. Patients are extremely impressed with our centers all under one roof design which allows us to evaluate and treat patients in one location thanks to our on site exam and procedure rooms, infusion center, gait lab and adjacent state of the art 3T MRI. We are also in the final stages of plans of adding Neuro-urology for quick assessment of any MS related bladder complaints as well as cognitive testing all within the center. We work to make the whole process easy for patients by providing assistance with appointments and scheduling to help patients accomplish multiple consultations in one visit.

Both centers provide patients access to the latest in emerging therapies available through our numerous clinical trials and research.

The MS Society saysthe model ofcomprehensive MS carebest treats the patient as whole. It involves the expertise of many different healthcare professionals each contributing in a unique way to the management of the disease and the symptoms it can cause.Coordinating the efforts of health professionals trained to treat MS from various disciplines provides patients with neurological and nursing care, individual and family counseling and education, physical, occupational, and speech therapies, and social services. An interdisciplinary approach to MS care facilitates coordination of services and continuity of care, while avoiding duplication and fragmentation for the patient and family. Comprehensive care embraces a philosophy of empowerment the person with MS is an active participant in planning and implementing healthcare and self-care activities. He or she is a consultant to the team, which is important because MS, like all chronic illnesses, will last a lifetime.

This formal recognition honors the Centers ongoing commitment to high-quality MS care. The Comprehensive MS Care Center distinction is appointed by a national committee, and the organization must demonstrate coordinated, multi-disciplinary care for MS. To receive this recognition, Hackensack Meridian Neuroscience Institute specialists have continually demonstrated a wealth of knowledge, experience, and the important attention to detail necessary in treating people living with MS.

I am proud that the MS Society recognized the significant benefit our Neuroscience Institutes comprehensive strategy has for patients,said Maria Coello, vice president of Care Transformation Services including Neurosciences, Hackensack MeridianHealth. It is further recognition of our doctors, team members and staffs commitment to allowing MS patients to live full and complete lives, by caring for the whole person, not just the neurological symptoms of the disease.

For more information, visit Hackensack Meridian Neuroscience Institutehere. To learn more about MS and the National MS Society, visitwww.nationalMSsociety.org.

See original here:
Hackensack Meridian Neuroscience Institute Recognized Nationally ... - Hackensack Meridian Health

WEDNESDAY, Nov. 15, 2023 (HealthDay News) -- Black women reporting having experienced interpersonal racism may have higher risk for having a stroke, according to a study published online Nov. 10 inJAMA Network Open.

Shanshan Sheehy, Sc.D., from the Slone Epidemiology Center at Boston University, and colleagues examined the association of perceived interpersonal racism with incident stroke among U.S. Black women. The analysis included 48,375 participants in the Black Women's Health Study with follow-up from 1997 through 2019.

The researchers identified 1,664 incident stroke cases, of which 550 were definite cases confirmed by neurologist review and/or National Death Index linkage. For those reporting experiences of racism in all three domains of employment, housing, and interactions with police, there was a 38 percent increase in incident stroke (95 percent confidence interval [CI], 1.14 to 1.67) and a 37 percent increase in definite cases (95 percent CI, 1.00 to 1.88) compared with that seen in women with no such racism experiences. A similar trend was seen for comparisons of women in the highest quartile of the everyday interpersonal racism score versus those in the lowest quartile (hazard ratio, 1.14 [95 percent CI, 0.97 to 1.35] for all incident stroke; hazard ratio, 1.09 [95 percent CI, 0.83 to 1.45] for definite cases).

"It is possible that the high burden of racism experienced by Black U.S. individuals may contribute to racial disparities in stroke incidence," the authors write.

One author disclosed financial ties to Qmetis.

Abstract/Full Text

Go here to see the original:
Experiencing Racism Increases Stroke Risk in Black Women, Study ... - HealthDay

A new Northwestern Medicine study has uncovered previously unidentified intracellular mechanisms in the peripheral nervous system that cause CharcotMarieTooth Type 2B disease, a rare congenital disorder that causes sensory deficits and muscle atrophy and weakness.

The findings improve the understanding of the origins of the disease and may also inform the development of new targeted therapies, according to the study published in the Proceedings of the National Academy of Sciences.

These findings are important as they highlight an essential role for properly regulated mitochondria-lysosome contact site dynamics and function in the axons of sensory peripheral neurons, and demonstrate that this may be an important pathway in the pathogenesis of Charcot-Marie-Tooth Type 2B disease, said Yvette Wong, PhD, assistant professor of in the Department of Neurologys Division of Movement Disorders and co-lead author of the study.

Charcot-Marie-Tooth Type 2 diseases are a group of hereditary neuropathic disorders characterized by the degeneration of axons in peripheral nerves.

CharcotMarieTooth Type 2B disease is specifically caused by mutations in a GTPase protein called Rab7, which leads to the degeneration of axons of peripheral sensory neurons. Wong and other Northwestern Medicine investigators previously found that mitochondria-lysosome contact sites can form to support essential crosstalk between mitochondria and lysosomes, and that the untethering of these contact sites is driven by Rab7s GTPase activity. In the context of CharcotMarieTooth Type 2B disease, Wong and colleagues also previously discovered that disease mutant Rab7 prevents the untethering of these contact sites, resulting in downstream defects in mitochondrial dynamics.

In the current study, Wong and colleagues aimed to determine in peripheral sensory neurons whether mitochondria-lysosome contact sites disrupted by mutant Rab7 lead to mitochondrial defects and whether those defects preferentially occur in axons in peripheral neurons, as observed in patients with the disease, or in the neuronal cell body.

The investigators created a new mouse model of Charcot-Marie-Tooth Type 2B disease mutant Rab7; the mice displayed sensory behavior defects and neuropathy but had normal motor behavior. Using super-resolution and live microscopy to study the peripheral sensory neurons from these mice, the investigators identified mitochondria-lysosome contact sites that could not efficiently untether in axons. Importantly, promoting the untethering of mitochondria-lysosome contact sites was sufficient to improve mitochondrial dynamics in the axons.

The findings suggest that targeted therapies which help improve mitochondria-lysosome contact site tethering dynamics and function may improve mitochondrial health in these axons, according to the authors.

These findings also suggest that mitochondria-lysosome contact sites may play an important role in other genetic forms of Charcot-Marie-Tooth Type 2 disease, which also exhibit axonal degeneration, as well as in other neurological disorders that have mitochondrial dysfunction or axonal degeneration, according to Daniela Maria Menichella, MD, PhD, 08, 11 GME, associate professor of Neurology in the Division of Neuromuscular Disease and senior author of the study.

Our study demonstrates a critical role for mitochondria-lysosome contact sites to maintain the health of peripheral nerves. Moreover, defects in this important pathway have been recently linked to the pathogenesis of multiple neurodegenerative diseases, including Parkinsons disease and lysosomal storage disorders, said Menichella, who is also an associate professor of Pharmacology.

According to the authors, next steps include understanding how defects in mitochondria-lysosome contact site dynamics and function contribute to the degeneration of peripheral neurons, uncovering new roles for mitochondria-lysosome contact sites, and identifying new pathways for how mitochondria and lysosomes interact with other organelles to maintain neuronal health and contribute to additional neurological disorders.

Together, this work provides important insights into mitochondria-lysosome contact site regulation in peripheral neuropathy and has important consequences for advancing the fields of organelle contact site biology and neurodegeneration, Menichella said.

NirupaDoris Jayaraj, senior research associate in the Meninchella laboratory, was co-lead author of the study. Co-authors include Dongjun Ren, a postdoctoral fellow in the Department of Pharmacology; Tayler Belton, a research technologist in the Wong laboratory; George Shum, a research technologist in the Wong lab; Hannah Ball, a student in the Driskill Graduate Program in Life Sciences (DGP) program and a member of the Wong lab; and Dimitri Krainc, MD, chair and the Aaron Montgomery Ward Professor of Neurology and director of the Simpson Querrey Center for Neurogenetics.

This work was supported by National Institutes of Health grants NINDS R00 NS109252, NINDS Diversity Research Supplement 3R00NS109252-04S2, NINDS R24 NS098523 and R37 NS054154, R01 NS104295-0, and NIH HEAL initiative supplement R01 NS104295-01 and R01 AR077691-01.

Read the original post:
Investigating the Pathogenesis of Rare Congenital Nerve Disorder ... - Feinberg News Center

Are compliments a part of your day-to-day life? (Getty Images) (Getty Images)

Did you know that giving and receiving compliments, when done regularly, does far more for our overall wellbeing than just providing some quick flattery?

Engaging in these acts of kindness on a regular basis (following World Kindness Day which fell earlier this week), really is worth it for the very real neurological impact it has on our brains and us.

That said, one in 10 Brits have never given or received a compliment, according to a new study something that needs to change (when done genuinely, of course).

And looking at the UK, when 1,5000 British adults were asked where is home to the most kind and complementary people, the majority vote (10%) said London. This may come as a surprise for those who believe 'it's much friendlier up north'...

Though Liverpool and Manchester did come in second place, and Newcastle third.

Here, Dr Ritika Suk Birah, HCPC accredited consultant counselling psychologist sheds some light on what actually goes on in our brains when exchanging compliments.

The most common emotions associated with well-intentioned compliments are happiness (43%), confidence (22%) and pride (21%), according to the study. Although in true British fashion, 20% of us do feel somewhat awkward, 17% feel embarrassed and 5% of Brits panic in the face of a compliment.

But while there's definitely a time and place for compliments, for those that are sincere and kind, it's probably worth us getting over any awkwardness to reap the benefits.

"When we smile and compliment each other it can have several beneficial effects on our self-esteem and overall wellbeing. Compliments serve as external validation reaffirming our sense of self-worth and competence," says the psychologist, enlisted by ScS, which conducted the survey.

"We can use neuroscience to understand that compliments ignite brain regions associated with reward and positive self-perception, such as the striatum and medial prefrontal cortex."

Story continues

"These neural activities trigger the release of endorphins and serotonin, two neurotransmitters known for their role in fostering feelings of joy, contentment and emotional wellbeing."

And whether you're the one dishing them out, or flattered by one you've received, the benefits work both ways.

"Receiving compliments can create a psychological positive feedback loop. When we feel good about ourselves, we are more likely to engage in positive behaviours, such as setting and achieving goals, which, in turn, reinforces our self-esteem," explains Dr Suk Birah.

"The act of giving compliments constructs a culture of mutual appreciation and respect, we strengthen social bonds and nurture positive interpersonal relationships."

Of course, we shouldn't need compliments all the time just to like ourselves, but they can certainly come as a welcome addition. "Compliments have transformative power in creating happiness, improving our overall sense of wellbeing which can lead to a more positive and emotionally fulfilling social environment," says Dr Suk Birah.

What was the last compliment you received or gave to someone else?

Read more: Half of women believe theyre just entering their 'confidence era'

Continued here:
Psychologist reveals the neurological impact of giving and receiving compliments - Yahoo Lifestyle UK

There has never been a more exciting time in Alzheimer care than today. Promising innovations in therapies and diagnostics for this most common form of dementia are emerging at a faster pace than at any other time in medicine. At the same time, science is revealing that, for some, preventive behavioral measures can meaningfully delay progression. These developments together provide greater reason for optimism for those at risk of Alzheimer than at any other time in recent memory.

And these medical achievements couldnt come at a better time. More than 6 million patients nationwide live with Alzheimer disease (AD). By 2050, this number could reach nearly 13 million with costs of care topping $1 trillion.1

Yet, this rapid pace of change also threatens to confuse providers and patients who may not be up to date on the latest science on Alzheimer. Dispelling long-perpetuated misunderstandings of this complicated condition may open more avenues leading to better outcomes.

#1: Only older patients need to worry about AD.

#2: AD is primarily an inherited genetic disease.

#3: Most patients dont want to know if they are at risk of developing AD.

#4: Only high-powered imaging tests can help evaluate for AD.

#5: Only pharmacological therapies can meaningfully address AD.

Fact: AD often begins in the brain in middle age sometimes decades before symptoms emerge. While age increases risk, it is not a direct cause of Alzheimer and patients of all ages can begin to take steps to potentially slow cognitive decline. A recent study conducted by the CDC showed pediatric patients can reduce their risk of developing AD later in life in a number of ways, from managing their blood pressure and blood sugar, to being physically active.2

Fact: Genetics are only one possible factor in the development of AD, and having a family history of Alzheimer does not necessarily doom one to developing the disease. At the same time, a lack of family history does not eliminate the possibility a person will develop Alzheimer. There are 2 categories of genes that influence whether a person develops a disease: risk genes and deterministic genes. While Alzheimer genes have been found in both categories, less than 1% of AD cases are believed to be because of deterministic genes.3

Even those who have these genes may never develop AD; risk genes increase the likelihood of developing a disease, but do not guarantee it will happen. Researchers have found several such genes that increase risk. Apolipoprotein (APOE) 4, one common form of the APOE gene, has shown to have the strongest impact on risk, as researchers estimate that between 40-65% of people diagnosed with Alzheimer have the APOE-e4 gene.3 Those who inherit copies of APOE-e4 from their parents have an increased risk of developing AD, but it is not a certainty. These individuals can still take steps to mitigate their risk by reducing environmental factors or taking preventative steps to better their condition.

Fact: A recent Harris Poll commissioned by Quest Diagnostics found that only 4 in 10 Americans surveyed said they would speak to their clinician right away if experiencing memory or cognitive loss, suggesting an aversion to being diagnosed with a dementia like Alzheimer. Yet, when asked directly, the majority (7 out of 10) expressed a desire to know if they have AD as early as possible to allow for treatment illustrating a willingness to confront the prospect of a scary medical diagnosis if treatment can enhance the odds of a favorable outcome.4

Fact: New diagnostics, including those using simple blood tests, are rapidly opening doors to accessible risk evaluation for many. These blood tests generally help assess -amyloid or tau, 2 brain proteins associated with Alzheimer pathology in the brain. Amyloid- creates plaques which may lead to tangles of tau in the brain. For this reason, many diagnostic companies, including Quest Diagnostics, are focused largely on tests for amyloid protein, given its potential to detect early stages of disease.5

Growing acceptance of blood tests is needed, as emerging pharmaceutical treatments for Alzheimer will require better tools to assess patients. This is because conventional tests, such as PET scans and those that use cerebral spinal fluid, are expensive and specialist dependent. Plus, there is a growing shortage of neurologists.6 Laboratory tests, when combined with other screening methods, can be a powerful tool in crafting an effective patient care plan in fact, in a survey of physicians, 84% said testing for early risk of AD will lead to earlier and improved disease management. Among U.S. adults, 86% agree, stating they believe blood tests for the early detection of Alzheimer risk will increasingly become a regular part of preventative care.7

Fact: For some, Alzheimer may be a preventive condition. New research shows it is possible to reduce risk of AD or at least slow progression. Some studies suggest people who exercise more, including walking an increased number of steps at an advanced pace, have better memory retention and are less likely to develop conditions like Alzheimer or dementia.8 Studies have also shown creative activities like playing games, learning an instrument or reading books may help preserve brain function.9 As a patient gets older, it can be more challenging to maintain social activity, though some research shows this can also help preserve mental function and slow mental decline.10 Yet, the same lifestyle choices and behaviors that can reduce risk of developing heart disease, diabetes and other chronic conditions may also offer some protection against Alzheimer. Addressing depression and hearing loss are other key steps to reduce risk.11

Fact: Cognitive decline is often not because of dementia and can be reversed. There are other potentially reversible causes of cognitive decline that can mimic dementia. These include things as minor as medication side effects or hormonal imbalances, and can be as severe as other chronic conditions like HIV. In 1 study, as many as one in 5 (19.17%) individuals (most over the age of 60 years) with cognitive issues were found to have a reversible condition, such as adverse effects from medication or hormone imbalances.12 Without screenings, conditions that mimic dementia may go undiagnosed in a patient and cause adverse health effects. If properly diagnosed, these conditions, may be treated to potentially slow or reverse any associated cognitive decline.13

Certain tools aim to address this. As an example, uMETHOD Health, a health technology company specializing in precision medicine for chronic diseases, recently worked with Quest Diagnostics to nationally debut a risk assessment and care plan service for patients with cognitive decline. The service, called RestoreU, employs artificial intelligence to crunch data on a persons lab test results and health history, including comorbidities, lifestyle habits and medications, to help identify if risk of cognitive decline is because of a reversible cause.14

With so much attention on emerging therapies for AD, it is easy to overlook the growing body of science suggesting a preventive care approach can help delay the onset of Alzheimer and other dementias in some patients. When it comes to conditions like Alzheimer and dementia, one thing remains clear: patients and providers both seek the ability to provide an early diagnosis and craft the best care plan possible. Though so many remain affected by cognitive conditions, there are steps that can be taken, as with any other health condition, to mitigate risk and ease symptoms. By speaking with a provider about these changes, patients may find these conditions more manageable than first anticipated.

See the article here:
Alzheimer Disease: Separating Fact from Fiction - Neurology Live

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

Read the original post:
Cardiac 18F-Dopamine PET: A Promising Predictor of Lewy Body ... - HealthDay

Months after the FDA approved valbenazine (Ingrezza; Neurocrine Biosciences) for the treatment of chorea associated with Huntington disease (HD), new interim data from the open-label extension (OLE) of the phase 3 KINECT-HD2 study (NCT04400331) continued to highlight the therapys longterm efficacy and safety. All told, improvements in chorea were observed at the first evaluation (week 2) when participants were taking the lowest dose of 40 mg, with efficacy sustained through week 50 at a maximal dose of 80 mg.1,2

After the completion of the phase 3 KINECT-HD study, adults with genetically confirmed motor-manifest HD entered the OLE where they received once-daily valbenazine starting at 40 mg for up to 156 weeks. In addition to safety evaluations, efficacy outcomes included change in Unified Huntingtons Disease Rating Scale Total Maximal (TMC) score, Clinical Global Impression of Change (CGI-C), and Patient Global Impression of Change (PGI-C). The data, which included outcomes up to week 50, were presented at the 30th Annual Meeting of the Huntington Study Group, held November 2-4, in Phoenix, Arizona.

Of 127 participants at the time of the analysis, 98 were from KINECT-HD. All told, mean TMC score reductions were observed by week 2 with valbenazine 40 mg (n = 118; 3.4 [3.1]) and sustained with maximal doses of 80 mg from week 8 (n = 110; 5.6 [3.6]) to week 50 (n = 66; 5.8 [4.1]). At week 50, 76.9% (50 of 65) of participants were CGI-C responders and 74.2% (49 of 66) were PGI-C responders. Among 125 patients who received treatment, 95.2% (n = 119) reported at least 1 treatment-emergent adverse event (TEAE) and 13.6% (n = 17) discontinued because of a TEAE. Falls (30.4%), fatigue (24.0%), and somnolence (24.0%) were among the most common TEAEs reported.

"These interim data provide insight on the clinically meaningful and sustained improvements participants are experiencing with INGREZZA for the treatment of chorea," Eiry W. Roberts, MD, chief medical officer at Neurocrine Biosciences, said in a statement. We look forward to analyzing additional data as they become available."

READ MORE: Patient Dosing Commenced in Phase 2 ASCEND Study of Parkinson Agent CVN424

Neurocrine also presented new substudy data from KINECT-HD using a wearable movement sensor, the first such study of its kind. Using the BioStamp nPoint system, participants wore 3 sensors (chest and anterior thighs) for 2, 7-day periods during the screening period and following the week 10 visit. A total of 27 patients (valbenazine: n = 12; placebo: n = 15) who wore the sensors for at least 5 hrs/day for at least 5 days during baseline and maintenance were included in the analysis. Results showed significant improvements in truncal chorea and gait asymmetry measures in the valbenazine (all P <.05) but not in the placebo group. Of note, 6 participants reported any sensor-related AE, all of which were mild.3

Valbenazine, a selective vesicular monoamine transporter 2 inhibitor, became the first such inhibitor FDA-approved for the treatment of chorea associated with HD in August 2023 based on results from the phase 3 KINECT-HD study and its OLE, KINECT-HD2. Similar in design, each study featured adults aged 18 to 75 years who had been diagnosed with either manifest HD or motor manifest HD who have sufficient chorea symptoms. In KINECT-HD, the agent met its primary end point, demonstrating a statistically significant placebo-adjusted reduction in Total Maximal Chorea (TMC) score of 3.2 units (P<.00001) from baseline to weeks 10 and 12.4

Read more from the original source:
Huntington Therapy Valbenazine Demonstrates Significant, Long ... - Neurology Live

Bruce Hughes, MD: Switching a little bit on this, I think its also incumbent upon us to not just talk about disease-modifying therapy and cognitive functioning, but we do know that physicality and physical exercise ties into mental health [treatment]. If the patients mental health is out of order, their physical health is never going to be maximally in order, so treating the whole patient is important. And then identifying what youre talking about, because I think we focus more here on cognition, but kind of tying in with that is fatigue, which is so hard to identify. Educating patients on cognitive tips is very important as far as not just your disease-modifying therapy, but things that you that help minimize the effects of the cognitive decline on your health.

Robert Naismith, MD: I agree. I think your mental health plays a huge role in the disease. We see this all the time when people are under stress, when people arent able to take care of themselves, they present with worsening. Thats something you really need to dig into and assess, and we see that all the time where people are trying to juggle parents who are not doing well and who are sick, and thats putting stress on the family or family dynamics between the spouse and is not the best, and this affects the disease. So I think what you brought up with exercise is an important thing that we talk about at every visit. Doing physical therapy as a tool to show you how to do stuff for yourself at home and then doing another visit to make modifications based upon the things that youve achieved with those exercises and really stressing [that] this is something thats going to help you do better, addressing mood. People have a lot of depression [and] anxiety, [and] sleep is an issue for a lot of people. This impacts how they feel and how the disease manifests itself in the fatigue, so we use a lot of antidepressants in practice. But not everybody feels like thats going to be the best thing for them, so we also have options for counseling. We have a list of counselors. One of the nice things is [that] people are now able to do counseling by , so they dont necessarily have to go to a place to do it, so a lot of my patients choose to pick a counselor in their area. They might do some in-person visits, they might do some [telehealth] visits, so I think the access is very good for that. But thinking about the whole patient in terms of their mood, their sleep, their comorbidities, exercise program, how theyre interacting with everybody, and if theres anything within your power to help that or get them to the professional that can help them do it together with you, those are the things that Im looking for my practice. As a multidisciplinary MS [multiple sclerosis] center I want to have the tools to say, well, this isnt my expertise, but I know someone who can help you with this; we need help to treat you in every way we can.

Bruce Hughes, MD: I think thats spot-on. The referral to mental health providers is big in multiple sclerosis management because unlike many patients, MS patients tend to have very good insight into their disease process, and to me, those are the ones who do the best with cognitive therapy and counseling. At your center, do you find much benefit in referrals to speech language cognitive therapy for ongoing assessment like what you would do with physical therapy or occupational therapy, or have you not found that quite as helpful?

Robert Naismith, MD: I think it depends upon the person, but we do make the recommendation when we have the referral for neurocognitive testing, thats going to be like a 2 or 2.5-hour battery where they can go through all the different domains of executive functioning, word finding, short-term memory, reading. Theyll go through all the different domains, and theyll check their baseline level so theyre able to get a real sense of their cognitive function, and also their mood. They also check for mood disorders as well. And then well have the specialist who does the testing explain everything to the patient and document and make a report. And then well also make a referral to speech cognitive therapy so that they can use those results and gain more insight and come up with strategies to adapt to them. It may also include a referral to vocational rehab if its going to affect their work issues and if the combinations need to be made so that theyre able to perform at their best. So it depends on the person, but we always offer with that neurocognitive referral a chance to see a speech cognitive therapist and also, if they are working, vocational rehab to try to make the accommodations that are going to help them be successful in the work setting.

Bruce Hughes, MD: I think that point is very good in that sometimes were identifying [whether it is] brain volume loss in the disease process or are there confounding variables on their cognitive functioning such as depression, such as sleep disturbance, which I think is huge and really underrecognized in the multiple sclerosis population. We should be doing a lot more assessment of sleep for whatever the cause of why theyre having sleep disturbance. Its just remarkably common. How do we how do we address and improve that?

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

Read more:
Improving Cognitive Awareness of Patients and Caregivers in MS ... - Neurology Live

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.

Read more:
Therapy Adjustments for Optimal, Early Intervention to Prevent ... - Neurology Live