CNS Connections - Fall 2024

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BUILDING THE FUTURE

Bringing CNS Members Together to Make Children’s Lives Better

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MAGAZINE

CONNECTING WITH...

CNS Connections is the official news magazine of the Child Neurology Society. The title references the passionate professional interest members share in neural connections and their commitment to connecting to and staying connected with the peers, colleagues, mentors, mentees – and, above all else, friends – in the field with whom they share a career, craft, calling, and community.

Child Neurology Society 1915 West Highway 36, Suite 174 Roseville, MN 55113 Tel: 651/486-9447 Fax: 651/486-9436 nationaloffice@childneurologysociety.org www.childneurologysociety.org

EDITOR

Daniel Bonthius, MD, PhD

MANAGING EDITOR

Monique Terrell

PROOF EDITOR

Julianne Bruce

DESIGN AND LAYOUT

Kimberlea Weeks | CEVA Design

Published 3 times yearly

2024: A Year of Growth, Connection, and Momentum

Reflecting on the past year feels like stepping back to admire a painting in progress. Each brushstroke—every effort, decision, and shared idea—has added depth to the Child Neurology Society (CNS) canvas, shaping 2024 into a year of growth and connection.

At the core of our progress was the commitment of our members, partners, and professional staff. Following a strong foundation in 2023, we celebrated a rebound in membership, welcoming new voices and creating a more inclusive environment. Our Annual Meeting marked a significant milestone, surpassing attendance benchmarks and showcasing the strength of our community.

We launched a Corporate Partner Program and refined our fundraising efforts, ensuring a sustainable foundation for the future. A highlight was the

opening of the CNS Education Center, providing valuable resources for professional development. Additionally, we launched the CNS Career Center to support members at all stages of their careers.

Behind the scenes, we improved our operations with new governance policies and partnerships that enhanced our financial strategy. We reinforced our reputation by making rejoining the Society more accessible, further establishing CNS as a trusted leader in child neurology.

As we lean into 2025, I am excited about what lies ahead. Our focus will remain on member engagement, financial sustainability, and our strategic vision. Together, we are building on our strong legacy—one story at a time. Thank you for being part of this journey.

With gratitude and optimism. •

QBuilding the Future: Vision and

With CNS President-elect Yasmin Khakoo

What is your biggest goal to accomplish as president of the Child Neurology Society?

The CNS needs to become the premier home for all child neurologists and others caring for children and young adults with neurologic conditions. Members need to see the value of joining and attending the Annual Meeting and utilizing our learning platforms throughout the year.

What are your other goals?

Our executive director has made great progress in revamping governance, creating guidelines for committee selection/function, and increasing transparency of the CNS structure. I will work with the Awards Committee to ensure that clear eligibility requirements are created. I will ensure that we address issues including fertility preservation, transition to retirement while being connected to the CNS community, and job choices for dual-career couples, single parents, or members with eldercare responsibilities. Additionally, we will address the needs of all members and affiliates—not only those pursuing academic and practice-based career paths, but also those interested

in industry, hospitalist, and even concierge medicine. I will ask our Research Committee to work with our members to find creative ways to obtain extramural funding, especially with our new US leadership.

Are there any new initiatives emerging for the CNS?

Our newly revamped educational platform is user-friendly and informative. The Genetics Curriculum is a brand-new initiative available to members and non-members. The Child Neurologist Career Development Program-K12 has broadened to include clinical projects and a separate Minority Research Scholar Program and continues to be a source of outstanding investigative child neurologists, neurologists, and neuroscientists. We plan to increase advocacy at the national level and research partnerships with other medical societies, including the American Academy of Neurology, the American Neurological Association, and the European Neurologic Society, among others. We will also partner more closely with the Association of Child Neurology Nurses (ACNN), who are essential to our team building and patient care, especially given the projected pediatric physician shortage in the next 5 years.

Priorities for the CNS President-elect

What are the biggest challenges facing child neurologists, and what can the CNS do to help them?

The biggest challenges we face as a community revolve around the state of healthcare and research funding in the coming years. With the incoming US administration, children’s health will be in danger should the appointees to the leadership roles of Health and Human Services, Center for Disease Control and Prevention, Food and Drug Administration, and the National Institutes of Health spread disinformation regarding vaccinations, infectious diseases, and research efforts.

Is “diversity, equity, and inclusion” an important issue for the CNS and the field of child neurology? What can child neurologists and the CNS do to advance the cause?

Yes, diversity, equity, and inclusion will always be important until we no longer have inequities in medicine, science, research, healthcare, and all aspects of life. I always say, “They don’t name a month unless there’s a problem.” Meaning that Black History Month, Women in Medicine Month,

Pride Month, and Developmental Disabilities Month would not be necessary if the playing field was level. We have already implemented some strategies to overcome these inequities: the recent creation of our LDEI Committee, ensuring committees are composed of a diverse group of members. We have made a concerted effort to include a variety of offerings at our Annual Meeting and webinars throughout the year; presenters are limited to one major presentation at the annual meeting to allow others to participate. We strongly encourage proposals and abstracts from different institutions, ranks, genders, ethnicities, and abilities. I would like to see more Spanish-language sessions.

What can child neurologists do to attract more medical students into our field?

We need to capture the attention of students as early as grade school through outreach into communities. Our institutions can offer to pay expenses for medical students to do rotations with us. Our CNS Junior Member offerings also attract potential child neurologists.

How do you envision working with the Child Neurology Foundation to advance child neurology?

I am excited to serve as a new Board member of the Child Neurology Foundation as part of my role as president-elect of the CNS. As we develop new therapies for previously untreatable neurologic conditions, survivorship in child neurology becomes a reality as pediatric oncology has for childhood cancer survivors. I will learn more about the CNF but hope we can work together to promote neurologic care across the lifespan and continue to develop advocacy programs.

CNS CONNECTIONS EDITOR

Child Neurology Synapses

Dang! Dengue Infection and Acute Necrotizing Encephalopathy of Childhood

Acute necrotizing encephalopathy of childhood associated with Dengue. Gupta, J et al. Neurology 2024; 103:e209954.

What the researchers did:

Dengue infection is caused by an arthropod-borne flavivirus that reaches humans via mosquito bites. The infection is most common in tropical and subtropical climates but has occurred in more temperate areas, as well. Most people infected with Dengue virus are asymptomatic, but others become substantially ill with symptoms that range from headache and body aches to hemorrhagic fever and shock. Acute necrotizing encephalopathy of childhood (ANEC) is a rapidly progressive

encephalopathy following a febrile viral illness. It is characterized by fever, depressed level of consciousness, seizures, elevated serum aminotransferases, thrombocytopenia, and characteristic neuroimaging findings of symmetrical abnormal signal intensity involving the thalami and other brain areas. The outcome of ANEC is often devastating, with high rates of morbidity and mortality. Dengue is one of the viruses that can lead to ANEC. However, the long-term outcome of children with ANEC due to Dengue is poorly studied. This group of researchers from India sought to characterize the prognosis of children with Dengue-induced ANEC.

What the researchers found:

The researchers prospectively studied a cohort of five children (aged 4.5 – 14 years) with ANEC associated with Dengue fever. They diagnosed Dengue via a positive Dengue nonstructural protein 1 (NS1) antigen test, and they diagnosed ANEC by documenting the clinical manifestations of fever, encephalopathy, transaminitis, thrombocytopenia, and characteristic MRI findings in the thalamus and elsewhere. The researchers followed the patients for at least six months following discharge. They found that all of these children were dramatically ill during the hospitalization. All were deeply encephalopathic and required prolonged hospital stays (mean duration 30 days). Most (4 of 5) required prolonged mechanical ventilation (mean duration 21 days). All of the children received immunomodulation with intravenous methylprednisolone, often followed by IV immunoglobulin. Despite the aggressive therapies administered to these children, their short-term responses were poor, and all five remained bedridden at the time of discharge. However, following discharge, all five of the patients experienced a substantial recovery. By six months of follow-up, all were ambulatory and fully independent in activities of daily living. All were back in school and, at worst, had minimal residual deficits, such as mild focal weakness or tremors.

What the research means:

This report provides another good example of how unpredictable and fascinating viral brain infections can be. Acute necrotizing encephalopathy of childhood (ANEC) associated with Dengue virus infection produced a catastrophic presentation and required a protracted hospital course. By the time of discharge, all remained bedridden. Yet, despite these seemingly terrible prognostic factors, all of the children had good neurologic outcomes by six months post-discharge. These results probably provide important clues regarding the ways in which Dengue virus interacts with brain tissue and with the immune system differently than some other viruses do. At a minimum, the results provide clear evidence that the ultimate outcome of a viral brain infection may be quite different than what would have been predicted based on earlier clinical conditions. • Link to CNS Synapses Library

CNS CONNECTIONS

EDITOR

Child Neurology Synapses

Phenobarbital Kills Neurons in the Developing Brain, While Lacosamide and Levetiracetam Do Not

Lacosamide and levetiracetam are not toxic to the developing mouse brain. Noguchi KK et al. Annals of Neurology 2024; 96: 812-818.

What the researchers did:

Neonatal seizures present child neurologists with a conundrum. On the one hand, child neurologists want to control the seizures. On the other hand, child neurologists want to avoid injuring the newborn’s brain with neurotoxic antiepileptic drugs (AEDs). Phenobarbital is currently the recommended first-line AED for neonatal seizures, as it is the most efficacious agent for seizures in this age group. However, preclinical studies have shown that phenobarbital (and other AEDs

with strong GABAA mimetic properties) cause degeneration of neurons and oligodendrocytes within the developing brains of rodents and nonhuman primates. Proof that this same pathologic effect occurs in humans is lacking, but clinical studies have suggested that phenobarbital and anesthetics with GABAA mimetic properties impair neurodevelopment. Thus, an alternative to phenobarbital for the treatment of neonatal seizures could be useful and protective. Lacosamide, a voltage-gated sodium channel blocker, is emerging as a treatment for neonatal seizures. Used alone, or in combination with levetiracetam, lacosamide is often effective for seizures in neonates and infants and is well-tolerated.

However, the question arises whether it, too, like phenobarbital, may cause neurodegeneration within the neonatal brain.

What the researchers found:

The team of researchers from Washington University in St Louis and the University of Wisconsin conducted a preclinical study exploring whether lacosamide, alone or in combination with levetiracetam, causes apoptosis in the neonatal mouse brain. Seven-day-old mice received single or repeat injections of saline (control group), phenobarbital (75 mg/kg), lacosamide (20-40 mg/ kg), levetiracetam (100 mg/kg), or the combination of lacosamide (40 mg/kg) and levetiracetam (100 mg/kg). The doses were chosen to produce serum drug levels that are therapeutic in humans. Six hours following the single or repeated injections, the animals were sacrificed. The brains were cut into sections and immunolabeled for activated caspace-3 (AC3), a marker for cells that are irreversibly committed to apoptotic cell death. To identify the cell types involved, the sections were fluorescently co-labeled with NeuN (a neuronal marker) or GFAP (an astrocyte marker). Oligodendroglia were identified by their shape and location within the white matter tracts. Apoptotic cells were counted stereologically. The researchers found that the saline-treated animals had only a small number of degenerating (AC3 positive) cells. In contrast, the phenobarbitaltreated animals had large numbers of apoptotic cells, which could be identified as neurons and oligodendroglia but not astrocytes. These phenobarbitalinduced apoptotic cells were present in high densities in multiple brain regions, including cortex, hippocampus, thalamus,

and amygdala. In further contrast, the animals treated with lacosamide, alone or in combination with levetiracetam, had only low levels of apoptotic cells that did not differ from the saline-treated controls. Thus, while phenobarbital induced apoptosis throughout the developing brain, lacosamide, levetiracetam, and their combination did not.

What the research means:

This study demonstrated that phenobarbital induces widespread and dense cellular apoptosis within the developing mouse brain. In contrast, lacosamide and levetiracetam, alone or in combination, do not. These results suggest that lacosamide, alone or combined with levetiracetam, may be less harmful than phenobarbital and should be explored more deeply as potential firstline treatments for neonatal and infantile seizures. However, this study does have limitations that must be kept in mind. First, the study was conducted in naïve animals who did not have seizures. The substantial neurophysiologic events that accompany seizures may interact with the anticonvulsants and lead to very different outcomes. Secondly, there are many potential neurotoxicities of AEDs beyond apoptosis. Consequently, while apoptosis may be a negative consequence of phenobarbital, other aberrant and unwanted effects could be even worse with lacosamide. Nevertheless, the results of this preclinical study give impetus to exploring lacosamide, levetiracetam, and perhaps other AEDs as potential replacements of phenobarbital as first-line treatment for neonatal seizures. •

Link to CNS Synapses Library

CNS CONNECTIONS

EDITOR

Child Neurology Synapses

Should Women Stop Taking Anticonvulsants During Early Pregnancy?

Effects of antiseizure medication withdrawal during the first trimester of pregnancy on seizure control and offspring outcomes. Fu Y et al. Epilepsia 2024; 65: 3186-3198.

What the researchers did:

Epilepsy is a perplexing problem that commonly complicates pregnancies. About 1% of all pregnancies are affected by epilepsy. The problem is perplexing because maintaining effective seizure control is important for maternal and fetal health, but exposure to antiepileptic drugs (AEDs) poses risks to the fetus. Those risks include teratogenicity; intrauterine

growth retardation; neurodevelopmental disorders; and fetal, neonatal, and infant death. Thus, there are strong theoretical arguments both to continue AEDs during pregnancy and to stop them. To address this issue, a group of researchers from a variety of hospitals across China conducted a large-scale prospective cohort study exploring seizure control and offspring outcomes among epileptic pregnant women in whom the AED was either continued throughout the pregnancy or stopped in the first trimester. The primary outcome investigated was deterioration in seizure control, defined as a greater than 50% increase in seizure frequency during

pregnancy, compared to nine months before pregnancy. Secondary outcomes investigated were adverse outcomes in the offspring, including low birth weight, major congenital malformations, neurodevelopmental delay, and fetal death.

What the researchers found:

The study included 695 pregnancies of women with epilepsy. Among these pregnancies, 14.2% withdrew the AEDs during the first trimester. For the remainder (85.8%), the AEDs were continued throughout the pregnancies. The researchers found that the incidence of worsened seizure frequency was higher in the AED withdrawal group (35.4%) than in the AED continuation group (26.3%). The risk of seizure deterioration after AED withdrawal was especially high among those women who had experienced seizures during the nine months before pregnancy. Regarding the postnatal assessments of the offspring, for those pregnancies in which a single AED was withdrawn, the incidence of adverse outcomes was not different in the AED withdrawal group than in the AED continuation group. However, the risk of neurodevelopmental delays increased significantly when two or more AEDs were withdrawn. Regardless of whether AEDs were withdrawn or not, seizure deterioration during pregnancy was associated with increased risk of fetal death.

What the research means:

The results of this study suggest that AED withdrawal during the first trimester of pregnancy does not protect the mother or fetus against adverse effects. Quite the contrary. AED withdrawal during the first trimester increases the risk of seizure deterioration, especially in those who experienced seizures during the nine months prior to pregnancy. Furthermore, worsening of seizures during pregnancy increased the risk of adverse offspring outcomes, especially fetal death. Thus, the results suggest that discontinuing AEDs during the first trimester is generally not a good idea. This study did not specifically address the issue of valproic acid, however. Stopping valproate before the pregnancy begins, if possible, and switching to a different AED remain sound practices. We child neurologists care for young women with epilepsy, some of whom will become pregnant, whether by design or not. Without medical advice, some of these pregnant young women will unilaterally and abruptly stop their AED out of fear that it may harm the fetus. This might be a very bad idea. This study underlines the importance of preconception counseling to address pregnancy preparation and optimization of AEDs to minimize maternal seizures and fetal harm. •

COMMUNITY

Child Neurology Foundation

2024 Annual Meeting Symposium Recap

The Child Neurology Foundation was thrilled to kick off the 53rd Child Neurology Society Annual Meeting in San Diego with an inspiring symposium titled “Caring for Children with Medical Complexity.” Led by the dynamic CNF PresidentElect Dr. M. Scott Perry of Cook Children’s Hospital, this symposium delved into the significant challenges faced by this vulnerable population within a healthcare system that is not designed for them. The symposium featured diverse insights from patients, caregivers, and medical providers, offering a holistic view of the issues at hand.

At the Child Neurology Foundation, we center the patient experience within all of our education. To open the symposium, parent Cristina Vargas shared the challenges she and her son, Juju, face every day. Her testimony grounded the rest of the talks with a specific point: families struggle around the clock with social, emotional, and medical challenges, and it is impossible to address all these things in a short medical appointment. However, it may impact the care you deliver to not help find solutions for

your patients, exemplifying the way that the growing challenges for child neurologists intersect with their patients. Speakers Dr. John R. Mytinger of Nationwide Children’s Hospital, Dr. Anne Marie Morse of Geisinger Medical Center, Jessica Nickrand, PhD of the Child Neurology Foundation, Monica Jones, JD, CNP from the Pediatric Epilepsy Surgery Alliance, and Dr. Ahmed T. Abdelmoity and Dr. JeanBaptiste LePichon of Children’s Mercy Kansas City, shared resources and practical strategies to maximize child neurologists’ impact on patients outside of clinical encounters. A driving theme throughout all the talks was embracing technology in your practice. Whether discussing artificial intelligence to improve note-taking accuracy and speed or learning about leveraging communication and care team modalities to improve care coordination, symposium participants learned how setting concrete goals with their teams and continual self-evaluation could lead to higher rates of success with medically complex patients. To paraphrase a warning from Dr. Morse: Doctors won’t be replaced by technology, but doctors who refuse to

Stephen Peters President Child Neurology Foundation
Link to CNF Website
(From left to right): Dr. John R. Mytinger; Jessica Nickrand, PhD; Dr. M. Scott Perry; Dr. Anne Marie Morse; Monika Jones, JD, CNP; Dr. Ahmed T. Abdelmoity; and Dr. Jean-Baptiste LePichon

engage with the technology that can improve patient care will be replaced by those who do engage with that technology. To emphasize this point, Dr. Abdelmoity and Dr. Le Pichon shared how they have developed a responsive feedback-driven improvement process to drive higher quality, patient-centered transitions to adult care. This integrated framework addresses the emotional, legal, and societal aspects of a young person’s transition, while also addressing their underlying neurologic conditions.

Speakers helped learners better understand the way that caring for children with medical complexities requires a team approach—including partnerships with patient advocacy organizations. As Dr. Mytinger presented to the symposium, multidisciplinary care programs can be beneficial in addressing challenges in this patient population, but innovative models that include the patient and their family and resource navigation can help stretch the limited resources of physicians within their practice.

Groups like the Child Neurology Foundation and the Pediatric Epilepsy Surgery Alliance have resources that

assist your patients in navigating some of their daily challenges. Referring a patient and their family who comes to you with questions about school resources, navigating a new diagnosis, or the emotional challenges that come with caregiving to these patient advocacy organizations will help the family meet their needs so that you can maximize the value of your interaction with your patients. Child Neurology Foundation data from the Neurology Social Services Network demonstrates that nearly 60% of inquiries for patient assistance are for emotional support in navigating the caregiver journey.

CNF is grateful for our partnership with the Child Neurology Society and was honored to partner on a symposium that addressed one of the most challenging topics in child neurology today. We value the feedback of the Child Neurology Society members and would like to hear from you how this topic impacts you and what future topics you would like to see us cover. Contact us today by sending an email to programs@childneurologyfoundation. org •

COMMUNITY

Timothy Feyma, MD

Pediatric Neurology, Gillette Children’s Specialty Healthcare Paid consultant to Acadia

Clinical Implications of Understanding Rett Syndrome as a Neurodevelopmental Disorder

Rett syndrome (RTT) is a complex neurodevelopmental disorder affecting approximately 1 in 10,000 to 15,000 female births worldwide.1,2 Although most often affecting females, RTT also occurs rarely in males.1,3 Clinical diagnosis requires a period of regression, often early in development, followed by stabilization.3,4

Cause of RTT

Most RTT cases are due to spontaneous mutations in the methylCpG-binding protein 2 (MECP2) gene on the X chromosome.5 While genetic testing is used to support a clinical diagnosis, “MECP2 mutations are not synonymous with RTT,” explains Dr. Feyma, co-director of Gillette Children’s Rett Syndrome Center of Excellence. “The presence of

MeCP2 Function Across Lifespan

these mutations alone is neither necessary nor sufficient for diagnosis.”1,4,5

Downstream effects

Functional MeCP2 proteins are essential for normal brain function and maintaining neuronal function throughout development, including activity-dependent synaptic plasticity.6 “Based on RTT mouse models,” Dr. Feyma notes, “we know that loss of Mecp2 function leads to deficits in synaptic maturation, neural circuit dysfunction, and excitatory and inhibitory imbalance.”7

Although the extent of the downstream effects of MeCP2 is still being researched, MeCP2 is known to impact several pathways, including growth factor signaling.7,9 Characteristic symptoms of

Adapted from Gulmez Karaca, et al. 2019.8

RTT may be attributed to downstream effects of the neuronal dysfunction resulting from MECP2 mutations.7,10 Dr. Feyma further explains that “MeCP2 regulates brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF1), which promote cell signaling pathways and play vital roles in synaptic and structural plasticity, making them important targets.”7,9,11 Lower levels of BDNF transcripts and IGF-1 in the brain were shown in studies of RTT patients.9,12 Patients exhibit a reduction in brain volume associated with smaller neurons and decreased dendritic arborization, and overall altered neural circuit structure.9 As a result, the neurodevelopmental delays typical of RTT follow, resulting in cognitive and motor dysfunction.6

Clinical presentation

While individual clinical presentation can vary widely, there are four main characteristics of RTT.1,4,9 “Patients with classic RTT present with a regression of purposeful hand use, while developing distinct stereotypic hand movements, such as wringing, clapping, or even mouthing,” Dr. Feyma elaborates. “Additionally, there is a loss of acquired spoken language, even if it’s just babbling, and gait abnormalities, including dyspraxia or loss of ambulation.”4

As RTT progresses, patients may demonstrate a range of motor, autonomic, and behavioral symptoms of varying severities.9,13 Management is often symptom based and dependent on the particular comorbidities. Dr. Feyma underscores the need for “individualized multidisciplinary intervention and support, as most people with RTT survive into middle age, requiring lifelong care.”1

Encouraging neuronal connections

“Initially, functional rescue from behavioral interventions, specifically early environmental enrichment, was demonstrated in juvenile and adult RTT mouse models,”14 mentions Dr. Feyma. “Based on current research, we now understand that despite the neurodevelopmental impacts, people living with RTT can benefit from a variety of therapeutic interventions. Unlike neurodegenerative diseases, neuronal loss is not a feature of RTT. With intervention, patients can develop critical skills, leading to symptomatic improvement, regardless of age or disease severity.”1,15-17

Patients with RTT require focused care, often participating in various therapies throughout their lifetimes.1

• Eye-gaze intervention studies have demonstrated improved psychosocial functioning and overall awareness, engagement, and expressiveness18,19

• Physical therapy can help preserve and restore movement and physical function at any age15,20,21

• Hydrotherapy and music therapy can also have a positive impact on children and adults20

Dr. Feyma stresses “it’s important to explore intervention strategies even in adult patients with RTT, as they are often able to see a positive impact with communication, physical, and occupational therapies.”

Recent advancements

While there is no cure, viable options are available to manage certain symptoms of RTT, in addition to ongoing research for potential therapies. Several clinical trials are in various stages of development, including those exploring gene therapy in RTT.22

References

1. Fu C, et al. BMJ Paediatr Open 2020;4(1):e000717.

2. Acadia Pharmaceuticals Inc. Data on file. RTT US Prevalence. March 2022.

3. Kyle SM, et al. Open Biol 2018;8(2):170216.

4. Neul JL, et al. Ann Neurol 2010;68(6):944-950.

5. Collins BE, et al. Neuropsychiatr Dis Treat. 2022;18:2813-2835.

6. Smeets EEJ, et al. Mol Syndromol. 2012;2(3-5):113-127.

7. Ehrhart F, et al. Orphanet J Rare Dis. 2016;11(1):158.

8. Gulmez Karaca K, et al. Int J Mol Sci. 2019;20(18):4577.

9. Pejhan S, et al. Biomolecules 2021;11(1):75.

10. Lopes AG, et al. Brain Sci. 2024;14(2):120.

11. Vahdatpour C, et al. Front Neurosci. 2016;10:450.

12. Itoh M, et al. J Neuropathol Exp Neurol. 2007;66(2):117-123.

13. Fu C, et al. BMJ Paediatr Open. 2020;4(1):e000731.

14. Gadalla KKE, et al. Biochem J. 2011;439(1):1-14.

15. Lotan M. ScientificWorldJournal. 2006;6:1504-1516.

16. Downs J, et al. Orphanet J Rare Dis. 2018;13(1):3.

17. Palmieri M, et al. Front Neurosci. 2023;17:1172805.

18. Townend GS, et al. J Dev Phys Disabil. 2016;28(1):101-112.

19. Vessoyan K, et al. Augment Altern Commun. 2018;34(3):230-241.

20. Fonzo M, et al. Brain Sci. 2020;10(7):410.

21. Banerjee A, et al. Brain. 2019;142(2):239-248.

22. Percy AK, et al. CNS Drugs. 2024;38(11):851-867.

@2024 Acadia Pharmaceuticals Inc. Acadia is a registered trademark of Acadia Pharmaceuticals Inc. All rights reserved. RETT-US-0139 11/24

Celebrating Our 2024 Corporate Partners

Excellence in Child Neurology

Annual Partners

Collective Innovation

These partners help create a dynamic environment where innovation thrives. Together, we strive for advancements that better the lives of children with neurological disorders.

Reflecting on Achievements

Thanks to our partners’ collaboration, CNS has reached significant milestones and driven initiatives delivering meaningful change.

Together, We Grow

As we conclude 2024, we extend our heartfelt thanks to these partners for their steadfast support. It’s through these partnerships that we continue to strengthen our impact and prepare for another promising year.

Whether you’re a child neurologist seeking your next career opportunity or an employer searching for top talent, the CNS Career Center is here to connect you.

Why Choose the CNS Career Center?

• Exclusive Listings: Access roles and candidates specifically in the child neurology field.

• Career Resources: Enhance your job search with tools to refine your résumé, prepare for interviews, and stay ahead.

• Personalized Job Alerts: Get updates on the latest opportunities that match your expertise.

This member benefit is designed to support your professional success and strengthen our child neurology community.

https://careercenter.childneurologysociety.org/career-resources

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