2018 Annual Meeting AAN Extra — Tuesday, Apr 24 by American Academy of Neurology

THE ANNUAL MEETING NEWS DAILY

Tuesday, April 24, 2018

IMPORTANT CLINICAL TRIALS DETAILED IN THIS MORNING’S PLENARY SESSION Experts will present on significant clinical trials conducted over the past year that affect patient care at this morning’s Clinical Trials Plenary Session. From expanding the time window for thrombectomy to trials of new treatments for Huntington’s disease, multiple sclerosis, and narcolepsy, attendees can expect to learn the latest updates in these trials and more. The session runs from 9:15 a.m. to 11:30 a.m. in South Exhibit Hall K.

Hall

The AAN announced on Monday the publication of a new guideline, Multiple Sclerosis and Disease-modifying Therapies, in the journal Neurology ®. A press conference was held for national and international media congregating at the convention center for the latest in neurology news. Continued on page 6 u

Deborah Hall, MD, PhD, FAAN Member, Science Committee Holly E. Hinson, MD, MCR Member, Science Committee Natalia S. Rost, MD, MPH, FAAN, FAHA Chair, Science Committee Continued on page 12 u

Hinson

Wednesday: Omalu, DeKosky to Present on First Chronic Encephalopathy in Pro Athletes

Press Conference Highlights New MS Guideline

Moderators:

Bennet Omalu, MBBS, MPH, MBA, will give a special presentation tomorrow along with Steven DeKosky, MD, FAAN, FANA, FACP, on their work to confirm Continued on page 7 u

Rost

INSIDE

AHA/ASA, AAN Combine for Tuesday’s Stroke Care Disparities Symposium

of” Headache 13 “Best Abstracts Featured in This Morning’s Session out New ePoster 19 Check Areas at Poster Sessions Invited Science 26 Today’s Examines Movement Disorders

In Multiple Sclerosis, when it comes to Brain Preservation

Grey Matters, Too JOIN US AT

Booth 932

Tuesday, April 24 Cover Important Clinical Trials Detailed

in This Morning’s Plenary Session

3 4 6 7

Press Conference Highlights New MS Guideline Wednesday: Omalu, DeKosky to Present on First Chronic Encephalopathy in Pro Athletes Tuesday’s AAN Section Meetings

20 ‘Cure One, Cure Many’ Is Theme of

The Vision of the AAN is to be indispensable to our members.

22 AAN Leaders Praise FAANs at

The Mission of the AAN is to promote the highest quality patient-centered neurologic care and enhance member career satisfaction.

Foundation Booth

Recognition Breakfast

24 The Gender Gap In Neurology 26 Today’s Invited Science Examines Movement Disorders

29 Find, Create New Career

Opportunities at Wednesday’s Advanced Leadership Workshop

Neurology Now Is Now Brain & Life—in English and en Español!

29 Compare Your Approach to Your

AHA/ASA, AAN Combine for Tuesday’s Stroke Care Disparities Symposium

30 Emerging Science Abstracts to Be

Wednesday: Omalu, DeKosky to Present on First Chronic Encephalopathy in Pro Athletes

13 “Best of” Headache Abstracts

Featured in This Morning’s Session

14 Today’s Experiential Learning Area Highlights

18 Order Annual Meeting On Demand

Colleagues in New ‘What Do I Do Now’ Sessions Presented Today and Wednesday

33 Quotable Quotes 34 Recollections of Past AAN Presidents

39 Tweets of the Day 39 Okuda Named Winner of Inaugural Brainstorm Competition

Now and Save

Contact Information: American Academy of Neurology 201 Chicago Avenue Minneapolis, MN 55415 USA Phone: (800) 879-1960 (Toll Free) or (612) 928-6100 (International) Fax: (612) 454-2744 Email: memberservices@aan.com Website: AAN.com AAN Executive Director/CEO: Catherine M. Rydell, CAE

Managing Editor: Angela Babb, CAE Editor: Tim Streeter Writers: Ryan Knoke, Sarah Parsons Designer: Jim Hopwood Photography: Will Evans Printing: Lithographix, Inc. Email: aannews@aan.com AANextra is published by the American Academy of Neurology. The American Academy of Neurology’s registered trademarks and service marks are registered in the United States and various other countries around the world. “American Brain Foundation” is a registered service mark of the American Brain Foundation and is registered in the United States.

19 Check out New ePoster Areas at Poster Sessions

Tuesday’s AAN Section Meetings 7:00 a.m.–8:00 a.m.

1:30 p.m.–2:30 p.m.

Neuroimaging Section LACC Petree Hall D

Autoimmune Neurology Section LACC Petree Hall D

Sleep Medicine Section LACC Petree Hall C

Ethics Section | LACC Petree Hall C

8:15 a.m.–9:15 a.m.

A.B. Baker Section on Neurological Education | LACC Petree Hall D

Neuroepidemiology Section LACC Petree Hall D Neurogenetics Section LACC Petree Hall C

12:00 p.m.–1:00 p.m. Global Health Section LACC Petree Hall C Neuromuscular Section LACC Petree Hall D

3:30 p.m.–4:30 p.m.

Geriatric Neurology Section LACC Petree Hall C

5:30 p.m.–6:30 p.m. LGBTQI Section | LACC Petree Hall C Pain & Palliative Care Section LACC Petree Hall D 

The American Academy of Neurology sincerely thanks Lithographix, Inc. for its outstanding service, steadfast professionalism, and high quality standards, as well as its generous donation of the 2018 Brain Health Fair program guide.

Neurology Now Is Now Brain & Life—in English and en Español! After 13 years of service to the public, the AAN’s awardwinning patient education magazine Neurology Now ® has been rebranded Brain & Life™. This free patient and caregiver resource has a fresh, clean look while still providing the same expert content your patients rely on. “After more than 10 years, we knew it was time for a makeover and an upgrade,” said Editor-in-Chief Orly Avitzur, MD, MBA, FAAN. “We wanted a publication that was fun to read, easy to understand, and chock full of inspirational stories. We wanted to build on the unparalleled expertise from neurologists our readers have grown to trust and respect. Enter Brain & Life, a modern Avitzur approach to brain health and living with neurologic conditions. We also wanted a website that would serve as a dynamic companion to the print magazine. We created BrainandLife.org, which debuts in conjunction with our first issue. Along with the latest stories from Brain & Life, it includes web-only content, past issues, videos, podcasts, and neurologist and patient blogs. BrainandLife.org also showcases additional resources and information from the AAN.” Avitzur explained the reason for the name change. “We knew our readers had come to appreciate Neurology Now, but the word “neurology” can be intimidating. With Brain & Life, we hope we will connect with new readers and build even greater public awareness of the field of neurology, brain health, and living with neurologic conditions.” In this month’s issue, actress Sharon Stone discusses the impact that her 2001 stroke had on her life and career. Other articles emphasize self-care for people living with neurologic disease, including proper exercise, pain management, and meditation. Also rolling off the presses is the first quarterly issue of Brain & Life™ en Español, featuring journalist Soledad O’Brien. This Spanish-language version of the magazine was well received when it was piloted last year. AAN member offices in areas with large Hispanic and Latino populations will receive free copies to distribute to their patients, and additional copies will be mailed to a growing subscriber base. The publication’s editor Joseph I. Sirven, MD, FAAN, said “It is Sirven estimated that more than 52 million Americans speak Spanish as either their primary or secondary language. Put another way, there are now more people who speak Spanish living in the USA than there are in all of Spain. So, it is with great excitement that we introduce the Brain & Life en Español—the Spanish language edition of Brain & Life. With its own bilingual editorial

Tuesday, April 24, 2018 • AANextra

board, Brain & Life en Español will be able to reach millions of Spanish speaking neurology patients throughout the USA and all of Latin America with the award-winning content we all love about Brain & Life.” Also, be sure to visit BrainandLife.org. The AAN’s new patient website centralizes our trusted resources into one convenient place. This is a great resource to access and share with your patients. AAN members may elect to receive multiple copies of Brain & Life to distribute to their patients, who also can subscribe for free. Visit BrainandLife.org to learn more or email BeGreen@ WasteFreeMail.com to adjust the number of copies you receive for your patients or to update your clinic address.

More Spanish-language Resources Available Brain & Life en Español is just one of a number of valuable resources that the AAN provides in the Spanish language. Others include: Selected clinical practice guidelines in Spanish at AAN.com/Guidelines/Home/ByLanguage 2018 Annual Meeting— Look for six education courses and four experiential learning area talks on a variety of topics, including MS, epilepsy, stroke, CNS infection and tropical medicine, and more—going on all week long and taught entirely in Spanish. Visit AAN.com/conferences-community/ annual-meeting/program-and-events/spanish-languagecurriculum to learn more 2018 Brain Health Fair—free resources and presentations in Spanish were available to public attendees at the April 20 event 

018 A P R I L/M AY 2

Exercise Find the Right Type and Amount for Your Condition Nerve Pain Smart Ways to Manage Neuropathy

After My Stroke In 2001, I Feel So Blessed and I’ve Learned So Much.” E H A R O N S TO N — AC TR E S S S

Rebound Headaches How to Break the Cycle

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Tuesday, April 24, 2018 • AANextra

Press Conference Highlights New MS Guideline Continued from cover

Lead author Alexander Rae-Grant, MD, said that according to the guideline, the question of whether to start a DMT, switch from one DMT to another, or stop a DMT depends on the benefits and risks of the medicines and the specific situation of each patient. The guideline highlights key findings that clinicians need to know: Careful risk management and personalization of treatment strategy are important. The guideline delineates the evidence supporting or not supporting use of the various DMTs compared with placebo and of several DMTs vs comparator DMTs, and offers guidance for starting, switching, and stopping DMT use. For several DMTs, the evidence is insufficient to determine efficacy but provides information regarding risk of adverse effects. 

Alexander Rae-Grant, MD, and Ruth Ann Marrie, MD, PhD, spoke at the press conference.

AHA/ASA, AAN Combine for Tuesday’s Stroke Care Disparities Symposium Recognizing that disparities in stroke care and treatment, particularly in underserved ethnic minorities, is a major health care issue, the AAN is excited to collaborate with the American Heart Association and American Stroke Association to host a two-hour symposium tomorrow that tackles this problem. The session will take place from 3:30 p.m. to 5:30 p.m. in 515B.

Bridging Racial and Ethnic Disparities in the Management of Stroke 3:30 p.m.–3:45 p.m. State of Racial and Ethnic Disparities in Stroke —Salvador Cruz-Flores, MD, FAAN 3:45 p.m.–4:00 p.m. What More Can be Done to Address Racial and Ethnic Disparities in Stroke? —Faculty 4:00 p.m.–4:15 p.m. Avenues to Engage in Stroke Disparities Research —Faculty

Tuesday, April 24, 2018 • AANextra

4:15 p.m.–4:30 p.m. Obstacles and Opportunities in Stroke Care Access Among Racial and Ethnic Minorities —Enrique C. Leira, MD, MS, FAAN

Breakthroughs in Engaging Minority and Rural Communities in Stroke Studies 4:30 p.m.–4:45 p.m. Learning About Your Community (and Establishing a Community Advisory Board) — Faculty

4:45 p.m.–5:00 p.m. Captivating the Community and Sustaining Ties —Bernadette Boden-Albala, MPH 5:00 p.m.–5:15 p.m. Building Trust with Your Community Through Communication —Brett M. Kissela, MD, MS, FAAN 5:15 p.m.–5:30 p.m. Dissemination of Results and Presenting Information — Faculty 

Wednesday: Omalu, DeKosky to Present on First Chronic Encephalopathy in Pro Athletes Continued from cover

the first case of dementia pugilistica/ chronic encephalopathy in an American football player. The presentation is on Wednesday from 1:00 p.m. to 2:15 p.m. in Concourse Hall 152/153. As chronicled in the 2015 film “Concussion,” Omalu’s story is one of triumph in the face of seemingly insurmountable odds. Born in eastern Nigeria during a civil war, Omalu and his family lived as refugees, yet he entered medical school at age 15 and became a physician by age 21.

Omalu’s new memoir, Truth Doesn’t Have a Side, will be available for purchase both before and after his presentation. Following Omalu’s presentation, he will be joined by DeKosky for a panel discussion. 

DeKosky is the Deputy Director of the McKnight Brain Institute in Gainesville, FL. In 2002, he was introduced to Omalu at the University of Pittsburgh. After looking at the case of the late Pittsburgh Steeler Mike Webster, they together confirmed the first case of dementia pugilistica/chronic encephalopathy. Four more cases followed. As the first doctors to identify chronic brain damage as a major factor in the deaths of some professional athletes, DeKosky and Omalu withstood dismissals, backlash, and pressure from peers and the National Football League.

COME CELEBRATE THE

1-YEAR ANNIVERSARY JOIN US AT BOOTH

1802

For patients with epilepsy 12 years of age and older for the treatment of partial-onset seizures (POS) with or without secondarily generalized seizures and adjunctive therapy in the treatment of primary generalized tonic-clonic (PGTC) seizures

RETHINK CO N V U L S I V E S E I Z U R E CO NTRO L AT B O OTH 17 15

HELP QUIET THE NOISE OF CONVULSIVE SEIZURES

Prescribed for

100,000 PATIENTS1*†

Approved in

Available in

COUNTRIES1†

FORMULATIONS2

TO LEARN MORE, VISIT FYCOMPA .COM/HCP Please see Important Safety Information, including a Boxed WARNING for Serious Psychiatric and Behavioral Reactions, on adjacent page. Please see Brief Summary of Prescribing Information on following pages.

* Worldwide figure for FYCOMPA® from 2012 through July 2017. Nearly 20,000 patients prescribed FYCOMPA in the United States. †Across different indications.

IMPORTANT SAFETY INFORMATION WARNING: SERIOUS PSYCHIATRIC AND BEHAVIORAL REACTIONS • Serious or life-threatening psychiatric and behavioral adverse reactions including aggression, hostility, irritability, anger, and homicidal ideation and threats have been reported in patients taking FYCOMPA® • These reactions occurred in patients with and without prior psychiatric history, prior aggressive behavior, or concomitant use of medications associated with hostility and aggression • Advise patients and caregivers to contact a healthcare provider immediately if any of these reactions or changes in mood, behavior, or personality that are not typical for the patient are observed while taking FYCOMPA or after discontinuing FYCOMPA • Closely monitor patients particularly during the titration period and at higher doses • FYCOMPA should be reduced if these symptoms occur and should be discontinued immediately if symptoms are severe or are worsening

SERIOUS PSYCHIATRIC AND BEHAVIORAL REACTIONS

SOMNOLENCE AND FATIGUE FYCOMPA caused dose-dependent increases in somnolence and fatigue-related events. Somnolence was reported in 16% and 18% of patients in the partial-onset seizure trials randomized to receive FYCOMPA at doses of 8 mg and 12 mg per day, respectively, compared to 7% of placebo-treated patients. Fatigue-related events were reported in 12% and 15% of patients in the partial-onset seizure trials randomized to receive FYCOMPA at doses of 8 mg and 12 mg per day, respectively, compared to 5% of placebo-treated patients. These adverse reactions occurred mostly during the titration phase. These adverse reactions were also observed in the PGTC seizure clinical trial. Patients should be advised against engaging in hazardous activities requiring mental alertness, such as operating motor vehicles or dangerous machinery, until the effect of FYCOMPA is known.

FALLS Falls were reported in 5% and 10% of patients in the partial-onset seizure clinical trials randomized to receive FYCOMPA at doses of 8 mg and 12 mg per day, respectively, compared to 3% of placebo-treated patients.

DRUG REACTION WITH EOSINOPHILIA AND SYSTEMIC SYMPTOMS (DRESS)

In the partial-onset seizures clinical trials, hostility- and aggression-related adverse reactions occurred in 12% and 20% of patients randomized to receive FYCOMPA at doses of 8 mg and 12 mg per day, respectively, compared to 6% of patients in the placebo group. These effects were dose-related and generally appeared within the first 6 weeks of treatment, although new events continued to be observed through more than 37 weeks. These effects in FYCOMPA-treated patients led to dose reduction, interruption, and discontinuation more frequently than placebo-treated patients. Homicidal ideation and/or threat have also been reported postmarketing in patients treated with FYCOMPA. The combination of alcohol and FYCOMPA significantly worsened mood and increased anger. Patients taking FYCOMPA should avoid the use of alcohol. Patients, their caregivers, and families should be informed that FYCOMPA may increase the risk of psychiatric events. Patients should be monitored during treatment and for at least one month after the last dose of FYCOMPA, and especially when taking higher doses and during the initial few weeks of drug therapy (titration period) or at other times of dose increases. Similar serious psychiatric and behavioral events were observed in the primary generalized tonic-clonic (PGTC) seizure clinical trial.

DRESS, also known as multiorgan hypersensitivity, has been reported in patients taking AEDs, including FYCOMPA. DRESS may be fatal or life-threatening. DRESS typically, although not exclusively, presents with fever, rash, lymphadenopathy, and/or facial swelling, in association with other organ system involvement. If signs or symptoms are present, immediately evaluate the patient and discontinue FYCOMPA if an alternative etiology for signs or symptoms cannot be established.

SUICIDAL BEHAVIOR AND IDEATION

FYCOMPA may decrease the efficacy of contraceptives containing levonorgestrel. Plasma levels of FYCOMPA were decreased when administered with moderate and strong CYP3A4 inducers, including, carbamazepine, phenytoin, or oxcarbazepine. Multiple dosing of FYCOMPA 12 mg per day enhanced the effects of alcohol on vigilance and alertness, and increased levels of anger, confusion, and depression. These effects may also be seen when FYCOMPA is used in combination with other CNS depressants.

Antiepileptic drugs (AEDs), including FYCOMPA, increase the risk of suicidal thoughts or behavior in patients. Anyone considering prescribing FYCOMPA or any other AED must balance the risk of suicidal thoughts or behavior with the risk of untreated illness. Epilepsy and many other illnesses for which AEDs are prescribed are themselves associated with morbidity and mortality and an increased risk of suicidal thoughts and behavior. Patients, their caregivers, and families should be informed of the risk and advised to monitor and immediately report the emergence or worsening of depression, suicidal thoughts or behavior, thoughts about self-harm and/or any unusual changes in mood or behavior. Should suicidal thoughts and behavior emerge during treatment, consider whether the emergence of these symptoms in any given patient may be related to the illness being treated.

DIZZINESS AND GAIT DISTURBANCE FYCOMPA caused dose-related increases in events related to dizziness and disturbance in gait or coordination. Dizziness and vertigo were reported in 35% and 47% of patients in the partial-onset seizure trials randomized to receive FYCOMPA at doses of 8 mg and 12 mg per day, respectively, compared to 10% of placebo-treated patients. Gait disturbance related events were reported in 12% and 16% of patients in the partial-onset seizure clinical trials randomized to receive FYCOMPA at doses of 8 mg and 12 mg per day, respectively, compared to 2% of placebo-treated patients. These adverse reactions occurred mostly during the titration phase. These adverse reactions were also observed in the PGTC seizure clinical trial.

WITHDRAWAL OF AEDs A gradual withdrawal is generally recommended with AEDs to minimize the potential of increased seizure frequency, but if withdrawal is a response to adverse events, prompt withdrawal can be considered.

MOST COMMON ADVERSE REACTIONS The most common adverse reactions in patients receiving FYCOMPA (≥5% and ≥1% higher than placebo) include dizziness, somnolence, fatigue, irritability, falls, nausea, weight gain, vertigo, ataxia, headache, vomiting, contusion, abdominal pain, and anxiety.

DRUG INTERACTIONS

PREGNANCY AND LACTATION Physicians are advised to recommend that pregnant patients taking FYCOMPA enroll in the North American Antiepileptic Drug (NAAED) Pregnancy Registry. Caution should be exercised when FYCOMPA is administered to pregnant or nursing women as there are no adequate data on the developmental risk associated with use in pregnant women, and no data on the presence of perampanel in human milk, the effects on the breastfed child, or the effects of the drug on milk production.

HEPATIC AND RENAL IMPAIRMENT Use in patients with severe hepatic or severe renal impairment is not recommended. Dosage adjustments are recommended in patients with mild or moderate hepatic impairment. Use with caution in patients with moderate renal impairment.

DRUG ABUSE AND DEPENDENCE FYCOMPA is a Schedule III controlled substance and has the potential to be abused and lead to drug dependence.

REFERENCES: 1. Data on file. Eisai Inc. Woodcliff Lake, NJ. 2. FYCOMPA US Prescribing Information. Woodcliff Lake, NJ: Eisai Inc.

Please see Brief Summary of Prescribing Information on following pages. FYCOMPA® is a registered trademark of Eisai R&D Management Co., Ltd., licensed to Eisai Inc. ©2018 Eisai Inc. FYCO-US2026 March 2018

FYCOMPA® (perampanel) tablets, for oral use, CIII FYCOMPA® (perampanel) oral suspension, CIII Initial U.S. Approval: 2012 Brief Summary of Full Prescribing Information dated July 2017 WARNING: SERIOUS PSYCHIATRIC AND BEHAVIORAL REACTIONS • Serious or life-threatening psychiatric and behavioral adverse reactions including aggression, hostility, irritability, anger, and homicidal ideation and threats have been reported in patients taking FYCOMPA. • These reactions occurred in patients with and without prior psychiatric history, prior aggressive behavior, or concomitant use of medications associated with hostility and aggression. • Advise patients and caregivers to contact a healthcare provider immediately if any of these reactions or changes in mood, behavior, or personality that are not typical for the patient are observed while taking FYCOMPA or after discontinuing FYCOMPA. • Closely monitor patients particularly during the titration period and at higher doses • FYCOMPA should be reduced if these symptoms occur and should be discontinued immediately if symptoms are severe or are worsening. WARNINGS AND PRECAUTIONS Serious Psychiatric and Behavioral Reactions In the controlled partial-onset seizure clinical trials, hostilityand aggression-related adverse reactions occurred in 12% and 20% of patients randomized to receive FYCOMPA at doses of 8 mg and 12 mg per day, respectively, compared to 6% of patients in the placebo group. These effects were dose-related and generally appeared within the first 6 weeks of treatment, although new events continued to be observed through more than 37 weeks. FYCOMPA-treated patients experienced more hostility- and aggression-related adverse reactions that were serious, severe, and led to dose reduction, interruption, and discontinuation more frequently than placebo-treated patients. In general, in placebo-controlled partial-onset seizure clinical trials, neuropsychiatric events were reported more frequently in patients being treated with FYCOMPA than in patients taking placebo. These events included irritability, aggression, anger, and anxiety, which occurred in 2% or greater of FYCOMPA-treated patients and twice as frequently as in placebo-treated patients. Other symptoms that occurred with FYCOMPA and were more common than with placebo included belligerence, affect lability, agitation, and physical assault. Some of these events were reported as serious and life-threatening. Homicidal ideation and/or threat were exhibited in 0.1% of 4,368 FYCOMPA-treated patients in controlled and open label trials, including non-epilepsy trials. Homicidal ideation and/or threat have also been reported postmarketing in patients treated with FYCOMPA. In the partial-onset seizure clinical trials, these events occurred in patients with and without prior psychiatric history, prior aggressive behavior, or concomitant use of medications associated with hostility and aggression. Some patients experienced worsening of their pre-existing psychiatric conditions. Patients with active psychotic disorders and unstable recurrent affective disorders were excluded from the clinical trials. The combination of alcohol and FYCOMPA significantly worsened mood and increased anger. Patients taking FYCOMPA should avoid the use of alcohol. Similar serious psychiatric and behavioral events were observed in the primary generalized tonic-clonic seizure clinical trial. In healthy volunteers taking FYCOMPA, observed psychiatric events included paranoia, euphoric mood, agitation, anger, mental status changes, and disorientation/confusional state. In the non-epilepsy trials, psychiatric events that occurred in perampanel-treated patients more often than placebo-treated patients included disorientation, delusion, and paranoia. Patients, their caregivers, and families should be informed that FYCOMPA may increase the risk of psychiatric events. Patients should be monitored during treatment and for at least 1 month after the last dose of FYCOMPA, and especially when taking higher doses and during the initial few weeks of drug therapy (titration period) or at other times of dose increases. Dose of FYCOMPA should be reduced if these symptoms occur. Permanently discontinue FYCOMPA for persistent severe or worsening psychiatric symptoms or behaviors and refer for psychiatric evaluation. Suicidal Behavior and Ideation Antiepileptic drugs (AEDs), including FYCOMPA, increase the risk of suicidal thoughts or behavior in patients taking these drugs for any indication. Patients treated with any AED for any indication should be monitored for the emergence or worsening of depression, suicidal thoughts or behavior, and/or any unusual changes in mood or behavior. Pooled analyses of 199 placebo-controlled clinical trials (mono- and adjunctive therapy) of 11 different AEDs showed that patients randomized to one of the AEDs had approximately twice the risk (adjusted Relative Risk 1.8, 95% CI: 1.2, 2.7) of suicidal thinking or behavior compared to patients randomized to placebo. In these trials, which had a median treatment duration of 12 weeks, the estimated incidence of suicidal behavior or ideation among 27,863 AED-treated patients was 0.43%, compared to 0.24% among 16,029 placebo-treated patients, representing an increase of approximately one case of suicidal thinking or behavior for every 530 patients treated. There were four suicides in drug-treated patients in the trials and none in placebo-treated patients, but the number is too small to allow any conclusion about drug effect on suicide. The increased risk of suicidal thoughts or behavior with AEDs was observed as early as 1 week after starting drug treatment with AEDs and persisted for the duration of treatment assessed. Because most trials included in the analysis did not extend beyond 24 weeks, the risk of suicidal thoughts or behavior beyond 24 weeks could not be assessed. The risk of suicidal thoughts or behavior was generally consistent among drugs in the data analyzed. The finding of increased risk with AEDs of varying mechanisms of action and across a range of indications suggests that the risk applies to all AEDs used for any indication. The risk did not vary substantially by age (5-100 years) in the clinical trials analyzed. Table 1 shows absolute and relative risk by indication for all evaluated AEDs. Table 1. Risk by indication for antiepileptic drugs in the pooled analysis Indication

Placebo Patients with Events per 1000 Patients

Drug Patients with Events per 1000 Patients

Epilepsy Psychiatric Other Total

1.0 5.7 1.0 2.4

3.4 8.5 1.8 4.3

Relative Risk: Incidence of Events in Drug Patients/ Incidence in Placebo Patients 3.5 1.5 1.9 1.8

Risk Difference: Additional Drug Patients with Events per 1000 Patients 2.4 2.9 0.9 1.9

The relative risk for suicidal thoughts or behavior was higher in clinical trials for epilepsy than in clinical trials for psychiatric or other conditions, but the absolute risk differences were similar for the epilepsy and psychiatric indications. Anyone considering prescribing FYCOMPA or any other AED must balance the risk of suicidal thoughts or behavior with the risk of untreated illness. Epilepsy and many other illnesses for which AEDs are prescribed are themselves associated with morbidity and mortality and an increased risk of suicidal thoughts and behavior. Should suicidal thoughts and behavior emerge during treatment, the prescriber needs to consider whether the emergence of these symptoms in any given patient may be related to the illness being treated. Neurologic Effects Dizziness and Gait Disturbance FYCOMPA caused dose-related increases in events related to dizziness and disturbance in gait or coordination. In the controlled partial-onset seizure clinical trials, dizziness and vertigo were reported in 35% and 47% of patients randomized to receive FYCOMPA at doses of 8 mg and 12 mg per day, respectively, compared to 10% of placebo-treated patients. The gait disturbance related events (including ataxia, gait disturbance, balance disorder, and abnormal coordination) were reported in 12% and 16% of patients randomized to

receive FYCOMPA at doses of 8 mg and 12 mg per day, respectively, compared to 2% of placebo-treated patients. Elderly patients had an increased risk of these adverse reactions compared to younger adults and pediatric patients. These adverse reactions occurred mostly during the titration phase and led to discontinuation in 3% of FYCOMPA-treated patients compared to 1% of placebo-treated patients. These adverse reactions were also observed in the primary generalized tonic-clonic seizure clinical trial. Somnolence and Fatigue FYCOMPA caused dose-dependent increases in somnolence and fatigue-related events (including fatigue, asthenia, and lethargy). In the controlled partial-onset seizure clinical trials, 16% and 18% of patients randomized to receive FYCOMPA at doses of 8 mg and 12 mg per day, respectively, reported somnolence compared to 7% of placebo patients. In the controlled partial-onset seizure clinical trials, 12% and 15% of patients randomized to receive FYCOMPA at doses of 8 mg and 12 mg per day, respectively, reported fatigue-related events compared to 5% of placebo patients. Somnolence or fatigue-related events led to discontinuation in 2% of FYCOMPA-treated patients and 0.5% of placebo-treated patients. Elderly patients had an increased risk of these adverse reactions compared to younger adults and pediatric patients. In the controlled partial-onset seizure clinical trials, these adverse reactions occurred mostly during the titration phase. These adverse reactions were also observed in the primary generalized tonic-clonic seizure clinical trial. Risk Amelioration Prescribers should advise patients against engaging in hazardous activities requiring mental alertness, such as operating motor vehicles or dangerous machinery, until the effect of FYCOMPA is known. Falls An increased risk of falls, in some cases leading to serious injuries including head injuries and bone fracture, occurred in patients being treated with FYCOMPA (with and without concurrent seizures). In the controlled partial-onset seizure clinical trials, falls were reported in 5% and 10% of patients randomized to receive FYCOMPA at doses of 8 mg and 12 mg per day, respectively, compared to 3% of placebo-treated patients. Falls were reported as serious and led to discontinuation more frequently in FYCOMPA-treated patients than placebo-treated patients. Elderly patients had an increased risk of falls compared to younger adults and pediatric patients. Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)/Multiorgan Hypersensitivity Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS), also known as Multiorgan hypersensitivity, has been reported in patients taking antiepileptic drugs, including FYCOMPA. DRESS may be fatal or life-threatening. DRESS typically, although not exclusively, presents with fever, rash, lymphadenopathy, and/or facial swelling, in association with other organ system involvement, such as hepatitis, nephritis, hematological abnormalities, myocarditis, or myositis sometimes resembling an acute viral infection. Eosinophilia is often present. Because this disorder is variable in its expression, other organ systems not noted here may be involved. It is important to note that early manifestations of hypersensitivity, such as fever or lymphadenopathy, may be present even though rash is not evident. If such signs or symptoms are present, the patient should be evaluated immediately. FYCOMPA should be discontinued if an alternative etiology for the signs or symptoms cannot be established. Withdrawal of Antiepileptic Drugs There is the potential of increased seizure frequency in patients with seizure disorders when antiepileptic drugs are withdrawn abruptly. FYCOMPA has a half-life of approximately 105 hours so that even after abrupt cessation, blood levels fall gradually. In epilepsy clinical trials FYCOMPA was withdrawn without down-titration. Although a small number of patients exhibited seizures following discontinuation, the data were not sufficient to allow any recommendations regarding appropriate withdrawal regimens. A gradual withdrawal is generally recommended with antiepileptic drugs, but if withdrawal is a response to adverse events, prompt withdrawal can be considered. ADVERSE REACTIONS Clinical Trials Experience Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in clinical practice. Partial-Onset Seizures A total of 1,038 patients receiving FYCOMPA (2, 4, 8, or 12 mg once daily) constituted the safety population in the pooled analysis of the placebo-controlled trials (Studies 1, 2, and 3) in patients with partial-onset seizures. Approximately 51% of patients were female, and the mean age was 35 years. Adverse Reactions Leading to Discontinuation In controlled clinical trials (Studies 1, 2, and 3), the rate of discontinuation as a result of an adverse reaction was 3%, 8%, and 19% in patients randomized to receive FYCOMPA at the recommended doses of 4 mg, 8 mg, and 12 mg per day, respectively, and 5% in patients randomized to receive placebo. The adverse reactions most commonly leading to discontinuation (≥1% in the 8 mg or 12 mg FYCOMPA group and greater than placebo) were dizziness, somnolence, vertigo, aggression, anger, ataxia, blurred vision, irritability, and dysarthria. Most Common Adverse Reactions Table 2 gives the incidence in the controlled clinical trials (Studies 1, 2, and 3) of the adverse reactions that occurred in ≥2% of patients with partial-onset seizures in the FYCOMPA 12 mg dose group and more frequent than placebo (in order of decreasing frequency for the 12 mg dose group). The most common dose-related adverse reactions in patients receiving FYCOMPA at doses of 8 mg or 12 mg (≥4% and occurring at least 1% higher than the placebo group) included dizziness (36%), somnolence (16%), fatigue (10%), irritability (9%), falls (7%), nausea (7%), ataxia (5%), balance disorder (4%), gait disturbance (4%), vertigo (4%), and weight gain (4%). For almost every adverse reaction, rates were higher on 12 mg and more often led to dose reduction or discontinuation. Table 2. Adverse Reactions in Pooled Placebo-Controlled Trials in Patients with Partial-Onset Seizures (Studies 1, 2, and 3) (Reactions ≥ 2% of Patients in Highest FYCOMPA Dose (12 mg) Group and More Frequent than Placebo) Placebo n=442 % Dizziness Somnolence Headache Irritability Fatigue Falls Ataxia Nausea Vertigo Back pain Dysarthria Anxiety Blurred vision Gait disturbance Weight gain Cough Upper respiratory tract infection Vomiting Hypersomnia Anger Aggression Balance disorder Diplopia Head injury Hypoaesthesia Pain in extremity Constipation

9 7 11 3 5 3 0 5 1 2 0 1 1 1 1 3 3 3 0 <1 1 1 1 1 1 1 2

4 mg n=172 % 16 9 11 4 8 2 1 3 4 2 1 2 1 1 4 1 3 2 1 0 1 0 1 1 0 0 2

FYCOMPA 8 mg n=431 % 32 16 11 7 8 5 3 6 3 2 3 3 3 4 4 1 3 3 2 1 2 5 1 1 0 2 2

12 mg n=255 % 43 18 13 12 12 10 8 8 5 5 4 4 4 4 4 4 4 4 3 3 3 3 3 3 3 3 3

Table 2. Adverse Reactions in Pooled Placebo-Controlled Trials in Patients with Partial-Onset Seizures (Studies 1, 2, and 3) (Reactions ≥ 2% of Patients in Highest FYCOMPA Dose (12 mg) Group and More Frequent than Placebo) (cont.) Myalgia Coordination abnormal Euphoric mood Confusional state Hyponatremia Limb injury Mood altered Arthralgia Asthenia Contusion Memory impairment Musculoskeletal pain Oropharyngeal pain Paraesthesia Peripheral edema Skin laceration

2 0 0 <1 <1 <1 <1 1 1 1 1 1 1 1 1 1

1 1 0 1 0 1 1 0 1 0 0 1 2 0 1 0

1 <1 <1 1 0 1 <1 3 2 2 1 1 2 1 1 2

3 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

Primary Generalized Tonic-Clonic Seizures A total of 81 patients receiving FYCOMPA 8 mg once daily constituted the safety population in the placebo-controlled trial in patients with primary generalized tonic-clonic seizures (Study 4). Approximately 57% of patients were female, and the mean age was 27 years. In the controlled primary generalized tonic-clonic seizure clinical trial (Study 4), the adverse reaction profile was similar to that noted for the controlled partial-onset seizure clinical trials (Studies 1, 2, and 3). Table 3 gives the incidence of adverse reactions in patients receiving FYCOMPA 8 mg (≥4% and higher than in the placebo group) in Study 4. The most common adverse reactions in patients receiving FYCOMPA (≥10% and greater than placebo) were dizziness (32%), fatigue (15%), headache (12%), somnolence (11%), and irritability (11%). The adverse reactions most commonly leading to discontinuation in patients receiving FYCOMPA 8 mg (≥2% and greater than placebo) were vomiting (2%) and dizziness (2%). Table 3. Adverse Reactions in a Placebo-Controlled Trial in Patients with Primary Generalized Tonic-Clonic Seizures (Study 4) (Reactions ≥ 4% of Patients in FYCOMPA Group and More Frequent than Placebo)

Dizziness Fatigue Headache Somnolence Irritability Vertigo Vomiting Weight gain Contusion Nausea Abdominal pain Anxiety Urinary tract infection Ligament sprain Balance disorder Rash

Placebo n=82 % 6 6 10 4 2 2 2 4 4 5 1 4 1 0 1 1

FYCOMPA 8 mg n=81 % 32 15 12 11 11 9 9 7 6 6 5 5 4 4 4 4

Weight Gain Weight gain has occurred with FYCOMPA. In controlled partial-onset seizure clinical trials, FYCOMPA-treated adults gained an average of 1.1 kg (2.5 lbs) compared to an average of 0.3 kg (0.7 lbs) in placebo-treated adults with a median exposure of 19 weeks. The percentages of adults who gained at least 7% and 15% of their baseline body weight in FYCOMPA-treated patients were 9.1% and 0.9%, respectively, as compared to 4.5% and 0.2% of placebo-treated patients, respectively. Clinical monitoring of weight is recommended. Similar increases in weight were also observed in adult and pediatric patients treated with FYCOMPA in the primary generalized tonic-clonic seizure clinical trial. Elevated triglycerides Increases in triglycerides have occurred with FYCOMPA use. Comparison of Sex and Race No significant sex differences were noted in the incidence of adverse reactions. Although there were few non-Caucasian patients, no differences in the incidence of adverse reactions compared to Caucasian patients were observed. Postmarketing Experience The following adverse reactions have been identified during post approval use of FYCOMPA. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure. Dermatologic: Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS). Psychiatric: Acute psychosis, hallucinations, delusions, paranoia, delirium, confusional state, disorientation, memory impairment. DRUG INTERACTIONS Contraceptives With concomitant use, FYCOMPA at a dose of 12 mg per day reduced levonorgestrel exposure by approximately 40%. Use of FYCOMPA with contraceptives containing levonorgestrel may render them less effective. Additional non-hormonal forms of contraception are recommended. Moderate and Strong CYP3A4 Inducers The concomitant use of known moderate and strong CYP3A4 inducers including carbamazepine, phenytoin, or oxcarbazepine with FYCOMPA decreased the plasma levels of perampanel by approximately 50-67%. The starting doses for FYCOMPA should be increased in the presence of moderate or strong CYP3A4 inducers. When these moderate or strong CYP3A4 inducers are introduced or withdrawn from a patient’s treatment regimen, the patient should be closely monitored for clinical response and tolerability. Dose adjustment of FYCOMPA may be necessary. Alcohol and Other CNS Depressants The concomitant use of FYCOMPA and CNS depressants including alcohol may increase CNS depression. A pharmacodynamic interaction study in healthy subjects found that the effects of FYCOMPA on complex tasks such as driving ability were additive or supra-additive to the impairment effects of alcohol. Multiple dosing of FYCOMPA 12 mg per day also enhanced the effects of alcohol to interfere with vigilance and alertness, and increased levels of anger, confusion, and depression. These effects may also be seen when FYCOMPA is used in combination with other CNS depressants. Care should be taken when administering FYCOMPA with these agents. Patients should limit activity until they have experience with concomitant use of CNS depressants (e.g., benzodiazepines, narcotics, barbiturates, sedating antihistamines). Advise patients not to drive or operate machinery until they have gained sufficient experience on FYCOMPA to gauge whether it adversely affects these activities. USE IN SPECIFIC POPULATIONS Pregnancy Pregnancy Exposure Registry There is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (AEDs), such as FYCOMPA, during pregnancy. Encourage women who are taking FYCOMPA during pregnancy to enroll in the North American Antiepileptic Drug

(NAAED) Pregnancy Registry by calling 1-888-233-2334 or visiting http://www.aedpregnancyregistry.org. Risk summary There are no adequate data on the developmental risk associated with use in pregnant women. In animal studies, perampanel induced developmental toxicity in pregnant rat and rabbit at clinically relevant doses. In the U.S. general population the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2-4% and 15-20%, respectively. The background risk of major birth defects and miscarriage for the indicated population is unknown. Oral administration of perampanel (1, 3, or 10 mg/kg/day) to pregnant rats throughout organogenesis resulted in an increase in visceral abnormalities (diverticulum of the intestine) at all doses tested; maternal toxicity was observed at the mid and high doses. In a dose-ranging study at higher oral doses (10, 30, or 60 mg/kg/day), embryo lethality and reduced fetal body weight were observed at the mid and high doses tested. The lowest dose tested (1 mg/kg/day) is similar to a human dose of 8 mg per day based on body surface area (mg/m2). Upon oral administration of perampanel (1, 3, or 10 mg/kg per day) to pregnant rabbits throughout organogenesis, embryo lethality was observed at the mid and high doses tested; the no-effect dose for embryo-fetal developmental toxicity in rabbit (1 mg/kg/day) is approximately 2 times a human dose of 8 mg per day based on body surface area (mg/m2). Oral administration of perampanel (1, 3, or 10 mg/kg per day) to rats throughout gestation and lactation resulted in fetal and pup deaths at the mid and high doses (associated with maternal toxicity) and delayed sexual maturation in males and females at the highest dose tested. No effects were observed on measures of neurobehavioral or reproductive function in the offspring. The no-effect dose for pre- and postnatal developmental toxicity in rat (1 mg/kg/day) is similar to a human dose of 8 mg per day based on body surface area (mg/m2). Lactation Risk summary There are no data on the presence of perampanel in human milk, the effects on the breastfed child, or the effects of the drug on milk production. Perampanel and/or its metabolites are excreted in rat milk, and are detected at concentrations higher than that in maternal plasma. The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for FYCOMPA and any potential adverse effects on the breastfed child from FYCOMPA or from the underlying maternal condition. Females and Males of Reproductive Potential Contraception Use of FYCOMPA may reduce the efficacy of hormonal contraceptives containing levonorgestrel. Advise women taking FYCOMPA who are using a levonorgestrel-containing contraceptive to use an additional non-hormonal form of contraception while using FYCOMPA and for a month after discontinuation. Pediatric Use The safety and efficacy of FYCOMPA for the treatment of partial-onset seizures in pediatric patients 12 years of age and older was established by three randomized double-blind, placebo-controlled, multicenter studies, which included 72 pediatric patients between 12 and 16 years of age exposed to FYCOMPA. The safety and efficacy of FYCOMPA for the adjunctive therapy of primary generalized tonic-clonic seizures in pediatric patients 12 years of age and older was established in a single randomized double-blind, placebo-controlled, multicenter trial (n=164), which included 11 pediatric patients 12 to 16 years of age exposed to FYCOMPA; an additional 6 patients were treated with FYCOMPA in the open label extension of the study. The safety and effectiveness of FYCOMPA in pediatric patients less than 12 years of age have not been established. Juvenile Animal Data Oral administration of perampanel (1, 3, 3/10/30 mg/kg/day; high dose increased on postnatal days [PND] 28 and 56) to young rats for 12 weeks starting on PND 7 resulted in reduced body weight, reduced growth, neurobehavioral impairment (water maze performance and auditory startle habituation) at the mid and high doses, and delayed sexual maturation at the high doses. CNS signs (reduced activity, incoordination, excessive grooming/scratching), pup death, decreased hindlimb splay, and decreased hindlimb grip strength were observed at all doses. Effects on pup body weight, pup growth, hindlimb splay, impairment in the water maze performance, and auditory startle persisted after dosing was stopped. A no-effect dose for postnatal developmental toxicity was not identified in this study. Oral administration of perampanel (1, 5,5/10 mg/kg/day; high dose increased on PND 56) to juvenile dogs for 33 weeks, starting on PND 42, resulted in CNS signs (incoordination, excessive grooming/licking/scratching, spatial disorientation, and/or ataxic gait) at all doses tested. Geriatric Use Clinical studies of FYCOMPA did not include sufficient numbers of patients aged 65 and over to determine the safety and efficacy of FYCOMPA in the elderly population. Because of increased likelihood for adverse reactions in the elderly, dosing titration should proceed slowly in patients aged 65 years and older. Hepatic Impairment Use of FYCOMPA in patients with severe hepatic impairment is not recommended, and dosage adjustments are recommended in patients with mild or moderate hepatic impairment. Renal Impairment Dose adjustment is not required in patients with mild renal impairment. FYCOMPA should be used with caution in patients with moderate renal impairment, and slower titration may be considered. Use in patients with severe renal impairment or patients undergoing hemodialysis is not recommended. DRUG ABUSE AND DEPENDENCE Controlled Substance FYCOMPA contains perampanel and is listed as a Schedule III controlled substance. Abuse Prescription drug abuse is the intentional non-therapeutic use of a drug, even once, for its rewarding psychological or physiological effects. Drug addiction, which develops after repeated drug abuse, is characterized by a strong desire to take a drug despite harmful consequences, difficulty in controlling its use, giving a higher priority to drug use than to obligations, increased tolerance, and sometimes physical withdrawal. Drug abuse and drug addiction are separate and distinct from physical dependence (for example, abuse may not be accompanied by physical dependence). Studies of human abuse potential were performed to evaluate the abuse potential of FYCOMPA (8 mg, 24 mg, and 36 mg) as compared to alprazolam C-IV (1.5 mg and 3 mg), and oral ketamine C-III (100 mg) in recreational polydrug users. Supra-therapeutic doses of FYCOMPA 24 and 36 mg produced responses for “Euphoria” that were similar to ketamine 100 mg and alprazolam 3 mg. For “High,” FYCOMPA 24 mg and 36 mg produced responses comparable to ketamine 100 mg and significantly higher than both doses of alprazolam on a visual analog scale (VAS). “Drug Liking,” “Overall Drug Liking,” and “Take Drug Again” for FYCOMPA were each statistically lower than ketamine 100 mg. In addition, for “Bad Drug Effects,” FYCOMPA 24 mg and 36 mg produced responses significantly higher than ketamine 100 mg. For “Sedation,” FYCOMPA 24 and 36 mg produced responses similar to alprazolam 3 mg and higher than ketamine 100 mg. Additionally, on VAS measures related to dissociative phenomena such as “Floating,” “Spaced Out,” and “Detached,” FYCOMPA at supra-therapeutic doses produced responses similar to ketamine 100 mg and greater than both doses of alprazolam tested. Of note, due to somnolence a number of subjects had missing data around Tmax of FYCOMPA. The above described data might represent an underestimate of FYCOMPA’s effects. The duration of effects of higher doses of FYCOMPA on the majority of measures was much greater than alprazolam 3 mg and ketamine 100 mg. In this study, the incidence of euphoria following FYCOMPA administration 8 mg, 24 mg, and 36 mg was 37%, 46%, 46%, respectively, which was higher than alprazolam 3 mg (13%) but lower than ketamine 100 mg (89%). Dependence Physical dependence is characterized by withdrawal symptoms after abrupt discontinuation or a significant dose reduction of a drug. The potential for FYCOMPA to produce withdrawal symptoms has not been adequately evaluated. OVERDOSAGE There is limited clinical experience with FYCOMPA overdose. The highest reported overdose (approximately 264 mg) was intentional. This patient experienced serious adverse reactions of altered mental status, agitation, and aggressive behavior and recovered without sequelae. In general, the adverse reactions associated with overdoses were similar to the reactions at therapeutic doses with dizziness reported most frequently. There were no reported sequelae. There is no available specific antidote to the overdose reactions of FYCOMPA. In the event of overdose, standard medical practice for the management of any overdose should be used. An adequate airway, oxygenation, and ventilation should be ensured; monitoring of cardiac rhythm and vital sign measurement is recommended. A certified poison control center should be contacted for updated information on the management of overdose with FYCOMPA. Due to its long half-life, the reactions caused by FYCOMPA could be prolonged.

Important Clinical Trials Detailed in This Morning’s Plenary Session Continued from cover

The topics and speakers are: Effects of IONIS-HTTRx in Patients with Early Huntington’s Disease, Results of the First HTT-lowering Drug Trial — Sarah J. Tabrizi, FRCP, PhD, FMedSci University College London, London, United Kingdom

Brain Oxygen Optimization in Severe Traumatic Brain Injury (BOOST) Phase 2 Trial: Towards Evidence-based in the Neurological Intensive Care Unit — Ramon R. Diaz-Arrastia, MD, PhD, FAAN Penn Presbyterian Medical Center, Philadelphia, PA

A Randomized, Placebo-controlled, Phase 3 Study of the Safety and Efficacy of Solriamfetol (JZP-110) for the Treatment of Excessive Sleepiness (ES) in Participants with Narcolepsy Types 1 and 2 (NT1/2) — Michael J. Thorpy, MD Montefiore Medical Center, Bronx, NY

Precision Medicine: Intracerebroventricular Enzyme Replacement Therapy with Cerliponase Alfa in Children with CLN2 Disease: Results from an Ongoing Multicenter Study — Emily C. De Los Reyes, MD Nationwide Childrens Hospital, Columbus, OH

Expanding the Time Window for Thrombectomy: Results of the DEFUSE 3 Study — Gregory W. Albers, MD Stanford University, Stanford, CA

A Phase 3, Randomized, Double-blind, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Eptinezumab for the Preventive Treatment of Chronic Migraine: Results of the PROMISE-2 Trial — Richard B. Lipton, MD, FAAN Albert Einstein College of Medicine, New York, NY

A Phase II Trial of Ibudilast in Progressive Multiple Sclerosis — Robert J. Fox, MD, FAAN Cleveland Clinic, Cleveland, OH

A Double-blind Placebo-controlled Study to Evaluate the Safety and Efficacy of FcRn-antagonist ARGX-113 (efgartigimod) in Generalized Myasthenia Gravis — James F. Howard Jr., MD, FAAN University of North Carolina, Chapel Hill, NC 

Patisiran, a RNAi Therapeutic, to Improve Outcomes in Hereditary Transthyretin-mediated (hATTR) Amyloidosis with Polyneuropathy — David D. Adams, MD, PhD APHP, Le Kremlin-Bicentre, France

Tuesday, April 24, 2018 • AANextra

“Best of” Headache Abstracts Featured in This Morning’s Session This morning’s “Best of” Scientific Platform Session will highlight the top four abstracts on headache, as rated by topic reviewers. The session is a perfect lead-in to the Clinical Trials Plenary Session that immediately follows.

“Best of” Session: Headache 8:00 a.m.–9:00 a.m. 515B 8:00 a.m.—Primary Results of PROMISE-1 (Prevention Of Migraine via Intravenous Eptinezumab Safety and Efficacy-1) Trial: a Phase 3, Randomized, Double-blind, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Eptinezumab for Prevention of Frequent Episodic Migraines Joel Saper, Richard Lipton, David Kudrow, Joe Hirman, David Dodick, Stephen Silberstein, George Chakhava, Jeff Smith 8:08 a.m.—Alterations in Regional Cerebral Blood Flow During the Premonitory Stage of Nitroglycerin-triggered Migraine Attacks, Assessed with Arterial Spin-labelled fMRI Nazia Karsan, Pyari Bose, Fernando Zelaya, Peter Goadsby 8:16 a.m.—Untangling the Burden of Menstrual Migraine from Headache Day Frequency: Results from the 2017 Migraine in America Symptoms and Treatment (MAST) Study Jelena Pavlovic, Michael Reed, Kristina Fanning, Sagar Munjal, Aftab Alam, Todd Schwedt, David Dodick, Dawn Buse, Richard Lipton 8:24 a.m.—Efficacy of Galcanezumab in Patients Who Failed to Respond to Preventives Previously: Results from EVOLVE-1, EVOLVE-2 and REGAIN Studies Qi Zhang, Dustin Ruff, Eric Pearlman, Sriram Govindan, Sheena K. Aurora 8:35 a.m. Panel Discussion/Meet the Investigators 

A N INDU S T RY THERAPEU T I C UPDAT E FROM G E H E A LT H CA R E “ Why aim for earlier diagnosis of neurodegenerative disorders?” We’ve all heard it. Now we’re talking about it. Catch this lively discussion on the impact of early diagnosis.

The great diagnosis debate View video of the debate online at: gehealthcare.com/talkingtime

#TalkingTime Saturday, April 21, 2018, 8:00 PM PT. Platinum Ballroom, JW Marriott Hotel

This event is not part of the 2018 American Academy of Neurology Annual Meeting. CME credits will not be given by any accredited organizations for attending this event. March 2018 JB56403US

Tuesday, April 24, 2018 • AANextra

Today’s Experiential Learning Area Highlights HeadTalks Neurology Game Show: Localize the Lesion 12:00 p.m.–1:00 p.m. Luis Torres, MD New this year! Localize the Lesion is a lively game show asking questions about patient symptoms and signs.

Tuesday, April 24, 2018 • AANextra

Controversies in Neurology: Is the Zombie Apocalypse Upon Us? Local Outbreaks, Bioterrorism, or Bioengineering Run Amok… 4:30 p.m.–5:30 p.m. WARNING: Includes live examinations of zombie patients! Recommended for mature audiences only! Neurologic centers are reporting sporadic zombie outbreaks around the US. Emergency and primary care personnel are dubious of its existence and increasingly calling for neurologic consultations, insisting it’s a neurologic condition without managing the much more serious systemic complications of the condition such as asystole and rabid hyperphagia. Bert B. Vargas, MD, FAAN; Joseph I. Sirven, MD, FAAN; Constantine Moschonas, MD, FAAN; and Jennifer Bickel, MD, FAAN, will dive right into the controversy, tackling provocative issues such as neurologist safety and quality of life—and how this epidemic has few neurologists to stop its spread. Faculty will debate novel reports of zombie occurrences since the 1960s. And live examinations of zombie patients demonstrating the various manifestations of this gravely serious condition will reveal localization of the pathology and therapeutic approaches to this malady.

Live Well: Taking Care of Your Patients Starts with Taking Care of You StrengthsFinder™ Social Hour 3:00 p.m.–3:45 p.m. Join Gallup Certified Strengths Coaches Julie Anderson and Keri Bischoff for an informal, interactive Strengths conversation. Briefly exploring the 34 themes of Strength, Anderson and Bischoff will share real and often humorous examples that reveal the insight and power of this perspective professionally and personally. Doing what you love to do exponentially increases your happiness and productivity. Discover a language for how you can be your best and how teamwork is enhanced when we all use our natural talents.

Maximize Your Value and Advocacy to Action What Is the AAN Doing for Small and Solo Practitioners? 2:30 p.m.–3:30 p.m.

Navigating Your Career Academic Career Panel: Find out How to Get Your Career Started 1:45 p.m.–2:15 p.m. Jennifer Molano, MD, FAAN, and Joseph E. Safdieh, MD, FAAN, will lead a lively panel who will share their experiences about how they navigated the academic environment to start their careers. Focus will be on the strategies to negotiate with your chair to make sure you have the resources you need to make sure you are poised for success.

Small and solo practitioners face different challenges from their academic and large group practice colleagues. AAN Board Member Elaine C. Jones, MD, FAAN, will discuss resources currently available to you and offer an opportunity for you to weigh in on how the Academy could better address those challenges.

The Member Experience: Personalize Your Journey Research Corner: Moving Neurology Forward Welcome to NINDS Day/Overview of NIH Funding with NINDS Director and NINDS Deputy Director 8:00 a.m.–8:30 a.m.

Get a New Profile Picture Want to update your profile picture? Stop by and we’ll take a new one for you! 

Get a preview of NIH Funding and NINDS opportunities by the NINDS’ Director Walter J. Koroshetz, MD, FAAN, and Deputy Director Nina F. Schor, MD, PhD, FAAN. Look for additional NINDS and NIH programming throughout the day, including: 12:40 p.m.–1:10 p.m.: NIH Funding and Professional Development Opportunities for Diverse Researchers 1:20 p.m.–1:50 p.m.: NIH Grant Review Process 2:00 p.m.–2:30 p.m.: NINDS Clinical Trials (new NIH definition) and networks, NeuroNext, StrokeNET, SIREN

Tuesday, April 24, 2018 • AANextra

I’M AFRAID TO FAINT AGAIN Look carefully. This may be the face of neurogenic orthostatic hypotension (nOH). If your patients with a pre-existing neurodegenerative disorder are suffering from dizziness or other symptoms that improve upon sitting, they could have nOH.1-3 Patients with nOH may experience symptoms that can make daily tasks a challenge.3,4 Understanding the symptoms commonly associated with nOH may help in diagnosis and may provide a path for appropriate symptom management.4 Access information about identifying and managing nOH in your patients and register for updates at NOHmore.com—your online resource for understanding why nOH matters. References: 1. Freeman R. Neurogenic orthostatic hypotension. N Engl J Med. 2008;358(6):615-624. 2. Kaufmann H, Malamut R, Norcliffe-Kaufmann L, et al. The Orthostatic Hypotension Questionnaire (OHQ): validation of a novel symptom assessment scale. Clin Auton Res. 2012;22(2):79-90. 3. Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clin Auton Res. 2011;21(2):69-72. 4. Low PA. Neurogenic orthostatic hypotension: pathophysiology and diagnosis. Am J Manag Care. 2015;21(suppl 13):s248-s257.

Order Annual Meeting On Demand Now and Save With so much excellent programming this week, selecting which programs to attend can be difficult. Don’t miss out on your favorites—and save money—by ordering AAN Annual Meeting On Demand before April 27! Attendees save up to $1,500 by ordering this week.* A CME-accredited comprehensive digital library, Annual Meeting On Demand gives you access to more than 500 hours** of presentations from the 2018 Annual Meeting education programs, including the syllabi for 200+ programs, within 24 hours from the completion of the live presentation. With Annual Meeting On Demand you can:

VISIT OUR BOOTH #509 The Mount Sinai Hospital is ranked No. 16 in Neurology & Neurosurgery by U.S. News & World Report, 2017-18. Our world-class specialists are commi ed to the discovery of new treatments for neurological conditions and hold faculty appointments at the Icahn School of Medicine at Mount Sinai, ranked among the nation’s top medical schools by U.S. News & World Report. • Comprehensive Stroke Center • Bendheim Parkinson and Movement Disorders Center • Corinne Goldsmith Dickinson Center for Multiple Sclerosis • Center for Headache and Facial Pain • Center for Cognitive Health and Alzheimer’s Disease Research • Parkinson’s Foundation Center of Excellence • Neuromuscular Disease Division • Neuro-Otology and Neurogenetics Division • Neuro-Infectious Diseases and NeuroAIDS Program • Epilepsy Program • Pediatric Neurology Division • Neuro-Oncology Program • Neuro-Ophthalmology Program • Health Outcomes and Knowledge Translation Research Division

1-800-MD-SINAI • mountsinai.org/neurology

Watch like you’re there in person with slides and synchronized audio Learn at your desk, in your car, or on the go with online access on any computer or mobile device Download PDFs of slides and MP3 files for even greater flexibility in accessing your content Earn credits with integrated CME testing right in your media player Participate without an internet connection by using your complimentary hard drive*** Order today! In Person: Visit the Annual Meeting On Demand Booth in the West Lobby Online: Orders.OnDemand.org/AAN/LosAngeles Phone: (800) 501-2303 *Savings vary by membership category. **Specific presentations within a session may not be available or may be audio only if the presenter has confidential patient information or otherwise declines to be recorded. ***Hard drive does not include all the functionality available online, such as Advanced Search, MP3/PDF downloads, Bookmarks, Recently Viewed, and CME testing. 

Check out New ePoster Areas at Poster Sessions New this year for the poster sessions, we’ve added semiprivate viewing areas for ePosters, allowing for a more interactive and dynamic engagement and discussion with presenters. Look for 12 ePosters each day, where you can delve into the data through touchscreen displays. Today’s Poster Session III will run from 11:30 a.m. to 7:00 p.m. in West Exhibit Hall A of the convention center, with presenter standby from 5:30 p.m. to 7:00 p.m.

091–172

173–200

ePosters

085–090

Again this year we’ve clustered all topic-related posters together into “neighborhoods” to enhance your discussions and make the posters easier to navigate. See the map for the neighborhood locations.

037–084

Aging and Dementia Lunchtime Poster Discussion Session

201–258

b1 g1 339–344 a1 ePosters

Poster Discussion

027–036

001–026

259–294

295–338

345–428

429–480

Poster Session 3

Join today’s lunchtime Poster Discussion Session at the poster discussion stage between 11:45 a.m. and 12:35 p.m., where a group of 10 abstracts will be presented by their authors in a five-minute data blitz with a moderator leading stimulating discussion on the content.

A. Research Methodology, Education, and History: 001 – 026

a1. Aging and Dementia Poster Discussion Session: 027 – 036 B. Movement Disorders: 037 – 084

b1. General Neurology ePoster Session: 085 – 090

Today’s ePoster Sessions: General Neurology and Research Methodology

C. Headache; Practice, Policy, and Ethics: 091 – 172 D. Aging, Dementia, Cognitive, and Behavioral Neurology: 173 – 200 E. Cerebrovascular Disease and Interventional Neurology: 201 – 258 F. Epilepsy/Clinical Neurophysiology (EEG): 259 – 294 G. Neuro Trauma, Critical Care, and Sports Neurology; Child Neurology and Developmental Neurology: 295 – 338

Be sure and check out the center of the poster hall for today’s interactive, touchscreen ePosters. 

g1. Research Methodology ePoster Session: 339 – 344 H. MS and CNS Inflammatory Disease: 345 – 428 I. Neuromuscular/Clinical Neurophysiology (EMG): 429 – 480

Remaining Poster Session Schedule Poster Session IV Wednesday: 11:30 a.m.–7:00 p.m. author standby from 5:30 p.m.–7:00 p.m. Poster Session V Thursday: 11:30 a.m.–7:00 p.m. author standby from 5:30 p.m.–7:00 p.m. Poster Session VI Friday: 11:30 a.m.–5:30 p.m. author standby from 4:00 p.m.–5:30 p.m.

Tuesday, April 24, 2018 • AANextra

‘Cure One, Cure Many’ Is Theme of Foundation Booth ‘Cure One, Cure Many’ is the guiding principle of the American Brain Foundation—one that sets it apart from other organizations raising money for a single brain disease, and one that more broadly unites the Foundation with all AAN members. It is an outlook grounded in science, based on an understanding that a cure for one brain disease will lead to cures for others. It is a philosophy that gives hope and understanding to families affected by multiple neurologic conditions and the many people who are impacted by brain disease. It is also the theme for this year’s Foundation booth, open each day of the Annual Meeting from 7:00 a.m. and 5:00 p.m. in the West Lobby of the Los Angeles Convention Center. All meeting attendees are encouraged to stop by the booth to meet staff and learn more about the Foundation’s important work, including the creation of the world’s first single neuroscience crowdfunding website at AmericanBrainFoundation.org. Visitors to the site can learn about current research in many areas of brain disease and either support a specific research project that most interests, moves, or motivates them, or make a general donation to support all efforts. Visitors can also learn about the available 2019 research awards.

Tuesday, April 24, 2018 • AANextra

The Foundation booth will also feature the Jenga GIANT challenge by which participants can try their hand at “outsmarting brain disease.” This fun, challenging, and interactive exercise figuratively illustrates the “Cure One, Cure Many” concept, with 54 different brain diseases inscribed on wooden blocks which are at first carefully interwoven to form a tower. As the blocks are slowly removed, the significance of their connectedness becomes increasingly evident until the game ends with them all tumbling to the ground. While at the booth, don’t forget to purchase your tickets for tomorrow evening’s Commitment to Cures fundraiser at the JW Marriott Los Angeles. Comedian Michael Pritchard will serve as the program emcee. The program will highlight 2018 Public Leadership in Neurology Award recipient Temple Grandin, PhD, and 2018 Commitment to Cures Award recipient DeMaurice Smith, executive director of the NFL Players’ Association. Acoustic guitarist, singer, composer, and American Brain Foundation Honorary Board Member Billy McLaughlin will provide memorable live performances before and after the event. Individual tickets are $125. 

VISIT US AT BOOTH #1202

TO LEARN MORE ABOUT GRT

GENE REPLACEMENT THERAPY:

A GENETIC EVOLUTION from Mendel’s work based in nature to notable advancements in medicine

We’ve come a long way since Mendel first laid the foundation of genetics— today, gene replacement therapy (GRT) is being investigated as a therapeutic approach that may have the potential to treat monogenic diseases at their source.1,2

References:1. Gayon J. From Mendel to epigenetics: history of genetics. C R Biol. 2016;339(7-8):225-230. 2. Naldini L. Gene therapy returns to centre stage. Nature. 2015;526(7573):351-360. © 2018 AveXis, Inc. All Rights Reserved. US-UNB-18-0039 04/18

AAN Leaders Praise FAANs at Recognition Breakfast AAN leadership—including Vice President Ann Tilton, MD, FAAN, and representatives of the Member Engagement Committee, the Member Application Review Subcommittee, and AAN executive staff—were on hand Sunday morning for a special Fellow Recognition Breakfast honoring all new 2017 FAAN members. These valued FAAN members took advantage of this exclusive opportunity to socialize with leaders and colleagues as they were recognized for their exemplary contributions to neurology. To find out if you for FAAN status, visit the Member Exprience Experiential Learning Area. 

Being a teaching hospital makes us stronger. Being a teaching hospital for two great medical schools makes us NewYork-Presbyterian Hosptial. What happens when two great medical schools bring their highly regarded faculties and groundbreaking research to one hospital? You get more innovation. A wider breadth of expertise. Greater diversity. And most importantly, better outcomes for patients. The physician faculties of Columbia and Weill Cornell have powered NewYork-Presbyterian to U.S. News & World Reportâ&#x20AC;&#x2122;s top ranking for New York hospitals for 17 straight years.

Learn more at nyp.org/amazingadvances

THE GENDER GAP IN NEUROLOGY If you’re a woman practicing medicine in a neurological specialty, chances are good that you’re not earning as much as you could be. More pointedly, you may not be earning as much as male counterparts doing the same work. In a 2015 article published in Medscape Medical News, an earnings differential of $37,000 between male and female neurologists was reported—one of the largest gaps in pay for any medical specialty. Nor is the gender gap limited to income. In 2014, an article published by the Association of American Medical Colleges noted only 11 percent of neurology department chairs at academic medical centers were women. These and other findings were presented to the AAN Board by the Academy’s Gender Disparity Task Force, or GDTF, in a final report dated February 2017. Charged with gathering data and recommending action to be taken by the AAN, the 11-person task force convened four times in as many months to examine gender disparities as they play out in compensation, professional advancement, leadership opportunities, and work/ life balance.

Does the AAN know women are making less than men? Elaine C. Jones, MD, FAAN, the Academy Board member who chaired the Gender Disparity Task Force, suggested the Board focus on the topic after a friend relayed this experience: As a neurologist providing hospital and clinical services as part of a larger group, the friend learned during a general meeting about the next year’s contract that she was earning $20,000 less than her male colleague doing the same work with the same credentials. As Jones relates, “She reached out to me as a Board member to ask, ‘Does the AAN know about this, that women are making less than men?’” At which point, Jones and the Board opted to create an inquiry into the subject on behalf of AAN members. “Some of us on the task force were surprised about the discrepancy, as I was when I first ran into it,” Jones says, noting that owning her own practice (Southern New England Neurology) may have shielded her somewhat. “When I started talking with women even in other professions, it was surprising how many had had this experience. It’s kind of a dirty secret.”

Task force results At first the committee thought it looked like a legislative issue, to be corrected by making new laws. They soon switched gears, however, partly because relevant laws already exist and partly from a commitment to identify specific areas the AAN could directly impact. As a brief recap, here are the main findings and recommendations of the Gender Disparity Task Force. Identified causes for disparities in compensation, professional advancement, leadership opportunities, and work/life balance: Lack of salary transparency, leading to female neurologists not being aware of their colleagues’ salaries and not having relevant data for negotiation.Absence of negotiating and networking by women, rooted in a difference in how the genders approach both tasks.

Tuesday, April 24, 2018 • AANextra

Bias and, in particular, implicit bias which can color major decisions without being detected. Penalty for work/life balance and family responsibility, based on the higher likelihood that women will assume caretaking roles in their personal lives.

Task force recommendations for the AAN:

Lead by example by reporting percentages of women involved in AAN leadership (currently 42 percent on the board and 34 percent on subcommittees), and by continuing to promote gender-friendly work practices. Continue to enhance leadership education options for female AAN members, such as the Women Leading in Neurology Program that begins Fall of 2017. Improve transparency by sharing neurology compensation and productivity data and developing resources that explain requirements for various career stages, while also leveraging relationships to encourage similar transparency from other medical associations and public institutions. Address bias by making available survey tools that reveal implicit biases, as well as by writing articles for AAN publications on the topic. Develop mentors by training men and women leaders to mentor women, by creating networking opportunities for women, and by highlighting female neurologists who have achieved leadership roles or professional success. Promote different practice options to support work/life balance. Offer a scholarship/research fund to support relevant scholarship on the subject. Explore legislative options that have been successful elsewhere while also updating the Code of Professional Conduct to reflect the AAN’s stance on gender disparity. Conduct further investigation and publish the results.

Why don’t women negotiate? Although Dr. Jones’ solo practice keeps her to one side of many of these issues, she relates how an experience serving as interim chair of medicine for her hospital provided insights into the situation. In that 18-month role, she was frequently involved in hiring new physicians. During that time, she says, “I definitely noticed the difference in process for men and women. The women coming in for jobs were less likely to negotiate, while the men were likely to negotiate.” Much of Jones’ sense of why that might be aligns with the findings of the report: Lacking data related to salaries makes it difficult to know what to negotiate for. But why aren’t men and women equally affected by this lack of information? Jones remembers that early in her career, pre-solo practice, her advisors cautioned her not to accept her hospital employment contract without negotiating—an idea that hadn’t even occurred to her. She gave the document to an attorney for review, then negotiated parts herself while leaving the more difficult sections for the lawyer to discuss with the hospital. Looking back, she is grateful for that experience. “Absolutely, it was difficult for me to negotiate,” she says. “It was uncomfortable. But I’m glad I had people advising me or I might not have done it.”

It’s not male vs. female—it’s something we can change Whether men are more likely to perceive their own value, or whether women have been more acculturated to avoid perceived conflict, are among the theories that abound for the difference between the way the two genders approach these issues. Whatever the roots of the situation might be, Jones is convinced the solution lies in women becoming more willing to advocate for themselves. And yet, she’s equally certain that the responsibility for change can’t rest with women alone. “I think we as women have to take charge of it because it’s affecting us. But it shouldn’t be up to women to change the system. We don’t have to make the solution, but we have to stop accepting it. We have to raise the issue.” At the same time, Jones cautions against framing gender disparities as male vs. female, noting that many of the underlying biases are implicit, and shared by both genders. She’s optimistic that a multi-pronged approach by the AAN as recommended by the task force will play a significant role in reducing the incidence of gender disparity and eventually eliminate it altogether. “I don’t think this is an insurmountable issue,” she says. “It’s pretty daunting on the national level, but within the neurology community, I think it’s something we can change. I’m very positive and hopeful.”

Six Tips for Negotiating Your Next Neurology Contract It’s galling to learn that you could have asked for more income or a better schedule when you accepted your neurology position. This is universally disappointing but when it happens to women, it may be the sign of something larger. According to numerous studies and theories, women may be more prone to leaving money on the table because of acculturation to avoid conflict, or from a sense that they will be perceived as pushy if they negotiate, or even from something as basic as not knowing how to conduct a negotiation. The following tips are useful to neurologists from either gender, but they will be especially important for women who may not have been exposed to the process before. Think holistically. Compensation is the most obvious and possibly the most important piece of your negotiation. But if you have specific schedule needs, the desire to tackle particular projects, or an interest in being supported for leadership roles, you need to raise those points as well. Arm yourself with data. Whether or not you decide to cite specific salary studies in a conversation with future employers, simply having the information will help with your frame of reference. If you are an AAN Junior member, you can access the Salary Calculator Tool at AAN.com/ careers. Or, consider asking your mentors and others such questions as, “What are you seeing for the salary range for first-year hospitalists?” etc. Create an advisory team. Speaking of mentors—who’s advising you? When it comes to professional careers, it’s helpful to have more than one person to turn to. Start now to ask a variety of people for permission to reconnect later for career advice when you need it. Continued on page 26 u

Use an attorney. This is a relationship you need to build early in your career, so you can access professional help each time you’re faced with a contract or other employment-related legal issue. Yes, you’ll pay an hourly fee that makes your breath catch, but remember: You’ve already invested untold dollars and hours in your career. Now it’s time to protect that investment. Brush up on steps for conducting a negotiation. A quick internet search will reveal multiple sources for negotiation steps, strategies, and practice dialogs. It’s a good idea to prepare yourself by bookmarking this information before you need it. Even better—run through some of the practice

scenarios so you can feel more confident when it’s time to actually negotiate. Motivate yourself by thinking of lifetime earnings. If a female neurologist in 2015 was earning $37,000 less than her male counterpart, and if she were to multiply that number—even without counting for inflation—by a mere 30 years in practice…you can do the math. By passing up the opportunity to negotiate in the first job, you rob your future self and your family of more than a million dollars. Let that number give you the courage you need to negotiate your next contract. 

Today’s Invited Science Examines Movement Disorders Today’s Invited Science platform session from 1:00 p.m. to 3:00 p.m. in 515B will feature encore presentations of “best of” abstracts previously presented at the International Parkinson and Movement Disorder Society Annual Meeting. Select abstracts will emphasize basic, clinical, and translational science as they evolve toward a more complete understanding of movement disorders with the overall goal of developing more effective prevention and treatment.

Abstracts and authors include:

1:00 p.m.–1:20 p.m. Tissue Engineered Nigrostriatal Pathway for Treatment of Parkinson’s Disease — John E. Duda, MD, Veterans Affairs Medical Center, Philadelphia, PA 1:20 p.m.–1:40 p.m. Which Clinical Features Predict Progressive Supranuclear Palsy Pathology? A Clinicopathological Study on 437 Autopsy Cases and a Literature Review — Gesine Respondek, MD, Technische Universität München, Munich, Germany 1:40 p.m.–2:00 p.m. Skin Nerve Phosphorylated a-synuclein Deposits in Idiopathic REM Sleep Behavior Disorder — Elena Antelmi, MD, University of Bologna, Bologna, Italy

Tuesday, April 24, 2018 • AANextra

2:00 p.m.–2:20 p.m. Results From a Phase 1b Multiple Ascending-dose Study of prx002, an Anti–alpha-synuclein Monoclonal Antibody, in Patients with Parkinson’s Disease — Joseph Jankovic, MD, FAAN, Baylor College of Medicine, Houston, TX 2:20 p.m.–2:40 p.m. The Effect of Early STN-DBS in PD Patients on Axial Symptoms: a 2-year Randomized Controlled Trial (EARLYSTIM-Gait Analysis) — Michael Barbe, MD, University Hospital Köln, Köln, Germany 2:40 p.m.–3:00 p.m. Exercise Alters Response of Reward Anticipation in the Ventral Striatum of Subjects with Parkinson’s Disease — Matthew Sacheli, Pacific Parkinson’s Research Centre, Vancouver, BC, Canada 

THE FIRST FDA-APPROVED TREATMENT INDICATED FOR ADULTS WITH TARDIVE DYSKINESIA (TD)1

ONE CAPSULE, ONCE DAILY1 Convenient, once-daily dosing without complex titration1

Not actual size

• INGREZZA 80 mg provided rapid and significant reductions in TD severity by 6 weeks1,2 —with continued reductions in TD severity through 48 weeks1,3 • Generally well tolerated in clinical trials across a broad range of TD patients1,2 • Selectively inhibits VMAT2, with no appreciable binding affinity for dopaminergic (including D2) or serotonergic receptors1

VMAT2, vesicular monoamine transporter 2.

Not an actual patient

I S I T T D O R A C U T E E P S ? | TA K E T H E T D C H A L L E N G E AT B O O T H # 1 0 2 2 EPS, extrapyramidal symptoms.

W W W. I N G R E Z Z A H C P. C O M

Important Information INDICATION & USAGE

INGREZZA® (valbenazine) capsules is indicated for the treatment of adults with tardive dyskinesia.

IMPORTANT SAFETY INFORMATION WARNINGS & PRECAUTIONS Somnolence INGREZZA can cause somnolence. Patients should not perform activities requiring mental alertness such as operating a motor vehicle or operating hazardous machinery until they know how they will be affected by INGREZZA.

QT Prolongation INGREZZA may prolong the QT interval, although the degree of QT prolongation is not clinically significant at concentrations expected with recommended dosing. INGREZZA should be avoided in patients with congenital long QT syndrome or with arrhythmias associated with a prolonged QT interval. For patients at increased risk of a prolonged QT interval, assess the QT interval before increasing the dosage.

ADVERSE REACTIONS

The most common adverse reaction (≥5% and twice the rate of placebo) is somnolence. Other adverse reactions (≥2% and >placebo) include: anticholinergic effects, balance disorders/falls, headache, akathisia, vomiting, nausea, and arthralgia. You are encouraged to report negative side effects of prescription drugs to the FDA. Visit MedWatch at www.fda.gov/medwatch or call 1-800-FDA-1088. Please see the adjacent page for brief summary of Prescribing Information and visit www.INGREZZAHCP.com for full Prescribing Information. REFERENCES: 1. INGREZZA [package insert]. San Diego, CA: Neurocrine Biosciences, Inc; 2017. 2. Hauser RA, Factor SA, Marder SR, et al. KINECT 3: a phase 3 randomized, double-blind, placebo-controlled trial of valbenazine for tardive dyskinesia. Am J Psychiatry. 2017;174(5):476-484. 3. Factor SA, Remington G, Comella CL, et al. The effects of valbenazine in participants with tardive dyskinesia: results of the 1-Year KINECT 3 extension study. J Clin Psychiatry. 2017;78(9):1344-1350.

for oral use

Brief Summary: for full Prescribing Information and Patient Information, refer to package insert. INDICATIONS AND USAGE

INGREZZA is a vesicular monoamine transporter 2 (VMAT2) inhibitor indicated for the treatment of adults with tardive dyskinesia.

WARNINGS AND PRECAUTIONS

Somnolence INGREZZA can cause somnolence. Patients should not perform activities requiring mental alertness such as operating a motor vehicle or operating hazardous machinery until they know how they will be affected by INGREZZA. QT Prolongation INGREZZA may prolong the QT interval, although the degree of QT prolongation is not clinically significant at concentrations expected with recommended dosing. In patients taking a strong CYP2D6 or CYP3A4 inhibitor, or who are CYP2D6 poor metabolizers, INGREZZA concentrations may be higher and QT prolongation clinically significant. For patients who are CYP2D6 poor metabolizers or are taking a strong CYP2D6 inhibitor, dose reduction may be necessary. For patients taking a strong CYP3A4 inhibitor, reduce the dose of INGREZZA to 40 mg once daily. INGREZZA should be avoided in patients with congenital long QT syndrome or with arrhythmias associated with a prolonged QT interval. For patients at increased risk of a prolonged QT interval, assess the QT interval before increasing the dosage.

Endocrine Disorders: blood glucose increased General Disorders: weight increased Infectious Disorders: respiratory infections Neurologic Disorders: drooling, dyskinesia, extrapyramidal symptoms (non-akathisia) Psychiatric Disorders: anxiety, insomnia During controlled trials, there was a dose-related increase in prolactin. Additionally, there was a dose-related increase in alkaline phosphatase and bilirubin, suggesting a potential risk for cholestasis.

DRUG INTERACTIONS

Drugs Having Clinically Important Interactions with INGREZZA Table 2: Clinically Significant Drug Interactions with INGREZZA Monoamine Oxidase Inhibitors (MAOIs) Clinical Implication:

Prevention or Management: Examples: isocarboxazid, phenelzine, selegiline Strong CYP3A4 Inhibitors Clinical Implication:

ADVERSE REACTIONS

The following adverse reactions are discussed in more detail in other sections of the labeling: • Somnolence • QT Prolongation Clinical Trials Experience Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.

Prevention or Management: Examples: Strong CYP2D6 Inhibitors

The safety of INGREZZA was evaluated in 3 placebo-controlled studies, each 6 weeks in duration (fixed dose, dose escalation, dose reduction), including 445 patients. Patients were 26 to 84 years of age with moderate to severe tardive dyskinesia and had concurrent diagnoses of mood disorder (27%) or schizophrenia/schizoaffective disorder (72%). The mean age was 56 years. Patients were 57% Caucasian, 39% African-American, and 4% other. With respect to ethnicity, 28% were Hispanic or Latino. All subjects continued previous stable regimens of antipsychotics; 85% and 27% of subjects, respectively, were taking atypical and typical antipsychotic medications at study entry. Adverse Reactions Leading to Discontinuation of Treatment A total of 3% of INGREZZA treated patients and 2% of placebo-treated patients discontinued because of adverse reactions. Common Adverse Reactions Adverse reactions that occurred in the 3 placebo-controlled studies at an incidence of ≥2% and greater than placebo are presented in Table 1. Table 1: Adverse Reactions in 3 Placebo-Controlled Studies of 6-week Treatment Duration Reported at ≥2% and >Placebo INGREZZA (n=262) (%)

Placebo (n=183) (%)

Concomitant use of INGREZZA with strong CYP2D6 inhibitors may increase the exposure (Cmax and AUC) to valbenazine’s active metabolite compared with the use of INGREZZA alone. Increased exposure of active metabolite may increase the risk of exposure-related adverse reactions.

Prevention or Management:

Consider reducing INGREZZA dose based on tolerability when INGREZZA is coadministered with a strong CYP2D6 inhibitor.

Examples:

paroxetine, fluoxetine, quinidine

10.9%

4.2%

Anticholinergic effects (dry mouth, constipation, disturbance in attention, vision blurred, urinary retention)

5.4%

4.9%

Balance disorders/fall (fall, gait disturbance, dizziness, balance disorder)

4.1%

2.2%

Headache Akathisia (akathisia, restlessness)

3.4% 2.7%

2.7% 0.5%

Vomiting Nausea Musculoskeletal Disorders

2.6% 2.3%

0.6% 2.1%

Arthralgia

2.3%

0.5%

Strong CYP3A4 Inducers Clinical Implication:

Prevention or Management: Examples: Digoxin

General Disorders Somnolence (somnolence, fatigue, sedation) Nervous System Disorders 1

Gastrointestinal Disorders

Within each adverse reaction category, the observed adverse reactions are listed in order of decreasing frequency.

Other Adverse Reactions Observed During the Premarketing Evaluation of INGREZZA Other adverse reactions of ≥1% incidence and greater than placebo are shown below. The following list does not include adverse reactions: 1) already listed in previous tables or elsewhere in the labeling, 2) for which a drug cause was remote, 3) which were so general as to be uninformative, 4) which were not considered to have clinically significant implications, or 5) which occurred at a rate equal to or less than placebo.

Concomitant use of INGREZZA with strong CYP3A4 inhibitors increased the exposure (Cmax and AUC) to valbenazine and its active metabolite compared with the use of INGREZZA alone. Increased exposure of valbenazine and its active metabolite may increase the risk of exposure-related adverse reactions. Reduce INGREZZA dose when INGREZZA is coadministered with a strong CYP3A4 inhibitor. itraconazole, ketoconazole, clarithromycin

Clinical Implication:

Variable and Fixed Dose Placebo-Controlled Trial Experience

Adverse Reaction1

Concomitant use of INGREZZA with MAOIs may increase the concentration of monoamine neurotransmitters in synapses, potentially leading to increased risk of adverse reactions such as serotonin syndrome, or attenuated treatment effect of INGREZZA. Avoid concomitant use of INGREZZA with MAOIs.

Concomitant use of INGREZZA with a strong CYP3A4 inducer decreased the exposure of valbenazine and its active metabolite compared to the use of INGREZZA alone. Reduced exposure of valbenazine and its active metabolite may reduce efficacy. Concomitant use of strong CYP3A4 inducers with INGREZZA is not recommended. rifampin, carbamazepine, phenytoin, St. John’s wort1

Clinical Implication:

Concomitant use of INGREZZA with digoxin increased digoxin levels because of inhibition of intestinal P-glycoprotein (P-gp).

Prevention or Management:

Digoxin concentrations should be monitored when co-administering INGREZZA with digoxin. Increased digoxin exposure may increase the risk of exposure related adverse reactions. Dosage adjustment of digoxin may be necessary.

The induction potency of St. John’s wort may vary widely based on preparation.

Drugs Having No Clinically Important Interactions with INGREZZA Dosage adjustment for INGREZZA is not necessary when used in combination with substrates of CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2E1, or CYP3A4/5 based on in vitro study results.

OVERDOSAGE

Human Experience The pre-marketing clinical trials involving INGREZZA in approximately 850 subjects do not provide information regarding symptoms with overdose. Management of Overdosage No specific antidotes for INGREZZA are known. In managing overdose, provide supportive care, including close medical supervision and monitoring, and consider the possibility of multiple drug involvement. If an overdose occurs, consult a Certified Poison Control Center (1-800-222-1222 or www.poison.org). For further information on INGREZZA, call 84-INGREZZA (844-647-3992). Distributed by: Neurocrine Biosciences, Inc. San Diego, CA 92130 INGREZZA is a trademark of Neurocrine Biosciences, Inc. CP-VBZ-US-0203v2 09/17

Find, Create New Career Opportunities at Wednesday’s Advanced Leadership Workshop Advanced Leadership Training: Preparing for Your Career’s Insurmountable Opportunities will take place Wednesday from 1:00 p.m. to 5:00 p.m. in 409AB and offer attendees a highly interactive opportunity to consider new strategies for approaching leadership in career and life. The session is free and included with Annual Meeting registration; however, seating is limited.

Griggs

The format will include panel discussions with neurologists “who have been there,” as well as small group and creative breakout discussions. Topics and issues that will be considered include mentoring, global opportunities, focusing on your mission, fostering inclusiveness and diversity, and supporting your passion. To add this program to your itinerary, visit the conference mobile app at AAN.com/view/MobileApp. 

Leider

The workshop will be led by former AAN President Robert C. Griggs, MD, FAAN, and Richard Leider, founder of Inventure— The Purpose Company, and one of America’s preeminent executive-life coaches. Leider is ranked by Forbes as one of the “Top 5” most respected executive coaches. Griggs and Leider will be joined by leaders from private practice and academia—representing many career stages—who will share their perspectives and offer ways of setting and reaching new goals, including consideration of how one can shift gears and pursue highly productive, generative, and creative activities as a practitioner, educator, or researcher.

Compare Your Approach to Your Colleagues in New ‘What Do I Do Now’ Sessions New “What Do I Do Now” pilot sessions will serve to further challenge and engage Annual Meeting attendees when faculty share a challenging real-life case before turning to audience members to ask, “What do I do now?” Attendees will be given the opportunity to weigh in on what they would do in a similar scenario before panel members explain how they actually handled the situation. Don’t miss these four informative and interactive new sessions taking place today and tomorrow: Tuesday, 1:00 p.m.–3:00 p.m. C107 What Do I Do Now?: Assessment and Management of Neuropsychiatric Symptoms in Neurocognitive Disorders 403B Wednesday, 7:00 a.m.–9:00 a.m. C137 What Do I Do Now?: Emergency and Inpatient Management of Migraine and Other Headache Disorders 408A

Wednesday, 1:00 p.m.–3:00 p.m. C149 What Do I Do Now?: Neurologic Consultations in Cancer Patients I 403B Wednesday, 3:30 p.m.–5:30 p.m. C164 What Do I Do Now?: Neurologic Consultations in Cancer Patients II 403B 

Tuesday, April 24, 2018 • AANextra

Emerging Science Abstracts to Be Presented Today and Wednesday Twenty-four Emerging Science abstracts will be presented today and tomorrow in plenary, platform, and poster sessions. Key aspects of the research were conducted after the October 23, 2017, abstract submission deadline and present new findings of sufficient scientific importance to warrant this expedited presentation and publication.

Clinical Trials Plenary Session Tuesday, 9:15 a.m.–11:30 a.m.

South Exhibit Hall K

A Double-blind Placebo-controlled Study to Evaluate the Safety and Efficacy of FcRn-antagonist ARGX-113 (Efgartigimod) in Generalized Myasthenia Gravis — James F. Howard, Jr., MD, FAAN, Chapel Hill, NC A Phase 3, Randomized, Double-blind, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Eptinezumab for the Preventive Treatment of Chronic Migraine: Results of the PROMISE-2 (Prevention of Migraine via Intravenous Eptinezumab Safety and Efficacy 2) Trial — Richard B. Lipton, MD, FAAN, Bronx, NY

Emerging Science Platform Session Tuesday, 5:45 p.m.–7:00 p.m.

Concourse Hall 152/153

INTREPID: A Prospective, Double Blinded, Multicenter Randomized Controlled Trial Evaluating Deep Brain Stimulation with a New Multiple Source, Constant Current Rechargable System in Parkinson’s Disease — Jerrold L. Vitek, MD, PhD, Minneapolis, MN ABX-1431, A First-in-Class Endocannabinoid Modulator, Improves Tics in Adult Patients with Tourette Syndrome — Kirsten Mueller-Vahl, MD, Hannover, Germany Longer-term Assessment of the Safety and Efficacy of Nusinersen for the Treatment of Infantile-onset Spinal Muscular Atrophy (SMA): An Interim Analysis of the SHINE Study — Diana Castro, MD, Dallas, TX RG7916 Significantly Increases SMN Protein in SMA Type 1 Babies — Giovanni Baranello, Milano, Italy

Tuesday, April 24, 2018 • AANextra

Effect of Fingolimod in Pediatric MS: Further Insights from Sensitivity, Supportive and Post-hoc Analyses from PARADIGMS — Kumaran Deiva, MD, PhD, Le Kremlin-Bicêtre, France MRI and Relapse Results for ALKS 8700 in Patients with Relapsing Remitting Multiple Sclerosis: 1-year Interim Results from the Phase 3 EVOLVE-MS-1 Study — Richard Leigh-Pemberton, MD, Waltham, MA Ezutromid Significantly Reduced Muscle Damage Whilst Maintaining Utrophin in Patients with Duchenne Muscular Dystrophy (DMD) after 24-weeks of Treatment — Francesco Muntoni, MD, London, United Kingdom Efficacy, Safety, and Tolerability of Ubrogepant for the Acute Treatment of Migraine: Results from a Single Attack Phase II Study, ACHIEVE I — Joel Trugman, Madison, NJ Efficacy and Safety of Erenumab in Episodic Migraine Patients with 2–4 Prior Preventive Treatment Failures: Results from the Phase 3b LIBERTY Study — Uwe Reuter, Berlin, Germany

Poster Session IV Wednesday, 11:30 a.m.–7:00 p.m.

West Exhibit Hall A

AVXS-101 Gene Replacement Therapy for SMA Type 1: Pivotal Study (STR1VE) Update — John W. Day, MD, PhD, Palo Alto, CA Effect of ZX008 (Fenfluramine HCl Oral Solution) on Total Seizures in Dravet Syndrome — Joseph Sullivan, San Francisco, CA

Transdermal Cannabidiol (CBD) Gel for the Treatment of Focal Epilepsy in Adults — John A. Messenheimer, Jr., MD, Moncure, NC ZX008 (Fenfluramine HCL Oral Solution) in Dravet Syndrome: Effect on Convulsive Seizure Frequency in Subjects Who Failed Treatment with Stiripentol Prior to Study 1 — Elaine Wirrell, MD, FAAN, Rochester, MN Eptinezumab Achieved Meaningful Reductions in Migraine Activity as Early As Day 1 and Were Sustained Through Week 12: Results From PROMISE-2 (PRevention Of Migraine via Intravenous eptinezumab Safety and Efficacy-2) Phase 3 Trial in Chronic Migraine — David B. Kudrow, MD, Santa Monica, CA Eptinezumab Reduced Migraine Frequency and Triptan/ Ergotamine Use Over Weeks 1-12, and Improved HIT-6 Scores at Months One and Three: Results from the Phase 3 PROMISE-2 Trial in Chronic Migraine — Stephen D. Silberstein, MD, FAAN, Philadelphia, PA Clinical Development of VX15/2503 Anti-Semaphorin 4D Antibody as a Potential Treatment for Huntington’s Disease — Elizabeth Evans, PhD, Rochester, NY A Randomized Trial of Deferiprone for Pantothenate KinaseAssociated Neurodegeneration (on behalf of the TIRCON Group) — Thomas H. Klopstock, MD, Munich, Germany Non-invasive Peripheral Nerve Stimulation for Symptomatic Relief of Hand Tremor in Essential Tremor — Rajesh Pahwa, MD, FAAN, Kansas City, KS

Natalizumab Extended Interval Dosing (EID) is Associated with a Significant Reduction in Progressive Multifocal Leukoencephalopathy (PML) Risk Compared with Standard Interval Dosing (SID) in the TOUCH ® Prescribing Program — Lana Zhovtis Ryerson, MD, New York, NY Week 48 Results from Study GNC-003: An International, Double-blind, Randomized, Placebo-controlled Phase IIb Trial to Assess the Efficacy, Safety, and Pharmacokinetics of GNbAC1 in Patients with Relapsing Remitting Multiple Sclerosis (CHANGE-MS—Clinical Trial Assessing the HERV-W Env Antagonist GNbAC1 for Efficacy in MS) — Hans-Peter Hartung, MD, FAAN, Dusseldorf, Germany Autologous Haematopoietic Stem Cell Transplantation in Treatment Naïve Patients with ‘Aggressive’ Multiple Sclerosis — Joyutpal Das, MBBS, Sheffield, United Kingdom B Cell Targeted Treatment in Myasthenia Gravis (BeatMG)—A Phase 2 Trial of Rituximab in Myasthenia Gravis: Topline Results — Richard J. Nowak, MD, New Haven, CT 

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QUOTABLE QUOTES

Paula Voinescu, MD Boston, MA What do you hope to gain from this meeting?

I'm both a clinician and researcher at Harvard. I feel that when you do neurology and subspecialize you focus your attention the most in your subspecialty, and a meeting like this offers the opportunity to really explore what's been going on in other areas. So, I feel like it's useful for me both as a clinician as a researcher to know what’s new in other subspecialties that I may have less time on a day-to-day basis to keep track. Lakshya Basumatary, MD Guwahati, India Have you had a chance to attend sessions that you were interested in?

I'm mostly interested in stroke and movement disorders, so in the morning I attended the movement disorders Hot Topics session and it was really good. There was lots of information on different controversies about whether we should start early L-dopa therapy for Parkinson’s disease or whether we can delay. There was some constructive debate and I think it will help lots of physicians and neurologists like me of the younger generation to explore more about these controversies. Overall, this conference has been designed to give more knowledge and more opportunity to learn about Parkinson’s, and it is very good.

What advice would you give to someone who was thinking of coming to the meeting for the first time?

It’s useful to browse the meeting program because there are so many things going on that it's hard to capture everything. But if you have specific interests in mind it is good to know where they are and kind of have a map to walk around.

Osawaye Osamwonyi, MBBS Abuja, Nigeria What are you looking forward to attending while you’re at the meeting?

Joshua Lukas, MD Miami, FL Are you finding the programs at the meeting that you are interested in learning?

Absolutely, specifically stroke and critical care. I’m trying to attend more of the emergency neurology lectures given that I'm starting real neurology in about two months and so they're extremely valuable. Especially what to do in those first critical hours. Plus, we have here the huge names, very famous neurologists in the books that I read every day, so every lecture has been inspirational. As an intern, do you feel you are getting what you'd like to get out of your AAN membership?

It’s more than I could possibly imagine. I started off as a third-year medical student and my first meeting was Vancouver—legendary! And I’ve been hooked ever since. I went last year to Boston and I'm here this year. It's been a networking opportunity. I've met people I’ve started research projects with and I'm still in touch with those people today.

This is my first meeting. I'm a senior resident neurology, and I want to be a part of AAN. It is one of the largest, if not the largest, in the world and I'm thinking that, being a resident in neurology, I should definitely get to know the personalities behind it. I am particularly interested in the history of the AAN and the fact that this is the 70th anniversary really caught my attention. I thought that it would be really special and I should actually come for this. And then meeting the foremost people in various subspecialties of neurology and residents from other parts of the world. It is very different from where I'm coming from, how practice is like, and the challenges. I went to the session for chief residents. I'm not a chief resident but I was just curious to know if the questions you ask were the same where I am. Truly, our circumstances are different but the essence of the thing is that people still have the same complaints: We’re working too much; the faculty say we’re not working enough; you don't know enough. And then, of course, you have different categories of people who want to still work and the chief resident is trying to see how he or she is going to balance that out. It's just a new experience for me and an exciting one at that. Do you think you'll attend future meetings?

I think the question is if I'll be missing any other ones. I plan to attend as many as much as possible!

What AAN programs have been useful for you?

The mentorship program is an invaluable asset.

Tuesday, April 24, 2018 • AANextra

Recollections of Past AAN Presidents

Richards in 1970.

Nelson G. Richards, MD, FAAN / President 1983–1985 Throughout 2018, the AAN is celebrating the history of the Academy during its 70th anniversary with a series of interviews of past presidents. The following excerpt is from a 2017 correspondence interview between Nelson G. Richards, MD, FAAN, (NR) and AANnews editor Tim Streeter (TS). Richards, who joined the AAN in 1957, was the first neurologist in private practice to be elected AAN president. He is retired and living in Virginia. TS: What motivated you to get involved in AAN leadership activities? NR: I had joined the American College of Physicians (ACP) and the practice management-oriented side by American Society of Medicine (ASIM). The Academy included both academic and practice management in one organization. The AAN was inviting participation. I started working with staff at the 1964 Annual Meeting in Denver and then became the local Annual Meeting chairman in Cleveland in 1965. I continued as chairman of this committee for a few years…. Dr. Foley, during his presidency in 1964, had talked with Dr. Herb Rosenbaum, from St. Louis, of the need for office-based neurologists at the AAN. Herb, with Dr. John Segerson of the Menninger Clinic, started organizing the Practice Committee. It was developed for the “grass-roots neurologist,” as Dr. Foley had suggested. I joined the committee. Education courses were developed for the

Tuesday, April 24, 2018 • AANextra

Annual Meeting, including the Coding for Procedures (CPT) and diagnosis codes (ICD-9-CM) for the insurance companies and government Medicare/Medicaid “third-party” carrier programs. I borrowed experienced staff from the American Society of Internal Medicine to aid us in organizing and recording efficient committee meetings and the structure of the board…. I carried this experience to the Academy organization during my presidency. Advice from their membership, staff, and executive director was very supportive in my understandings of medical organizations and committees. Advice came along during difficult times at the Academy. The relationship of the ASIM, with the more academic ACP, was very similar to the Academy, where academics and practice are in our one organization. Indeed, the ACP and ASIM have joined each other. I used my observations at ASIM for the structure of the Academy. TS: Dr. John Conomy said that you “brought the community of practicing neurologists into the mainstream of the organization and eventually into the leadership and conscience of the AAN.” What were the obstacles you faced? Who were some of the leaders who held differing views?

Cohen, the immediate past president, was very helpful and became a good friend. TS: What were the challenges of being a practicing neurologist in those days? NR: There were few referrals for the office-based neurologist. Neurological consultations were felt to be “diagnose and adios.” Detailed neurological examination was needed and the formulation of the problem, but few neurodiagnostic procedures were available. Previous neurological education had usually been minimal for most doctors… TS: Was it a challenge to get the first practice management course into the Annual Meeting in 1981? NR: There was some resistance to include practice management within the Annual Meeting. Documentation of practice was related to the proper coding numbers for the patient’s insurance. Medicare/Medicaid were the “third-party payers.” The need of coding by ICD-9 and CPT were poorly understood in many practices. Efficient office management was needed, usually with the additional employment of personnel. The challenge was there. Budgets were tight with additional help being needed.

TS: You were the first practicing neurologist to become AAN NR: I did not feel any obstacles president in 1983. How did that and found much support in come about? changes I suggested. Academic neurologists were helpful in the understanding of our objectives not to replace but complement academic and private practices’ relationships. Some of the eastern neurologists did express some reservation in the need of an additional society in the middle of America. I asked five of the recent presidents to be available to give me suggestions and advice when needed. Maynard Richards and Executive Director/CEO Catherine M. Rydell in 2003.

NR: The Academy was for all neurologists, including those in office-based practice. The courses in practice were popular. An officebased neurologist was needed. The activity of the Practice Committee may have been a source for a practicing neurologist. TS: Was it difficult to get the Executive Board to adjust the schedule of the Annual Meeting to better accommodate practitioners? NR: No, I had great support from the previous presidents and chairmen of the Education Committee. When we placed the courses at both ends of the scientific papers

presentation it was based on the desire that all partners at home should get access to the meeting. This was developed to make it possible for those members who came to the meeting to return home and allow their associates, who were at home in their active practice, to come to meetings.

a difficult job. The AAN was growing in membership and organizational activities. He, and his small staff, organized and set up the conventions. He was always pleasant with the various problems. He needed help. He was basically a CPA. TS: There were only a dozen or so employees on staff when you were president. Did that impede the Academy’s efforts to serve its members, or was that a “simpler time” back then?

TS: Can you talk about Stanley Nelson when he was executive director? What was his style and his contribution to the success of the AAN? NR: He was working with a very small staff and had little contact with the membership for doing

NR: It was a simpler time. I had a new basic change in the Academy to one similar to the ASIM in function and activity. Staff and members worked together with almost no resistance. With the two-year president’s appointment, the first year was involved with structure and committee selection, and the second year, there was the application of the action of the appointed committee. It was really a great time. Visit AAN.com/view/AANhistory to read the complete transcript of Richard’s interview and learn more about how the AAN evolved in the 1960s and 1970s. 

Richards, Long-range Planning Retreat, 1991.

Richards, fifth from left, at 1968 Annual Meeting.

Richards, at far left, during 1968 Annual Meeting entertainment.

Tuesday, April 24, 2018 • AANextra

INDUSTRY THERAPEUTIC UPDATE FROM ADAMAS PHARMACEUTICALS, INC. HOW CAN WE

FIGHT DYSKINESIA IN

PARKINSON’S DISEASE? Join us for personal and professional perspectives on Parkinson’s disease, with a focus on dyskinesia. This dynamic program features a roundtable discussion among leading experts in the treatment of dyskinesia in Parkinson’s disease, as well as a heartfelt keynote presentation by the daughter of the late, great Muhammad Ali, who lived with Parkinson’s disease for years before he was diagnosed. Don’t miss this opportunity to hear engaging personal and professional perspectives on the impact and management of Parkinson’s disease, with a focus on dyskinesia.

TUESDAY, APRIL 24TH 2018

7:00 PM–10:00 PM REGISTRATION BEGINS AT 6:30 PM

San Diego Ballroom • Westin Bonaventure Hotel • Los Angeles, CA COMPLIMENTARY DINNER WILL BE SERVED

GOCOVRI (amantadine) extended release capsules is the first and only medicine approved by the FDA for the treatment of dyskinesia in patients with Parkinson’s disease receiving levodopa-based therapy, with or without concomitant dopaminergic medications.

IMPORTANT SAFETY INFORMATION CONTRAINDICATIONS

GOCOVRI is contraindicated in patients with creatinine clearance below 15 mL/min/1.73 m2. WARNINGS AND PRECAUTIONS Falling Asleep During Activities of Daily Living and Somnolence: Patients treated with Parkinson’s disease medications have reported falling asleep during activities of daily living. If a patient develops daytime sleepiness during activities that require full attention (eg, driving a motor vehicle, conversations, eating), GOCOVRI should ordinarily be discontinued or the patient should be advised to avoid potentially dangerous activities. Suicidality and Depression: Monitor patients for depression, including suicidal ideation or behavior. Prescribers should consider whether the benefits outweigh the risks of treatment with GOCOVRI in patients with a history of suicidality or depression.

PRESENTERS

KEYNOTE SPEAKER

Rajesh Pahwa, MD

Laverne & Joyce Rider Professor of Neurology Kansas Medical Center Chief, Parkinson Disease & Movement Disorder Division Director, Parkinson Foundation Center of Excellence Kansas City, KS

Daniel E. Kremens, MD, JD Associate Professor of Neurology Department of Neurology Sidney Kimmel Medical College at Thomas Jefferson University Philadelphia, PA

Stuart Isaacson, MD

Associate Professor of Neurology Herbert Wertheim College of Medicine Florida International University Miami, FL Director, Institute for Neurodegenerative Diseases of Florida Parkinson’s Disease and Movement Disorders Center of Boca Raton Alzheimer’s and Memory Disorders Center of South Florida Boca Raton, FL

MARYUM ALI Daughter of Muhammad Ali “My Father’s Journey, and What It Means to Me”

IMPORTANT SAFETY INFORMATION (cont.) WARNINGS AND PRECAUTIONS (cont.) Hallucinations/Psychotic Behavior: Patients with a major psychotic disorder should ordinarily not be treated with GOCOVRI because of the risk of exacerbating psychosis. Observe patients for the occurrence of hallucinations throughout treatment, especially at initiation and after dose increases. Dizziness and Orthostatic Hypotension: Monitor patients for dizziness and orthostatic hypotension, especially after starting GOCOVRI or increasing the dose. Withdrawal-Emergent Hyperpyrexia and Confusion: Rapid dose reduction or abrupt discontinuation of GOCOVRI, may cause an increase in the symptoms of Parkinson’s disease or cause delirium, agitation, delusions, hallucinations, paranoid reaction, stupor, anxiety, depression, or slurred speech. Avoid sudden discontinuation of GOCOVRI. Impulse Control/Compulsive Behaviors: Patients may experience urges (eg, gambling, sexual, money spending, binge eating) and the inability to control them. It is important for prescribers to ask patients or their caregivers about the development of new or increased urges. Consider dose reduction or stopping medications. ADVERSE REACTIONS The most common adverse reactions (>10%) were hallucination, dizziness, dry mouth, peripheral edema, constipation, fall, and orthostatic hypotension. DRUG INTERACTIONS Other Anticholinergic Drugs: The dose of GOCOVRI should be reduced if atropine-like effects are observed. Drugs Affecting Urinary pH: The pH of the urine has been reported to influence the excretion rate of amantadine. Monitor for efficacy or adverse reactions under conditions that alter the urine pH. Alcohol: Concomitant use with alcohol is not recommended, as it may increase the potential for CNS effects such as dizziness, confusion, lightheadedness, and orthostatic hypotension. Please see Brief Summary of full Prescribing Information on the next page.

Please visit us at Booth 703 For more information and to preregister for this program, please visit

www.fightdyskinesia.com Seating is limited, so preregistration is recommended. This promotional, non-CME program is intended only for healthcare professionals involved in the treatment of people with Parkinson’s disease. This is not an AAN-endorsed event.

GOCOVRI™ (amantadine) extended release capsules Brief Summary of full Prescribing Information. See full Prescribing Information. Rx Only. INDICATIONS AND USAGE: GOCOVRI is indicated for the treatment of dyskinesia in patients with Parkinson’s disease receiving levodopa-based therapy, with or without concomitant dopaminergic medications. CONTRAINDICATIONS: Contraindicated in patients with creatinine clearance below 15 mL/min/1.73 m2 WARNINGS AND PRECAUTIONS: Falling Asleep During Activities of Daily Living and Somnolence: Patients treated with Parkinson’s disease medications have reported falling asleep while engaged in activities of daily living, including the operation of motor vehicles, which sometimes has resulted in accidents. Patients may not perceive warning signs, such as excessive drowsiness, or they may report feeling alert immediately prior to the event. In controlled clinical trials, somnolence and fatigue were reported in 4% vs. 1% of patients treated with GOCOVRI or placebo, respectively. Before initiating treatment with GOCOVRI, advise patients of the potential to develop drowsiness and specifically ask about factors that may increase the risk for somnolence with GOCOVRI, such as concomitant sedating medications or the presence of a sleep disorder. If a patient develops daytime sleepiness or episodes of falling asleep during activities that require full attention (e.g., driving a motor vehicle, conversations, eating), GOCOVRI should ordinarily be discontinued. If a decision is made to continue GOCOVRI, patients should be advised not to drive and to avoid other potentially dangerous activities. There is insufficient information to establish that dose reduction will eliminate episodes of falling asleep while engaged in activities of daily living or daytime somnolence. Suicidality and Depression: In controlled clinical trials, suicidal ideation or suicide attempt was reported in 2% vs. 0%; depression or depressed mood 6% vs. 1%; confusional state 3% vs. 2%; apathy 2% vs. 0%, in patients treated with GOCOVRI or placebo, respectively. Monitor patients for depression, including suicidal ideation or behavior. Prescribers should consider whether the benefits outweigh the risks of treatment with GOCOVRI in patients with a history of suicidality or depression. Hallucinations/Psychotic Behavior: Patients with a major psychotic disorder should ordinarily not be treated with GOCOVRI because of the risk of exacerbating psychosis. In controlled trials, the incidence of patients who experienced visual hallucination, auditory hallucination, delusions, illusions, or paranoia was 25% vs 3%; hallucinations caused discontinuation of treatment in 8% vs.0%; in patients treated with GOCOVRI or placebo, respectively. Observe patients for the occurrence of hallucinations throughout treatment, especially at initiation and after dose increases. Dizziness and Orthostatic Hypotension: In controlled clinical trials, 29% vs. 2% experienced dizziness, syncope, orthostatic hypotension, presyncope, postural dizziness or hypotension; and 3% vs. 0% discontinued study treatment because of dizziness, postural dizziness, or syncope; in patients receiving GOCOVRI or placebo, respectively. Monitor patients for dizziness and orthostatic hypotension, especially after starting GOCOVRI or increasing the dose. Concomitant use of alcohol with GOCOVRI is not recommended. Withdrawal-Emergent Hyperpyrexia and Confusion: A symptom complex resembling neuroleptic malignant syndrome (characterized by elevated temperature, muscular rigidity, altered consciousness, and autonomic instability), with no other obvious etiology, has been reported in association with rapid dose reduction, withdrawal of, or changes in drugs that increase central dopaminergic tone. Abrupt discontinuation of GOCOVRI may cause an increase in the symptoms of Parkinson’s disease or cause delirium, agitation, delusions, hallucinations, paranoid reaction, stupor, anxiety, depression, or slurred speech. If possible, avoid sudden discontinuation of GOCOVRI. Impulse Control/Compulsive Behaviors: Patients can experience intense urges to gamble, increased sexual urges, intense urges to spend money, binge eating, and/or other intense urges, and the inability to control these urges while taking one or more of the medications, including GOCOVRI, that increase central dopaminergic tone. In some cases, these urges were reported to have stopped when the dose was reduced or the medication was discontinued. Because patients may not recognize these behaviors as abnormal, it is important for prescribers to specifically ask patients or their caregivers about the development of such urges, and to consider dose reduction or stopping GOCOVRI treatment. ADVERSE REACTIONS: Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice. GOCOVRI was evaluated in two double-blind, placebo-controlled efficacy trials of similar design and population: Study 1 (123 patients) and Study 2 (75 patients). The study population was approximately 56% male and 94% white, with a mean age of 65 years (age range from 34 years to 82 years). The mean duration of levodopa-induced dyskinesia was 4 years (range 0.1 to 14 years). Active treatment started at 137 mg once daily for one week, followed by a dose increase to 274 mg once daily. The treatment duration was 25 weeks for Study 1 and 13 weeks for Study 2. Study 1 was stopped prematurely unrelated to safety, with 39/100 patients (safety population) treated with GOCOVRI for 24 weeks. The most common adverse reactions reported in >10% of GOCOVRI-treated patients and more frequently than on placebo were: hallucination, dizziness, dry mouth, peripheral edema, constipation, falls, and orthostatic hypotension. The overall rate of discontinuation because of adverse reactions was 20% vs. 8% for patients treated with GOCOVRI or placebo, respectively. Adverse reactions that led to treatment discontinuation in at least 2% of patients were hallucination (8% GOCOVRI vs. 0% placebo), dry mouth (3% GOCOVRI vs. 0% placebo), peripheral edema (3% GOCOVRI vs. 0% placebo), blurred vision (GOCOVRI 3% vs.0% placebo), postural dizziness and syncope (GOCOVRI 2% vs. 0% placebo), abnormal dreams (GOCOVRI 2% vs. 1% placebo), dysphagia (GOCOVRI 2% vs. 0% placebo), and gait disturbance (GOCOVRI 2% vs. 0% placebo). Pooled Analysis of Adverse Reactions Reported for ≥ 3% of Patients Treated with GOCOVRI 274 mg (N=100) or placebo (N=98), respectively: Psychiatric disorders: visual and/or auditory hallucination (21%, 3%); anxiety and/or generalized anxiety (7%, 3%); insomnia (7%, 2%); depression/depressed mood (6%, 1%); abnormal dreams (4%, 2%); confusional state (3%, 2%). Nervous system disorders: dizziness (16%, 1%); headache (6%, 4%); dystonia (3%, 1%). Gastrointestinal disorders: dry mouth (16%, 1%); constipation (13%, 3%); nausea (8%, 3%); vomiting (3%, 0%). General disorders and administration site conditions: peripheral edema (16%, 1%); gait disturbance (3%, 0%). Injury, poisoning and procedural complications: fall (13%, 7%); contusion (6%, 1%) Infection and infestations: urinary tract infection (10%, 5%). Skin and

subcutaneous tissue disorders: livedo reticularis (6%, 0%); pigmentation disorder (3%, 0%). Metabolism and nutrition disorders: decreased appetite (6%, 1%). Vascular disorders: orthostatic hypotension, including postural dizziness, syncope, presyncope, and hypotension (13%, 1%). Eye disorders: blurred vision (4%, 1%); cataract (3%, 1%); dry eye (3%, 0%). Musculoskeletal and connective tissue disorders: joint swelling (3%, 0%), muscle spasm (3%, 0%). Reproductive system and breast disorders: benign prostatic hyperplasia—all male (6%, 2%). Respiratory, thoracic and mediastinal disorders: cough (3%, 0%). Other clinically relevant adverse reactions observed at <3% included somnolence, fatigue, suicide ideation or attempt, apathy, delusions, illusions, and paranoia. Difference in the Frequency of Adverse Reactions by Gender in Patients Treated with GOCOVRI. Adverse reactions reported more frequently in women (n=46) vs. men (n=54), were: dry mouth (22% vs.11%), nausea (13% vs. 4%), livedo reticularis (13% vs. 0%), abnormal dreams (9% vs. 0%) and cataracts (7% vs. 0%), respectively. Men vs. women reported the following adverse reactions more frequently: dizziness (20% vs. 11%), peripheral edema (19% vs. 11%), anxiety (11% vs. 2%), orthostatic hypotension in (7% vs. 2%) and gait disturbance (6% vs. 0%), respectively. Difference in the Frequency of Adverse Reactions by Age in Patients Treated with GOCOVRI. Hallucinations (visual or auditory) were reported in 31% of patients age 65 years and over (n=52), vs.10 % in patients below the age of 65 years (n=48). Falls were reported in 17% of patients age 65 and over, vs. 8% of patients below age 65. Orthostatic hypotension was reported in 8% of patients age 65 and over, compared to 2% of patients below age 65. DRUG INTERACTIONS: Other Anticholinergic Drugs: Products with anticholinergic properties may potentiate the anticholinergic-like side effects of amantadine. The dose of anticholinergic drugs or of GOCOVRI should be reduced if atropine-like effects appear when these drugs are used concurrently. Drugs Affecting Urinary pH: The pH of the urine has been reported to influence the excretion rate of amantadine. Urine pH is altered by diet, drugs (e.g., carbonic anhydrase inhibitors, sodium bicarbonate), and clinical state of the patient (e.g., renal tubular acidosis or severe infections of the urinary tract). Since the excretion rate of amantadine increases rapidly when the urine is acidic, the administration of urine acidifying drugs may increase the elimination of the drug from the body. Alterations of urine pH towards the alkaline condition may lead to an accumulation of the drug with a possible increase in adverse reactions. Monitor for efficacy or adverse reactions under conditions that alter the urine pH to more acidic or alkaline, respectively. Live Attenuated Influenza Vaccines: Due to its antiviral properties, amantadine may interfere with the efficacy of live attenuated influenza vaccines. Therefore, live vaccines are not recommended during treatment with GOCOVRI. Inactivated influenza vaccines may be used, as appropriate. Alcohol: Concomitant use with alcohol is not recommended, as it may increase the potential for CNS effects such as dizziness, confusion, lightheadedness, and orthostatic hypotension, and may result in dose-dumping. USE IN SPECIFIC POPULATIONS: Pregnancy: There are no adequate data on the developmental risk associated with use of amantadine in pregnant women. Based on animal data, may cause fetal harm. Lactation: Amantadine is excreted into human milk, but amounts have not been quantified. There is no information on the risk to a breastfed infant. The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for GOCOVRI and any potential adverse effects on the breastfed infant from GOCOVRI or from the underlying maternal condition. Pediatric Use: Safety and effectiveness of GOCOVRI in pediatric patients have not been established. Geriatric Use: In Phase 3 clinical trials, the mean age of patients at study entry was 65 years. Of the total number of patients in clinical studies of GOCOVRI, 46% were less than 65 years of age, 39% were 65-74 years of age, and 15% were 75 years of age or older. Hallucinations and falls occurred more frequently in patients 65 years of age or older, compared to those less than 65 years of age. No dose adjustment is recommended on the basis of age. GOCOVRI is known to be substantially excreted by the kidney, and the risk of adverse reactions may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal function. Renal Impairment: GOCOVRI is contraindicated for use in patients with end-stage renal disease (creatinine clearance values lower than 15 mL/min/1.73 m2). A 50% dose reduction of GOCOVRI dosage to a starting daily dose of 68.5 mg daily for a week, followed by a daily maintenance dose of 137 mg is recommended in patients with moderate renal impairment (creatinine clearance between 30 and 59 mL/min/1.73 m2). For patients with severe renal impairment (creatinine clearance between 15 and 29 mL/min/m2), a daily dose of 68.5 mg is recommended. Overdosage: Deaths have been reported from overdose with amantadine immediaterelease. The lowest reported acute lethal dose was 1 gram of amantadine hydrochloride (equivalent to 0.8 g amantadine). Acute toxicity may be attributable to the anticholinergic effects of amantadine. Drug overdose has resulted in cardiac, respiratory, renal, or central nervous system toxicity. Pulmonary edema and respiratory distress (including adult respiratory distress syndrome, ARDS) have been reported with amantadine; renal dysfunction, including increased BUN and decreased creatinine clearance, can occur. Central nervous system effects that have been reported with overdose include agitation, aggressive behavior, hypertonia, hyperkinesia, ataxia, tremor, disorientation, depersonalization, fear, delirium, psychotic reactions, lethargy, and coma. Seizures may be exacerbated in patients with prior history of seizure disorders. Hyperthermia has occurred with amantadine overdose. For acute overdosing, general supportive measures should be employed along with immediate gastric decontamination if appropriate. Give intravenous fluids if necessary. The excretion rate of amantadine increases with acidification of urine, which may increase the elimination of the drug. Monitor patients for arrhythmias and hypotension. Electrocardiographic monitoring may be needed after ingestion because arrhythmias have been reported after overdose, including arrhythmias with fatal outcomes. Adrenergic agents, such as isoproterenol, in patients with an amantadine overdose has been reported to induce arrhythmias. Monitor blood electrolytes, urine pH, and urinary output. Although amantadine is not efficiently removed by hemodialysis, this procedure may be useful in the treatment of amantadine toxicity in patients with renal failure. Gocovri, the Gocovri logo, Adamas, and the Adamas logo are trademarks of Adamas Pharmaceuticals, Inc. or its related companies. © 2018 Adamas Pharmaceuticals, Inc. or its related companies. All rights reserved. GOC-0202 03/18

TWEETS OF THE DAY Abhimanyu Mahajan @amahajan001

Excellent experience answering questions by Med students. This is a great initiative by the AAN to get students more interested and aware in neurology. #AANAMAbhimanyu Mahajan added,

Dr Joe Safdieh @BrainHealthMD

Wow what a crowd at the @AANMember Medical Student Symposium. About 200 students here. These students are so curious about the field and are asking great questions! #AANAM

Daniel C. Potts, MD @DanielCPotts

Kara Stuart Lewis @DrKSLewis

At #AANAM in Los Angeles. Brilliant and energetic plenary session from Dr. Maisha Robinson from Mayo Jacksonville on neuropalliative care. Reminder that palliative care is not ONLY end of life care.

Honored to have been asked to display the watercolors of my father, Lester E. Potts, Jr., an #artist who lived with #Alzheimers, at the American Academy of Neurology @ AANMember Annual Meeting Innovation Hub in LA #AANAM #Dementia #BringingArtToLife #EndTheStigma

Okuda Named Winner of Inaugural Brainstorm Competition Darin T. Okuda, MD, FAAN, took home the grand prize at Monday’s inaugural Brainstorm: A Competition for the Innovator in All of Us for his innovative idea “3-Dimensional Phenotyping: The Next Revolution in Medicine.” Okuda’s effort involves an innovative approach to understanding the threedimensional characteristics of brain lesions resulting from a variety of disease states that improve patient education, provide advancements in our diagnostic and clinical surveillance capabilities, and allow for a better understand of the biology of disease. The exciting “Shark Tank”-style competition had contestants vying for the $1,500 grand prize through presentation of their inventive solutions to challenges related to neurologyrelated issues in front of a panel of

judges. The judges provided constructive feedback before turning it back to the contestants who had to think quickly before presenting refinements and improvements. Congratulations to Dr. Okuda!  Okuda

The 2018 AAN Annual Meeting

MS Industry Therapeutic Updates from Biogen

Advancing MS Treatment: An Individualized Approach

Three Unique Sessions and Panel Discussions Running Simultaneously Tuesday 24 April 2018, 19:00–21:00 (dinner provided) New Frontiers in the Early Diagnosis of MS Chairperson: Xavier Montalban, MD, PhD Panelists: Bianca Weinstock-Guttman, MD, and Timothy L. Vollmer, MD, FAAN JW Marriott, Los Angeles, CA, USA Platinum Ballroom, Salon C, Level 2

Looking Beyond the Symptoms to Customize MS Care Chairperson: Jens Kuhle, MD, PhD Panelists: Mar Tintoré, MD, PhD, and Claire Riley, MD JW Marriott, Los Angeles, CA, USA Platinum Ballroom, Salons H-J, Level 2

Planning for the Future in the MS Treatment Journey Chairperson: Gavin Giovannoni, MBBCh, PhD, FCP (Neurol., SA), FRCP, FRCPath Panelists: Jiwon Oh, MD, PhD, and Timothy West, MD JW Marriott, Los Angeles, CA, USA Gold Ballroom 4, Level 1

M-GMS-US-00800

April 2018