transmitter NEURO A PUBLICATION OF SANTA BARBARA NEUROSCIENCE INSTITUTE AT COTTAGE HEALTH

FALL 2018

Differentiating Between Psychogenic Non-Epileptic and Epileptic PAGE 4

Cottage Children’s Medical Center Clinic: An Individualized Approach to Care PAGE 8

A Look at Amyotrophic Lateral Sclerosis PAGE 6 NEUROtransmitter • fall 2018

Table of Contents

4 Differentiating Between Psychogenic Non-Epileptic and Epileptic Seizures BY MICHAEL GIBBS, MD

6 Amyotrophic Lateral Sclerosis: A Look at This Motor Neuron Degenerative Disease Making Recent Headlines BY KAREN DaSILVA, MD

8 Cottage Children’s Medical Center Concussion Clinic: An Individualized Approach to Care BY REBECCA PIFER, MSN, BSN, and PENNY MORGAN OVERGAARD, PHD, RN

11 Saving the : The 11TH Annual Neuroscience Symposium of The Central Coast, Program Details

Thomas H. Jones, MD About Santa Barbara Cottage Hospital and Cottage Health Executive Medical Editor The not-for-profit Cottage Health is the parent organization of Santa Barbara Cottage Philip R. Delio, MD Medical Editor, Hospital (and its associated Cottage Children’s Medical Center and Cottage Rehabili­ Sean Snodgress, MD tation Hospital), Santa Ynez Valley Cottage Hospital and Goleta Valley Cottage Hospital. Medical Editor, Neuroradiology Traci Rodriguez The Santa Barbara Neuroscience Institute at Cottage Health is a physician-led initiative Executive Editor established to focus on medical conditions over the full cycle of care. The Institute Gary D. Milgram, MBA, RN Administrative Editor aims to deliver the highest value to the patient by incorporating best prac­tices, Gary Hopkins applying resources judiciously, and measuring and reporting outcomes relentlessly. Managing Editor Albert Chiang+Deja Hsu Art Directors Maria Zate Advisory Editor To be added to the mailing list, please contact Traci Rodriguez at [email protected].

2 NEUROtransmitter Fall 2018 Dear Colleagues, i want to take this opportunity to draw your attention to Director of Surgery and Professor of Neurosurgery- the interesting articles in this edition of NEUROtransmitter and Biobehavioral Sciences at the Semel Institute highlighting some of the exceptional work being done by our for Neuroscience and Human Behavior at the University of colleagues here in Santa Barbara, but also to invite you to California Los Angeles, and Dr. Jeff Victoroff, Associate attend our 11th annual Saving the Brain Conference, which Professor of Neurology and Psychiatry at the Keck School of takes place on Nov. 2. Medicine at the University of Southern California. Dr. Fried, This issue of the magazine includes an in-depth discussion whose research and clinical work is dedicated to the treatment by Dr. Michael Gibbs, a neurologist with subspecialty of intractable disorders and epilepsy, will speak on “The training in the diagnosis and management of epilepsy, on Changing Landscape of Epilepsy Surgery.” Dr. Victoroff, an differentiating between psychogenic non-epileptic and internationally known expert in traumatic brain injury, will epileptic seizures. Dr. Karen DaSilva, a neurologist and speak on “Concussive Brain Injury: The Revolution.” expert in neuromuscular diseases, presents an update on Closer to home, Dr. Ty Vernon, a clinical psychologist and current diagnostic techniques and available treatments for autism expert who serves as Director of the Koegel Autism ALS. In their article, Rebecca Pifer, Center at the University of California MSN, BSN, and Penny Morgan Santa Barbara, will talk about “Early Overgaard, PHD, RN, from Social Development in Autism.” the Cottage Children’s Medical Also sharing their expertise Center Concussion Clinic, provide and experience at this year’s a timely look at the services – conference are my colleagues Dr. including preventive education, John Park, neurosurgeon and evaluation, diagnosis and specialized Medical Director of the Brain and management of concussion – Spinal Program at Santa Barbara provided by the clinic to young Neuroscience Institute at Cottage athletes in our community. Health, Dr. Robert Taylor, If you haven’t already done so, neuro-interventionalist/vascular I encourage you to register for this neurologist at the and year’s Saving the Brain neuroscience THOMAS H. JONES, MD Neurovascular Center of Central symposium, which once again features California and Medical Director nationally recognized guest speakers of Neurocritical Care at Cottage as well as local experts from Santa Barbara Cottage Hospital. Health, Dr. Rohit Sharma, a surgical intensivist/acute Our objective this year – and every year – is to provide care physician and Associate Director of Trauma Services conference attendees with a glimpse into the latest advances in at Cottage Health, and Dr. Philip Delio, a neurologist at the field of neuroscience research as they apply to clinical care. Neurology Associates of Santa Barbara and Medical Director I am especially pleased to welcome as our keynote speaker of Stroke Services at Cottage Health. Dr. Greg Albers, The Coyote Foundation Professor of I look forward to seeing you at this year’s conference. You Neurology and Neurological Sciences at Stanford Medical will find more information about the symposium, including Center. In his address – “How the Stroke Stopwatch was how to register, at the back of this issue. Shattered” – Dr. Albers, the principal investigator of the DEFUSE 3 trial, will describe the study’s groundbreaking Sincerely, research that expanded the treatment window for ischemic stroke from six to 24 hours, using specially designed imaging THOMAS H. JONES, MD software that allows physicians to see stroke in real time. Neurosurgeon and Medical Director Our other visiting speakers are Dr. Itzhak Fried, Santa Barbara Neuroscience Institute at Cottage Health

Fall 2018 NEUROtransmitter 3 Differentiating Between Psychogenic Non-Epileptic and Epileptic Seizures

BY MICHAEL GIBBS, MD

sychogenic non-epileptic seizures (PNES) medically unexplained symptom. Seventy-five percent of are a type of non-epileptic seizure and are PNES patients have post-traumatic stress disorder (PTSD), misunderstood by many people outside of the field with 30 percent of those individuals having suffered from of epilepsy. Even among neurologists who do not sexual abuse and 25 percent from physical abuse. PNES is Pspecialize in epilepsy, PNES is commonly misdiagnosed. seen in a significant number of active and former military While abnormal electrical brain activity is always seen with members who have experienced a blast injury of some kind. epileptic seizures, non-epileptic seizures – sometimes referred to as “non-epileptic events” to avoid with the PNES Versus Other Non-Epileptic Seizures term “seizures” – may exhibit many different alterations of Non-epileptic seizures encompass a broad range of seizure- awareness or experience. like events, with their own specific indicators. For example, syncope, with or without , usually is triggered by a Prevalence of PNES precipitating event, such as a psychological stressor or another The estimated prevalence of PNES is factor such as a history of low blood pressure approximately 33 per 100,000 population, which or on standing. Syncope often makes PNES about as common as multiple involves some body stiffening and can be difficult sclerosis and Parkinson’s disease. PNES patients to distinguish from epileptic seizures. Syncope are predominantly women and the mean age at patients also do not generally show the same post- onset is 31. While PNES is not seen in young ictal confusion and agitation that persons with children, there seems to be no upper age limit to epilepsy experience. the disease. Other non-epileptic seizures may include Forty-six percent of PNES patients have hypoglycemic episodes in which patients exhibit some previously been diagnosed with or MICHAEL GIBBS, MD stiffening or shaking, breath-holding spells in children, , and 57 percent have at least one other cataplexy (a sleep phenomenon), or even a paroxysmal

4 NEUROtransmitter Fall 2018 movement disorder. Complex can also be considered a type of non- f i r s t c a s e s t u d y epileptic seizure. EEG Monitoring Helps PNES, however, is the largest Diagnose Non-Epileptic Seizure in Patient category of non-epileptic seizures. Between 30 and 40 percent of Observed in an EMU, a female ictal cry at onset, with a stop-start patients in the epilepsy monitoring patient having a seizure exhibited quality to it. In epileptic seizures, unit (EMU) at Santa Barbara several that the individual typically experiences Cottage Hospital receive a diagnosis initially indicated the seizure tonic contraction of their diaphragm of PNES. might be epileptic. She had eye and lets out a single, large ictal cry. opening at onset, consistent with Additionally, the patient had tonic Etiology of PNES an epileptic seizure, and appeared pulling on the left face but clonic PNES is listed in the Diagnostic to have a seizure . She also had movements in the right arm, which and Statistical Manual of Mental some clonic jerking, with elbow has no anatomical basis in the brain Disorders-5th Edition as a subtype of a flexion of her right hand, at the since they are different electrical functional neurologic disorder, meaning onset and the movement seemed phenomena and should not be it is an experiential and behavioral to be rhythmic. Asynchronous or occurring at the same time. manifestation of distress that is arrhythmic movement typically is a psychiatric in origin. While PNES does sign of non-epileptic seizure. DIAGNOSIS: EEG monitoring of the not appear to have an organic basis, Features that were consistent patient helped determine that the recent studies using improvements with a non-epileptic seizure were an seizure was non-epileptic. in imaging techniques have shown anatomical changes in PNES patients’ compared to controls. supplementary motor area, as well as the precentral and A functional connectivity study using diffusion tensor postcentral gyrus, of individuals with PNES. imaging showed increased connectivity between motor and Clearly, PNES is not simply a , or a form emotional processing regions and the posterior insula in the of malingering. At the same time, it is not caused by excessive brains of PNES patients compared to controls. A separate synchronous discharges in the brain, as is the case with epilepsy. study showed atrophy in the anterior cingulate cortex and Continued on page 10

Signs and Symptoms of PNES • Eye closure at onset – This is the most specific sign of PNES. It is estimated to be present in 80 percent of PNES cases. • Crying – In PNES, this can occur either prior to, directly after or, especially, during a convulsive event. Crying occurs very rarely during epileptic seizures. However, it can occur during frontal lobe epileptic seizures. • Asynchronous or side-to-side movements – Asynchronous or arrhythmic movements are also very characteristic of PNES. • Pelvic thrusting – Repeated perispinal lumbar contractions are often present during PNES, but are not seen during epileptic seizures. • Absence of progressive stages – Epileptic seizures have a beginning, middle and end. For example, they may start with a tonic contraction that transitions to clonic features before the seizure ends. The absence of progression through stages is an indication of PNES. • Long duration – The average epileptic seizure lasts just over one minute. If the seizure continues for a longer duration – for example, 30 minutes or an hour – it is more likely to be PNES.

Fall 2018 NEUROtransmitter 5 Amyotrophic Lateral Sclerosis: A Look at This Motor Neuron Degenerative Disease Making Recent Headlines

BY KAREN DaSILVA, MD

n the last six months, two leaders in very different some, it can start with just weakness in one foot; in others, it paths of life were taken by amyotrophic lateral sclerosis can start with weakness of both shoulders, or atrophy of the (ALS) – renowned theoretical physicist and author intrinsic hand muscles, or weakness of speech. Stephen Hawking and former San Francisco 49ers Ireceiver Dwight Clark. Yet, until the Ice Bucket Diagnosing ALS Challenge, which raised $115 million for the While the diagnosis can be made on strictly ALS Association in the summer of 2014, clinical history and exam, the combination of relatively few members of the public even knew these findings is not typically present at the onset this disease existed. of the initial symptoms. Definite ALS consists ALS is an unrelenting neurodegenerative of evidence of upper motor neuron and lower disease that causes motor neuron death. It can motor neuron disease affecting three different vary in onset location and overall prognostic segmental regions of the body (segments include course.While in some patients it can start with bulbar, thoracic, upper extremities/cervical, and the glossopharyngeal nerves, in others it can start KAREN DaSILVA, MD lower extremities/lumbar). However, it is not with the motor nerves in the L5 myotome. In uncommon for a patient to present with variances

6 NEUROtransmitter Fall 2018 of the broader disease process – that is, motor neuron disease. Currently Available Treatments As an example, a patient can present with a pure lower Two disease-modifying agents are currently available. motor neuron disease affecting only one segment (muscle Rilutek (Riluzole) was the first agent (oral tablet) made cramps, fasciculations, atrophy in more than one myotome available, and while its mechanism of action is not entirely in a segment, such as foot drop with iliopsoas weakness). As clear, it inhibits glutamate release and inactivates voltage- such, clinicians are frequently pressed to exclude mimickers dependent sodium channels. The second agent – edaravone such as lumbar radiculopathy or large fiber polyneuropathy. (radicava) (intravenous infusion) – was released about a The typical work-up will include MRIs of the brain and/or year ago. Again, the exact mechanism of action for this agent spine, serum studies and possible cerebrospinal fluid (CSF) is unknown but it essentially works as an anti-oxidant to studies to exclude mimickers, and electromyography (EMG) reduce tissue injury in neurons. and nerve conduction studies (NCS) to look for supportive Further treatments involve implementing a evidence of denervation and rule out mimickers. multidisciplinary care support including physical, To date, there is still no biomarker for the disease. A occupational, and speech therapy, pulmonary function complete understanding of the pathophysiology and etiology monitoring with early non-invasive ventilatory support, of the majority of the sporadic forms of the disease remains nutrition with emphasis on weight maintenance, and unknown. However, ALS is a neurodegenerative disease that community support. selectively affects motor neurons throughout the central and A number of other treatments are undergoing research peripheral nervous systems. trials at many centers worldwide. These include various This is frustrating for the patient, family and clinician. stem cell-targeted therapeutics – from neurotrophic While the majority of cases are thought to be sporadic in secreting mesenchymal stem cells to embryonic astrocytic nature, there is an increasing identification of genetic types of stem cell implantation. For familial forms, ongoing trials on this disease. Superoxide dismutase, or SOD1, was among the intrathecal administration of an antisense oligonucleotide originally identified genetic types. More recently, C9orf72 compound against superoxide dismutase 1 (SOD 1) are has been identified as a genetic subtype that can underlie not being conducted. only familial but also, interestingly, sporadic forms of ALS. At this time, genetic etiologies still compromise less than 25 For more information on the Santa Barbara Neuroscience percent of cases. Institute at Cottage Health, visit www.cottagehealth.org/neuro

c a s e s t u d y If Motor Neuron Signs Present in At Least One Spinal Region, with No Alternative Explanation, Consider ALS

A 61-year-old woman presented intrinsic hand. An MRI scan showed evidence of chronic denervation originally with a few months left cervical spine nonfocal. On exam, in multiple myotomes of the left upper extremity weakness. Onset she had spasticity of the left upper lumbosacral with fasciculations, was gradual; the patient went to extremity with weakness throughout but no further active denervation. a chiropractor initially. However, and atrophy throughout left hand There was no evidence of active after experiencing progressive muscles and triceps. The exam also denervation or reinnervation in the weakness and left shoulder , showed fasciculations throughout thoracic paraspinal region. Within she went to Neurosurgery. An muscles of the left upper extremity, the next year, she developed MRI brain scan at Santa Barbara brisk reflexes throughout biceps/ bulbar symptoms with dysarthria, Cottage Hospital showed prior triceps/ finger flexors, and intact tongue fasciculations, weakness, right hemispheric stroke in motor sensation to light touch and cold and atrophy. cortex (T2+) with diffusion positive throughout left upper extremity. To consider ALS, motor neuron corticospinal tracts. She was EMG of the left upper extremity signs must be present in at least diagnosed with stroke and placed revealed a combination of acute one spinal region (bulbar, cervical, on Plavix. However, progression of denervation and reinnervation in the thoracic, lumbar); progression weakness continued. Evaluation left C5-6, C8, T1 myotomes. EMG must occur with no alternative with a physiatrist noted atrophy of of the left lower extremity showed explanation available.

Fall 2018 NEUROtransmitter 7 Cottage Children’s Medical Center Concussion Clinic: An Individualized Approach to Care

BY REBECCA PIFER, MSN, BSN, and PENNY MORGAN OVERGAARD, PHD, RN

ild traumatic brain provider trained in the evaluation and removal from physical activity for as long injury (mTBI), more management of prior to as six to eight weeks. Based on studies, commonly called returning to physical activity. this has been significantly shortened. concussion, occurs when Initially, during the acute symptomatic Mthe impact of the brain against the Cottage Children’s Medical period, we now begin treatment with skull causes structural or functional Center - Concussion Clinic cognitive rest criteria for typically damage.1,2 Each year, an estimated 40 The Cottage Concussion Clinic 24 to 48 hours. Next, we progress million children participate in organized emphasizes diagnosis and individualized through a personalized return-to- sporting events.3 The Centers for treatment plans in which we follow academics protocol in which we carefully Disease Control and Prevention (CDC) patients’ progress weekly until they coordinate with the school system to estimates up to 3.8 million sports- are returned to baseline function. help ensure academic success. Finally, related concussions occur annually in the Historically, initial treatment strategies when the individual is symptom free, we U.S. Thirty percent of all concussions recommended a defined period of begin a stepwise graded return-to-play occur between the ages of 5 and 19, and cognitive rest therapy or “brain rest” protocol designed to safely return the as many as 50 percent go unreported.4 often as long as seven to 10 days and patient to physical activity. Younger athletes may be particularly The concussion clinic also at risk as very little is known about provides an individualized the effects of concussive injury on the approach to the care of our more developing brain. However, we do complex patient cases in which know that a history of one concussion post-concussion symptoms (PCS) is associated with an up to 5.8 times develop. The treatment then higher risk for sustaining subsequent becomes a collaborative approach concussions.4,5 California state law utilizing multidisciplinary mandates that any individual suspected pediatric specialists in neurology, of having a concussion be removed psychology and rehabilitative immediately from all physical activity Rebecca Pifer, MSN, BSN, and Penny Morgan services, with the goal of returning and assessed by a licensed health care Overgaard, PhD, RN the patient to baseline function.

8 NEUROtransmitter Fall 2018 Concussion Signs: Loss of consciousness (even brief), seizure, disorientation, incoherent speech, appears dazed, confused, forgetful, asks repetitive questions, more clumsy, answers slowly, mood/behavior/personality change, .

Concussion Symptoms: PHYSICAL: , head pressure, nausea, vomiting, , balance problems, visual problems, fatigue, sensitivity to lights/noises, dazed, stunned, neck pain. COGNITIVE: feeling “foggy”/slowed down, difficulty concentrating, difficulty remembering, forgetful, confusion, answers slowly, repetitive speech, slowed reaction time. EMOTIONAL: irritable, sad, nervous, more emotional. SLEEP DISTURBANCE: drowsiness, sleeping more/less than usual, difficulty sleeping.

Post-Concussion Syndrome* : history of concussion with persistent symptoms lasting longer than four weeks. DEMOGRAPHIC RISK FACTOR: female, adolescent age. MEDICAL RISK FACTOR: history of concussion, prolonged recovery, mood disorder (ADHD, depression, anxiety, seizure disorder), , chronic pain, psychiatric illness, substance abuse. INJURY RISK FACTOR: severe impact, double impact, prolonged duration of initial symptoms, major visual symptoms after initial injury, loss of consciousness, amnesia of event, abnormal neurobehavioral testing.

*Possible risk factors for the development of post-concussion syndrome with the limited data currently available.

Medication? testing. This testing is important. In the 2. Giza, C. C., & Hovda, D. A. (2014). Of note, a majority of individuals (80 event of a concussion, the data provided The new neurometabolic cascade of concussion. to 90 percent) who sustain a concussion Neurosurgery, 75(0 4), S24. not only help identify a concussion, but 3. Pfister, T., Pfister, K., Hagel, B., Ghali, W. A., have resolution of symptoms within also help medical professionals provide a & Ronksley, P. E. (2015). The incidence of seven to 10 days of injury.6,7 Therefore, more comprehensive and individualized concussion in youth sports: a systematic review the routine use of medication is approach to concussion management. and meta-analysis. British Journal of Sports Medicine, bjsports-2015. unnecessary and should be avoided as Baseline testing offers a unique 4. Harmon, H., Drezner, J., Gammons, M., there is no evidence-based research opportunity to individualize education Guskiewicz, K., Halstead, M., Herring, S., regarding effective pharmacological and increase concussion awareness overall Kutcher, J., Panama, A., Putukian, M., Roberts., W. treatments to speed the recovery (2013). American Medical Society for sports through primary health promotion, Medicine position statement: concussion in sport. from or to treat concussion. The only counsel individuals and their parents about British Journal of Sports Medicine, bjsports-2013. exceptions are the use of over-the- the risk of concussion based on personal 5. Buzas, D., Jacobson, N. A., & Morawa, L. G. (2014). counter, low-dose Tylenol for Concussions from 9 youth organized sports: history and by sport, discuss risk reduction Results from NEISS hospitals over an 11-year during the acute symptomatic period or in sports, and encourage reporting. time frame, 2002-2012. Orthopaedic Journal of if the individual has prolonged severe Sports Medicine, 2(4), 2325967114528460. symptoms that are negatively impacting 6. McCrory, P., Johnston, K., Meeuwisse, W., Conclusion Aubry, M., et al. (2005). Summary and agreement their quality of life in such a way that The Cottage Concussion Clinic is a grant- statement of the 2nd International Conference on the potential benefits of the treatment funded resource available to offer not only Concussion in Sport, Prague 2004. British Journal outweigh the risk of the medication. of Sports Medicine, 39(4), 196-204. preventive education, but also evaluation, 7. Mihalik, J. P., Stump, J. E., Collins, M. W., Lovell, diagnosis and specialized management of M. R., Field, M., & Maroon, J. C. (2005). Proactive Approach concussion to youth throughout the Tri- Posttraumatic migraine characteristics in athletes The Cottage Concussion Clinic offers Counties. There is no cost to patients. following sports-related concussion. Journal of baseline testing as a proactive measure Neurosurgery, 102(5), 850-855. taken prior to the start of a sports season. References Baseline testing includes information 1. Graham, R., Rivara, F. P., Ford, M. A., & Spicer, C. M. (Eds.). (2014). Sports-related concussions For more information on the Santa about the athlete’s history, graded symptom in youth: improving the science, changing the Barbara Neuroscience Institute at Cottage checklists, cognitive function and balance culture. National Academies Press. Health, visit www.cottagehealth.org/neuro

Fall 2018 NEUROtransmitter 9 monitored. For some patients, just s e c o n d c a s e s t u d y Patient with Mixed being in a hospital environment is stressful enough to trigger a seizure. Diagnosis Experiences Both Epileptic and EMU monitoring allows us to Non-Epileptic Seizures accurately diagnose PNES patients, reduce future exposure to anti- The female patient is initially seizure after her medications were epileptic drugs, and direct them to observed lying on her back removed. She was observed having beneficial treatments. throughout the seizure, a focal onset that progressed to a experiencing asynchronous generalized tonic-clonic seizure. Treatment for PNES abdominal contractions but She had a tonic left mouth pull One quality, randomized clinical exhibiting no tonic stiffening at onset. Initially, she exhibited trial for treatment of PNES1 elsewhere. In the middle of the a slight fencer position (a sign helps inform the management of event, she uttered an emotional of a focal onset) then flexion these patients. Participants in the ictal cry that clearly expressed a and extension of both arms that four-armed trial were given 1) of distress. There was reverted back to flexion at the start Sertraline (an SSRI), 2) cognitive some confusion when she was of the clonic phase, which included behavioral therapy (CBT) only, admitted about whether she had rhythmic jerking. 3) Sertraline plus CBT, and 4) had an epileptic or non-epileptic standard medical care. seizure. The seizure under DIAGNOSIS: The patient was CBT, a form of talk therapy observation was diagnosed as given a mixed diagnosis, meaning specifically aimed at trying to non-epileptic. she had both epileptic and non- control non-epileptic seizures, The patient had another epileptic seizures. was by far the most successful intervention. With CBT only, there was a 51 percent reduction in Continued from page 5 PNES. With CBT and Sertraline, there was a 59 percent reduction in seizures. With The role of EMU Monitoring Sertraline only and standard medical care, there was no Continuous video-EEG monitoring in the EMU is critical if reduction in seizures. there is any diagnostic uncertainty or if a patient continues to have seizures despite being on seizure medication. Conclusion Between 5 to 10 percent of patients with PNES are given a While PNES, like any other psychiatric disease, is often mixed diagnosis, meaning they experience both epileptic and difficult to treat, there is a treatment, even if it is not perfect. non-epileptic seizures. These patients are especially difficult The prognosis is much better if we can identify the disease to treat since the different may be difficult to early. People who have had PNES for years are much less distinguish. EMU monitoring allows us to characterize the likely to respond to CBT. PNES patients and their families two types of seizures to help direct treatment and educate should be educated about their diagnosis and referred to CBT, family members to identify the differences. with or without an SSRI such as Sertraline. My recommendation is to admit patients to the EMU 1. LaFrance, W. Curt, et al. “Management of Psychogenic Nonepileptic Seizures.” for monitoring if they experience at least one seizure per Epilepsia, 4 Mar. 2013, onlinelibrary.wiley.com/doi/abs/10.1111/epi.12106. week. PNES patients typically have more frequent seizures than that. We often use suggestion, photo stimulation For more information on the Santa Barbara Neuroscience or hyperventilation to provoke events that can then be Institute at Cottage Health, visit www.cottagehealth.org/neuro

10 NEUROtransmitter Fall 2018 On behalf of the Santa Barbara Neuroscience Institute, you are cordially invited to attend

PROGRAM DETAILS FRIDAY, NOVEMBER 2, 2018 saving the brain 7:00 am to 4:30 pm The Hilton Santa Barbara Beachfront Resort (Formerly Fess Parker Doubletree) THE 11TH ANNUAL NEUROSCIENCE Santa Barbara, CA 93103 SYMPOSIUM OF THE CENTRAL COAST

More information about this year’s symposium can be found at www.cottagehealth.org/stbFRIDAY, NOVEMBER 2,. Program 2018 • agenda 7:00 amsubject to 4:30 to change. pm

TIME TOPIC The HiltonSPEAKER Santa Barbara Beachfront Resort 0700 Registration / Continental Breakfast / Vendor Fair (Formerly Fess Parker Doubletree) 0745 Welcome and Overview Santa Barbara,Thomas CA H. Jones,93103 MD, Neurosurgeon, Neurosurgical Associates of Santa Barbara; Medical Director, Santa Barbara Neuroscience Institute at Cottage Health

0800 The Changing Landscape of Epilepsy Surgery Itzhak Fried, MD, Director of Epilepsy Surgery, Featuring nationally recognized guest speakers andProfessor local experts of Neurosurgery-Psychiatry and Biobehavioral Sciences, Semel Institute for in the neurosciences from Santa Barbara Cottage Hospital. Neuroscience and Human Behavior

0845 Surgery in theRegistration is $150.00 (beforeJohn October Park, 26) MD, PhD, Neurosurgeon and Intraoperative MRI: An UpdateRSVP online at cottagehealth.org/stbMedical Director, Brain and Spinal Tumor Program, Santa Barbara Neuroscience Institute at Cottage Health

0930 Concussive Brain Injury: The Revolution Jeff Victoroff, MD, Associate Professor of Neurology and Psychiatry, Keck School of Medicine, University of Southern California

1015 Break / Vendor Fair

1045 Keynote Speaker Greg Albers, MD, The Coyote Foundation How the Stroke Stopwatch was Shattered Professor of Neurology and Neurological Sciences, Stanford Medical Center, DEFUSE 3 Trial Principal Investigator

1145 Case Study Review: Neurointerventional Robert Taylor, MD, Neurointerventionalist/ Stroke and Treatment in the Real World Vascular Neurologist, Stroke and Neurovascular Center of Central California; Medical Director, Neurocritical Care at Cottage Health

1230 Lunch / Vendor Fair

1330 Early Social Development in Autism Ty Vernon, PhD, Director of the Koegel Autism Center, University of California Santa Barbara

1415 Pulmonary/Ventilator Management in the Neuro ICU Rohit Sharma, MD, Surgical Intensivist/Acute Care Physician, Associate Director, Trauma Services at Cottage Health

1500 Stretch Break

1515 “How Can I Get Smarter?”: Philip R. Delio, MD, Neurologist, Neurology Memory and Cognitive Enhancement Associates of Santa Barbara; Medical Director, Stroke Services at Cottage Health

1600 Evaluations and Drawing

Fall 2018 NEUROtransmitter 11 Nonprofit Org. US POSTAGE PAID Santa Barbara, CA Permit No. 35 Santa Barbara Cottage Hospital 400 West Pueblo Street P.O. Box 689 Santa Barbara, CA 93102-0689

On behalf of the Santa Barbara Neuroscience Institute, you are cordially invited to attend saving the brain THE 11TH ANNUAL NEUROSCIENCE SYMPOSIUM OF THE CENTRAL COAST

FRIDAY, NOVEMBER 2, 2018 • 7:00 am to 4:30 pm The Hilton Santa Barbara Beachfront Resort (Formerly Fess Parker Doubletree) Santa Barbara, CA 93103

Featuring nationally recognized guest speakers and local experts in the neurosciences from Santa Barbara Cottage Hospital. Registration is $150.00 (before October 26) RSVP online at cottagehealth.org/stb