Stroke Awareness and Health Fair

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Stroke Warning Signs:

  • Sudden numbness or weakness of the face, arm, or leg, especially on one side
  • Confusion, trouble speaking or understanding
  • Partial loss of vision in one or both eyes
  • Difficulty in walking, dizziness, loss of balance or coordination
  • Sudden, severe headaches

Tom Chivington was sorting some paperwork when he suddenly felt dizzy. A former college tennis coach, he considered himself in excellent health. He and his wife, Georgie, were both sports enthusiasts and avid travelers. Because he had seen a doctor about the same sensations just five days earlier, Chivington knew just what to do: He called 911.

“I had a stroke. The first time was a warning sign. When I felt the same symptoms the second time, I knew to call 911 and get to the hospital right away,” said Chivington, 70, who three years later shows no symptoms of his stroke. Chivington shared his experience at the annual Stroke Awareness and Health Fair in late May, a half-day community education program sponsored by the Stanford Stroke Center. The program included presentations from Stanford stroke specialists on prevention, treatment and rehabilitation.

The message was clear: Stroke can happen to anyone.

Timing is Everything
A stroke occurs when a blood vessel carrying oxygen to the brain suddenly bursts or becomes blocked, explained Anna Finley Caulfield, MD, a clinical assistant professor of neurology. Ischemic stroke, the more common of the two types of stroke, is caused by blockage of an artery in the brain. Hemorrhagic stroke occurs when a blood vessel breaks and leaks blood in or around the brain. Strokes can cause paralysis, language disturbances, coordination or balance difficulties, confusion or sensory loss.

But a rapid response can make all the difference, said JJ Baumann, RN, MS. The symptoms of a stroke manifest suddenly, so it’s crucial to act quickly. “You have about three hours to recognize what’s happening, get to a hospital, get a CT, and get drug treatment,” she said. “That’s a lot to happen in a short time. Most people just don’t get to the hospital fast enough, so it’s important to know the signs and call 911.”

Baumann said that only 50 percent of stroke patients call 911 and arrive at the hospital via ambulance. If patients call 911they are able to see a physician faster because the emergency department is prepared with experts who are trained to recognize the symptoms of stroke. She suggested that family members and coworkers learn to recognize the symptoms and remember the term FAST (face-arm-speech-time).

New Options
Every second the brain survives without blood flow, damage is done. The window of opportunity after a stroke is small-treatment is most effective within three hours of the onset of signs and symptoms. But that window is expanding.

“The reality is that not everyone can make it to the emergency room during that ‘golden window,’” said Greg Albers, MD, director of the Stroke Center and the Coyote Foundation professor of neurology.

Albers, an internationally recognized stroke expert, is studying the possibility of using clot-busting medications such as tissue plasminogen activator (tPA) up to six hours after the onset of certain kinds of stroke.

He also described promising breakthroughs in mechanical technologies, including a new clot retriever system called Penumbra, which was approved by the FDA in January 2008.  It uses a suction device that can remove a clot in less than 20 seconds. Another corkscrew-like device called the MERCI (mechanical embolus removal in cerebral ischemia) retrieval system, made up of a wire that is threaded up through an artery to the site of the blockage and retrieves the clot. Studies show that about 50 percent of patients benefit from this system up to eight hours after the onset of a stroke

“The technology is improving rapidly, and we have some new, positive options,” said Albers. “But we need to know what’s going on in the brain before we act so we can identify the patients who will have good outcomes after the three-hour window.”

Preventive Measures
While certain risk factors for stroke-age, gender, race, genetics-cannot be controlled, most people can take active measures to prevent its occurrence, said Neil Schwartz, MD, PhD, a clinical assistant professor of neurology. “There are modifiable factors that play an important part in stroke onset,” he said, “and there are multiple ways to control high blood pressure, cholesterol, smoking, inactivity and obesity.”

Schwartz described several studies that tracked the effects of drugs and behavior modification on preventing stroke. One study showed that stroke patients who used atorvastatin, a drug used to lower cholesterol, were 16 percent less likely to have another stroke; another demonstrated the direct effect of lowering high blood pressure on stroke occurrence. Other trials continue to track the benefits of preventive medication.

“It important that patients get involved in clinical trials to help us learn more about what works and what doesn’t” he said.

Recovery and Rehabilitation
Stroke is the No. 1 cause of disability in the U.S. Regaining and improving function after a stroke is of primary importance to restore independence and to enhance quality of life.

“Rehabilitation is about retraining the person. The patient needs to learn to utilize remaining function in a way that won’t develop into poor movement or behavior,” said Jeffrey Teraoka, MD, a clinical associate professor of orthopedic surgery, who discussed new interventions that range from drug therapy to virtual reality.

Patients often benefit from devices such as a supported gait harness, which helps patients focus on movement mechanics by holding their weight, somewhat like a baby jumper swing. He described animal studies using cognitive stimulants, like adrenaline enhance dopamine, that appear to enhance recovery. Today rehabilitation also includes virtual reality games, which are easy, accessible and safe, and provide positive reinforcement that can reduce the monotony of traditional therapy.

“Rehabilitation is designed to maximize function,” said Teraoka. “Be cautious what you invest in. Your treatment requires diligence, creativity and patience.”

For Tom Chivington, recovery was as much about outlook as action.

“I remember lying there and thinking, ‘Why me?’ and ‘Do I really want to live like this?’ Dr. Albers leaned down and said to me, ‘You know you can recover from this.’ I realized then the importance of attitude. That, and the support of friends.”

About the Stanford Stroke Center
The Stanford Stroke Center was one of the first centers of its kind in the United States and was one of the first to be designated a primary stroke center by The Joint Commission, a not-for-profit organization that accredits more than 15,000 health care organizations in the U.S. Stanford was the 15th hospital and the second academic hospital in the country to be stroke certified, an acknowledgment of its excellence in stroke care.

The Center incorporates a multidisciplinary approach to stroke care. It’s staffed 24 hours a day with neurologists, neurosurgeons, radiologists and rehabilitation experts, who use the latest technology when patients come in with signs or symptoms of stroke. In addition to utilizing cutting-edge technology for emergency stroke care, the Center is involved in studies to improve existing therapies and to develop new techniques for treating, diagnosing and preventing stroke.

Stroke Statistics

  • About 700,000 Americans suffer from a stroke each year-that’s someone every 45 seconds.
  • Twice as many women die from a stroke than from breast cancer
  • The incidence of stroke rises dramatically with age; the risk doubles for each decade after age 55.
  • About 5 percent of people over age 65 have had at least one stroke.
  • High blood pressure is a factor in 70 percent of all strokes.

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Updates on Dementia: Translating Research into Practice

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At a Glance:

  • Alzheimer’s disease is not just one disorder with one specific set of symptoms
  • Studies show other disorders, such as frontotemporal dementia and mild cognitive impairment, show similar symptoms but affect different parts of the brain than Alzheimer’s
  • Research is leading to new understanding of cognitive decline, which in turn may identify new targets for therapy and possible prevention

Dementia is a brain disorder that seriously affects a person’s ability to carry out daily activities. The most common form of dementia among older people is Alzheimer’s disease, which initially involves the parts of the brain that control thought, memory and language. As more and more of the brain is affected, areas that control basic life functions, like swallowing and breathing, become irreversibly damaged.

Although scientists are learning more every day, they still do not know what causes Alzheimer’s, and there is no cure. New understanding, improved treatments and viable preventive strategies are becoming ever more crucial: Increasing numbers of people are joining the more than 5 million Americans already living with Alzheimer’s disease, and its prevalence is expected to double by 2020.

More than 400 physicians, nurses, social service workers, caregivers and community members attended the 10th annual Updates on Dementia: Translating Research into Practice, a conference held at Stanford in early June that featured experts in clinical research and elder care who covered topics that included sexuality, bathing and hygiene, ethnic and cultural sensitivity, and gay and lesbian issues. The event was moderated by Victor Henderson, MD, MS, a professor of Health Research and Policy and a member of the Stanford Center on Longevity.

Transition Phase
“It’s a burgeoning crisis, and if we don’t do anything about it the population curves indicate that tens of millions of people will have it over the next 20 to 30 years,” said Ronald Petersen, MD, PhD, director of the Mayo Clinic Alzheimer’s Disease Research Center, who spoke on Mild Cognitive Impairment: The Current Status. “If we are to have an impact on Alzheimer’s disease, we will need to prevent the whole process. This will require predictive testing before symptoms develop and interventions to slow its progression.”

Petersen’s presentation focused on mild cognitive impairment (MCI), a transitional period between normal function and the onset of Alzheimer’s. This condition does not fit the criteria for dementia because although patients show diminished memory and judgment, most abilities are preserved and normal activities are maintained. The challenge, he said, is that there are no specific tests, and the indices, such as verbal recall, fall into the expected profiles of aging.

Mild cognitive impairment falls into two patterns, he said. Approximately 10 percent of the people with amnesiac MCI, in which memory is affected, develop Alzheimer’s disease, while only 1 to 2 percent of the patients with non-amnesiac MCI-those with no memory impairment but with cognitive complaints-do not go on to acquire the disease.

“We have been tracking patterns of impairment over the years,” Petersen said. “We can measure the degree of shrinkage in the hippocampus. The volume of the brain shows a greater degree of atrophy in amnesiac MCI. By documenting serial progression using magnetic resonance imaging, we may be able to use and track disease-modifying therapies.”

Petersen also discussed the potential of using biomarkers, including proteins such as amyloids and apo-E, to study the patterns of impairment.

“Is MCI just early Alzheimer’s? Not always, and it’s still too soon to be sure of the connections,” he said. “Our future progress will depend on getting a diagnosis earlier so we can figure out ways to intervene or at least delay onset or prolong the transitional stage. There are lots of variabilities in the studies and, in the meantime, we must reassess the criteria.”

Molecular Connections
Research is showing that Alzheimer’s is just one disease related to cognitive decline, according to Bruce Miller, MD, director of the Memory and Aging Center at UCSF, who spoke on Frontotemporal Dementia and Other Non-AD Dementia.

Frontotemporal dementia (FTD) refers to a group of diseases that are commonly misdiagnosed as Alzheimer’s-an important distinction because these diseases are treated differently. Patients with FTD have different behaviors early on that appear to last longer.

The symptoms of FTD include apathy, indifference, repetitive mannerisms and addictive behavior, such as gambling and overeating. These behaviors affect a different part of the brain, making it relatively easy to separate FTD from Alzheimer’s. At the same time, FTD is a social disorder, and input from caregivers is important because its victims have poor self perception. People who are misdiagnosed can end up in the legal system, under psychiatric care or as social pariahs.

“It’s not so much how we label the disease as much as knowing what molecule is responsible,” he said. “These are not pure disorders. They have mixed pathologies, which means that people are starting to think of new ways to intervene. Lots of problems are neurochemical, so I think this is a very promising period.”

Many cognitive disorders relate closely to other disorders: For example, Parkinson’s puts people at high risk for dementia but not necessarily Alzheimer’s, and most Alzheimer’s patients eventually develop symptoms similar to Parkinson’s. And 65 percent of patients with REM (rapid eye movement) sleep behavior disorder, in which the motor system is not turned off during deep sleep, develop some kind of Parkinsonian disorder. These connections all point to potential points of intervention, Miller said.

“The circuitry in the brain is breaking down, but it is the part that affects social behavior and regulation rather than memory,” said Miller. “It’s a social disorder. There is no amyloid accumulation in the brain as you would see in Alzheimer’s disease. This is important because it requires different interventions and the need to monitor and evaluate therapies.”

Other speakers during the day-long conference discussed Love, Sex and Alzheimer’s; Caring for Someone with Dementia when you are Lesbian, Gay, Bisexual or Transsexual; and Bathing Without a Battle. Handouts offered lists of local and national resources, and descriptions of Alzheimer-related clinical trials.

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The Humbling History of Multiple Sclerosis

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MRI snapshotPresented by: Jeffrey Dunn, MD
Associate Director, Stanford Multiple Sclerosis Center

Lecture Overview:

  • The symptoms of multiple sclerosis have been described since the 1300s, but it wasn’t until the early 20th century that a unified picture emerged
  • The biggest breakthroughs in understanding and treating MS have taken place when researchers and physicians work together
  • While excellent therapies currently exist, advanced imaging and technologies like proteomics are leading to the promise of more targeted and effective treatments

In the late 1300s outside Rotterdam, a young woman suddenly collapsed, suffering limb weakness, face pain and vision problems. Her symptoms were well documented as her health deteriorated, and she was later canonized as St. Lidwina, the patron saint of ice skating. She also appears to have been the first documented case of multiple sclerosis-a theory substantiated when her body was exhumed for study 650 years later.

Augustus d’Este, an illegitimate son of King George III, kept a detailed journal for more than 20 years that documented his health problems, even though, in 1822, no one yet knew what condition he had. He described his symptoms so clearly that later researchers were able to definitively diagnose him as having multiple sclerosis.

“Over the years, individual cases of MS have been reported in great detail,” said Jeffrey Dunn, MD, co-director of the Stanford Multiple Sclerosis Center, who discussed the past, present and future of MS at a presentation sponsored by The Health Library on May 15. “But it wasn’t until physicians and researchers started to compare notes and share experiences that a unified view of multiple sclerosis emerged.”

That first cohesive perspective of MS-one that connected the symptoms with anatomical changes-was introduced in 1869 by Jean-Martin Charcot, who is considered the father of modern neurology. He meticulously tracked the symptoms of one of the patients in the Paris hospital where he worked and taught. The autopsy of her brain revealed hard nodules, which he called sclerosis of plaques.

Additional reports throughout the 1800s described “strange cases” of this new disease, but it was considered rare, a perception that changed dramatically: By 1950, neurologists considered MS one of the most common neurological diseases in America.

“It’s important to look forward because the future of multiple sclerosis is one of hope,” said Dunn. “But we can understand the future better by looking at the past.”

MS appears to be more common among people of Northern European descent, although it is becoming more common in people with Latino backgrounds. While factors such as fat in the diet, industrial development, toxic exposure, vitamin D and viral exposure have all been attributed to inducing MS, its probable cause is most likely a combination of genetic and environmental factors, said Dunn

“No two cases are alike, which is one of the most challenging aspects of MS, but most cases present in a certain way,” he said. “Monthly MRIs show MS progression and plaques as white spots that show up and then disappear, like fireflies. Symptoms relapse in about 85 percent of cases, and the disease does tend to slow down over time. But MS is not only different in each patient; it changes over time even within an individual in many cases. Even more problematically, there are no biomarkers for the disease and no metrics for disability.”

Physicians learned to recognize MS because of improved technologies, such as magnetic resonance imaging (MRI), and because there were more neurologists with the skills to make the difficult diagnosis. Today there are six FDA-approved treatments for MS, and despite the challenges from new limitations on using placebos in clinical trials, Dunn said there are almost 70 new therapies in various stages of trials, many of which will be tested at Stanford.

Dunn explained the strategies and the trial-and-error studies behind several of the current therapies, some of which were originally designed as chemotherapies, treatments for other diseases and even carpet dye.

“The biggest advances in discovery take place when clinical care and research are combined together and allowed to interface,” said Dunn. “New technology like advanced microscopic techniques and proteomics, which maps proteins, gives us the chance to translate discoveries to humans and positions us to find specific therapies.”

About the Multiple Sclerosis Center at Stanford Hospital & Clinics

The Multiple Sclerosis Center provides comprehensive, specialty care, using state-of-the-art techniques to diagnose, evaluate, manage and treat adult patients with MS. Its team of neurologists offers particular expertise in diagnostic and treatment challenges, combining individualized care with promising clinical research opportunities. One of only two dedicated MS centers in the Bay Area, its physicians and staff offer a unique depth of knowledge for MS patients.

The Center provides:

  • comprehensive patient care
  • neurological tests and assessments
  • access to clinical trials
  • state-of-the-art technologies, including MRI and electrodiagnostics
  • a localized clinical immunology infusion service
  • information on new treatments and current research
  • recommendations for follow-up services

The Multiple Sclerosis Center is located on the third floor of the Boswell Building of Stanford Hospital & Clinics in the Neuroscience Clinic, Room A301.

Hours are 8:30 am-5 pm Monday-Friday.

Tel: 650-723-6469

About the Speaker
Dr. Dunn is the associate director of Stanford’s Multiple Sclerosis Center and an associate professor of neurology and neurological sciences. He is a board-certified neurologist specializing in the diagnosis, treatment and clinical research of multiple sclerosis and demyelinating disease.

With a focus on clinical care, he also conducts research on combination therapy and emerging immunotherapy and has worked as a principal investigator for clinical research studies sponsored by the NIH and other organizations. Dr. Dunn served as president and chief medical officer of the “MS Hub,” a novel regional care center at Evergreen Healthcare in Kirkland, Washington, before joining Stanford in early 2008.

Dr. Dunn earned his MD from Temple University and did his specialty training in neurology at the University of Washington.

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Alzheimer’s and Communication

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Presented by: Judith L. London, PhD
Licensed Clinical Psychologist
Author, Connecting the Dots
February 24, 2010

Lecture Overview:

More than 5 million Americans are living with Alzheimer’s disease (AD), a long-term progressive disease that affects memory, intellectual ability, judgment, and behavior, depriving people of their independence and ability to communicate. Alzheimer’s accounts for 70 percent of all types of dementia, and more than half of these cases are in the middle to late stages, when individuals require extensive help with daily activities and lose the ability to respond to their environment.

There’s no known cause of AD, a slow but irreversible mental decline that lasts an average of seven years but that can linger for as long as 20. People in mid- to late-stage Alzheimer’s can no longer survive in society without an extensive support system.

“So many people mistakenly assume that there’s nothing left as the disease advances, and don’t bother trying to connect and communicate on a meaningful level,” said Judith London, PhD, a clinical psychologist specializing in dementia, who spoke at a presentation sponsored by the Stanford Health Library. “But when you focus on what’s still there rather than what’s gone and reach out, you discover the part that’s still there and very much alive.”

London, who worked extensively in public long-term health facilities, described how Alzheimer’s precipitates damage to the neurons in the brain, preventing cells from communicating with each other.

“You can help ‘connect the dots’ of scattered information and memories in a meaningful way. You become the connector, and help the person express him or herself,” she said.

Because Alzheimer’s patients often feel isolated, it’s up to the visitor or caregiver to initiate interactions. The easiest first step, London advised, is to make eye contact: Get into their field of vision and say who you are. “Start with a smile,” London advised, “and approach the person as you would want to be treated-with respect, kindness, and dignity.”

Make sure you can be seen and heard: Speak slowly and clearly, and use gestures, she said, and use anything you know about the person’s interest or background as a basis to communicate. Use the person’s name, not a nickname or term of endearment, to help validate their identity.

“They also often have poor vision and hearing, which adds to their sense of isolation,” said London. “Don’t assume they are no longer interested in engaging.”

She also suggested that instead of using distraction when people are repeating themselves to try to help them express what’s on their mind. “They are reacting to something that is emotionally important to them,” she said. “Be positive about their efforts to make a connection and communicate.”

London suggested that visitors carefully observe the immediate circumstances to find possible triggers for episodes of depression, paranoia, or anger. If you can identify a pattern by examining what happened right before, during, and after an incident, the time it occurred, and who else was involved, you may be able to alter the circumstances to head off an outburst. She advised caregivers to not take accusations personally.

In group therapy with dementia patients, London found that that people responded to personal questions and empathy even when they seldom initiated a dialog.

“Unconscious memory is still present in those with Alzheimer’s and is the last part of memory to go. People with late-stage Alzheimer’s can understand even when they cannot let you know in a direct way,” London said. “When you reach out to connect and communicate, the person will connect back with you.”

About the Speaker
Judith London, PhD, is a clinical psychologist licensed in New York and California who has worked with patients with Alzheimer’s and other forms of dementia for more than 20 years. A former adjunct professor at New York University, she now conducts seminars on Alzheimer’s, dementia, and maintaining brain health. She is the author of Connecting the Dots: Breakthroughs in Communication as Alzheimer’s Advances.

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How is Your Memory? Evaluating Memory and Its Relationship to Alzheimer’s Disease

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Presented by: Wes Ashford, MD, PhD
Clinical Professor, Psychiatry and Behavioral Sciences (affiliated)
Senior Research Scientist, Stanford/ VA Aging Clinical Research Center
May 19, 2010

Lecture Overview:

    MRI brain scan

  • While mild forgetfulness affects most people as they age, serious memory problems affect your ability to participate in everyday activities.
  • See your doctor if you have concerns about memory and forgetfulness.
  • Alzheimer’s is a type of dementia that progresses slowly over time and causes irreversible changes in the brain.
  • Brain imaging for dementia is pointing to specific patterns of amyloid plaque and neurofibrillary fiber build-up in the brain, and these patterns appear to be associated with genetic makeup.

Dementia is a medical condition that impairs memory and thinking processes, from remembering words to how to behave. While everyone forgets words or a person’s name at times, the condition is not dementia unless it is severe enough to interfere with a person’s ability to carry out daily activities and it declines over time.

The most common form of dementia among older people is Alzheimer’s disease, which initially involves the parts of the brain that control memory, and language. The disease was first diagnosed in 1907 in a patient with what are now considered classic symptoms of the disease. Her brain had both senile plaques (filled with a protein called beta-amyloid) and neurofibrillary tangles (made up of tau protein) that affected specific regions of the brain.

The cognitive decline associated with dementia and Alzheimer’s disease is an issue not only for affected individuals but also for society. New understanding, improved treatments, and viable preventive strategies are becoming more crucial since more than 5 million Americans are already living with Alzheimer’s disease, and its prevalence is expected to double by 2020.

“The problem is that it is difficult to recognize when people have a problem,” said Wes Ashford, MD. PhD, a clinical professor of psychiatry and behavioral sciences, at a presentation sponsored by the Stanford Health Library. “People with a memory problem often try to cover it up, and as much as 90 percent of patients are misdiagnosed early in the disease course. After a certain point they don’t recognize that they have a memory problem and by then they need to be in a nursing home.”

Making Connections
Ashford has spent his career researching the process of memory loss associated with aging. He and the other members of the group at the Stanford/VA Aging Clinical Research Center are involved in a variety of studies to measure the effectiveness of medications, mood, sleep, and other factors on disease progression. He has developed a simple memory test that can help track changes over time, using colorful images to detect early signs of memory loss.

Ashford explained that the brain is constantly creating new connections among its billions of neurons as it registers new information. As dementia progresses, the brain no longer maintains this neural network, affecting first short-term memory and then older, more established connections. Brain autopsies show that the hippocampus, the part of the brain involved in forming and maintaining memories, shrinks dramatically and becomes riddled with amyloid plaques and neurofibrillary tangles.

“Plaques and tangles occur in very specific areas of the brain that are responsible for learning and storing new information,” Ashford said, adding that plaques appear to be associated with Alzheimer’s disease, while tangles show a closer relationship with the dementia that accompanies Alzheimer’s in its later phases. “The disease progresses in a variable but measurable fashion, following a specific pattern. It may progress slowly but it tracks logically, and eventually old memories become destroyed.”

Genetic Differences
By using different imaging technologies, such as MRI, PET, and CT scans, scientists have been able to follow the progression of dementia and Alzheimer’s, and found that genetic factors play a significant role the age when patients develop brain patterns associated with amyloid plaques and with neurofibrillary tangles.

“We can actually see where the tangle develops and where the amyloid is depositing,” said Ashford. “We can track progression over time while it is still considered mild cognitive impairment, before it is officially dementia.”

For one common genotype (20 percent of the population), there is a 40 percent chance of developing Alzheimer’s by age 76; another genotype (one that affects only 2 percent of the population) has 10 times greater chance of having the disease by age 67; another group appears to develop Alzheimer’s only after age 95.

For Ashford, these studies may help to measure the early progression of disease and then identify a way to prevent its development in the people who would most benefit from intervention. Though a genetic approach to prevention is not on the immediate horizon, these studies do point to the possibility of targeted interventions based on genotype.

“If we can understand the genetics better, we will be able to understand how Alzheimer’s develops and the best method and timing to make changes,” he said. “To make progress we need diagnostic and treatment centers for humans and accessible genetic testing.”

In the meantime, other factors have been shown to decrease the risk of Alzheimer’s, such as maintaining a healthy lifestyle, interacting with others through social activities, keeping the brain exercised through games and learning, and keeping up with screening tests for high blood pressure and cholesterol.

About the Speaker
J. Wesson Ashford, MD, PhD, is a senior research scientist at the Stanford/Veterans Affairs Aging Clinical Research Center and a clinical professor of Psychiatry and Behavioral Sciences at Stanford. He is also the director of the War Related Illness and Injury Study Center at the VA Palo Alto Health Care System. Ashford received his MD and his PhD in neuroscience from UCLA, where he was a founding member of the Neurobehavior Clinic and the first chief resident and associate director on the Geriatric Psychiatry Inpatient Unit. He joined Stanford and the VA Palo Alto in 2003.

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Epilepsy: A Patient Story

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Damon Weems had dreams of becoming a pilot until epilepsy consumed his life. With the determination of his barnstormer grandfather, Damon refused to give up. He believed a seizure-free life was possible.

weems1.jpgAfter a frightful cycle of multiple medication adjustments and dreaded setbacks, Damon eventually found Dr. Robert Fisher at the Stanford Epilepsy Center. “I am so grateful to be given a new life by the Stanford team. I would like to help those who have given up hope. I never dreamed it was possible to be seizure free, but finally I am,” Damon said recently.

For more than 20 years, epilepsy controlled Damon’s life. As seizures sliced through his quality of life, Damon was forced to leave his training with the Air National Guard. He grieved the loss of his career for many years, while his family and friends were increasingly scared by his regular grand mal seizures.

A self-described “adrenaline junkie,” Damon still had many goals to fulfill. This positive attitude prompted him to redouble his efforts to wrestle control of his life that epilepsy had taken. He stopped playing the guitar and piano, and could no longer travel to Bluegrass music festivals. He had tried unsuccessfully to hide his seizures and even completely re-directed his life by becoming a trial attorney. However, repeated seizures in the courtroom eventually set him back, even with understanding judges who called a recess whenever Damon had a seizure. With a family to support, life seemed to be a dangerous string of career failures, recurring car accidents, and relentless social embarrassment. Everything Damon wanted in life had been taken—everything, that is, except hope. He managed to keep his spirits up and kept looking for an answer.

Damon’s treatment at Stanford began with a medication change, a regular occurrence that people with epilepsy and their families are used to living through. “There is always a honeymoon with a new medicine,” Damon said. Although the medication gave him some relief, he still had seizures that affected every aspect of his life—he could no longer drive, his seizures were becoming even more frequent, and he was recovering after years of a failed attempt to self-medicate with alcohol. Yet, Damon refused to be slowed down. Damon had gained sufficient faith in Dr. Fisher to consider surgery—a particularly difficult decision because some years earlier he had had an unsuccessful surgery at another hospital. Epilepsy surgery involves the removal of seizure-related brain tissue without harming other delicate brain structures. It was a chance Damon was willing to take.“

In his quiet reassuring way, Dr. Fisher gave me hope there was much to explore and perhaps other things to accomplish,” Damon said. He underwent more testing to be sure of his condition prior to a second and highly successful surgery, performed by Dr. Gary Heit, a neurosurgeon no longer at Stanford. Dr. Fisher gave up his summer vacation to be with Damon. “He was not only on my side. He was at my side,” Damon says of the summer of his surgery. “I will be forever grateful.”

Today, at 61, Damon can drive, and he can play music again. He can spend time outdoors as he has always wanted. In addition he proudly helps guide the careers of his two sons, both lawyers with their father’s passion. Damon is exceedingly grateful to his wife who weathered the many storms his epilepsy brought into their life together. “She gave up nice summer vacations in order to take care of me” he says. Damon thanks Dr. Fisher and the entire Stanford team for never giving up hope and bringing him to a seizure-free life, of which he simply says, “I’ve never been this happy.”

The Masquerading Headache:Chronic Daily Migraine, Positional Headache, POTS, or Spinal Fluid Leak? Why It Hurts When You Stand Up

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Presented by: Ian Carroll, MD, MS
Assistant Professor of Anesthesiology
January 14, 2016

People who are suffering severe recurring headaches, neck pain, nausea, vomiting, dizziness, ringing in the ears, diffuse pain, fatigue, or brain fog may have a fixable condition that frequently goes unrecognized. The key to the diagnosis is recognizing that these symptoms get worse the longer the person is upright.

For some patients symptoms are rapidly progressive when someone becomes upright and rapidly relieved by lying down, but for others the postural symptoms are subtle. For these patients, headache, dizziness or other symptoms may only happen or be recognizably worse late in the day. In contrast, mornings for these patients after being recumbent all night are often better than the rest of the day. Doctors often recognize the first group, but fail to properly recognize the second pattern.

Ian Carroll, MD, thinks many can be helped if they find a doctor who recognizes the cause: a cerebrospinal fluid (CSF) leak.

Spinal fluid leaks occur when there is a tear or leak of the covering called the dura that surrounds the spinal cord and the brain. The dura functions like a watertight bag holding spinal fluid that bathes and protects the spinal cord and the brain. If the dura is pierced or torn, the fluid can leak. That can lower pressure around the brain, leading to “orthostatic” headaches that occur when someone stands up or sits up.

The telltale signs are headaches, neck pain, nausea, vomiting, dizziness, ringing in the ears (tinnitus), diffuse pain, fatigue, or brain fog that are worse when standing upright or late in the day (after patients have been upright for many hours). Patients can sometimes experience weird symptoms that make them worry they have a neurologic disease such as multiple sclerosis or visual disturbances, double vision, patchy numbness or tingling in the face or limbs, unusual smells (experienced as smelling odors that others don’t), and disturbances of taste like a persistent metallic taste in the mouth. Sometimes CSF leaks come with nausea, chronic fatigue and a racing pulse called tachycardia. The headaches have left some people without relief, trying to cope with an “invisible” disability that can ruin careers and rob them of a normal life, said Dr. Carroll, an assistant professor of anesthesiology, perioperative and pain medicine.

Disabling headaches from spinal fluid leaks have been in the news recently when the head coach of the Oakland-based Warriors professional basketball team, Steve Kerr, went on medical leave for several months while he recovered from this. Dr. Carroll said he hasn’t been involved in Kerr’s medical care, but he has seen plenty of other patients struggling with similar symptoms.

Spinal fluid leaks can often occur from whiplash injuries in a car accident or other physical trauma, but surprisingly many patients cannot identify a preceding trauma. Sometimes CSF leaks result from medical procedures like surgery or a spinal tap. Most doctors do not know that spinal taps can leak chronically or that leaks can present other than as a severe headache that is completely and rapidly relieved by lying down. Some cases occur spontaneously in people who have unusual connective tissue in their bodies and don’t know it, Dr. Carroll said.

People with CSF leaks are usually misdiagnosed. They’re told they have chronic migraines, chronic fatigue syndrome, fibromyalgia, or less known conditions like Chiari malformation, Tarlov cysts or POTS (postural orthostatic tachycardia syndrome).  A positive tilt table test and autonomic testing do not rule out a CSF leak as the underlying cause of the syndrome.

Dr. Carroll developed the hunch that some headaches were caused by spinal fluid leaks after his own family experience. After his young daughter had a spinal tap to evaluate some unrelated symptoms, she started getting headaches when she wasn’t lying down. “When she sat up, she screamed in pain,” he said. After the headaches persisted, she was treated for spinal fluid leaks and got better. That got his attention.

Then he read a New York Times column written by a Yale internist, Dr. Lisa Sanders, about a young woman who had endured 3 months of intractable headaches that started after she had whiplash. She later developed dizziness when upright, and  her pulse jumped from 74 when she was lying down to 130 when sitting up.

She was diagnosed with POTS, or postural tachycardia syndrome, a condition thought to be caused by blood vessels not constricting enough to keep blood flowing to the brain when a person stands up. Dr. Carroll suspects this patient and others were misdiagnosed and more likely had a CSF leak. He then began wondering if people at Stanford were being misdiagnosed as well. One of the reasons is that spinal fluid leaks may not show up on standard medical tests.

When spinal fluid pressure is extremely low inside the skull, it can show up on standard MRI tests. But many times the pressure drop may not be enough to cause MRI findings but are still enough to cause headaches, nausea and other symptoms, Dr. Carroll said. He has seen multiple headache patients whose MRI scans looked normal, but when they were given treatment to fix a spinal fluid leak, their headaches stopped.

Most physicians are trained to rely on MRI scans to determine if spinal fluid leaks are causing headaches, so they may miss this, Dr. Carroll said. “Most doctors think they know about this problem, but what they know is wrong,” he said.

Based on the patients he has seen, he said, “Most people are not extreme leakers. A lot of leaks may be more subtle.”

Another test, called a CT myelogram, is more likely to detect leaks and more commonly see the things that leak, such as aneurysms in the dura called meningeal diverticula or perineural cysts, Dr. Carroll said. But even that doesn’t show some leaks, in his experience.

Based on the patients he has seen, Dr. Carroll outlined three major causes of tears in the dura that cause spinal fluid leaks. A major cause, already widely known, can be any medical procedure that pierces the dura. That can be spinal surgery, a spinal tap or even the epidural anesthesia that some women get in childbirth. A headache that develops the day after any of these procedures is called a “post-dural puncture headache,” or PDPH, and is caused by a single leak. In most cases, a next-day headache after any of these procedures often goes away on its own as the dura heals and the leak stops. If it doesn’t stop, a treatment called a “blood patch” can be done that seals the leak in 90 percent of cases, Dr. Carroll said.

Two other causes of headaches from spinal fluid leaks are spontaneous, Dr. Carroll said. The first is a bone spur or any bony calcification that pierces the dura. People with degenerative changes in their spine can have bulging spinal discs that calcify and can then poke through the dura to cause a leak at a single site or multiple sites, he said. CT myelograms can detect bone spurs, but some patients with unexplained headaches may not get this test or their doctor doesn’t understand the connection between an “osteophyte” (bone spur) reported from the CT myelogram of the spine and the patient’s headache or neurologic symptoms.

A third cause is having unusual connective tissue that leaves the dura thinner and more susceptible to tearing or leaking, Dr. Carroll said. This kind of connective tissue is unusually stretchy. People who have it may be unusually flexible or appear “double-jointed” compared to most.

“If you have connective tissue that’s extra stretchy and flexible, the bag that holds your fluid in is thinner and more susceptible to having a tear or leak,” Dr. Carroll said. A small whiplash injury or fall could trigger the leak without being detected. “People are wondering why you’re having all these headaches and neck pains after a car accident. They don’t go looking down in your back,” he said.

Patients with Ehlers-Danlos, Marfan syndrome, neurofibromatosis, and adult polycystic kidney disease are all known to have weaker connective tissue and be more susceptible to having undiagnosed CSF leaks. Other tipoffs that may indicate unusual connective tissue are being very tall (above 6-foot-2), having scoliosis, having many bulging discs throughout the spine, or diffuse arthritis.

People who are so hyperflexible they can bend their bodies into difficult poses for gymnastics or ballet that others can’t do may have the type of connective tissue difference linked to spinal leaks. Having cataracts earlier in life than usual—by age 40 or 50, rather than 65—can also be a tipoff for connective tissue differences.

This kind of unusual connective tissue won’t show up on an MRI, so it may go undetected and lead doctors to miss spinal fluid leaks that can occur at multiple sites in the spinal dura, Dr. Carroll said. He explained that research suggests that 30 percent to 40 percent of patients with spontaneous CSF leaks have more than one leak when they are diagnosed. This seemingly unlikely occurrence can happen because the connective tissues in these patients are inherently weaker than normal.

When a patient has a spontaneous leak the conventional treatment for a spinal-leak headache­—a blood patch on the dura—has a roughly 30 percent chance of stopping the headache with the first patch, Dr. Carroll said. If further patches don’t work, other options to fix a leak include fibrin “glue” seals or surgery to close any defects in the dura.

He is working with other physicians at Stanford and elsewhere to examine more patients with unexplained headaches that fit the profile of spinal fluid leaks: daily headaches that worsen when standing up (or late in the day), as well as nausea and dizziness. In the past 6 months, he’s found 26 people who had unexplained or misdiagnosed headaches who were helped by blood patches or other treatment for spinal fluid leaks.

He wants to find more. He urges friends and family of people suffering from unexplained chronic headaches to contact him at Stanford if they show the tipoff symptoms. If people with headaches feel much better every day in the morning after sleeping all night lying down, that’s another tipoff, Dr. Carroll said. Patients can help establish the diagnosis themselves by simply spending 24 hours lying flat.  People who are leaking will feel that day is one the best days in a long time.

“Having lives derailed by intractable headaches is a tragedy, but it is a much greater tragedy when the person has an unrecognized CSF leak that could be fixed  easily if only recognized. We can help them be back at work, and live life again more fully,” he said.

About the speaker:
Ian Carroll received his MD from Columbia University and did his internship and residency at Stanford University School of Medicine. He also received an MS in clinical epidemiology from Stanford. He is board certified in pain medicine and anesthesia by the American Board of Anesthesiology, and in addiction medicine by the American Board of Addiction Medicine. He has received research grants from the NIH, the Foundation for Anesthesia Education and Research (FAER), and Stanford University. He also received a faculty award for teaching excellence in Stanford’s pain management division. He has previously lectured on neuropathic pain for the Stanford Health Library.

About the Stanford Pain Management Center
Clinicians and researchers at the Stanford Pain Management Center have made major advances in the understanding of chronic pain as a distinct disease that fundamentally alters the nervous system. The center’s work has earned it a designation as a Center of Excellence by the American Pain Society.

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Non-Pharmalogic Treatment of Pain

Posted By SHL Librarian

Presented by: Ravi Prasad, PhD
Clinical Associate Professor of Anesthesia
February 27, 2014

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The pain that comes from hitting a finger with a hammer or touching a hot stove serves an important purpose, warning our bodies to respond to danger. But for more than 100 million adult Americans, the pain never seems to go away.

Chronic pain affects more Americans than diabetes, heart disease, and cancer combined. It is one of the largest causes of disability in the United States, costing greater than $500 billion each year in lost productivity and health care treatment.

“The purpose of pain is to act as a warning system to protect the body from harm,” said Ravi Prasad, PhD, the assistant chief of the Division of Pain Medicine, who spoke at a presentation sponsored by the Stanford Hospital Health Library. “It alerts you to react in order to avoid damage. The problem is, that is not true of all kinds of pain.”

Different Categories
There are two types of pain. Acute pain has a specific cause that can usually be resolved by following a protocol, such as taking medication or undergoing a procedure.  The pain is a direct reflection of harm. For example, a fall can lead to a fractured ankle that can be put in a cast, treated short-term with mild painkillers, and/or strengthened with physical therapy.

Chronic pain, on the other hand, does not always have a specific or identifiable origin, and the brain continues to send out pain messages even though there is no longer a stimulus for danger. “It’s a like a false alarm to the body. The pain is real, but it is not a sign of active harm. There’s no imminent threat and yet it persists with no fixed endpoint,” he said. “Many people suffer for months or even years without any evidence of ongoing physical damage.”

For most people, life is filled with multitudes of activities and interests, from family to work to hobbies. For people suffering from chronic pain, that one aspect of life starts to take over everything else and becomes the central focus.

Facets of Treatment
“Acute pain and chronic pain are two different beasts. Using acute modalities to treat chronic pain is a disservice to the patient: It can lead to false hope and disappointment when standard approaches don’t deliver results,” Dr. Prasad said. “Chronic pain needs to be perceived and treated like other chronic conditions, using similar paradigms to optimize the condition.”

Treatment for chronic conditions like diabetes, high blood pressure, or asthma involve both behavior and lifestyle modification, and patients need to incorporate all recommendations.

“It’s a matter of balance— you can’t just pick and choose the things you like or think might work. Stress and emotions have a powerful effect on chronic pain as well, so it’s not just a matter of diet or exercise or movement. Treatment involves a multifaceted approach to improve quality of life,” he said.

The first step is medical optimization, a careful analysis by a medical specialist to make sure the condition is indeed chronic and not caused by an undiagnosed disease. Options can include surgical treatment or injection therapies, or the physician also may use pharmacologic interventions by prescribing the most appropriate medication(s) at the most appropriate level. In conjunction, they usually incorporate physical reconditioning with physical therapists to offset the tendency to minimize using the painful area or to overcompensate by favoring other parts.

Like other chronic conditions, behavior and lifestyle modification are fully integrated into treatment as well. These non-pharmacologic strategies include psychological and behavior-based therapies that incorporate the mind-body connection, such as biofeedback, breathing and relaxation training, and cognitive behavioral therapy.

Mind and Body
Pain is a complicated process that involves an intricate interplay of chemicals and signals in the body’s sympathetic and parasympathetic nervous system. The process serves as an on-off switch, a feedback system of excitation and inhibition—“the “fight or flight” response. When the sympathetic nervous system activates, it raises blood pressure, heart rate, and muscle tension. The parasympathetic system brings these functions back to normal.

Because pain’s effect on the brain affects the same regions associated with basic emotions, feelings like stress or anxiety can amplify the suffering.

“Stress and pain are intrinsically connected, “said Dr. Prasad. “The nervous system’s reaction to stressors is directly involved with physiological changes. The body doesn’t discriminate between physical and emotional stressors: The physiological response pathway is the same, whether we are responding to a threatening dog or an argument with a spouse. It creates a vicious cycle.”

The challenge with chronic pain, he added, is how to break the cycle since the pain itself cannot be alleviated. One of the most successful strategies is the application of breathing exercises, focusing in deep and slow inhalations and exhalations. Deep breathing activates the parasympathetic nervous system, cueing the brain to slow things down after a stressful event. But the process requires some mental discipline and concentration for it to work.

“It’s not just a psychological trick,” he said. “It’s a physiological response. It’s also a distraction since it helps to refocus your attention away from the pain. The pain still exists, but you’re giving your body a reprieve to stop the feedback system.”

He also emphasized the benefit of cognitive restructuring to learn how to reinterpret the situation and override one’s automatic reaction to a stimulus. Thoughts control emotional, physical, and behavioral responses, so changing perspective can have a powerful impact on outcomes. The process is not easy, he warned, since automatic responses tend to develop over a lifetime, and habits are hard to break.

Studies show that cognitive restructuring helps to reduce perception of pain as well as levels of anxiety and depression, he said, and shows an improved sense of control since its users are better able to recognize their triggers for pain episodes.

“It’s not as simple as, ‘Think positive,’ but there are ways to break the cycle by targeting your thoughts and asking some fundamental questions about their usefulness. Ask, ‘Is this helpful?’ or ‘Is this accurate?’ It can eventually lead to a different set of automatic thoughts,” he said. “The pain is still there but it may reduce the loop of activation.”

About the Speaker
Ravi Prasad, PhD, is a clinical associate professor of anesthesiology, perioperative, and pain medicine, assistant chief of the Division of Pain Medicine, and director of the Stanford Comprehensive Interdisciplinary Pain Program. He received his PhD from Texas Tech University and completed his internship at Salt Lake City Veterans Affairs Medical Center in Utah and his fellowship at Kaiser Permanente in San Francisco.

About the Stanford Pain Management Center
The Stanford Pain Management Center is an integrated, comprehensive program that treats more than 12,000 patients a year.. A team of anesthesiologists, physiatrists, neurologists, psychologists, nurses, and physical therapists assess each patient’s type and degree of pain, and develop personalized treatment plans. The Center is one of only a few institutions in the country that have received consecutive Center of Excellence awards from the American Pain Society.

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Update on Stroke

Posted By SHL Librarian

Presented by: Greg Albers, MD
Director, Stanford Stroke Center
May 15, 2014

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About 780,000 Americans suffer from a stroke each year—someone every 45 seconds. It’s the fourth leading cause of death in the U.S. but the greatest cause of long-term disability. Most people do not die from a stroke but its effects cause more than half of all neurologic hospitalizations. The direct and indirect costs from lost work and lost productivity are enormous.

Though it can occur at any age, the risk of stroke doubles for each decade after age 55, and the aging Baby Boomer population is expanding the number of the most susceptible people.

“Stroke is incredibly common,” said Greg Albers, MD, director of the Stanford Stroke Center and the Coyote Foundation Professor of Neurology, who spoke at a presentation sponsored by the Stanford Hospital Health Library. “Almost everybody’s lives have been touched by stroke in one way or another.”

Stroke is defined as a brain injury that occurs from an abrupt disruption of blood flow to the brain. Ischemic stroke, the more common of the two types of stroke, is caused by a clot that blocks an artery in the brain. Hemorrhagic stroke occurs when a blood vessel breaks and leaks blood in or around the brain. Strokes can cause paralysis, language disturbances, coordination or balance difficulties, confusion, or vision loss.

Types of Stroke
An ischemic stroke occurs when a blood vessel becomes blocked with cholesterol deposits, a condition known as atherosclerosis. A thrombotic stroke is caused by a clot that forms inside a blocked blood vessel in the brain; an embolic stroke is caused by a clot that forms elsewhere in the body and travels toward the brain until it becomes lodged in a narrow artery. Since there’s no bleeding, ischemic strokes typically doesn’t hurt and many occurs during sleep therefore the exact time of onset is unclear. About 85 percent of strokes are ischemic and 15 percent are caused by hemorrhage.

The less common hemorrhagic stroke usually stems from years of hypertension (high blood pressure) that eventually causes blood vessel walls inside the brain to weaken and rupture.

“A blocked artery and a ruptured artery are two very different problems that require different solutions,” said Dr. Albers.

Vessel Network
Two carotid arteries supply blood to the front of the brain, and two vertebral arteries supply blood to the back of the brain. A loop of arteries at the base of the brain, called the Circle of Willis, helps determine how well the brain can compensate for a blocked vessel. Some people have a genetic advantage in which a complete Circle of Willis can provide a protective back-up system to compensate for a blocked vessel. The system is made less efficient by smoking or unhealthy lifestyle habits.

The junctions where these arteries come together at the Circle of Willis may develop weak spots that can balloon out, creating sacs called aneurysms that can leak or rupture.

About 25 percent of ischemic strokes occur because of atherosclerosis in the large vessels in the neck. About 20 percent are caused by a heart embolism, and another 20 percent stem from small vessel atherosclerosis in the brain. About one third are undetermined, creating a diagnostic and treatment challenge for stroke specialists.

Location, Location, Location
The symptoms of stroke depend on which vessel is blocked. A stroke in the anterior parts of the brain will often cause numbness, weakness, and partial vision loss. In the left hemisphere  it will typically cause language or speech problems; in the right side it can cause a condition called neglect, in which the person is unaware of his or her neurologic deficits. A stroke in the left hemisphere will affect the right side of the body, and vice versa. A stroke in the posterior part of the brain can lead to bilateral weakness, vertigo, double vision, or blindness.

Behavioral risk factors include smoking, alcohol abuse, diet, and inactivity. Contributing physiological factors include high blood pressure, high cholesterol, atrial fibrillation, diabetes, and prior stroke or a TIA.

A transient ischemic attack, or TIA, is a clot in the brain that dissolves before it has done any damage. A TIA does not cause disability, but the risk of a significant stroke within the next 48 hours is about 5 percent and a warning of more potential trouble ahead.

Control Factors
“Controlling high blood pressure is our most powerful tool for controlling stroke,” Dr. Albers said. “In general, the lower, the better”. Controlling blood pressure can reduce the risk of stroke by 30 to 40 percent.”

Multiple studies have shown that statins reduce risk of stroke in patients with coronary artery disease and high cholesterol. Dr. Albers cited the SPARCL study that found that a high dose of a statin medication reduced the risk of stroke and was well tolerated, with side effects (such as muscle aches) comparable to that of the placebo group.

Studies also have shown that quitting smoking can reduce risk by almost 50 percent within one year, and controlling cholesterol levels can decrease risk by about 20 percent. Dr. Albers suggested that for patients with atherosclerosis, LDL cholesterol (the “bad” cholesterol) should be lowered to below 80 to100 mg/dL.

After the cause of a stroke is determined, different medications are prescribed based on the type of stroke. For most patients with an ischemic stroke, regular use of an antiplatelet agent such as aspirin or clopidogrel (Plavix) can help prevent blood clots from forming. If atrial fibrillation is the cause, anticoagulants, such as warfarin (Coumadin), are typically prescribed.

New Options
While the FDA has approved the use of a clot-busting medication called tissue plasminogen activator (tPA) for up to three hours after a stroke, many people do not recognize the symptoms and do not make it to the emergency room in time. Dr. Albers and his Stroke Center associates typically give tPA up to 4.5 hours after the onset of certain kinds of stroke.

“The reality is that not everyone can make it to the emergency room during that ‘golden window,’” he said. “There’s only a small window of opportunity, so if you think you are experiencing a stroke, call 911 and go the emergency room immediately. You need to act quickly because we need to take some images and do some tests before starting treatment, and that takes time.”

About the Stanford Stroke Center
The Stanford Stroke Center was one of the first centers of its kind in the United States and was the first to be designated a comprehensive stroke center by The Joint Commission, a not-for-profit organization that accredits more than 15,000 health care organizations in the U.S.

The Center incorporates a multidisciplinary approach to stroke care. It’s staffed 24 hours a day with neurologists, neurosurgeons, radiologists, and rehabilitation experts, who use the latest technology when patients come in with signs or symptoms of stroke. In addition to utilizing cutting-edge technology for emergency stroke care, the Center is involved in studies to improve existing therapies and to develop new techniques for treating, diagnosing, and preventing stroke.

About the Speaker
Gregory Albers, MD is director of the Stanford Stroke Center and the Coyote Foundation Professor of Neurology and Neurological Sciences. A nationally known stroke expert, his research and clinical work focuses on the treatment and prevention of cerebrovascular disorders and the use of diffusion and perfusion MRI to expand the treatment window for ischemic stroke. Dr. Albers received his MD from University of California, San Diego, School of Medicine and did his internship, residency and stroke fellowship at Stanford. He is Board Certified in Neurology and in Vascular Neurology by the American Board of Psychiatry and Neurology.

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Advances in Surgical and Nonsurgical Treatment of Brain Tumors

Posted By SHL Librarian

Presented by: Steven D. Chang, MD
Professor, Neurosurgery
Stanford University Medical Center

October 30, 2014

There is a delicate balance when it comes to treating brain tumors. How do you effectively destroy the cancer cells while avoiding damage to the nearby normal cells? How can you operate on such a complex organ without causing neurological problems?

The answer lies in new tools and technologies that involve less invasive procedures that use computers and robotics, and more refined use of radiologic imaging, said Steven D. Chang, MD, a professor of neurosurgery, who spoke at a presentation sponsored by the Stanford Health Library. The optimal strategy depends on the individual and the type of brain cancer that needs to be treated, and is individualized for each patient.

Glioblastoma, for example, is an extremely aggressive form of brain cancer that affects more than 15,000 people each year. These tumors are highly malignant, and because the cells reproduce quickly patients usually survive only a few months without treatment.

Surgical Procedures
In the past, glioblastoma was treated solely with basic surgical techniques. Today an innovation known as an interoperative MRI scanner (iMRI) allows a surgeon to conduct an imaging scan while the patient is still in the operating room to ensure that all visible cancerous cells have been removed. The OR team can access the MRI images during the procedure without having to move the patient out of the operating room.  This process maximizes the chance of removing as much tumor as possible and improves patient outcome.

The system can be set up in several ways, with the imaging instruments on a sliding mechanism on the ceiling, in an adjacent room, or integrated into the operating room bed. “We can take a picture of the skull to see if we have done the best job possible,” Dr. Chang said. “It’s a powerful tool to have available.”

A recent study of 44 glioblastoma patients found that almost half had a residual tumor after the surgeon thought the procedure was complete. The iMRI allows the surgeon to continue to resect the tumor after the scan for the complete removal of all radiographically visible cancer cells before the skull is closed up.

Another advanced surgical strategy is an awake craniotomy, in which language function directly tested during the procedure by having the patient speak to the surgical team during the tumor resection. This procedure is used when the tumor lies close to the language center of the brain as a way to preserve speech. The patient is sedated without a general anesthesia for initial comfort and then awakened once the brain is exposed.

Since the brain has no pain receptors, there is no discomfort during the actual surgery. The neurosurgeon is able to map the brain’s speech areas as the patient speaks and interacts. If speech is affected during the electrical stimulation and mapping that area of the brain is marked and preserved. This approach is especially useful since many tumors look like normal brain tissue, said Dr. Chang.

Diffusion tensor imaging (DTI) is a type of magnetic resonance imaging that maps the internal structure of the brain. The brain’s neurons are intrinsically interconnected like the branches of a major highway. DTI creates a complex and detailed map of the white matter tracts, which are the internal neurological pathways of the brain. The resulting image shows where the neurons intersect so the surgeon can avoid critical areas.

Dr. Chang showed an image of a tumor that abutted the neurological pathways involved in motor function; DTI enabled the team to plan the surgical approach in a direction that avoided these crucial nerve tracts. In another example, DTI was used to identify and avoid the neural tracks in the back of the brain essential to vision, preserving the patient’s sight.

Another useful technique is a functional MRI (fMRI), which depicts the patterns of activity and creates detailed maps that show which parts of the brain are involved in a particular neurologic process. During the MRI scan, the patient performs a series of tasks, such as speaking, answering questions, and moving the hands to activate the parts of the brain involved in motor, speech reception, and expressive function. The MRI shows the patterns of activation so critical function can be spared while removing the tumor. This powerful tool is especially helpful for patients who have had a previous injury or for those who are bilingual since the site of activity may be moved from its normal location.

Noninvasive Procedures
The CyberKnife is a robotic radiosurgery system that delivers beams of high-dose radiation with extreme accuracy to treat tumors. It combines computerized imaging with radiation therapy from a linear accelerator to precisely deliver radiation in the three-dimensional pattern of a tumor.

This noninvasive technology is used as an outpatient procedure so patients are back to work or school almost immediately. It is also often more cost-effective compared to surgery or traditional radiotherapy and does not interfere with other treatments such as chemotherapy.

“It is extremely precise and can be used to treat inaccessible tumors,” said Dr. Chang. “It can be used as an alternative to conventional surgery or radiation therapy, and in conjunction with these strategies as part of a multimodality treatment plan.”

The CyberKnife, which was invented by Stanford neurosurgeon Dr John Adler, incorporates a robotic delivery system that can deliver images in real time, which means it can accommodate a patient’s movements during treatment. Multiple radiation beams are used, with each beam focused on the target for an accrued impact. Originally designed to treat brain tumors, it is now used for prostate, pancreas, spine, lungs, and liver. More than 7,000 patients have been treated with the two CyberKnifes at Stanford.

This type of radiosurgery is also an important tool for peri-optic tumors, which are difficult to treat because of their location so close to the optic nerve. Studies have shown that vision is preserved—and in some cases improved—after treatment with the CyberKnife. A similar challenge is addressed with acoustic neuromas, which are accessible for surgery but located right alongside the hearing nerve.

Dr. Chang said that these advances are due in large part because Stanford’s experienced neurosurgeons work as a team with specialists in radiology, pathology, oncology, radiation oncology, and other professionals to improve outcomes and quality of life for people with brain cancer.

About the Speaker
Steven D. Chang, MD, is the Robert C. and Jeannette Powell Professor in the Neurosciences, director of the Stanford Neurogenetics Program and the Stanford Neuromolecular Innovation Program, and co-director of the Stanford Cyberknife Program. A noted expert in radiosurgery technology, Dr. Chang is at the forefront of refining new strategies for using radiation to treat brain cancer. He received his MD and completed his internship, residency, and fellowship at Stanford. He is board certified by the American Board of Neurological Surgery.

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