Brain imaging in Parkinson’s disease

Traditional brain imaging with CT and MRI scans do not show changes in the brain when someone has Parkinson’s disease and are generally not helpful in diagnosis.  A new kind of brain scan, called a DaT scan, does show changes in persons with Parkinson’s disease and may someday become an important tool in diagnosing Parkinson’s.

The dopamine transporter, or DaT, scan uses a chemical that labels the dopamine transporter in the area of the brain known as the striatum. Dopamine is a neurochemical that is decreased in persons with Parkinson’s disease.

The dopamine transporter, which moves dopamine in and out of cells, is also decreased in the striatum in persons with Parkinson’s disease and related disorders. The chemical that labels the transporter is injected into the vein and can be imaged by using something called single photon emission computerized tomography, or SPECT scanning. This technique has been registered in the European Union since 2000 for differentiating a diagnosis of essential tremor and a parkinsonian syndrome. It was approved by the Food and Drug Administration in 2011 for this same indication and recently became available at the OHSU Brain Institute.

There are a number of things that are important to know about DaT scanning. DaT scans are not able to distinguish between idiopathic Parkinson’s disease (typical Parkinson’s disease) and the syndromes known as atypical parkinsonian syndromes. These include progressive supranuclear palsy, multiple system atrophy, and cortical basal degeneration. There also can be some uncertainty in the interpretation of scans. In one fairly large study, even after DaT scanning, about 10 percent of persons had not received a clear diagnosis or there was disagreement between the scan and the physician’s diagnosis. The data we have at this time indicate a diagnosis made by a clinician based on an exam, or a radiologist based on a DaT scan, is about as likely to be correct or incorrect. Neither is perfect.

DaT scans may become a critical tool is assisting in the diagnosis of Parkinson’s disease and related disorders. However, at this point, Parkinson’s disease is still something a physician, ideally a neurologist, must diagnosis. For classic cases of Parkinson’s disease, it is unlikely that most neurologists would order a DaT scan as they would feel confident in the diagnosis.

It is again important to state that the DaT scan is not going to be helpful in differentiating Parkinson’s disease from the related atypical parkisnonian syndromes. Still, if you are curious if a DaT scan may be appropriate for you, it is best to talk with your neurologist and discuss the pluses and minuses of pursuing this testing.

Amie Peterson, M.D.
Assistant Professor of Neurology
OHSU Parkinson Center of Oregon
OHSU Brain Institute

OHSU Brain Institute experts at the cutting edge of treating stroke

With stroke, time is brain. When people suffer strokes, they need certain medical treatments within a limited amount of time, or their brains can be so damaged that they will have permanent disabilities.

That’s why the OHSU Telemedicine Network is so vital in stroke treatment for hundreds of thousands of rural Oregonians. The network allows experts with the Oregon Stroke Center at the OHSU Brain Institute to use a two-way audio-video robot to collaborate with physicians at hospitals throughout Oregon seeing patients who might have suffered strokes. The network allows the OHSU stroke experts to quickly assess a patient’s condition through the audio-video link and prescribe immediate treatments if they are needed.

Read more about it at OHSU’s 96K blog.

New technology also is allowing doctors to see inside the brains of stroke victims in new ways — and help patients completely recover from stroke in cases where a full recovery would have been impossible before.

The technology allows stroke experts to see which parts of the brain have been too injured by the stroke to save, and which parts were affected by low blood flow but can be saved if treated immediately. You can also read more about this life-changing technology at the 96K blog.

The surgery that changed my life: controlling the seizures

Leigh with her mom Leslie

Seventeen-years old, waking up on a Sunday morning wondering who I was, where I was, and how I became that way. That was the first time memory loss had become part of my life.

However, it was not the first time I had been overcome by confusion. In fact, that cycle began at age four — on the night I had my first epileptic seizure.

Epilepsy is a neurological condition that produces seizures affecting one’s mental and physical functions. The night my epilepsy began, I was sleeping in my room when my parents heard me breathing rather oddly. When they went to check on me, my eyes were rolled back, I was smacking my lips, and my body was limp. When I woke up, I was in the hospital.

All my life, I have taken medicine to control my seizures. Between the ages of 4 and 12, I would have grand mal or tonic clonic seizures, which would occur a couple times each year. As I continued to grow, my seizures changed to complex partial and nocturnal seizures, which eventually resulted in severe memory loss.

Medicine has kept me stable and safe, and thus, I never minded taking it. However, the medicine began to become less affective and by the time I was 21 years old, I began having more seizures than usual. The problem with this is that every time an epileptic seizure occurs, there is a possibility that damage can be done to the brain. Therefore, the change that would soon occur in my life would be brain surgery.

When I first heard this, I laughed. I have always looked at epilepsy as an adventure — as the factor that simply makes me special. I have never thought of myself as disabled or sickly, and always try to remember that it could be worse. With these thoughts, I disassociated myself from the idea of brain surgery, thinking that it would always be unnecessary. However, the circumstances continued changing. My seizures began occurring two or three times per day, rather than once a month.

The daily seizures were complex partial seizures, during which I would shake and drool, lasting from 30 seconds to 2 minutes. Afterward I would speak very slowly, be somewhat confused and forgetful, and my head would hurt immensely, always in the same area. Because the seizures were happening so often, I had to convince myself to follow through with the brain surgery, which occurred on September 17, 2012.

My surgery was performed by Dr. Kim Burchiel, head of the neurological surgery department at within the OHSU Brain Institute. The surgery lasted four hours and went extremely well. I spent five days in the hospital and improved a little bit each day. I was told from the beginning that it will take me at least a year to recover, and that I need to be patient.

It has been six months since surgery, and my seizures have changed immensely. I now have about two or three seizures per week, as opposed to every day, and can usually predict when they will occur. I also stay awake during the process and no longer lose my memory. Although my seizures still cause headaches and slow speech, I am continuing to improve each week, and am very thankful for all that has occurred.

I have received so much support throughout my experience as an epileptic, which is why I began volunteering for the Epilepsy Foundation Northwest. Because I was able to go to college and major in sociology and Spanish, I have always wanted to use my skills to support other cultures. Group support is extremely important in regard to any illness, which is why I would like to continue supporting and helping others who have experienced epilepsy.

Although I do not know what will happen in regard to the stability of my seizures, I have decided to look at this change as a positive factor and use my past experience to help others who need inspiration.

Leigh Schommer, Portland

Schommer, 24, is currently studying and teaching English in Puebla, Mexico. The story of her epilepsy, her brain surgery and recovery was recently chronicled by the Oregonian.

So what is a Comprehensive Stroke Center anyway?

Wayne Clark, M.D.
Director, Oregon Stroke Center

This week the Oregon Stroke Center at the OHSU Brain Institute was very pleased to receive the following notification from our hospital accreditation organization: “Effective Immediately The Joint Commission has officially certified OHSU as a Comprehensive Stroke Program!”

OHSU is the first hospital in the Pacific Northwest and one of only 27 hospitals in the U.S. to receive this certification.

Well, this all does sound exciting — but what does it mean for a patient who is having a stroke? Taking a step back, there are several different levels of treatment for someone who is having a stroke that is being caused by a blocked artery in the brain. The first is to make sure basic care is provided for the patient. Are they breathing safely? Is their blood pressure too high or low? What kind of stroke is happening and when did it occur?

These needs can be met at excellent, local “stroke ready” hospitals around the state. Here the patient is first examined and decisions are made on whether the patient should be treated locally or whether he or she needs to be transferred to facilities for more advanced care. Some of these local hospitals can give the specific stroke treatment “clot buster” therapy — “tissue plasminogen activator,” or TPA —  in an attempt to open up the artery causing the stroke. The decision to give TPA often involves discussing the case with a remote stroke specialist by phone or more recently by using video “telestroke” evaluations. OSHU currently has a nine-hospital “telestroke” network where we can evaluate the patient and assist local hospitals around the state. After the TPA is started, the patient is frequently transferred to a larger hospital for further care and and management.

The next level of stroke care capability is a “primary stroke center.” These hospitals have been certified by The Joint Commission — a non-profit that accredits more 20,000 health care organizations across the country — to be fully capable of delivering acute stroke treatment, including TPA, and providing extensive evaluation and detailed management of the patient. This includes having intensive care beds and being able to provide rehabilitation services. Currently, 14 hospitals in Oregon are primary stroke center certified. OHSU has been a primary stroke center since 2007.

However, for many patients, TPA alone may not be sufficient. In these cases, more advanced “interventional” techniques are required to try to pull out the clot that is causing the stroke. In addition there are other types of stroke that can be caused by an artery breaking inside the brain (a cerebral hemorrhage) or an artery popping on the surface of the brain (a subarachnoid hemorrhage). For these very critical patients, specialized “neurointerventionalists” and cerebrovascular neurosurgeons are required to stop the bleeding, using special clips or coils. In addition, the patients need to be managed very closely in a specialized neurosciences intensive care unit. This is where a “comprehensive stroke center” is required.

To meet the Joint Commission criteria, the Oregon Stroke Center had to prove that we had all of these capabilities — 24 hours a day, 365 days a year. In addition, we had to demonstrate that our complication rates for all these procedures were better than the national guidelines. Another big part of the comprehensive stroke center criteria is that we monitor the care and outcome of our patients not only in the hospital but during outpatient follow-up for three months!

Having this hierarchical hospital approach to stroke care — stroke ready, primary stroke center, comprehensive stroke center — allows patient throughout the state to start receiving immediate appropriate treatment locally while providing a tertiary referral center for advanced stroke care for Oregon.

Wayne Clark, M.D.
Director, Oregon Stroke Center
OHSU Brain Institute

 

 

Autism rates increasing — but why?

Autism spectrum disorders are severe neurodevelopmental disorders affecting young children that are usually detected in the first years of life. Autism is now recognized as one of the most common developmental disorders — likely to affect about 10,000 youth under age 18 in Oregon.

Meanwhile, epidemiological studies have shown increasing rates of autism in most countries.  On Tuesday, April 2, as part of the OHSU Brain Awareness Season lecture series, I will speak about my work over the last 25 years in studying autism. And I will talk about the factors that might account for the upward trends and rates, including the role of prenatal factors or childhood immunizations.

Major progresses have been achieved in the last few years with large-scale genetic studies on autism. An increased proportion in cases of autism — about 25 percent — can now be traced back to known genetic causes.

The new genetic discoveries are paving the way for identifying novel treatments and drug therapies currently under development that might become available in the not-too-distant future.

The outcome of autism has changed since the development of early intensive behavior programs that can significantly improve the developmental trajectories of children with autism — provided that they are accessed early and with sufficient intensity. On Tuesday, I will also talk about treatments that work and how available those treatments are.

Capitalizing on existing strengths in basic and clinical sciences, OHSU is now  developing a Center for Excellence in Autism that will act as a resource center for health-care providers and families in the community while contributing through research to a new understanding of the causes and treatments of autism.

Eric Fombonne, M.D.
Professor of Psychiatry
Director, Autism Research Center, OHSU Brain Institute

False hopes and real risks with Alzheimer’s ‘treatments’

“What do I have to lose?”

I hear this question regularly from patients who want to try the latest “breakthrough” in Alzheimer’s research featured on television or YouTube.  These are typically things that either have been tested in animals with no human studies or things that have been tested haphazardly in small numbers of patients and then vigorously hyped.

For example, curcumin is a component of curry that has been tested in animals, with a single small negative study in human subjects, but is well publicized and recommended in the lay media. Bexarotene is a drug approved for skin cancer that showed impressive results in animals and is now in human testing.

A videotape of a single Alzheimer’s patient using coconut oil went viral and has everyone asking about it. A report of a single patient with a great response to the spinal injection of Enbrel has also been widely disseminated, with some physicians wondering if we should be trying this. Intravenous immunoblobulin, or IVIG — a product derived from blood — has been tested in an encouraging study in 36 patients, but it will really take the results of a larger study (which will be reported this summer) to know whether it can really be recommended.

In each case, the drug is currently available, either as an approved supplement or as a drug which is Food and Drug Administration-approved for other indications. So there is a temptation to try it without real proof that it is effective for Alzheimer’s: “What do I have to lose?”

In the case of curcumin and coconut oil, the answer is: “nothing.” I don’t push these treatments. But if my patients ask about them, I tell them: “Go ahead, give it a try.” I wish I could say that they come back with glowing reports, but sadly I have not heard much encouraging news.

My response is very different when I’m asked about Enbrel, IVIG, or bexarotene. In each of these cases, there is the possibility of significant side effects. Each of these requires a doctor and a prescription, and in the absence of good evidence in human subjects, I do not prescribe them.

Even for patients with Alzheimer’s, there is a lot to lose. Our patients have the capacity for a good quality of life for many years after diagnosis, and we can and should promote sensible, simple measures for improving quality of life rather than promote desperate attempts with real risks.

Joseph Quinn, M.D.
Professor of Neurology
Layton Aging & Alzheimer’s Disease Center
OHSU Brain Institute

Deep Brain Stimulation: life-changing treatment for tremors, and maybe more

Functional neurosurgery is surgery intended to improve brain function.  These procedures have been applied to the treatment of pain, movement disorders, epilepsy, and behavioral disorders.

In the past, the techniques were mostly targeted destruction of brain tissue or pathways. In very specific areas, destroying brain tissue could actually help — by decreasing a person’s tremors from movement disorders, for instance. Now with deep brain stimulation technology, these techniques are being replaced by reversible, and non-damaging approaches. During my presentation on March 25, 2013 at Portland’s Newmark Theater, as part of OHSU’s Brain Awareness Season lecture series, I will discuss the history of this field, its current status and directions for the future.

Stereotaxis is the method we use to direct surgery to discrete points in the brain. Literally it means “touching a point in space.” Effectively, with stereotactic neurosurgery, we consider a brain in three dimensions and assign a specific “address” for every point within that brain.

In 1946, the technique of stereotactic neurosurgery was applied to patients, having been used in animals almost 30 years previously. In the first years, operations were conducted in patients with Parkinson’s disease, pain, and “emotional disorders.”

Stereotaxis opened up a new field of neurosurgery, which thrived for more than 20 years, mostly for the treatment of movement disorders in Parkinson’s and in other conditions. During this time, all of the commonly performed operations were designed to produce a small area of damage in a highly precise area of the brain — damage that could then diminish symptoms of movement disorders. In the late 1960s, when levodopa was discovered as a drug treatment for Parkinson’s disease, stereotactic surgery almost disappeared, except in a few centers. It took about 20 more years for neurologists to realize that levodopa did not cure Parkinson’s disease, and that it had a number of toxic effects.

In the mid-1970s, a new type of surgery was developed: deep brain stimulation, or DBS. These systems were fashioned after heart pacemakers. And, as for the heart, the systems required implantation of a wire electrode in the brain and a generator to power the electrode. This was a new technology that seemed to be able to influence brain function reversibly, without damaging the brain. Because it was reversible, it could also be tested by a trial of stimulation before actually implanting a full system. DBS was used to try to control chronic pain, and although initially it appeared to work, experience over the next decade was not promising, and it fell into disuse.

By the mid-1980s, a new application of DBS came to the forefront: for movement disorders. Based on the targets of earlier destructive operations, and the concept that stimulation at these brain sites would have positive effects in patients with Parkinson’s disease and tremor, the field of DBS was reborn.

Over the next 20 years, DBS technology would be proven to be superior to the best medical therapy available in advanced Parkinson’s disease, and for the treatment of severe familial tremors. It is now a standard and widely accepted treatment for these disorders, and has almost completely replaced the historic destructive approaches.

Today, new applications for DBS are being considered and tested, and more sophisticated ways of implanting the electrodes are emerging. DBS is being tested for a number of conditions, including refractory depression, obsessive-compulsive disorders and epilepsy. These clinical trials are in process, and the results of these investigations should be available in the next year or two. If DBS helps any one of these diagnoses, it will dramatically change its treatment.

Other possible applications of DBS are being considered and preliminary studies for Alzheimer’s disease, and even severe obesity, have been conducted. The impact of effective surgery for either of these two conditions would have enormous financial implications in the next several decades, with potential health care savings measured in the hundreds of billions of dollars.

The advent of DBS technology poses the bioethical question of whether our ability to modify brain function should be uncritically applied to medical and behavioral disorders. To state it another way: “Just because we can do it, should we do it?” This will be a quandary for society, the legal system and our future health care systems to debate.

My hope is that this will serve as an introduction to my presentation, and that we can continue this discussion on the blog long after the lecture.

Kim Burchiel, M.D., F.A.C.S.
John Raaf Professor and Chairman of Neurological Surgery
OHSU Brain Institute

Learning in Honolulu: understanding risks — and prevention — for strokes

Aloha from HawaiiEvery February, healthcare providers and researchers from all over the world meet for the American Stroke Association’s annual International Stroke Conference. This year the conference was hosted in Honolulu, Hawaii and I was honored to attend and present three of my own papers on stroke.

The conference was huge. There were so many interesting topics covered simultaneously that I ended up having to read about some of them afterwards. But there were a few things I thought our audience might find interesting.

One of the main topics of the conference was whether emergent blood clot retrieval through mechanical means was a beneficial treatment in acute stroke. This is a highly debated topic, and many centers, including the OHSU’s Oregon Stroke Center, do perform this procedure, as it is still considered a standard of care at advanced stroke centers. I won’t get into the details of the studies, because that will get into pages of discussion.

There were many other interesting tidbits of information that I picked up from the conference. There was a study from New Zealand that suggests that cannabis use or a lifestyle that includes cannabis use may double your stroke risk. Another study showed that the “Southern diet” — packed with fatty, fried, salty and sugary foods — also increases stroke risk. I guess people should think twice before having the deep fried snickers bars sold at the fairs. More importantly, don’t use cannabis then eat fried chicken.

The one study that really influenced me during my attendance at the conference was called the EMBRACE study. It is a study that was done in Canada looking at patients with cryptogenic stroke. Cryptogenic stroke is a fancy term meaning “we did a stroke evaluation and still don’t know what caused your stroke.” Up to 30 percent of strokes are cryptogenic. Atrial fibrillation, which is an irregular heart rhythm, is a significant risk factor for stroke, and it often occurs silently as it comes and goes. Many people can have normal heart rhythms the majority of the time, but then briefly go into atrial fibrillation. So it’s possible that it’s missed when a patient is seen at the doctor’s office.

Therefore, if this arrhythmia is suspected, patients are often sent home with a rhythm-monitoring device for up to 30 days. More commonly, it’s done for only two days.

This study showed that one in six patients older than 55 with a cryptogenic stroke or transient ischemic attack – not a stroke but an episode where blood flow to a part of the brain stops briefly — had previously undiagnosed atrial fibrillation that was only identified after wearing a 30-day event monitor. This basically showed that the two-day monitor that we commonly use is not good enough, and some patients need longer monitoring.

Hormozd Bozorgchami, M.D.
Instructor, Oregon Stroke Center
OHSU Brain Institute

The neuroscience of memory, and how it matters in court

When I was 6 years old, I ran into a door frame and had to have stitches on my forehead. I remember that I was running to answer the phone. I remember thinking “oh no, I’m going to hit that door frame!” And, of course, I remember that after the stitches were put in, the doctors put a bandage on my teddy bear’s forehead to cheer me up.

But … do I really “remember” all of this? How much of this “memory” comes from my parents re-telling this story over the years, and how much was originally encoded in the memory neurons in my brain? I wouldn’t bet my life on being able to distinguish between the two. And I certainly would not bet someone else’s life on it.

Recently, the New Jersey Supreme Court took a new stance on how memory should be judged for accuracy in the courtroom. Rather than trying to account for imperfect memories from eyewitnesses, the new ruling focuses on educating the jury about the potential falsity of memories. The instructions include the statement that “human memory is not foolproof. Research has revealed that human memory is not at all like a video recording that a witness need only replay to remember what happened. Human memory is far more complex.” More specifically, jurors will be instructed about influences on memory that could be relevant in a crime scene, such as how stress can decrease an eyewitness’s memory recall abilities, and how most people have difficulty correctly identifying a person of a different race. These new instructions are largely based on scientific research findings from the fields of neuroscience and cognitive psychology.

While many of the details of memory consolidation and recall are still a mystery, scientists do have evidence from brain scan studies about distinct brain regions that are active during different phases of memory processing. Using functional magnetic resonance imaging, scientists have discovered that many of the same brain regions are active when a person is recalling a “false” memory and a “true” memory. This presents a major hurdle for extending these neuroimaging techniques to assess the accuracy of eyewitness accounts in a courtroom setting. Furthermore, most of the laboratory research involves simple object or facial recognition and recall within a short experimental session, and with no real world context. That is very different from the complicated emotional effects that factor in to witnessing a crime, combined with the time delay of months or even years between the initial event and the court date.

For these reasons, it likely is too early to extend these neuroimaging techniques to determine the accuracy of eyewitness accounts in a courtroom setting. However, as scientists learn more about the essential basics of how memories are stored in the brain, we can (and should) use this knowledge to educate jurors. Cognitive psychologists have uncovered many of the basics of memory formation and recall, extinction of memories, and memory “reconsolidation.” (In other words, each time my mom retells the story of how I got stitches, the memory is re-coded in my brain, with potentially new or different information attached to it.) By educating jurors on the nature of memory, the New Jersey Supreme Court is taking a huge leap forward in incorporating scientific discoveries on the basics of memory to ensure a more accurate and fair legal system. Our hope is that this bridge between neuroscience research and the law community continues to gain support.

Kateri Spinelli, Ph.D.
Post doctoral fellow, Dept. of Neurology
OHSU Brain Institute

 

All pain is in your brain

Where is your pain?

The short answer is simple: in your brain. It may seem as if it’s in your broken finger, or the toe you just stubbed on the door, or in your aching tooth. But it’s not. Pain is a sensory experience, and resides in your brain.

ouch, pain, brain, all pain is in the brainTo consider why I say that, ask yourself: does an anesthetized patient feel pain during a surgical procedure?  The answer (assuming the patient is properly anesthetized of course!) is that he or she feels no pain. Yet surgery always involves some degree of tissue damage. In the days before anesthesia, patients generally avoided surgery at almost all costs, and most procedures were horribly painful. (Anyone who has read the seventeenth century Diary of Samuel Pepys cannot forget his description of being trussed up for an excruciating surgical procedure that he underwent for removal of bladder stones. Modern surgery would not be possible without anesthesia.)

What this little thought experiment reminds us is that pain is not the same thing as injury. You can sustain an injury (or undergo a surgical procedure), but unless your brain processes that information, there is no pain. Pain, by definition, is a conscious experience.

Given that pain happens in our brains, it might seem as if pain could be eliminated very easily if only we could somehow block activity in the brain’s “pain center.” Unfortunately, it is not as simple as that. Most important, there is no focal point, no “center” for pain in the brain. There is no one region that specifically produces pain when stimulated, no one region that can be lesioned to eliminate pain permanently.

Instead, information about injury is processed across a network of brain regions sometimes referred to as the “pain matrix.” Different nodes in this matrix seem to play various roles in the pain sensation. Some parts of the brain seem to be more important for processing the location or degree of injury. That is, they let you know that it’s your finger, not your toe, and tell you how bad it is. Other parts of the brain contribute to the emotional and cognitive aspects of the pain sensation. For example, elements of the pain matrix that include the frontal lobes of the brain are important for the suffering element of pain and for evaluating its significance for our lives. (Will I be able to work after this injury? Does this mean my cancer is coming back?) This appraisal of how an injury and its consequences fit in with a person’s overall experience is an important part of pain.

Any sensation of pain therefore arises not from the activity of a “pain neuron” or “pain center,” but reflects activity distributed across a wide brain network. This can make pain management extremely complicated. But approaches to pain treatment that take the distributed nature of pain processing into account have more hopes of succeeding. It’s a very big topic – and one that I’ll be touching on over the coming months.

Mary Heinricher, Ph.D.
Professor, departments of Neurological Surgery and Behavioral Neuroscience
OHSU Brain Institute

 

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