Vitamin D, mood and memory in persons with Parkinson’s disease

Vitamin D has become a hot topic in recent years. For many years, vitamin D has been known to play a role in bone health. More recent research suggests it may have a much broader role in multiple body systems.

In regard to the brain, we know that there are receptors for vitamin D in most parts of the human brain. In persons without Parkinson’s disease, some research suggests vitamin D may be related to mood and cognitive function. These data are somewhat limited, however, and a definitive conclusion has not been drawn.

To look more closely at mood, memory and their relationship with vitamin D in persons with Parkinson’s, some colleagues and I conducted an observational study of 286 people with Parkinson’s. We did testing of cognitive function and mood and had blood drawn. When correcting for age, disease duration, and Parkinson’s disability, we found associations between vitamin D concentrations and several measures of language function. These included how many animals or vegetables a person could name in one minute, known as verbal fluency, and how good they were at remembering a list of words. This relationship — between higher vitamin D levels and better language function — was present in those persons with Parkinson’s who were not demented, but not present in those with dementia. In regard to mood, a self reported scale of depression showed an association with vitamin D concentrations — again, just in the non-demented subset of Parkinson’s patients.

It appears that there may be a relationship between vitamin D and cognition and mood in persons with Parkinson’s. Cause and effect cannot be determined from this type of study. It is possible, for example, that persons with Parkinson’s who are depressed are less likely to get outside and therefore have lower vitamin D concentrations.

To determine if a relationship truly exists, good intervention studies are needed to see what happens to cognition and mood when vitamin D concentrations are increased in persons with Parkinson’s. Currently we are pursuing a research project looking at this with a joint OHSU and Portland VA Medical Center study. We hope to have results in the next year or two.

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

A toast to your health

There’s possibly no better time to highlight this research story than on New Year’s eve: a drink or two a day — a glass of wine, a glass of beer — might also keep the doctor away.

That’s what colleagues and I found in a study published this month in the journal Vaccine. We studied the drinking behaviors of rhesus macaque monkeys, who were given 22-hour-a-day access to a mixture of alcohol and water — and allowed to drink or not drink it. What we found after 14 months of study: the immune system of the monkeys that drank “moderate” amounts of alcohol were actually bolstered — more than the monkeys who drank more heavily and more than a control group of monkeys who drank a low-calorie sugar solution. We defined “moderate” drinking as monkeys who had a blood alcohol level of 0.02 to 0.04 percent (A blood alcohol level of 0.08 percent is the limit for humans to be able to legally drive a vehicle.).

The media coverage of our work — which has been extensive, in USA Today, Time, The Daily Beast and elsewhere — has focused on the happy news that drinking in moderation might help boost our immune system and help us fight off infection. But my colleague, Ilhem Messaoudi Powers (formerly at OHSU, now at the University of California-Riverside), and I want our research to go beyond that. We want to better understand how our body is reacting to moderate alcohol to actually have this effect. The goal would be to then find new, alcohol-free ways — maybe new medications — to boost the immune system, in generally healthy people and in people with immunodeficiency.

Of course, based on what we’ve found, it looks like people might be able to get that boost by enjoying their New Year’s Eve with that glass of wine, as well.  But remember — it’s all about moderation.

Kathy Grant, Ph.D.
Professor of Behavioral Neuroscience
OHSU Brain Institute


Ask our expert: Aging & declining mental ability

Q: Does getting older always mean losing mental ability?

A: Part of normal brain aging may mean a slowing of mental processing, especially in your memory. Although many patients ask, it’s difficult to prescribe any particular type of mental exercise for your brain, though learning things that get you out of your normal routine can help, such as learning a new language or trying a different type of puzzle.

But your best option is physical activity: Research has shown that aerobic exercise — such as walking, swimming, biking or hiking — for about 30 minutes a day, five times a week can promote the release of growth factors in the brain that create new cells.

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

Do you have a question you’d like one of our expert to answer? Share it with us in the comments section below.

How our brains wash away the gunk during sleep

You wake on Saturday morning, drag your body out of bed and survey your home. You had entertained houseguests the night before, and it shows. Friends and family had filled your home, loud voices and much conversation echoed within your walls and everyone went home much later than you had planned. And now it is time to pay the piper. A full Saturday’s worth of dishwashing, floor scrubbing and shelf wiping stares you back in the face.

Such is our common experience, something each of us can likely relate to. New research, however, suggests that your brain may feel the same way at the end of a long day of thinking.

The brain is just like any other organ in the body in that the spaces in between its cells must be regularly swept clean to keep things running smoothly. Yet it has remained a bit of mystery how the brain accomplishes this task.

See, in the rest of the body, the lymphatic system takes care of most of this cleaning of the spaces between cells. The brain, however, has no lymphatic system.

In the summer of 2012, our research team reported in the journal Science Translational Medicine the discovery of a clever anatomical pathway by which the brain accomplishes this task of cleaning out the spaces between cells. Basically, it uses spaces on the outside of blood vessels as a dedicated set of plumbing that allows cerebrospinal fluid, or CSF, that surrounds the brain to wash through the brain, essentially flushing debris and waste out. This washing depended on water movement through support cells in the brain called “glial cells.” Thus we termed this brain-wide clearance pathway the “glymphatic system.”

Anyone who has every pulled an all nighter, or has had young children, knows that after a night with little or no sleep, not only do you feel more tired, but your mind is foggier. Why a good night’s sleep leaves the mind clear and crisp, and indeed why we would need sleep at all (since it represents “wasted” time not doing something more productive), has been one of the persistent mysteries in neuroscience.

In a study published last week in the journal Science, our team reported findings that may shed light on this question. By imaging the flushing of fluid through the brains of live mice that were awake or naturally asleep using a technique called 2-photon microscopy, we found that the rate of cleaning in the brain differed dramatically between the waking brain and the sleeping brain.

When the brain is asleep, we found that its cells shrink in order to open up the spaces between them, which allows CSF to flush through the sleeping brain at about 20 times the rate seen in the waking brain. This translated to a doubling in the efficiency of waste clearance from the sleeping versus waking brain. These findings suggest that part of the function of sleep is restorative – that it provides the brain an opportunity to tidy up and clean out the day’s accumulated waste when the activities of waking life aren’t getting in the way. It’s like cleaning up on a Saturday after Friday night’s houseguests have left.

These new findings do not simply illuminate a potential purpose of sleep, but may inform our understanding of the role of sleep disturbances in the setting of neurodegenerative diseases like Alzheimer’s disease. Alzheimer’s disease is believed to be caused by the buildup of plaques made up of a protein called amyloid beta in the aging brain. Two recent studies published in the journal JAMA Neurology have shown that in human patients that haven’t yet developed Alzheimer’s disease, poorer sleep quality is associated with greater buildup of amyloid beta plaques. Whether this is because bad sleep promotes amyloid beta accumulation, or whether low-level brain damage caused by amyloid beat promotes sleep disturbance has not been clear. However, our study suggests that one of the functions of sleep is the clearance of amyloid beta, and supports the idea that the inability to get proper sleep could promote the development of neurodegeneration.

While this most recent study was led by Dr. Maiken Nedergaard at the University of Rochester Medical Center in New York, follow-on studies are currently underway here at OHSU. In January of this year, I was recruited from the University of Rochester to come to OHSU and establish a research program based in part upon my work in this brain-wide, waste-clearance pathway. Bringing this research here to OHSU was made possible in large part by the generous gift from Phil and Penny Knight establishing the Knight Cardiovascular Institute at OHSU, of which I am now a part.

Using 2-photon microscopy and other approaches, we are working to define how this waste-clearance system becomes impaired in the aging brain and the contribution that damaged, aging blood vessels in the brain make to this process. The goal is to find key steps in this degenerative process that could be targeted with drugs to stop the failure of amyloid beta clearance and the accumulation of amyloid beta plaques in the brain.
With a lot of smart people working together, we hope that the discoveries that we’ve made so far in mice will translate to new opportunities to change the course of Alzheimer’s disease in patients.

Jeffrey Iliff
Assistant Professor of Anesthesiology and Peri-Operative Medicine
Knight Cardiovascular Institute

OHSU Brain Institute


Lewy body dementia — a less-known cause of cognitive problems

Not all people with cognitive problems have Alzheimer’s disease. While Alzheimer’s is the most common reason for memory problems as people get older, there are other types of dementia.

Lewy body dementia or Lewy body disease is a much less common cause of cognitive problems and is seen in about seven in a thousand people over the age of 65. People with LBD tend to have trouble with visual spatial function and executive function. Executive function involves the ability to carry out complex tasks that have multiple steps, such as baking a cake. Early in the course of the disease, persons with LBD often have a fairly good memory. For example, remembering a list of words told to them five minutes before.

People with LBD may also have hallucinations or delusions. They may see people who are not present or have false beliefs such as thinking their house belongs to someone else. They often fluctuate in their degree of cognitive problems, having some days when they seem to do very well and others when they really struggle.

On a physical exam, the doctor may see some features similar to Parkinson’s disease such as slowed walking, smaller movements and handwriting, and stiffness. It is also common that people with LBD have a history of a disorder of sleep called REM sleep behavior disorder, or RBD. RBD often starts many years before cognitive problems develop. In RBD, people act out their dreams (which occur during REM sleep) and can injure themselves and their bed partner.

Unfortunately, there are not perfect treatments for LBD. But medications called cholinesterase inhibitors can help some patients. Rivastigmine is the one that has been studied the most extensively. Memantine is a different type of medication that may help some patients as well.

One of the most important things to be aware of is that people with LBD can respond very poorly to many typical antipsychotic medications, such as haloperidol and chlorpromazine. These medications are often used to treat delusions and are also given frequently for agitation. The typical ones should be avoided in LBD. There are two antipsychotics — quetiapine and clozapine — that can be used if delusions and hallucinations are problematic. If the parkinsonian features are prominent, a medication used to treat Parkinson’s disease, levodopa, may also be tried.

People with cognitive problems as well as RBD or hallucinations may have Lewy body dementia — not Alzheimer’s Disease. In this type of dementia, a neurological consultation is often particularly helpful.

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

Designing a migraine-free lifestyle — especially for women

One in five women in America suffer from migraine headaches. In the throes of a migraine attack, simple head movement intensifies the pain. Eating or exercising is out of the question. Sometimes a migraine sufferer can’t even get out of bed.  There are 28 million Americans who have these disabling headaches — three times as many women as men. Almost half of them don’t see a doctor, don’t know their headaches are migraine or are trying to treat them on their own.

Beat a migraineThere are many new treatment options to keep migraineurs on the tennis court, at their son’s soccer game and alert and energetic at the office or factory … and not in bed! Consulting a physician is the first step. But there are many ways to avoid migraine triggers in everyday life.

What people with migraine experience as a headache is actually the final stage of a complex process. Many factors appear to set off, or “trigger,” the cascade of events in the brain. Migraine triggers include an odd array of sensory inputs, as well as substances contained in certain foods and beverages. Recognizing and avoiding specific triggers can enable migraine sufferers to craft a headache-free lifestyle.

Practical Tips for Preventing Migraine

• Wake up early on Saturday and Sunday. Get up the same time each day, even if you have stayed out late the night before. Change in sleep routine can make you vulnerable to morning headache. And, when you sleep in till noon on Sunday, you’ll most likely drink less coffee or tea, putting you in “mini-caffeine withdrawal” and inviting a headache.

• Drink water instead of diet soda. Diet drinks contain artificial sweeteners, such as aspartame, and many have caffeine, both of which can trigger migraine headache.

• Use the money you’ve saved on diet drinks to purchase sunglasses with photochromic lenses that automatically darken when exposed to UV rays. Wear prescription sunglasses while driving. Even on an overcast day (which NEVER happens in Portland, of course!) glare from the windshield and reflected light from nearby cars can cause you to squint, tensing the muscles of your scalp and face. Many individuals with migraine are exquisitely sensitive to light, called photophobic; and bright, reflected light while driving, or on computer screens placed near windows, can precipitate headache.

• Begin your exercise routine with a slow and gentle warm up. Abrupt vigorous exercise can rapidly increase blood flow to the brain and dilated vessels throb and may set in motion the cascade of changes in blood vessels and electrical activity of nerve cells that characterize what’s happening in your brain during migraine pain.

• Watch for abrupt changes in weather. The medical literature is controversial about barometric pressure or wind patterns being true provokers of headache, but most of my patients report a sensitivity to weather pattern change. While of course we can’t alter the weather, we can be vigilant about avoiding other migraine triggers, such as lack of sleep or red wine, during rapid weather fluctuations. Often it’s a combination of two or more migraine triggers that actually result in full-blown migraines.

• Be wary of common food “triggers” of migraine. Culprits include wine (especially red), aged cheese such as Brie, blue, cheddar (pizza!), MSG, aspartame, peanuts or peanut butter, processed and preserved foods such as luncheon meats, and onions. Not all of these foods serve as triggers for all migraineurs. But being a food-detective, keeping a brief food diary for a week or two, can be a smart preventative move.

• Be especially cautious with alcohol. Alcohol serves as a cerebral vasodilator, activating nerve endings that supply these vessels as they expand, triggering vascular headache. In addition, alcohol acts as a diuretic; dehydration can compound many types of head pain.

• Avoid dehydration. Dehydration, in children as well as adults, makes nausea and vomiting from any cause, including migraine, worse.  Sufficient water intake, especially when exercising, can protect against the headache and accompanying nausea of migraine symptoms. A feeling of thirst is not an early indicator of your body’s volume status. By the time you feel thirsty, your plasma volume is already low. Your best guide to your body’s hydration status is the color of your urine. It should be pale yellow. Any darker means you need to increase your daily water intake. Remember many foods have high water content: watermelon and celery, of course, but also many fish, such as salmon, and eggs.

There are many factors we can’t control that influence headache vulnerability, such as genetics and hormonal changes. But fortunately, we are able to modify many aspects of our lifestyle to reduce migraine frequency and intensity.

Tarvez Tucker, M.D.
Associate Professor of Neurology and Neurocritical Care
OHSU Brain Institute






Scientists ‘create’ a tiny brain

For the first time, scientists have grown a brain in a dish.

In a study published in the journal Nature last month, Austrian researchers used human induced pluripotent stem cells or embryonic stem cells and a combination of specialized growth conditions to produce “cerebral organoids.”

Within these organoids, the authors can define many, but not all, of the discrete brain regions found in the human brain. The organization of these regions in relation to one another is not the same as in a human brain, and the connectivity between brain regions is not intact. Nonetheless, some of these regions, including the cerebral cortex, are internally organized exactly as they would be in the human brain. The organoids are developmentally similar to a 9-week old embryo (about the size of a pea), making them a great model for studying early human brain development.

The authors used these miniature brains to make a new discovery about the molecular basis of a disease called microcephaly, where brain size is severely reduced. This disease has been difficult to study using animal models, because the brain regions that malfunction in the human disease don’t exist in many other animals. Importantly, the researchers used induced pluripotent stem cells isolated from the skin of human patients with microcephaly to grow the diseased organoids. Modeling the disease in this way, the researchers come as close as possible to a tailored view of the malfunction that occurred in these same patients during brain development in utero.

The authors do emphasize that it is impossible to grow an entire human brain in a dish — so we are a far cry from Mary Shelley’s Frankenstein. But there is no doubt that cerebral organoids will be a great tool to study many of the complicated pathways that converge for early development of the human brain to proceed properly. By studying these processes in a dish in the lab, scientists have the benefit of examining development in real-time, instead of relying on snap shots from tissue isolated during different developmental time points. Researchers can also manipulate the growth and nutrient environments of the organoids, as well as perform genetic manipulations and drug treatments to tease apart different aspects of brain development. Future studies using these miniature brains may even pave the way for new therapeutic treatments for some developmental diseases.

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

Should MS drugs cost more than $40,000 a year?

I have been treating people with multiple sclerosis, or MS, for 30 years. While some people with MS have a very mild case — we call that “benign” MS — most do not.  Typically, people develop the illness as young adults and have to contend with the illness for decades. Untreated, over time, most people with MS become permanently disabled. Many lose the ability to walk, become too disabled to work, have thinking problems and a host of other physical, psychological and social problems that result from the illness.

I don’t like MS and am tired of seeing people’s lives limited by the illness.

For the first 10 years of my career, I had no medications that I could prescribe to control MS. But in 1993, the first drug that could alter the course of the disease was approved by the Food and Drug Administration for treating early MS. Now there are 10 FDA-approved drugs for treating MS. None of these drugs cures the illness and none reverses damage that has already happened. They do control the illness and I have no doubt that they help people with MS, particularly if started early. I see far fewer people with MS becoming disabled than I did during the first 10 years of my career when we had no medications. These medications clearly are beneficial to people with MS when used properly.

The MS medications have side effects, and sometimes these are very serious. Some require injecting yourself one or more times a week. Some suppress the immune system, which may cause long-term side effects. However, when used properly, people with MS can take these medications safely and the treatments are definitely better than the illness.

There is a problem, however. These medications are incredibly expensive. The medications all cost more than $40,000 a year! And since the medications are not cures, people take these medications year after year. I am often asked by patients with MS: “Why do these medicines cost so much?” And my answer is: “I don’t know.”

How drug prices for medications are set is a secret. The usual answer from the pharmaceutical companies is that it costs lots of money to develop the drugs and get final FDA approval. But that is only part of the answer. The cost of developing the drugs first released by the FDA for treating MS — Betaseron, Avonex and Copaxone — have long since been recovered, yet the price of these drugs keeps going up. When these drugs were first introduced in the mid-1990s, their cost was about $15,000 a year.  They now cost more than $40,000. Had their cost just kept up with inflation, they should cost half that amount.

What about competition? Shouldn’t that be bringing the prices down? Well, just the opposite has occurred. In the past few years, each new drug that has come on the market has had a higher price than already approved drugs and this has resulted in prices for all the drugs going up. In 2010, when the first oral drug for MS — Gilenya  — was released, it cost more than any other MS drug, at $48,000 a year. This led to increases of all of the older drugs by as much as 39 percent.. And the prices have only continued to rise. It seems that the pharmaceutical companies making these drugs are charging more and more because they can get away with it.

All of the pharmaceutical companies have programs to reduce the impact of these costs for patients. For those with private insurance, the companies have co-pay caps. For the uninsured and underinsured, they provide drugs at reduced cost or even free. Unfortunately, people on Medicare are not eligible for these programs, which affects not only older patients but also younger patients who have become disabled and qualify for Social Security Disability and Medicare.

These programs reduce some of the impact of the cost of these medications on the individual patient but they do nothing to reduce the cost to our health care system. There are over 500,000 Americans with MS and over half of them are on these medications. These medications cost our health care system billions of dollars per year.

Is there anything that we can do about these high costs? Patients, doctors and national organizations, like the National MS Society, need to speak out about the cost of these drugs. The NMSS has created a toolkit to help people engage the media or public officials on policies and programs that impact people living with multiple sclerosis. Engaging in these issues has never been easier — all you need is a computer with Internet access. For many with MS who are unable to leave home, such a toolkit can serve as their platform — whether they start a petition, join a patient group, blog about the desire for affordable medication or write their member of Congress.

Physicians need to speak out too. Oncologists at Memorial Sloan-Kettering Cancer  Center recently refused to prescribe a new cancer drug because it was too expensive and not superior to other less expensive drugs. Recently, more than 100 oncologists —  including the OHSU Knight Cancer Institute’s Brian Druker — published a paper in the journal Blood, which is the journal for the American Society for Hematology. They argued that the cost of medications for cancer were often too high and that the high prices may be harming patients. Neurologists need to take a similar position with regard to medications for MS and other expensive medications for neurologic diseases.

We have made significant advances in treating MS over the past 20 years but we need to work together to break down barriers to care, improve access to quality health services and support funding for more MS research.  With your help and voice, we can turn MS issues, like more affordable treatments, into national priorities.

Dennis Bourdette, M.D.
Professor and Chair, Department of Neurology
OHSU Brain Institute

From laboratory to farm: a scientist’s visit to the local herb farm

As a basic scientist, most of my neuroscience training and research has focused on the underlying biological mechanisms of disease. During the past year, I have started working with a natural compound in my research on Parkinson’s disease. Curcumin, the active ingredient in turmeric spice, can act as an anti-oxidant and anti-aggregation agent, and may have a positive effect on the Lewy bodies found in Parkinson’s patients.

At first, I was a bit skeptical about natural compounds and alternative therapies. But as I’ve read more of the literature, attended conferences, and talked with other researchers in the field, I have hope that research on natural compounds could lead to potential therapies. However, for most compounds, many more studies are needed. For a clinician’s perspective on recommending natural compounds to his Alzheimer’s patients, see Dr. Joe Quinn’s post from a few months ago.

I and a few other OHSU scientists recently took an educational trip to the herbal supplement company Oregon’s Wild Harvest farm in Sandy, Ore. Prior to this trip, I had very little knowledge about how herbs were processed into supplements, or into the compounds that I use in the lab. My colleagues and I gave short presentations on our research projects involving natural compounds, and the Oregon’s Wild Harvest staff were engaged with and curious about our experimental findings. We then took a tour of the farm and production facilities. I was impressed with the streamlined process of testing the herbs for quality control, drying and combining particular herbs into supplements, and finally packaging the supplements into capsules for bottling and labeling — all done in a few small buildings on a family-owned farm, practically right in my own back yard.

It just so happened that Oregon’s Wild Harvest, or OWH, was producing its turmeric supplement during my visit, which I was very curious about since it is the natural compound I’m investigating in Parkinson’s. It was interesting and informative to compare notes with the company’s staff about which turmeric forms they put in their supplements and why.

Observing the front end of herbal supplement production gave me a new perspective on how my research is connected to the bigger picture. As a neuroscientist, I always strive to see the “connections” between my research in the lab and other sectors of society. I now have a better understanding of how curcumin is transformed from the root of a plant to the compound I use in the laboratory. It was refreshing to interact with the founders and staff of OWH, who approach natural compounds from the farmer’s and manufacturer’s point of view — a perspective that is good to keep in mind as my research progresses forward.

While natural supplements and alternative therapies are becoming more main stream, clinical trials using natural compounds, including curcumin, to treat neurological diseases have been disappointing thus far. However, a few of the scientific studies currently underway at OHSU are giving some exciting positive results. As the scientific community continues to investigate potential therapeutic applications for natural compounds, I believe it’s important for us to also stay connected to where and how these compounds are derived.

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

What causes a migraine?

“I have a pounding headache!”

We’ve all heard that lament – from a friend or family member, and very likely felt one ourselves. That throbbing, pounding head pain that makes it hard to think, much less do everything we need to do.

According to surveys, more than 10 percent of the U.S. population suffers from migraine headaches. Women are more frequent sufferers than men, with up to 25 percent of women experiencing migraines, but less than 10 percent of men. Migraines often have a range of symptoms, including nausea, light sensitivity, and a visual disturbance called an “aura.” But the predominant and common symptom among almost all migraine sufferers is headache pain. Available treatments for migraine pain leave much to be desired. Relief is rarely complete, and most patients have to try several drugs before finding one that is at least partially effective.

Plus, the treatments themselves can cause headaches! This phenomenon, referred to as “medication overuse headache” or MOH, is very common. As the individual takes his or her headache medicine more and more frequently, the medicine itself causes more and more headaches, a painful vicious cycle that can be broken only by stopping all drug treatment. MOH can be triggered even by over-the-counter agents like aspirin.

So what causes headaches? Migraines have long been referred to by doctors as “neurovascular” headaches, because the pain had been thought to arise from distension of the blood vessels in the head. This theory was based in part on the pulsing character of the pain, which was attributed to stretching of the vessels as the heart beats. In addition, although the brain itself lacks pain sensors, patients undergoing brain surgery reported pain when vessels inside the head were stimulated. Further bolstering this idea, many of the drugs that have been used for migraine treatment can constrict blood vessels, and some drugs that dilate blood vessels can cause headaches, at least in some people.

However, this idea of blood vessels as the source of headache has recently been viewed with increasing skepticism by headache researchers. Not all effective anti-migraine agents constrict blood vessels in the head, and evidence that blood vessels were dilated during migraine was weak at best. On top of this, a couple of recent studies have found that the throbbing pain of the migraine is not in synch with the heartbeat.

With the demise of the blood vessel theory, we are now starting to recognize that migraine is a disorder of the brain itself. The throbbing character of migraine pain was recently found to be correlated with certain brain waves, the so-called “alpha” waves, although this has so far been studied only in one patient. There are also a whole host of migraine triggers, ranging from foods to hormones, to light and stress. The tremendous variety of stimuli that can trigger a migraine implies that there are many brain systems that feed into the pathways that ultimately give rise to headache. We also know that people with migraine can be more sensitive to many sensations, even between migraine attacks.  This implies that the “migraine brain” is more alert and poised to respond to any input. We also know from animal studies that the pain-facilitating system in the brain contributes to headache-related pain. (See my earlier blog post about how your brain controls pain.)

What does all of this mean for migraine sufferers? The demise of the blood vessel theory is important, because it tells us that we should focus our attention on the brain itself when trying to help migraine patients. The fact that the source of the pain is the brain also means patients and their doctors should consider the full range of factors that can trigger pain in a “migraine brain” — things like diet, stress, exercise, hormones, or even just bright light.

Finally, without adequate treatment, occasional migraines can become more and more frequent, due to changes in the brain itself. This makes it important to seek treatment — if necessary from a headache specialist — to control migraines before they become a chronic daily event.

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

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