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Friday, April 17, 2015




On Saturday, the American Academy of Neurology (AAN) kicks off its 67th annual meeting, where researchers will present results from studies on a wide range of neurologic illnesses, including multiple sclerosis (MS), epilepsy, Alzheimer’s disease, ALS, Parkinson’s, autism, stroke, migraine, chronic pain, and more.


To whet your appetite, we’re previewing some of the exciting MS research that will be presented at the meeting. Look for more meeting coverage from Neurology Now and Neurology Today throughout the week.


A Promising New Drug

An investigational MS drug may help repair myelin, the fatty tissue that protects nerve cells in the brain which is damaged in MS, according to a new study.


Diego Cadavid, MD, senior director of Biogen Idec in Cambridge, MA, and a Fellow of the AAN, and colleagues tested an experimental antibody called anti-LINGO-1 against a placebo in 82 people with a first case of acute optic neuritis, a condition that involves damage to the optic nerve fibers in one eye; researchers estimate that half of those who develop this condition will go on to have MS. The researchers found that people who received the anti-LINGO-1 antibody had some restored function to the optic nerve, compared with people who took a placebo.


This suggests the drug may trigger remeylination (or restoration of myelin) of the nerve cells, which has the potential to slow or even stop the progression of the disease, the authors said. More studies will be needed to see whether these changes in nerve function translate to an improvement in symptoms, Dr. Cadavid said in a news release.


Read the study abstract here.


Coffee May Reduce MS Risk

People who drink lots of caffeine appear to be at a lower risk of developing MS, according to two new studies, one conducted in Sweden and the other in the US.


In both studies, researchers found that people who drank four or more cups of coffee each day (six in the Swedish study) in the previous year had a 33 percent lower risk of developing MS compared with non-coffee drinkers. The lower risk was similar for people who had a high caffeine intake for five or 10 years before the study began.


The results suggest that caffeine “may have protective effects for the brain,” although it’s still unclear why that’s the case, said study author Ellen Mowry, MD, MCR, an assistant professor of neurology at Johns Hopkins University School of Medicine in Baltimore, MD in a news release.


Read the study abstract here and learn more about the research on our Neurology News blog.


People with MS May Lack Key Nutrients

Women with MS have lower levels of five antioxidant and anti-inflammatory nutrients essential to maintaining good health, compared with women without the condition, according to new research. Restoring the balance of these key nutrients may offer new ways to treat the symptoms of MS, study author Sandra D. Cassard, ScD, a research associate at the Wilmer Eye Institute of Johns Hopkins University in Baltimore, MD, said in a news release.


Comparing the nutrition habits of 27 women between the ages of 18 and 60 with relapsing-remitting MS and 30 women without MS, Dr. Cassard and colleagues found that the women with MS had lower levels of food folate (also known as vitamin B9, found in beans, lentils, some citrus fruits, and dark, leafy greens), vitamin E, magnesium, lutein and zeaxanthin (found in eggs, broccoli, corn, and leafy greens like spinach, kale, and collard greens), and quercetin (found in many fruits and veggies, including capers, radish leaves, dill, cilantro, fennel, and red onion).


Since MS is a disease that causes chronic inflammation, getting the appropriate levels of anti-inflammatory nutrients “may help prevent the disease or help reduce the risk of attacks for those who already have MS,” Dr. Cassard said.


Read the study abstract here and learn more about the research on our Neurology News blog.


For updates from the AAN Annual meeting, follow Neurology Now on Twitter, Facebook, and Google+.

Wednesday, April 15, 2015




Depression and diabetes are a double whammy when it comes to dementia risk, according to a study published today in the journal JAMA Psychiatry. Researchers found that people who were depressed and had type 2 diabetes had a 117 percent higher risk for dementia than people with neither condition.


In Western countries like the United States, 8 to 14 percent of people have type 2 diabetes, and about 25 percent of the general population will experience an episode of major depression during their lifetime, according to figures cited in the study. And up to 20 percent of people have both type 2 diabetes and depression.


Depression, Diabetes, and Dementia in Danes

Researchers in Denmark and the US looked at a database of more than 2.4 million Danish citizens who were at least 50 years old and free from dementia when the study began in 2007. They collected data on these participants between 2007 and 2013. Overall, 477,133 individuals (or 19.4 percent) had a diagnosis of depression, 223,174 (9.1 percent) had type 2 diabetes, and 95,691 (3.9 percent) had both conditions.


During the study period, 59,663 people (2.4 percent) developed dementia. Of that group, 15,729 people (26.4 percent) had depression, 6,466 (10.8 percent) had type 2 diabetes, and 4,022 (6.7 percent) had both conditions.


Depression and Diabetes Spike Dementia Risk

The researchers calculated that people with type 2 diabetes were at a 20 percent greater risk for developing dementia compared with people who were neither depressed nor had diabetes. Those with depression had an 83 percent higher risk. And those who had both conditions were at the greatest risk of developing dementia, with a 117 percent higher risk than people with neither condition.


Adequate screening and treatment for both depression and diabetes could help reduce the risk for later dementia, and potentially lighten the public health load of dementia worldwide, the researchers wrote.


Take Action Now

“The co-occurrence of diabetes mellitus and depression, especially in persons younger than 65 years, poses an important hazard to healthy brain aging and cognitive fitness in the later years of life,” Charles F. Reynolds, III, MD, UPMC endowed professor of geriatric psychiatry and a professor of neurology, behavioral and community health sciences, and clinical and translational science at the University of Pittsburgh, wrote in an invited commentary.


It hasn’t been proven that treating depression and diabetes can reduce dementia risk, but existing research does point to a link, Dr. Reynolds said. This study reinforces the need for patients, with the help of their physicians, to adopt lifestyle habits that may reduce depression, diabetes, and dementia risk.


Exercising regularly, eating a healthy diet (there’s even evidence that specific diets reduce the risk for Alzheimer’s disease), drinking alcohol in moderation, getting sufficient sleep, staying socially active, and taking appropriate medications to manage medical conditions have all been linked in past research to better brain health, Dr. Reynolds said.


For expert advice on treating depression and reducing your risk of dementia, read “5 Ways to Diminish Your Dementia Risk.”


To learn more about how depression and diabetes are linked to dementia, browse our archives here.

Monday, April 13, 2015



More than 4 million Americans each year experience injuries such as headache, neck pain, stiffness, or tenderness as a result of whiplash, which occurs when the head or neck is jerked violently out of alignment with the spine, usually as the result of a car crash. While most people make a full recovery, about one-quarter may develop long-term chronic pain, muscle weakness, disability, or post-traumatic stress disorder (PTSD). And doctors have had a hard time predicting which of their patients will not fully recover.


But now, a new magnetic resonance imaging (MRI) technique could make that determination easier—and may provide relief for those with whiplash-related chronic pain or PTSD, according to a study published in the journal Spine.


Clues in the Cervical Muscles

Researchers from Northwestern University in Chicago used a special MRI technique to measure the water-to-fat ratio in the cervical multifidus muscles of the neck in 36 people who had experienced a whiplash-related injury approximately one week earlier. After three months, the researchers asked them to report on their level of pain and disability (recovered, mild, or severe) and complete a questionnaire to determine whether they had PTSD.


In past studies, the research team had found that people with whiplash injuries who went on to develop chronic pain, disability, and PTSD had more fat in the neck muscles—an abnormality that signals rapid muscle wasting, or atrophy—one to three months after the injury. People who made a full recovery by three months or who had only mild symptoms did not have this abnormality.


In the current study, the researchers were able to detect this water/fat imbalance in some patients as early as one or two weeks after their injury, even though none of the patients had the abnormality at the start of the study. And those who had more fat in their neck muscles—in addition to other suspected predictors of chronic pain such as older age (over 35 years) and higher initial scores on tests of pain and psychological distress—tended to be the ones who went on to develop long-term pain or PTSD.


Early Detection Means Early Treatment

“We haven’t found an effective treatment for people with chronic whiplash, and I think it’s because we haven’t really figured out what’s wrong with them,” said study author James Elliott, PT, PhD, an assistant professor of physical therapy and human movement sciences at the Northwestern University Feinberg School of Medicine, in a news release. Patients who experience chronic pain and have PTSD are less likely to benefit from physical therapy, for instance, he said. “They may require a more concerted effort for pain management from their physician and help from a psychologist.”


Since routine MRI scans do not pick up on this water/fat abnormality, doctors may want to consider using this specialized MRI technique in patients who show other signs of an increased risk for chronic pain or PTSD, the researchers wrote.


It’s unclear why some patients develop the abnormality and others don’t. It may appear in response to an additional injury that goes undetected, Dr. Elliot proposed, but “what has actually been injured remains to be seen. Now we know to look more deeply into the problem.”


For more coverage of the latest research into chronic pain, browse our archives here.

Friday, April 10, 2015




You can never be too rich or too thin, the old adage goes. But a new study, published in The Lancet Diabetes & Endocrinology, suggests that when it comes to dementia risk, you can be too thin.


The new study is the largest so far to look at the link between Body Mass Index (BMI) and dementia risk, drawing data from nearly 2 million patients aged 40 and older who were seen in clinics in the United Kingdom between 1992 and 2001. The patients were an average of 55 years old at the start of the study period and had a median BMI of 26.5 kg/m2, which is within the “overweight” range. (For more information about BMI and how to calculate it, visit the National Institutes of Health.) Over about nine years of follow-up clinic visits, 45,507 people were diagnosed with dementia.


As BMI Goes Down, Dementia Risk Goes Up

The researchers found that people who were underweight (with a BMI of less than 20 kg/m2) around middle age were 34 percent more likely to be diagnosed with dementia than people in the normal weight range (with a BMI of between 20 and 25 kg/m2). Compared to people with a BMI close to the study average of 26 to 27 kg/m2, underweight patients had, on average, a 64 percent higher risk of developing dementia.


On the other end of the BMI spectrum, the researchers found that people who were classified as very obese (with a BMI of more than 40 kg/m2) were 29 percent less likely to be diagnosed with dementia than people with a normal BMI. These associations remained the same even after the researchers accounted for other factors that may influence dementia risk such as age, alcohol intake, or smoking.


The ‘Obesity Paradox’

The researchers couldn’t explain why being overweight or obese was linked to a lower risk for dementia in their study, especially since some past research has suggested the opposite. “Many different issues related to diet, exercise, frailty, genetic factors, and weight change could play a part,” said Nawab Qizilbash, MD, a clinical epidemiologist and head of OXON Epidemiology in London, in a news release.


Dr. Qizilbash said he and his colleagues plan to do more research to try to understand this “obesity paradox.” Study author Stuart Pocock, PhD, a professor of medical statistics at the London School of Hygiene and Tropical Medicine, added that if they can come to understand why these people with a high BMI had a lower dementia risk, “it’s possible that further down the line, researchers might be able to use these insights to develop new treatments for dementia.”


In the meantime, don’t take the study as an invitation to chow down on junk food—these findings are far from conclusive, wrote Deborah Gustafson, MD, PhD, a professor of neurology at SUNY Downstate Medical Center in Brooklyn, NY, in an accompanying editorial. Past research has turned up conflicting evidence on whether a high BMI is linked to an increased risk for dementia. Some studies have hinted at a link, but some have failed to find one, she wrote.


The current study, Dr. Gustafson said, is certainly “not the final word on this controversial topic.”


To learn more about risk factors for dementia, browse our archives here.


Image via Thinking Tree on Flickr.

Thursday, April 09, 2015



Left image shows a normal brain scan; middle image shows a suspected CTE subject and right image shows an Alzheimer's case. More red and yellow colors demonstrate more abnormal brain proteins (tau and amyloid). Image: PNAS/David Geffen School of Medicine at UCLA.


In the past few years, national media attention has revolved around several high-profile cases of athletes who committed suicide and were later found to have chronic traumatic encephalopathy (CTE), a degenerative brain disease that appears in people with a history of repeated traumatic brain injury (TBI). It is believed to cause progressive cognitive and behavioral changes such as memory loss, confusion, dementia, suicidal behavior, depression, personality changes, and even physical symptoms like tremors or an abnormal gait.


Currently, the only way to diagnose the disease is after a patient’s death, when doctors can perform an autopsy to look for an accumulation of tau proteinwhich is also observed in people with Alzheimer’sin regions of the brain that control mood, cognition, and motor function. In living patients, doctors may suspect CTE based on cognitive, behavioral, and motor changes, combined with a history of TBI.


Now, researchers at the University of California, Los Angeles, have found a way to detect possible signs of this devastating condition in the brains of living people.


PET Scans Reveal Protein Pattern

For the study, published in the Proceedings of the National Academy of Sciences, 14 former NFL players suspected to have CTE based on their cognitive and behavioral symptoms received positron emission tomography (PET) scans using a special chemical tracer that allowed the researchers to track how tau protein was spread throughout their brains. The researchers administered the same PET scans to 24 people with Alzheimer’s disease and 28 healthy people.


All of the former football players had similar patterns of tau deposits throughout their brains, concentrated mainly in the subcortical region and the amygdalaareas that govern learning, memory, behavior, and emotions. This pattern appeared consistent with that of tau accumulation observed in people with an autopsy-confirmed diagnosis of CTE, the researchers said.


The brains of the Alzheimer’s patients had a different pattern of tau accumulationone that involved areas of the cerebral cortex, which governs cognitive abilities like memory, thinking, and attention.


“We found that the imaging pattern in people with suspected CTE differs significantly from healthy volunteers and those with Alzheimer’s,” said study author Julian E. Bailes, MD, director of the Brain Injury Research Institute and chairman of neurology at NorthShore Neurological Institute in Evanston, IL, in a news release.


The Way Forward

The findings are very preliminary, and Dr. Bailes and his colleagues cautioned that the observed tau accumulations do not definitively prove that the 14 retired NFL players have CTE. Larger studies conducted at multiple centers throughout the country will be needed to test this technology and validate the findings, they said. Involving patients who have experienced other types of brain injury, such as veterans with blast-induced TBI, will also be crucial.


But Dr. Bailes said the findings do suggest that PET scans may be helpful for differentiating trauma-related cognitive issues from those caused by Alzheimer’s disease. And, he added, the results could ultimately help doctors diagnose the condition and even test possible treatments.


To learn more about chronic traumatic encephalopathy, browse our archives here.