Stroke: Why Blood Pressure and Stress Matter

Dr. Guy McKhann, famous neurologist, once wrote that back in his early practice, his response to a stroke patient was, "Take two aspirin and call me to set up your rehabilitation program."

Now health professionals are taking a more aggressive, proactive approach to stroke prevention.

Learn about stroke and the brain in easy-to-read language. Look here!

• Blood pressure is a major determinant of stroke risk, and a current large-scale NIH study is examining whether recommending more aggressive blood pressure control than is suggested by current guidelines would further reduce risk of major stroke or incidence of cognitive decline related to vascular dementia.  Results from this study have the potential to impact clinical practice significantly.

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	Stroke YESTERDAY Until the 1950s, little was known about stroke and virtually nothing could be done for stroke victims. Death from stroke was 4 times what it is today. By 1960, the incidence and mortality from stroke began to gradually decline as treatable risk factors such as hypertension and smoking were identified. During the 1970s, further decline in stroke mortality was achieved through management of risk factors and significant clinical advances such as computer tomography for early diagnosis of ischemic or hemorrhagic stroke, the demonstration of the effectiveness of aspirin for ischemic stroke and prevention, and assessment of brain metabolism using Position Emission Tomography (PET) scanning. TODAY Fewer people are dying of stroke today—age-adjusted stroke mortality rate has decreased 70 percent since 1950, and has decreased 33 percent since 1996, which indicates the trend persists.  As the population ages, further advances are needed to keep pace. Over 6 million people in the United States have survived a stroke but live with its impact every day. In 1995, an NIH-funded clinical trial established the first (and only) FDA-approved treatment for acute ischemic stroke. The drug tPA (tissue plasminogen activator), currently approved for delivery within 3 hours of stroke symptoms, reduces the risk of disability and maximizes the potential for patient recovery. A recent analysis estimated that tPA can provide considerable cost savings if used in just 20 percent of all ischemic stroke patients in the US — nearly $74 million for the first post-stroke year alone.  Improving utilization through current stroke awareness campaigns will lead to better outcomes for stroke patients and substantial cost savings. Blood pressure is a major determinant of stroke risk, and a current large-scale NIH study is examining whether recommending more aggressive blood pressure control than is suggested by current guidelines would further reduce risk of major stroke or incidence of cognitive decline related to vascular dementia.  Results from this study have the potential to impact clinical practice significantly. A large, NIH-funded clinical trial compared the effectiveness of a common surgical procedure, carotid endarterectomy, with carotid stenting, which is a newer intervention, to determine which resulted in the best outcomes for stroke patients. This provided clinicians with valuable risk-benefit information when considering optimal treatment courses with their patients. A number of devices can be deployed within the blood stream to remove clots from brain arteries and to dilate narrowed brain arteries.  NIH clinical trials are ongoing to learn whether these devices will improve functional outcome in stroke patients. Observational cohort studies have improved our understanding of cultural and ethnic disparities that continue to exist in stroke occurrence, risk factors and mortality.  Geographic variation has been thought to contribute to the high stroke mortality in the southeastern United States Stroke Belt.  However, a NIH-funded national population-based cohort study (REasons for Geographic And Racial Differences in Stroke) (http://www.regardsstudy.org) found that exposure to the Stroke Belt during adolescence or early adulthood was more predictive of hypertension than was current residence in the Stroke Belt.  This study clearly indicates that preventive measures must begin early in life. TOMORROW A major objective is the control of blood pressure. The assessment of antihypertensive therapies will result in the identification of specific treatments to lower blood pressure and preempt primary and secondary stroke. NIH clinical trials will continue to generate evidence to help clinicians and patients decide on the best prevention, treatment, and rehabilitation strategies by comparing the effectiveness of different approaches. New therapies will emerge as investigators continue to explore and develop new approaches to treat acute stroke and minimize ischemic damage, providing patients and physicians with more therapy options and a better chance of survival and recovery. As results from large NIH cohort studies continue to improve our understanding of genetic and behavioral influences on stroke risk and occurrence, informed development of more tailored primary and secondary prevention strategies will improve stroke awareness and risk factor management, and will help reduce disparities in stroke incidence and outcomes. Results from a European study suggested that tPA is effective in a subset of patients beyond the currently approved 3-hour time-to-treatment window, providing an opportunity to offer the therapy to more patients.  Advances in neuroimaging may allow clinicians to identify eligible patients at all time points, and to use stroke profiles to better predict outcomes and response to therapy. New approaches are currently being tested for the treatment of brain hemorrhage.  If successful, this would lead to the first clinically directive intervention available for the most fatal type of stroke. Contact: NINDS Brain Resource and Information Network, PO Box 5801 Bethesda, MD 20824, (800) 352-9424 National Institute of Neurological Disorders and Stroke (NINDS):http://www.ninds.nih.gov/

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Page Last Updated on March 29, 2013
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Poverty itself can be harmful to health, education

At the height of the recession in 2012, nearly one in four American children were living in poverty.

Today, five years after America went through the worst economic crisis since the Great Depression, children are still more likely to live in poverty than adults. In fact, while the national poverty rate sits at 14 percent, for children, it’s 18 percent.

Learn about the brain, stress, and health in easy-to-read language.

The problem is particularly acute for children of color. While white children experience poverty at a rate of 11 percent, around 27 percent of Hispanic children, 31 percent of black children and 34 percent of Native American children in America today are growing up poor.

There are the obvious side-effects of growing up in poverty: deprivation, worry, and sometimes hunger and the risk of homelessness.

But just as troubling, experts say, is that growing up in a poor household is linked with long-term consequences in educational outcomes, physical health and brain development that can follow a child well into adulthood. Here are just a few ways how:

Children who grow up poor are more likely to be poor as adults

According to a study, around five percent of adults who never experienced poverty as children were poor at ages 20 and 25. If they were poor anywhere from one to seven years as a kid, that number went up to approximately 13 percent. For those who spent eight to 14 years in poverty as children, 46 percent were poor at age 20, and 40 percent were poor at age 25.

The longer you grow up in poverty, the harder it is to graduate

One factor at play for why poor children go on to struggle as adults is education. Whether it’s because they didn’t have access to good schools, or their parents didn’t have the time or resources to help them, children who grow up in poverty often start at a disadvantage that can make it harder to achieve later in life.

In a 2017 report from the Urban Institute, researchers found that 62 percent of children who spent at least half their childhoods in poverty went on to attain a high school diploma by age 20. By comparison, that number was 90 percent for those who never experienced poverty.

The gaps only widen when it comes to college. 

Overall, the Urban Institute found that only 16 percent of kids who spent half their childhoods poor were either consistently working or in school and mostly out of poverty by their late 20s.

Growing up poor can carry long-term health implications

Poverty itself can be dangerous. Children growing up poor are more likely to be injured in accidents, and five times more likely to die due to accidents, according to the American Academy of Pediatrics.

Children in poor neighborhoods are at increased risk of cycling accidents, pedestrian injuries, falls, burns, poisonings and chemical burns.

But the risks go deeper than that. Research shows that children who grow up in poverty are also more likely to develop chronic illnesses such as asthma or obesity — the latter can lead to further health problems, including diabetes and heart disease. Poor children are also more likely to be sedentary and exposed to tobacco, which in turn may increase the risk of heart and lung problems when they grow up.

Poverty can also harm a child’s brain development and lifelong mental health

“There are definite impacts [of poverty] on physical health,” said Benard Dreyer, former president of the American Academy of Pediatrics, in an interview with FRONTLINE. “But in addition, and perhaps more importantly, there’s an impact on brain development and the ability to succeed in life.”

Dreyer was referring to a growing body of research that shows exposure to “toxic” stress can actually impact a child’s brain development.

All children experience stress, and caring adults or support networks can help them cope and figure out how to respond. However, the constant stresses of living in an impoverished household — and in some cases, dealing with abuse or neglect — can create a toxic stress response.

Such levels of stress “impact children’s brain development in the first couple of years of life,” said Dreyer, and can result in permanent changes to brain structure and function. These changes can manifest as increased anxiety, impaired memory and mood control – making it harder to learn, solve problems, follow rules and control impulses. The release of stress hormones can also create a “wear and tear” effect on the child’s organs, including the brain.

Source: PBS/Frontline

Autism's Puzzles

Learn brain basics in easy-to-read language.

What is autism spectrum disorder?

Autism spectrum disorder (ASD) refers to a group of complex neurodevelopment disorders characterized by repetitive and characteristic patterns of behavior and difficulties with social communication and interaction. The symptoms are present from early childhood and affect daily functioning.

The term “spectrum” refers to the wide range of symptoms, skills, and levels of disability in functioning that can occur in people with ASD. Some children and adults with ASD are fully able to perform all activities of daily living while others require substantial support to perform basic activities. The Diagnostic and Statistical Manual of Mental Disorders (DSM-5, published in 2013) includes Asperger syndrome, childhood disintegrative disorder, and pervasive developmental disorders not otherwise specified (PDD-NOS) as part of ASD rather than as separate disorders. A diagnosis of ASD includes an assessment of intellectual disability and language impairment.

ASD occurs in every racial and ethnic group, and across all socioeconomic levels. However, boys are significantly more likely to develop ASD than girls. The latest analysis from the Centers for Disease Control and Prevention estimates that 1 in 68 children has ASD.

What are some common signs of ASD?

Even as infants, children with ASD may seem different, especially when compared to other children their own age. They may become overly focused on certain objects, rarely make eye contact, and fail to engage in typical babbling with their parents. In other cases, children may develop normally until the second or even third year of life, but then start to withdraw and become indifferent to social engagement.

The severity of ASD can vary greatly and is based on the degree to which social communication, insistence of sameness of activities and surroundings, and repetitive patterns of behavior affect the daily functioning of the individual.

Social impairment and communication difficulties
Many people with ASD find social interactions difficult. The mutual give-and-take nature of typical communication and interaction is often particularly challenging. Children with ASD may fail to respond to their names, avoid eye contact with other people, and only interact with others to achieve specific goals. Often children with ASD do not understand how to play or engage with other children and may prefer to be alone. People with ASD may find it difficult to understand other people’s feelings or talk about their own feelings.

People with ASD may have very different verbal abilities ranging from no speech at all to speech that is fluent, but awkward and inappropriate. Some children with ASD may have delayed speech and language skills, may repeat phrases, and give unrelated answers to questions. In addition, people with ASD can have a hard time using and understanding non-verbal cues such as gestures, body language, or tone of voice. For example, young children with ASD might not understand what it means to wave goodbye. People with ASD may also speak in flat, robot-like or a sing-song voice about a narrow range of favorite topics, with little regard for the interests of the person to whom they are speaking.

Repetitive and characteristic behaviors
Many children with ASD engage in repetitive movements or unusual behaviors such as flapping their arms, rocking from side to side, or twirling. They may become preoccupied with parts of objects like the wheels on a toy truck. Children may also become obsessively interested in a particular topic such as airplanes or memorizing train schedules. Many people with ASD seem to thrive so much on routine that changes to the daily patterns of life — like an unexpected stop on the way home from school — can be very challenging. Some children may even get angry or have emotional outbursts, especially when placed in a new or overly stimulating environment.

What disorders are related to ASD?

Certain known genetic disorders are associated with an increased risk for autism, including Fragile X syndrome (which causes intellectual disability) and tuberous sclerosis (which causes benign tumors to grow in the brain and other vital organs) — each of which results from a mutation in a single, but different, gene. Recently, researchers have discovered other genetic mutations in children diagnosed with autism, including some that have not yet been designated as named syndromes. While each of these disorders is rare, in aggregate, they may account for 20 percent or more of all autism cases.

People with ASD also have a higher than average risk of having epilepsy. Children whose language skills regress early in life — before age 3 — appear to have a risk of developing epilepsy or seizure-like brain activity. About 20 to 30 percent of children with ASD develop epilepsy by the time they reach adulthood. Additionally, people with both ASD and intellectual disability have the greatest risk of developing seizure disorder.

How is ASD diagnosed?

ASD symptoms can vary greatly from person to person depending on the severity of the disorder. Symptoms may even go unrecognized for young children who have mild ASD or less debilitating handicaps. Very early indicators that require evaluation by an expert include:

• no babbling or pointing by age 1
• no single words by age 16 months or two-word phrases by age 2
• no response to name
• loss of language or social skills previously acquired
• poor eye contact
• excessive lining up of toys or objects
• no smiling or social responsiveness

Later indicators include:

• impaired ability to make friends with peers
• impaired ability to initiate or sustain a conversation with others
• absence or impairment of imaginative and social play
• repetitive or unusual use of language
• abnormally intense or focused interest
• preoccupation with certain objects or subjects
• inflexible adherence to specific routines or rituals

Health care providers will often use a questionnaire or other screening instrument to gather information about a child’s development and behavior. Some screening instruments rely solely on parent observations, while others rely on a combination of parent and doctor observations. If screening instruments indicate the possibility of ASD, a more comprehensive evaluation is usually indicated.

A comprehensive evaluation requires a multidisciplinary team, including a psychologist, neurologist, psychiatrist, speech therapist, and other professionals who diagnose and treat children with ASD. The team members will conduct a thorough neurological assessment and in-depth cognitive and language testing. Because hearing problems can cause behaviors that could be mistaken for ASD, children with delayed speech development should also have their hearing tested.

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What causes ASD?

Scientists believe that both genetics and environment likely play a role in ASD. There is great concern that rates of autism have been increasing in recent decades without full explanation as to why. Researchers have identified a number of genes associated with the disorder. Imaging studies of people with ASD have found differences in the development of several regions of the brain. Studies suggest that ASD could be a result of disruptions in normal brain growth very early in development. These disruptions may be the result of defects in genes that control brain development and regulate how brain cells communicate with each other. Autism is more common in children born prematurely. Environmental factors may also play a role in gene function and development, but no specific environmental causes have yet been identified. The theory that parental practices are responsible for ASD has long been disproved. Multiple studies have shown that vaccination to prevent childhood infectious diseases does not increase the risk of autism in the population.

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What role do genes play?

Twin and family studies strongly suggest that some people have a genetic predisposition to autism. Identical twin studies show that if one twin is affected, then the other will be affected between 36 to 95 percent of the time. There are a number of studies in progress to determine the specific genetic factors associated with the development of ASD. In families with one child with ASD, the risk of having a second child with the disorder also increases. Many of the genes found to be associated with autism are involved in the function of the chemical connections between brain neurons (synapses). Researchers are looking for clues about which genes contribute to increased susceptibility. In some cases, parents and other relatives of a child with ASD show mild impairments in social communication skills or engage in repetitive behaviors. Evidence also suggests that emotional disorders such as bipolar disorder and schizophrenia occur more frequently than average in the families of people with ASD.

In addition to genetic variations that are inherited and are present in nearly all of a person’s cells, recent research has also shown that de novo, or spontaneous, gene mutations can influence the risk of developing autism spectrum disorder. De novo mutations are changes in sequences of deoxyribonucleic acid or DNA, the hereditary material in humans, which can occur spontaneously in a parent’s sperm or egg cell or during fertilization. The mutation then occurs in each cell as the fertilized egg divides. These mutations may affect single genes or they may be changes called copy number variations, in which stretches of DNA containing multiple genes are deleted or duplicated.  Recent studies have shown that people with ASD tend to have more copy number de novo gene mutations than those without the disorder, suggesting that for some the risk of developing ASD is not the result of mutations in individual genes but rather spontaneous coding mutations across many genes.  De novo mutations may explain genetic disorders in which an affected child has the mutation in each cell but the parents do not and there is no family pattern to the disorder. Autism risk also increases in children born to older parents. There is still much research to be done to determine the potential role of environmental factors on spontaneous mutations and how that influences ASD risk.

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Do symptoms of autism change over time?

For many children, symptoms improve with age and behavioral treatment. During adolescence, some children with ASD may become depressed or experience behavioral problems, and their treatment may need some modification as they transition to adulthood. People with ASD usually continue to need services and supports as they get older, but depending on severity of the disorder, people with ASD may be able to work successfully and live independently or within a supportive environment.

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How is autism treated?

There is no cure for ASD. Therapies and behavioral interventions are designed to remedy specific symptoms and can substantially improve those symptoms. The ideal treatment plan coordinates therapies and interventions that meet the specific needs of the individual. Most health care professionals agree that the earlier the intervention, the better.

Educational/behavioral interventions: Early behavioral/educational interventions have been very successful in many children with ASD. In these interventions therapists use highly structured and intensive skill-oriented training sessions to help children develop social and language skills, such as applied behavioral analysis, which encourages positive behaviors and discourages negative ones. In addition, family counseling for the parents and siblings of children with ASD often helps families cope with the particular challenges of living with a child with ASD.

Medications: While medication can’t cure ASD or even treat its main symptoms, there are some that can help with related symptoms such as anxiety, depression, and obsessive-compulsive disorder. Antipsychotic medications are used to treat severe behavioral problems. Seizures can be treated with one or more anticonvulsant drugs. Medication used to treat people with attention deficit disorder can be used effectively to help decrease impulsivity and hyperactivity in people with ASD. Parents, caregivers, and people with autism should use caution before adopting any unproven treatments.

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What research is being done?

The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a component of the National Institutes of Health (NIH), the leading supporter of biomedical research in the world.  NINDS and several other NIH Institutes and Centers support research on autism spectrum disorder. 

Where can I get more information?

For more information on neurological disorders or research programs funded by the National Institute of Neurological Disorders and Stroke, contact the Institute's Brain Resources and Information Network (BRAIN) at:

BRAIN
P.O. Box 5801
Bethesda, MD 20824
800-352-9424
http://ninds.nih.gov

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#MeToo, part 3. Top 10 Things a Gay Rapist Accomplishes

Top 10 Things a Gay Rapist Accomplishes:

1. Seals a temporary lack of self-confidence of the victim to permanence.

2. Ruins routine sleep, making you need meds for the most natural of body functions.

3. Makes victim reach for comfort on the most elemental level, including eating.

4. So victim is susceptible to drugs, sex, overeating.

5. Having reached stage 4, diabetes can be achieved.

6. Once diagnosed with diabetes, victim, now adult watches in horror that Affordable Care Act will be killed by Trump.

7. Depression, diabetes, and sleep meds make partner deeply uncomfortable, completing the stress cycle to perpetuate more stress.

8. Having no self-esteem, said victim does not attend to financial matters and faces bleak financial future, further eroding relationship with partner, who, for clarity, has contributed to support of household beyond his share.

9. Further eroding of self-confidence when victim cannot talk to anyone, particularly LGBT, about a major part of his life.

10. Victim thinks, constantly, of man's inhumanity to man and where does his situation fit. Little feedback received convinces him that, well, take a place in line. Others have it much worse. And keep setting those useless therapy appointments, for which you've paid $ thousands over decades.

#MeToo 2. When You're Gay, You Blame the Victim

I so want to tell my story, but even today, 34 years later, it haunts me and depresses me. A gay rape follows you ceaselessly.

My perp was a former high school teacher. It staggered me when it happened and stings my self-confidence today.

My friend Art, who committed suicide in 1992, was eccentric and wise at the same time. He knew that being gay in America was difficult, "whether or not you choose to deal it or not." Adding one of the most demeaning violations of body and soul brings about a special inner silencing. It is your soul dying, like a tree, from the inside out.

I find it still nearly impossible to be coherent about what happened.

I had broken up with my first boyfriend. The hurt lasted all summer of 1982, when I choose to go out on a Saturday night to the bar in North Jersey where we had met. I was tired of the trips to NYC and Westchester and Connecticut, even, to socialize.

I got to the bar in Jersey that night and there was my ex's car in the parking lot. I panicked and drove home. Lonely and scared, I called my old teacher with whom I'd remained in contact over the years. I was comfortable enough to come out to him while still in school, but he never returned in kind, and by word and deed I knew he was gay. Yet, he was the only friend I could think to call and he immediately invited me (for the first time) to his apartment in NYC for a drink and some talk. I rushed there at the chance.

It didn't take long--five minutes--before he had stripped, cornered me, and forced himself on me. I was on his bed and stayed there, frozen in fear and disbelief for five or more hours. This was his version of intimacy. At 26, I had an emotional maturity of half that age. Like many gay kids, I missed out on the social rites of dating, sexual experience, and emotional expression.

Really, his was like animal behavior. He thought, after knowing me for a decade, that that was all I wanted or needed. It is the most profound form of pathological narcissism. The victim is an object, not even human, does not exist for the perpetrator.

When you're gay and raped, there really are no places to go. Women can at least, at the very least, have a social understanding of the emotions and the devastation. Gay men do not have such an ephemeral place. We have depression, overeating, drugs, and dangerous, casual sex as options to block the pain.

In 2015, I went back to the Fordham Prep reunion for my class of 1975. Surreally, pictures of my perpetrator flashed on a slideshow that seemed 100 times normal size. There were other teachers, other students, but all I could see was him.

It made a difficult night even worse. I heard about a lawyer who was suing the many perpetrators at this Jesuit school. I contacred him and he took my case. I had a long phone interview and filled out a long document. Hoping for some justice, I found out a year later that the lawyer had been lying. I had no case because I was not a student at the time of the rape, he blandly told me. The school was not responsible because I was an adult that night. It was a doublecross and I suspect this lawyer, representing the law firm that took down the Boston Archdiocese priests (use Google), was either incompetent or guilty of malpractice.

The road to nowhere continues from that night in 1982. Either you switch into extreme denial, flattening out your emotions for a sort of emotional death, or you medicate with food or drugs or sex.

The gay community has sadly neen incapable of providing support, weighed down by their own baggage of stress and denial. I love the community and have met some wonderful people. But emotional trauma, up to now, had reduced its ability to be supportive in significant ways. I believe and hope this is changing.

So, if you survive (and suicide ideation is never far from my mind), you live in a zombie-like state. And if gay people can't understand, trust me that straight people can't ever comprehend.

Blame the victim is all people can do, gay or straight. It's in the books.

#MeToo Pt. 1: Where do you go if you're a gay man?

"I'm sick and tired of being sick and tired." --Fannie Lou Hamer

On a Saturday night in August, 1983, I, a 26-year old gay male, was abused and raped by my former high school English teacher. (He was gay, too).  It was the worst experience of my life. I became a different person that night.

I've followed closely the current wave of revelations, by mostly women, of assaults from powerful white men. Each revelation takes me back to that apartment on Riverside Drive and the gut-wrenching emotional pain I experienced the next day and in bursts over more than 34 years.

A character in a favorite show, Six Feet Under, once said to a business rival, "There are things much worse than death." I believe I am familiar with them.

The rape and abuse on that night robbed me of any sense of an already fragile self-confidence. Family, friends, work colleagues, and shrinks alike comment frequently on this deficit.

"Where is your anger?" pleaded/questioned one therapist for whom I had forked over more money than I could afford. Relationships, never easy in the gay world, burned out suddenly and rapidly. In jobs, I worked below my capabilities and when I was lifted up by some enlightened people filled with grace, I burned out on the job and walked away.

The last 10 years have been spent in a relationship strained to the limit. Scrapping to earn money, I have found myself at food pantries and bottle return machines. Without my partner's financial support, SNAP, and Obamacare, I don't know where I'd be. I do not denigrate all these supports; neither are they ennobling. They dig the hole of self esteem as much as provide food and medicine.

Wherever that place would be, what happened in the late summer of 1983 rides along with me, never exorcised.

To the Kevin Spaceys, Harvey Weinsteins, Donald Trumps, Louis CKs of recent note, you must somehow learn the devastation of your assaults. Not in the moment, not the next day, but throughout a lifetime.

I understand the character in Six Feet Under: There are things worse than death.

End of Part 1.

Parkinson’s Disease: A Looming Pandemic

NEWS   Parkinson's disease is a progressive disorder of the nervous system that affects movement. It develops gradually, sometimes starting with a barely noticeable tremor in just one hand. But while a tremor may be the most well-known sign of Parkinson's disease, the disorder also commonly causes stiffness or slowing of movement.

In the early stages of Parkinson's disease, your face may show little or no expression, or your arms may not swing when you walk. Your speech may become soft or slurred. Parkinson's disease symptoms worsen as your condition progresses over time.

Although Parkinson's disease can't be cured, medications may markedly improve your symptoms. In occasional cases, your doctor may suggest surgery to regulate certain regions of your brain and improve your symptoms.--Mayo Clinic

New research shows that the number of people with Parkinson’s disease will soon grow to pandemic proportions.  In a commentary appearing today in the journal JAMA Neurology, University of Rochester Medical Center neurologist Ray Dorsey, M.D. and Bastiaan Bloem, M.D., Ph.D., with Radboud University Medical Center in the Netherlands, argue that the medical community must be mobilized to respond to this impending public health threat.

“Pandemics are usually equated with infectious diseases like Zika, influenza, and HIV,” said Dorsey.  “But neurological disorders are now the leading cause of disability in the world and the fastest growing is Parkinson’s disease.”

Learn the essentials of the brain, in easy-to-read form. CLICK HERE!

The piece builds upon the Global Burden of Disease study, also co-authored by Dorsey, which appeared in The Lancet Neurology in September and showed that neurological disorders are now the leading source of disability globally.  That study tracked the prevalence of neurological diseases like Parkinson’s, Alzheimer’s, stroke, epilepsy, meningitis, encephalitis, multiple sclerosis, and migraine, both globally and by country. 

In their commentary, the authors point out that between 1990 and 2015, the prevalence of Parkinson’s more than doubled and it is estimated that 6.9 million people across the globe have the disease.  By 2040, researchers believe that number of people with Parkinson’s will grow to 14.2 million as the population ages and the rate of growth will outpace Alzheimer’s.  These estimates are likely conservative due underreporting, misdiagnosis, and increasing life expectancy.  

To combat this growing pandemic, the authors argue that the medical community should pursue the same strategies that, in 15 years, transformed HIV from an unknown and fatal illness into a highly treatable chronic condition.  

“People with HIV infection simply demanded better treatments and successfully rallied for both awareness and new treatments, literally chaining themselves to the doors of pharmaceutical companies,” said Bloem. “Today, HIV has become a treatable, chronic disease. This upcoming increase in the number of Parkinson patients is striking and frankly worrisome. We feel it is urgent that people with Parkinson’s go to the pharmaceutical industry and policymakers alike, demanding immediate action to fight this enormous threat.”

The authors contend that the Parkinson’s community must come together and focus its activism in support of: developing a better understand the environmental, genetic, and behavioral causes and risk factors for Parkinson’s to help prevent its onset; increasing access to care – an estimated 40 percent of people with the disease in both the U.S. and Europe do not see a neurologist and the number is far greater in developing nations; advocating for increases in research funding for the disease; and lowering the cost of treatments – many patients in low-income countries do not have access to drugs that are both lifesaving and improve quality of life. 

“For too long the Parkinson’s community has been too quiet on these issues,” said Dorsey.  “Building on the AIDS community’s motto of ‘silence=death,’ the Parkinson’s community should make their voices heard.  The current and future burden of this debilitating disease depends upon their action.”

“Too many people have Parkinson’s today and more will face diagnoses tomorrow,” said Todd Sherer, Ph.D., CEO of The Michael J. Fox Foundation for Parkinson’s Research.  “We all — government, patient organizations, researchers, doctors and patients — must work together for better care for those living with this disease and research toward a future without Parkinson’s.”

This article has been republished from materials provided by University of Rochester Medical Center. Note: material may have been edited for length and content. For further information, please contact the cited source.

FASD: Alcohol and the Precious Fetal Brain

Alcohol is the leading known environmental agent capable of causing physical birth defects.

Fetal Alcohol Spectrum Disorders

YESTERDAY Alcohol’s ability to cause birth defects was recognized more than three decades ago by U.S. researchers, and it is now the leading known environmental teratogen (an agent capable of causing physical birth defects). In a 1981 advisory, the U.S. Surgeon General suggested that pregnant women should limit their alcohol intake – although no recommended level of intake was specified. Fetal alcohol syndrome (FAS) is one of the most serious consequences of heavy drinking during pregnancy. FAS is a devastating constellation of birth defects characterized by craniofacial malformations, neurological and motor deficits, intrauterine growth retardation, learning disabilities, and behavioral and social deficits. While the prevalence of FAS in the U.S. is between 0.5-2.0 cases per 1000 births, it is more common in other parts of the world. For example, in parts of South Africa where heavy drinking prevails, the incidence of FAS exceeds 60 cases per 1000 individuals. It is estimated that for every child born with FAS, three additional children are born who may not have the physical characteristics of FAS but who, as a result of prenatal alcohol exposure, still experience neurobehavioral deficits that affect learning and behavior. TODAY The umbrella term "Fetal Alcohol Spectrum Disorders (FASD)" is now used to characterize the full range of prenatal alcohol damage varying from mild to severe and encompassing a broad array of physical defects and cognitive, behavioral, and emotional deficits. The earliest stages of life are periods of great vulnerability to the adverse effects of alcohol. Embryonic The earliest stages of life are periods of great vulnerability to the adverse effects of alcohol. Embryonic and fetal development are characterized by rapid, but well-synchronized patterns of gene expression, which makes the embryo/fetus particularly vulnerable to harm from alcohol. Research shows that patterns of exposure known to place a fetus at greatest risk for FASD include drinking four or more drinks per occasion, and drinking more than seven drinks per week. The outcomes attributable to prenatal alcohol exposure for the children of women drinking in this manner include deficits in growth, behavior, and neurocognition, including deficits in arithmetic, language and memory, visual-spatial abilities, attention, and speed of information processing. Imaging and neurobehavioral research in individuals with FAS and FASD reveals that some brain regions appear to be most sensitive to prenatal alcohol while other areas apparently are spared adverse effects. Particularly vulnerable regions include the frontal cortex, hippocampus, corpus callosum, and components of the cerebellum, including the anterior vermis. Despite a number of prevention efforts, including point of sale warning signs and bottle labeling, national surveillance data indicate that in 2005, 12% of pregnant women admitted drinking alcohol in the previous month and 2% were binge drinking. Data from prenatal clinics and postnatal studies suggest that 20-30% of women drink at some time during pregnancy. A majority of women in the U.S. reduce or abstain from alcohol once pregnancy is recognized but almost half of pregnancies in the U.S. are unplanned. More than 12% of women who are not using contraception and are at risk of becoming pregnant drink at levels that exceed 7 drinks per week or 4 or more drinks per occasion. In a 2005 update of the Surgeon General’s advisory of 1981, the U.S. Surgeon General advised pregnant women and women who may become pregnant to abstain from drinking alcohol to eliminate the chance of giving birth to a baby with FASD. The Surgeon General’s 2005 advisory states: A pregnant woman should not drink alcohol during pregnancy. A pregnant woman who already has consumed alcohol during her pregnancy should stop in order to minimize further risk. A woman who is considering becoming pregnant should abstain from alcohol. Health professionals should routinely inquire about alcohol consumption by women of childbearing age, inform them of the risks of alcohol consumption during pregnancy, and advise them not to drink alcoholic beverages during pregnancy. Health professionals may offer brief office-based interventions to women at risk for an alcohol-exposed pregnancy or who are drinking during pregnancy, or may refer them to an alcohol treatment specialist. Women who continue to have difficulty refraining from alcohol after a brief intervention and those who are alcohol dependent should be referred to an alcohol treatment specialist. A number of effective tools are available for assessment of at-risk drinking and intervention guidelines for women of childbearing age. Currently, NIH and other agencies and organizations recommend that primary care providers screen all women of childbearing age for alcohol use. TOMORROW Ongoing research seeks to find more effective ways to prevent and treat FASD. The broadest approach involves universal prevention measures targeted to the global community of men and women, and conveys general education on risks and information to abstain from alcohol in pregnancy. Current research also includes multilevel interventions involving case management of high risk individuals and brief interventions using motivational interviewing and community reinforcement. Screening, brief intervention, and referral for treatment (SBIRT) approaches have emerged as a significant tool for addressing alcohol and other substance use in primary and prenatal care settings. SBIRT has been endorsed by the NIH, the American College of Obstetricians and Gynecologists, and other federal agencies and professional societies. Ongoing NIH research on computer-delivered brief interventions is beginning to show promising effects in the area of prenatal substance use, with early results suggesting that computer-delivered SBIRT may be implemented efficiently and at low cost in community settings. Other ongoing efforts to minimize the damage caused by prenatal alcohol exposure include studies of pharmacological intervention during pregnancy. This approach may be applicable when there is alcohol exposure before a woman recognizes that she is pregnant, or otherwise fails to stop drinking during the pregnancy. Early-stage clinical trials are underway to assess the ability of choline supplementation as well as several behavioral interventions to mitigate learning and behavioral deficits in children with FASD. In addition, basic science investigations are exploring a number of other potential therapeutic interventions, such as dietary choline supplementation during pregnancy to prevent FASD. Researchers are also using animal models of FASD to explore several promising approaches to reversing or ameliorating neurobehavioral deficits. For example, recent animal studies examining the effects of neonatal binge alcohol exposure on the performance of a motor task suggest that complex motor skill training may help reverse performance deficits resulting from such exposure. NIAAA also seeks to launch an initiative to establish more precise estimates of FASD prevalence through creation of a standardized diagnostic system among affected children. While multiple studies designed to examine the risk factors for and effects of FASD have estimated the overall prevalence of FASD in the U.S., results of these studies suggest disparities due to relatively high rates of FASD in selected heavily drinking groups. There is a substantial need to determine a more accurate prevalence of FASD in broader communities exhibiting more variable risk. Source: National Institute on Alcohol Abuse and Alcoholism

Fetal Alcohol Spectrum Disorders

YESTERDAY

• Alcohol’s ability to cause birth defects was recognized more than three decades ago by U.S. researchers, and it is now the leading known environmental teratogen (an agent capable of causing physical birth defects). In a 1981 advisory, the U.S. Surgeon General suggested that pregnant women should limit their alcohol intake – although no recommended level of intake was specified.
• Fetal alcohol syndrome (FAS) is one of the most serious consequences of heavy drinking during pregnancy. FAS is a devastating constellation of birth defects characterized by craniofacial malformations, neurological and motor deficits, intrauterine growth retardation, learning disabilities, and behavioral and social deficits.
• While the prevalence of FAS in the U.S. is between 0.5-2.0 cases per 1000 births, it is more common in other parts of the world. For example, in parts of South Africa where heavy drinking prevails, the incidence of FAS exceeds 60 cases per 1000 individuals.
• It is estimated that for every child born with FAS, three additional children are born who may not have the physical characteristics of FAS but who, as a result of prenatal alcohol exposure, still experience neurobehavioral deficits that affect learning and behavior.

TODAY

• The umbrella term "Fetal Alcohol Spectrum Disorders (FASD)" is now used to characterize the full range of prenatal alcohol damage varying from mild to severe and encompassing a broad array of physical defects and cognitive, behavioral, and emotional deficits.

• The earliest stages of life are periods of great vulnerability to the adverse effects of alcohol. Embryonic

• The earliest stages of life are periods of great vulnerability to the adverse effects of alcohol. Embryonic and fetal development are characterized by rapid, but well-synchronized patterns of gene expression, which makes the embryo/fetus particularly vulnerable to harm from alcohol.
• Research shows that patterns of exposure known to place a fetus at greatest risk for FASD include drinking four or more drinks per occasion, and drinking more than seven drinks per week. The outcomes attributable to prenatal alcohol exposure for the children of women drinking in this manner include deficits in growth, behavior, and neurocognition, including deficits in arithmetic, language and memory, visual-spatial abilities, attention, and speed of information processing.
• Imaging and neurobehavioral research in individuals with FAS and FASD reveals that some brain regions appear to be most sensitive to prenatal alcohol while other areas apparently are spared adverse effects. Particularly vulnerable regions include the frontal cortex, hippocampus, corpus callosum, and components of the cerebellum, including the anterior vermis.
• Despite a number of prevention efforts, including point of sale warning signs and bottle labeling, national surveillance data indicate that in 2005, 12% of pregnant women admitted drinking alcohol in the previous month and 2% were binge drinking. Data from prenatal clinics and postnatal studies suggest that 20-30% of women drink at some time during pregnancy. A majority of women in the U.S. reduce or abstain from alcohol once pregnancy is recognized but almost half of pregnancies in the U.S. are unplanned. More than 12% of women who are not using contraception and are at risk of becoming pregnant drink at levels that exceed 7 drinks per week or 4 or more drinks per occasion.
• In a 2005 update of the Surgeon General’s advisory of 1981, the U.S. Surgeon General advised pregnant women and women who may become pregnant to abstain from drinking alcohol to eliminate the chance of giving birth to a baby with FASD.
• The Surgeon General’s 2005 advisory states:
  
  
  • A pregnant woman should not drink alcohol during pregnancy.
  • A pregnant woman who already has consumed alcohol during her pregnancy should stop in order to minimize further risk.
  • A woman who is considering becoming pregnant should abstain from alcohol.
  • Health professionals should routinely inquire about alcohol consumption by women of childbearing age, inform them of the risks of alcohol consumption during pregnancy, and advise them not to drink alcoholic beverages during pregnancy.
  • Health professionals may offer brief office-based interventions to women at risk for an alcohol-exposed pregnancy or who are drinking during pregnancy, or may refer them to an alcohol treatment specialist. Women who continue to have difficulty refraining from alcohol after a brief intervention and those who are alcohol dependent should be referred to an alcohol treatment specialist.
• A number of effective tools are available for assessment of at-risk drinking and intervention guidelines for women of childbearing age. Currently, NIH and other agencies and organizations recommend that primary care providers screen all women of childbearing age for alcohol use.

TOMORROW

• Ongoing research seeks to find more effective ways to prevent and treat FASD. The broadest approach involves universal prevention measures targeted to the global community of men and women, and conveys general education on risks and information to abstain from alcohol in pregnancy.
• Current research also includes multilevel interventions involving case management of high risk individuals and brief interventions using motivational interviewing and community reinforcement.
• Screening, brief intervention, and referral for treatment (SBIRT) approaches have emerged as a significant tool for addressing alcohol and other substance use in primary and prenatal care settings. SBIRT has been endorsed by the NIH, the American College of Obstetricians and Gynecologists, and other federal agencies and professional societies. Ongoing NIH research on computer-delivered brief interventions is beginning to show promising effects in the area of prenatal substance use, with early results suggesting that computer-delivered SBIRT may be implemented efficiently and at low cost in community settings.
• Other ongoing efforts to minimize the damage caused by prenatal alcohol exposure include studies of pharmacological intervention during pregnancy. This approach may be applicable when there is alcohol exposure before a woman recognizes that she is pregnant, or otherwise fails to stop drinking during the pregnancy.
• Early-stage clinical trials are underway to assess the ability of choline supplementation as well as several behavioral interventions to mitigate learning and behavioral deficits in children with FASD. In addition, basic science investigations are exploring a number of other potential therapeutic interventions, such as dietary choline supplementation during pregnancy to prevent FASD.
• Researchers are also using animal models of FASD to explore several promising approaches to reversing or ameliorating neurobehavioral deficits. For example, recent animal studies examining the effects of neonatal binge alcohol exposure on the performance of a motor task suggest that complex motor skill training may help reverse performance deficits resulting from such exposure.
• NIAAA also seeks to launch an initiative to establish more precise estimates of FASD prevalence through creation of a standardized diagnostic system among affected children. While multiple studies designed to examine the risk factors for and effects of FASD have estimated the overall prevalence of FASD in the U.S., results of these studies suggest disparities due to relatively high rates of FASD in selected heavily drinking groups. There is a substantial need to determine a more accurate prevalence of FASD in broader communities exhibiting more variable risk.

Source: National Institute on Alcohol Abuse and Alcoholism