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Jack Sisson's TBI Blog
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Tuesday, November 27, 2012
Reminder: Progress Doesn't Always Go Forward
Whatever the medical problem, we all like the idea of simply taking a pill over more heavy-handed approaches like surgery, transplantation, chemotherapy, and radiation. It's just so simple, right -- open the mouth, toss the little thing in, and swallow? For treating neurological problems in particular, nothing may seem more logical: sure, an awful lot of wiring comes into play... but it's mostly just chemicals, right? You should be able to just add more of a chemical, or introduce a new one, to fix some inner imbalance?
The US military in particular has been investigating the use of a drug commonly called citicoline (WebMD) for treatment of traumatic brain injuries.
Not that anyone expects a "cure," of course, especially one to be simply gulped down in battlefield emergencies. But citicoline has seemed (in both rats and humans) to halt some of the chemical effects on the brain of various injuries -- not just head trauma, but ischemic stroke, glaucoma, and so on. Best of all: it's a naturally-occurring drug, marketed under various brand names but not subject to patent restrictions... and (at least in the US) requires no prescription. A quick search online confirmed that it's inexpensive and widely available from "regular" sources. You don't have to obtain citicoline from a furtive retailer with an office on the sidewalk at a poorly-lit street corner.
But a recent study in Europe of over two thousand patients (published in the Journal of the American Medical Association, or JAMA) reveals that citicoline is no more effective than placebos in the treatment of TBIs. The study followed the progress of over two thousand patients, including more than 1,200 in the US, over the course of 90 days' treatment. This is disappointing news, for TBI treatment not just here but around the world. (The study's author says citicoline is approved for use as a TBI treatment in almost sixty countries.)
One interesting angle to the report, by the way: although they didn't sponsor the study, a Spanish manufacturer of citicoline supplied the samples used in the testing. Good to be reminded that pharmaceutical testing doesn't always lead to results beneficial to the commercial interests of the parties behind it.
Sunday, November 25, 2012
Citicoline Supplement Doesn't Help Treat Brain Injury, Study Finds
From U.S. News and World Report:
The 'nutraceutical' had been widely used to ease trauma damage, but research shows no effect
The supplement citicoline does nothing to help improve brain function in patients with traumatic brain injury, a new study finds.
In the United States, citicoline is widely available at health food stores as a nutraceutical -- a product that reportedly provides health and medical benefits -- and is used by patients with a range of neurologic disorders.
Citicoline is also approved for treatment of traumatic brain injury, but such use had not been evaluated in a large, randomized clinical trial, noted Dr. Ross Zafonte, of Harvard Medical School, Spaulding Rehabilitation and Massachusetts General Hospital in Boston, and colleagues.
Their phase 3 clinical trial included more than 1,200 patients with mild, moderate or severe brain injuries. The patients started taking either citicoline or an inactive placebo within 24 hours of their injury and continued the therapy for 90 days.
Brain function tests conducted after the treatment period showed little difference between the two groups of patients. Rates of improvement ranged from about 35 percent to 86 percent in the citicoline group, similar to 36 percent to 84 percent observed in the placebo group.
A second evaluation, conducted six months after the brain injury, again revealed little difference between patients who took citicoline and those who took the placebo, according to the study published in the Nov. 21 issue of the Journal of the American Medical Association.
One expert said the study findings are disheartening.
The lack of any therapeutic effect "is another disappointment for individuals with traumatic brain injury," said Wayne Gordon, vice chair of the department of rehabilitation medicine at the Mount Sinai School of Medicine in New York City. He said "it highlights the fact that traumatic brain injury as an injury is not 'one-size-fits-all' and research is needed to develop approaches to the better classification of brain injury."
The study authors agreed, saying their findings suggest that the "worldwide use of citicoline for traumatic brain injury should now be questioned."
Dr. Danny Liang is a neurosurgeon at the Cushing Neuroscience Institute, part of the North Shore-LIJ Health System, in Manhasset, N.Y. He said that the new study "gives the medical community the most objective way to evaluate this potential therapy."
However, "this was a well-designed study that unfortunately gave disappointing results," Liang said.
The U.S. National Institute of Neurological Disorders and Stroke has more about traumatic brain injury.
Link to U.S. News and World Report.
Head trauma awareness up, but many NFL players are tuning it out
When the NFL and the NFL Players Association completed their 10-year labor deal last year, they agreed to commit more than $100 million over its duration to medical research, primarily that of brain injuries.
Since NFL commissioner Roger Goodell was questioned at congressional hearings in 2009 about the league’s approach to concussions and whether head injuries in football can be linked to brain disease, the league has toughened its standards and improved its methods for diagnosing and treating concussed players.
There are campaigns by Steelers coach Mike Tomlin about awareness, and even Hall of Fame safety Ronnie Lott is a spokesman for the league’s cause.
Concussion awareness has never been greater in the eyes of the NFL. But the win-at-any-cost culture of among most players seemingly still exists. Despite the potential long-term effects of repeated blows to the head, players are loathe to take themselves out of a game for medical precautions.
• Steelers safety Ryan Clark suffered two concussions in a 15-day span — and didn’t miss a game.
• Teammate Troy Polamalu has been diagnosed with “eight or nine” concussions over his career but told “The Dan Patrick Show” during the offseason that he lied about having concussions in the past. “Yes, I have, for sure,” Polamalu said, noting that he has chosen to play injured despite the team’s medical staff advising him otherwise.
• Steelers linebacker James Harrison has estimated he had a dozen unreported concussions during his career.
• San Francisco quarterback Alex Smith stayed in the game for several plays after he suffered a concussion against St. Louis two weeks ago.
• The next night, Chicago quarterback Jay Cutler played seven snaps after his concussion.
• Steelers running back Isaac Redman was diagnosed with a concussion during last week’s game against Baltimore and said he was “woozy” as late as Tuesday. He passed a concussion test and was on the practice field the next day. He was cleared a day later and will be on field Sunday against the Browns.
• Chicago linebacker Brian Urlacher said recently he would cover up a concussion if it meant staying on the field.“There’s a lot of risk, but there’s a lot of reward in (football),” Clark said. “You can provide a great life for your family. You get great relationships. We get paid well. But you know there’s going to be some risk to it, especially if you play the way that I play it.”
‘Why Would You Tell?’
One hundred and 58 players are on the season-ending injured reserve list but only five because of concussions, with the biggest name being Detroit running back Jahvid Best.Yet there are 14 players on this weekend’s injury report with concussions. Five are listed as probable, and two of those are expected to play Sunday and have not missed a game.
Last week, Sporting News released the results of a survey of 103 players from 27 teams that asked whether they would hide concussion symptoms to stay on the field. Fifty-six percent said yes.
Former Steelers running back Willie Parker said it’s a similar mentality today as he played from 2004-09.“For me, it was the team first,” said Parker, who signed with the Steelers as an undrafted rookie free agent and fought to beat out a future Hall of Famer (Jerome Bettis) and a notable free agent signee (Duce Staley). “That’s how I looked at it. You don’t want to let your brother next to you down.
"Will that mentality change?"
“Not if you have any fight in you,” said Parker, who broke a leg toward the end of the 2007 season and never was the same. “You have to have fight in you, hunger in you and that dog in you. If you get a concussion, why would you tell? Why would you say something?”
Saturday, November 24, 2012
Can We Prevent Alzheimer's Disease?
Three Steps The Science Suggests You Can Take To Reduce Your Risk
Thursday, November 22, 2012
Army launches campaign to dispel myths about vets with PTSD and TBI
From The Washington Post:
The Army has launched a “Hire a Veteran” education campaign aimed at debunking myths about hiring veterans with post-traumatic stress or traumatic brain injury.
Recent research by the Society for Human Resource Management, which is partnering with the Army in the campaign, has shown some employers are concerned about the impact of PTSD and TBI on a veteran’s job performance, as well as the cost of accommodating these veterans in the workplace.
About 42 percent of employers in a SHRM membership survey believe their companies would face challenges in hiring veterans suffering from PTSD or other mental health issues.
“The myth is they’re not going to be successful,” said Tim Isacco, chief operating officer for Orion International, a firm specializing in placing veterans in the private sector, said at a news conference Monday at the National Press Club. “They will be.”
The campaign includes a video and online employer toolkit that can be downloaded at www.wtc.army.mil/employers.
“The first step is to help employers to understand that not all veterans need accommodations,” said Jeff Pons, chief human resources and strategy officer for the society. “And when they do — for PTSD or other disabilities — many of those accommodations can easily be made.”
Only 13 percent of employers were very familiar with resources on where to find veteran job candidates, according to Pon. “That’s not acceptable,” he said.
“Reasonable accommodations for our wounded warriors entering into the workplace are not difficult, expensive or a burden, especially when compared to the value these outstanding individuals bring,” said Brig. Gen. David J. Bishop, commander of the Army’s Warrior Transition Command.
The campaign is aimed at removing the stigma associated with PTSD and TBI, Bishop said.
“People think it’s some kind of tremendous burden, to the point they can’t even mention the words, like it’s a dirty name,” Isacco said.
Former Army staff sergeant Paul “Rob” Roberts, who suffered serious burns and a traumatic brain injury when his squad was hit by a roadside bomb while on patrol in Chamkani, Afghanistan, in 2009, wanted to continue working for the federal government after retiring from the Army.
With the help of the Army’s Wounded Warrior Program, Roberts was able to land an internship with the Drug Enforcement Agency. “The internship with the DEA taught me that even though I am a little bit slower, I am still a value part of the team,” he said at Monday’s press conference.
“I’m too young to be retired,” added Roberts, 30, who now works for the Federal Bureau of Investigation. “People need a sense of purpose, or they start to shut down and wither away.”
Read The Washington Post here.
We wish all our readers a safe, healthy and peaceful Thanksgiving.
We have much to be thankful for,
although we might not always remember that.
It's nice to have a day to think about what's really important
and give thanks for our many blessings.
Wednesday, November 21, 2012
Alzheimer's Disease: You Can Reduce Your Risk
From The Huffington Post:
If I told you how to reduce your risk of developing Alzheimer's Disease (AD), would you do it? My work as a geriatrician, seeing Alzheimer's patients and counseling hard-pressed families, makes me hope so.
My many conversations with people over 50, at dinner parties and elsewhere, who dread losing their memory, independence and self-control to Alzheimer's, make me hope so.
The fact that a recent poll suggested Alzheimer's is America's second most feared disease (after cancer), makes me hope so.
Amid all the difficult news about dementia, this may be one of the best reasons for hope: Contrary to widespread misconception, you have the power to lower your odds of getting dementia, even if specific medical interventions to prevent AD have yet to be identified.
Like every physician, I wish we had a treatment that could prevent or reverse this cruel disease that now afflicts more than 5 million Americans. But we don't, at least not yet. The hard truth is that, while there are medications that help slow the progression of symptoms in the early and middle stages of dementia (cholinesterase inhibitors, including Donezepil, brand name Aricept), nothing turns back the clock once Alzheimer's symptoms take hold.
What we do have, right now, is considerable knowledge about the risk factors that make it more or less likely that a person will develop Alzheimer's in the first place.
Most physicians now believe that the damage done by Alzheimer's is irreversible and that the best hope lies in preventing it. This is particularly true for people at higher risk. I believe passionately that we should all know what those risks factors are and work to turn them in our favor.
AD risk factors that you cannot change
There are two kinds of risk factors: those you can't control and those you can. Here are some risks factors that you should be aware of, even if you can't change them.
Family History: Having one parent with AD doubles your risk; two parents with AD puts you at five times greater risk.
Age: About 5 percent of Alzheimer's patients have early onset disease, but the vast majority of cases are late-onset. Seventy-four is the most common age for detection. Dementia is never an inevitable part of aging, but getting older is a risk factor. The number of Alzheimer's cases doubles every five years after age 65 and AD risk hits about 50 percent after age 85.
Genetics: People with two copies of the apolipoprotein (ApoE4) gene appear to be at about 10 to 15 times greater risk, and one copy triples the risk. That said, having one or even two copies of the gene does not mean you will definitely develop Alzheimer's. For this reason, most physicians do not recommend taking the blood test for ApoE4, except in research settings. (A different variant of the same gene, ApoE2, provides some protection against the disease.) New genes that increase risk continue to be identified, holding out promise for greater understanding of basic mechanisms, and, therefore, hope for prevention.
Multiple mutations of a number of genes are the most common cause of early-onset AD (before age 60). Members of these unfortunate families with such mutations definitely will develop AD.
On the bright side, earlier this year researchers reported an exciting discovery: a rare gene mutation that appears to offer strong protection against Alzheimer's, even for people at high genetic risk.
Being a woman: More women than men develop Alzheimer's Disease. Although women outlive men, and age is a powerful risk factor, the weight of evidence suggests that women are still at slightly higher risk than men. And there is no doubt that women bear the major burden of caregiving for persons of both sexes with AD.
Down's Syndrome: About half of all people with Down's Syndrome will develop symptoms of Alzheimer's by their 50s, but almost all at autopsy show the typical pathologic features of AD.
Continue reading for risk factors that you can change.
Tuesday, November 20, 2012
TBI Simulations via Supercomputer
Artificial intelligence, or AI, was at one time the Holy Grail of computer science. (It probably still is, in some inner circles -- maybe under another name.) It turns out that crafting a device capable of "thinking" must remain more or less on the back burner until we know more solidly what goes on in the original "thinking" machine: the human brain. As that understanding grows, and we can more closely simulate what happens at neuron Y when neuron X fires, we can turn some of our attention to the opposite problem: what happens at neuron Y when neuron X fails to fire -- as in a traumatic brain injury.
Even this presents one huge problem: the brain contains many, many more than just two neurons. Even a powerful desktop computer can't recreate all the interactions, the stimuli and responses, the changes over time in a moderately complex neural activity. Instead, we turn to supercomputers: machines capable of modeling the most complex, large-scale systems, both natural and man-made -- climate, astronomy, the genetic code, economics... and the traumatically injured brain.
Such a project recently in the news is a joint effort by the Sandia National Laboratories and the University of New Mexico. The research focuses on injuries sustained by the head as a result of nearby explosions, with the longer-term goal of improving military and sports helmet design. Researchers pursued two dovetailing lines of inquiry:
How complex are the phenomena being studied? According to one report:
Immediately following blast waves, soldiers can suffer brief losses of consciousness, but more damage evolves weeks later... The symptoms -- headaches, memory loss, mood disorders, depression and cognitive problems -- can prevent sufferers from working, he said.
There's another important avenue of investigation with the Sandia/UNM project. Most TBI studies, understandably, focus on injuries sustained from the top, front, sides, and back of the head. In recent combat, though, many brain and related injuries are coming from the bottom: the improvised explosive devices (IEDs) in Iraq and Afghanistan have often sent shock waves into the brain from below. Thus, the Sandia/UNM research has also modeled previously ignored portions of cranial anatomy: the jaw, mouth and palate, and cheekbones.
The YouTube video below comes from Sandia's YouTube channel. Says its description:
These computer simulations contain a computer model of a human's head. The images show the deposition of compressive energy in the brain during frontal blasts. These models combined with University of New Mexico's clinical observations are being used to identify energy thresholds that should lead to better military and sports helmet designs.
Sunday, November 18, 2012
NFL Board Paid $2M to Players While League Denied Football-Concussion Link
The NFL’s retirement board awarded disability payments to at least three former players after concluding that football caused their crippling brain injuries — even as the league’s top medical experts for years consistently denied any link between the sport and long-term brain damage.
The board paid at least $2 million in disability benefits to the players in the late 1990s and 2000s, documents obtained in a joint investigation by ESPN’s “Outside the Lines” and FRONTLINE show. The approvals were outlined in previously unpublished documents and medical records (pdf) related to the 1999 disability claim of Hall of Fame center Mike Webster.
The board’s conclusion that Webster and other players suffered brain damage from playing in the NFL could be critical evidence in an expanding lawsuit against the league filed in the U.S. District Court in the Eastern District of Pennsylania. The lawsuit (pdf), which involves nearly 4,000 former players, alleges that the NFL for years denied the risks of long-term brain damage and “propagated its own industry funded and falsified research to support its position.”
Bob Fitzsimmons, a Wheeling, W.Va., lawyer who represented Webster in his disability case and is co-director of the Brain Injury Research Institute, described the retirement board’s conclusions as “the proverbial smoking gun.”
“It’s pretty devastating evidence,” said Fitzsimmons, who is not part of the lawsuit against the NFL. “If the NFL takes the position that they didn’t know or weren’t armed with evidence that concussions can cause total disability — permanent disability, permanent brain injury — in 1999, that evidence trumps anything they say.”
The NFL declined to comment for this story, but league spokesman Greg Aiello emphasized in an email that the retirement board is independent, and that its decisions “are not made by the NFL or by the NFL Players Association.”
The seven-member NFL retirement board is composed of three owner representatives, three player representatives, and a non-voting representative of the NFL commissioner. Among its duties is deciding individual disability claims.
The NFL, which has filed a motion to dismiss the lawsuit, in recent years has denied that it concealed information about the risks of chronic brain injury and says it has updated its policies as concussion research has evolved over the past two decades.
Yet in a series of scientific papers from 2003 to 2009, members of the NFL’s Mild Traumatic Brain Injury Committee wrote that “no NFL player” had experienced chronic brain damage from repeated concussions. The committee, first formed in 1994, asserted that NFL players were different than boxers, whose susceptibility to brain injuries caused by the sport has been documented since the 1920s.
“Professional football players do not sustain frequent repetitive blows to the brain on a regular basis,” members of the NFL committee wrote in a December 2005 paper in Neurosurgery, the official journal of the Congress of Neurological Surgeons.
However, board documents obtained by Outside the Lines and FRONTLINE show that the NFL retirement board determined in 1999 that repeated blows to the head had left Webster, who spent most of his 17-year career with the Pittsburgh Steelers, “totally and permanently” disabled. The board based its finding on the diagnoses of five doctors, including a Cleveland neurologist hired by the board to examine the player. The doctors described Webster as “childlike” and showing signs of dementia.
“The Retirement Board determined that Mr. Webster’s disability arose while he was an Active Player,” wrote Sarah E. Gaunt, director of the NFL’s retirement plan, in a May 8, 2000 letter to Fitzsimmons. The medical reports, she wrote, “indicate that his disability is the result of head injuries he suffered as a football player with the Pittsburgh Steelers and Kansas City Chiefs.”
The board granted “total and permanent” disability benefits to two other players — one in 1996 (pdf) — who claimed their mental impairment stemmed from “repetitive trauma to the head or brain from League football activities,” according to documents provided by the NFL board as part of a 2004 lawsuit seeking additional compensation for Webster’s family. The board redacted the players’ names; the documents were stamped “confidential.”
Interviews and documents from additional cases suggest that other retired players also received long-term disability benefits for brain injuries related to football, but ESPN and PBS could not verify those cases.
Webster died at age 50 in 2002. After his death, he was the first NFL player to be diagnosed with Chronic Traumatic Encephalopathy, a degenerative brain disease that has since been found in more than a dozen deceased NFL players.
The league first acknowledged in December 2009 that repeated concussions could lead to long-term mental impairment.
Saturday, November 17, 2012
Study: Soccer Players Without Concussions Still Have Brain Changes
A small study of professional soccer players found that even those who have never experienced a concussion still have changes in the white matter of their brains, likely from routine and unprotected headers.
The brain‘s white matter is made up of nerves and their myelin protective coating (similar to the insulation that blankets electrical wire) that play a significant role in connecting brain regions and establishing neural networks that are critical to cognition. Previous studies have investigated how concussions lead to changes in this white matter, but a new study lead by Dr. Inga K. Koerte of Harvard Medical School in Boston, is one of the first to look at how even blows to the head that aren’t considered concussions may lead to traumatic brain injury.
In the study, the researchers compared bran scans of 12 male soccer players from German elite-level soccer clubs who had not experienced a concussion, to brain scans of 11 competitive swimmers who had similarly never experienced repetitive brain trauma. The research team used high-resolution diffusion tensor imaging (DTI), which looks at the brain microscopically and is much more effective at catching white matter changes than the standard MRI.
The researchers found surprising alterations in the white matter that were “consistent with findings observed in patients with mild TBI, and suggesting possible demyelination [nerve disorder].” Even though the players had no concussions, their brains told a different story of damage, including changes to the myelin sheaths surrounding nerves.
“Although our study is small, it is the first to look at soccer players with no symptoms and no diagnoses of concussions,” says Koerte. “We think it is an important finding not just for soccer players, but other athletes of other sports too.”
While concussions have long been a part of professional sports such as boxing and football, researchers are still struggling to define concussions clinically, and research into brain changes resulting from repetitive blows to the head is a relatively new area of research. “[Brain damage from repetitive blows] would have tremendous public health implications,” says Dr. Jeffrey Bazarian, an associate professor of emergency medicine at URMC. “If players are damaging their brains, it is a large public health issue because everyone, even at a young age, hits their head like this. But right now we really don’t have enough information.” Bazarian was not involved with the study, but has also used DTI to assess mild brain injury in high school football and hockey players.
Link to a related story: Frequent Soccer-Ball Headers Linked to Brain Injury
Friday, November 16, 2012
Report: Deaths rose after nursing home evacuations
From USA Today:
A new study about nursing home evacuations during hurricanes exposes grave consequences suffered by the most vulnerable residents and flaws within government guidelines for the relocations.
A 218% increase in the mortality of residents with severe dementia is cited in a three-year study of 21,255 residents living in nursing homes along the Gulf Coast within 30 days of an evacuation, and a 158% increase in deaths within 90 days.
The authors' report Thursday at the Gerontological Society of America's annual meeting in San Diego comes seven months after a government study cited "gaps'' in the evacuation plans of nursing homes that could compromise health and safety.
"We don't know why these deaths are occurring after evacuations,'' says Lisa Brown, a lead author of the dementia study and a professor of aging studies at the University of South Florida-Tampa. "This is the first report to quantify the deaths. It tells us we need to think through evacuations."
Though physical safety is emphasized in government guidelines, Brown says, "there's a shortfall when it comes to mental health issues. Dementia, depression and anxiety are not being dealt with."
The authors wrote that 50% to 70% of about 1.6 million adults living in nursing homes have Alzheimer's disease or a related dementia.
"Sheltering in place'' is the preferred method for dealing with residents, Brown says, because of the risks of relocation. There was a four-fold spike in evacuations from Hurricane Katrina in 2005, when about 140 patients drowned in nursing homes, through Hurricane Gustav in 2008.
Wednesday, November 14, 2012
Caregivers for relatives with dementia need help and support
From the Cleveland Plain Dealer:
Caring for a family member with a debilitating illness such as dementia can be an exhausting responsibility.
Nearly 65 million Americans provide the day-to-day needs of ailing family members at least 20 hours weekly, according to AARP. Of those, 15 million take care of people with Alzheimer's disease, a brain disorder that results in loss of memory and intellectual functions.
In many cases, these caregivers, generally family members, are not getting paid and not getting much physical or emotional relief. Fatigue can be a danger, whether the care is given in their own home or a relative's home, experts say. Or even making decisions long distance.
"Most people who are providing care tend to be doing it in isolation, and their journey can be very lonely," said Eric Hall, president and CEO of the Alzheimer's Foundation of America.
Other family members sometimes don't know how to react, and friends tend to back away, leaving the caregiver alone," he said. "There is no cure, there is no silver bullet. It comes down to care. The question is: What do we do now to support the families?"
Experts say that caregivers need to avoid burnout by learning about the illness, asking for help, being organized, setting aside time for themselves and facing their own emotions. Often, there is one person in the family who takes on a large part of the responsibility.
Happily sacrificing but exhausted
Jeff Jenkins, 50, spends his days as a nurse at the Cleveland Clinic caring for critically ill patients and his evenings at home caring for his mother.
"My mother sacrificed everything for me," the Avon Lake resident said. "I want to do the same. It's my choice."
That's why Jenkins, a divorced father of three daughters, decided to keep his mother at home rather than in a care facility.
Though he has help at home when he's at work, Jenkins said, the routine can be draining.
"Sometimes I don't have any time to unwind. It's like my drive home is my only downtime," Jenkins said.
Though she has not been formally diagnosed, Jenkins' 78-year-old mother, Victoria Jenkins, likely has dementia, he said. Jenkins first noticed a change in his mother four years ago following surgery to repair her broken wrist after a fall.
"She wasn't enjoying things that she typically enjoyed. She was an avid reader, but began saying, 'I really can't get into this book. I don't know what's going on,' " he said.
This was a noticeable change because his mother, who had worked in the bridal boutique of a department store and then in food service for a school system, had always been active and independent.
Jenkins said his mother would be more confused and scared in a facility. She's more likely to maintain her abilities longer living at home.
In-home support good for caregiver
More people appear to be choosing the in-home route.
The at-home senior-care industry has been growing by about 15 percent annually in the past several years, said Larry Mason, executive director of Senior Helpers of Northeast Ohio. The agency provides nonmedical personal care and companionship.
Mason said about 40 percent of the people his employees look after have dementia or Alzheimer's.
Families, who often pay out of pocket, contract for outside help from a few hours a week to around the clock. Hourly rates for this nonmedical care can be as much as $25.
Experts say that caregivers who regularly schedule activities outside the house ultimately lengthen the time they can do the job effectively.
Jenkins agreed. "Church is big for me. It gets me back in order so I can function and not lose my mind."
Monday, November 12, 2012
Mixing Meds and Alcohol: Just How Dangerous Is It?
Most psychiatric drugs bear some version of the warning: “Do not drink alcoholic beverages when taking this medication.”
In reality, though, many people taking psych meds drink anyway. They have various reasons: not wanting to curtail their fun, not putting much stock in the warnings, or simply thinking it’s easier to take a proffered drink than explain why they’re turning it down.
Doctors oftentimes don’t bother to talk to patients about potential dangers. Or they tell patients not to drink, but don’t explain why. To make matters worse, because of a lack of studies on the subject, patients inclined to do their own research will have a hard time just how risky it is to drink while taking various kinds of psychiatric medications (I’ve written elsewhere about this troubling lack of evidence).
A widely publicized study that came out last month in the journalNeurology underscores the problem. The findings, which pooled data from 16 studies, showed that people taking SSRI antidepressants like Zoloft or Celexa were 40 percent more likely to suffer a type of stroke caused by bleeding in the brain and 50 percent more likely to suffer any bleeding in the skull.
The overall risks remained tiny (this kind of rare stroke occurs in just 26 out of every 100,000 people in a given year, and taking SSRIs could be expected to increase the likelihood by about 1 person out of 10,000).
As a journalist, I’m skeptical of exaggerating dangers – especially since this study didn’t even look at at alcohol use directly, and because the risk of suffering brain hemorrhages is so low overall.
But as someone who has taken SSRIs for many years and done my fair share of college and post-college heavy drinking, I have to confess to being slightly unsettled by these warnings.
I also didn’t find it particularly reassuring that the lead authorsuggested that heavy drinkers might want to switch to a different kind of antidepressant, such as Wellbutrin or an older tricyclic drug like Pamelor or Elavil. Both Wellbutrin and alcohol increase the likelihood of seizure, which makes combining them extra-risky (something I only learned after years of doing just that). And tricyclics carry their own risks when combined with alcohol.
The obvious answer, you might say, is simply to be safe, not sorry. In the absence of studies examining the relationship between alcohol, particular psychiatric medications and specific negative health outcomes, it’s probably wiser to abstain from drinking if the drug you’re taking warns against it.
Thursday, November 08, 2012
Dementia deaths more than double in a decade
Is it just me or is the United Kingdom paying proportionately more attention to dementia and its societal consequences than the United States? Maybe it's just a product of Google and the various other search engines I use, but for a country much smaller than the Southeastern United States, they seem to publish more articles on the subject and conduct more studies than any other like-sized country. Like the headline for this article, which should be major news anywhere. Does Britain have an epidemic of dementia? And if so, is it part of a worldwide trend? Do these numbers extrapolate globally? What in the world could cause brain disease to double in just 10 years? Can the fact that we're living longer really cause the number of such deaths to double in just a decade? Any ideas out there?
From The Telegraph:
The proportion of people dying of dementia has more than doubled in a decade, official figures show, and by 2021 one in eight of all deaths could be due to the brain disease
Every tenth woman in England and Wales now dies of dementia (10.3 per cent), according to mortality figures for 2011 from the Office for National Statistics, up from 4.3 per cent in 2001.
In men, the proportion of deaths from dementia has risen from 2.0 to 5.2 per cent over the course of the decade.
Should these rises be sustained, it will mean that by 2021 about 12 per cent of all deaths will be attributed to dementia.
Experts said the figures were a “scary” reminder of the scale of the dementia timebomb facing Britain
At the moment some 800,000 people in Britain are living with dementia, including about 500,000 from the most common type, Alzheimer’s. Less than half (43 per cent) have received a formal diagnosis. One million are expected to have dementia by 2021.
Professor Clive Ballard, head of research at The Alzheimer’s Society, said the increase in deaths attributed to dementia was due both Britain's ageing population and to a greater understanding that the disease did actually kill people.
He said: “Dementia is getting more common, because people are living longer.
“There’s an exponential increase in dementia with age. One in 20 people at 65 have it, but that increases to one in five at 80, one in three at 90 and one in two at 95.
“So once you get more and more people living beyond 80, you will get more people dying from dementia.”
He also said doctors were now far more likely to record dementia as the underlying cause of death, due to a better understanding of it.
He explained: “In very severe Alzheimer’s, people get bed-bound, can’t clear their chests properly and become very vulnerable to infections like pneumonia.
“Whereas 10 years ago a doctors might have put ‘pneumonia’ as the cause of death on the death certificate of someone with dementia, now they are more likely to put ‘pneumonia and dementia’.”
People with Alzheimer's were also "much more prone" to strokes because the amyloid proteins associated with the disease in the brain also tended to block blood vessels.
Just as doctors had realised for years that people with end-stage cancer were really killed by the disease, rather than the final trigger such as an infection or a heart attack, so they were now accepting a similar thing happened in those with dementia.
Given that one in three 65-year-olds will develop dementia during the rest of their lives, Prof Ballard thought predictions that one in eight could be dying of the disease by 2021 might prove on the low side.
“If we assume that half of those with dementia will die of it, that suggests a sixth of all deaths could be due to the disease,” he said.
“The proportion of the increase is quite scary, and that’s why we need to have a plan now, rather than burying our heads in the sand.
Tuesday, November 06, 2012
Alzheimer's may have a genetic component
Researchers said Tuesday they had seen the earliest-ever warning signs of Alzheimer's Disease -- among a high-risk group of 20-somethings -- in the ongoing quest for early detection and prevention.
A major problem in the search for a cure for this debilitating form of dementia is that symptoms appear years after irreversible brain decay has already set in.
For the study, a team of scientists from the United States and Colombia tested 18- to 26-year-old members of an extended Colombian family that share a common ancestor and a genetic predisposition to develop an inherited form of Alzheimer's.
One in three members of the clan carry a gene mutation that will lead to a rare form of the disease which hits people in their 40s, unlike the common variant which presents much later.
A brain scan comparison found that individuals who carry the errant gene have less grey matter in certain areas of the brain than those who don't, scientists wrote in The Lancet medical journal.
They also found that those with the mutation had higher levels in their cerebrospinal fluid of a protein called amyloid beta, implicated in the plaque build-ups found on the brains of Alzheimer's sufferers.
The findings "suggest that neurodegenerative changes occur more than 20 years before symptom onset and somewhat earlier than was suggested by findings from previous MRI studies," Nick Fox of the University College London's Dementia Research Centre said in a comment on the study.
Alzheimer's disease causes two-thirds of dementia cases -- attacking one in 200 people -- the rate is increasing as the world's population ages.
Trial participants, 20 with the fateful gene mutation and 24 without, were not told whether they had it or not. All had normal cognitive abilities at the time of the study.
"The findings... could ultimately lead to improved early detection and better clinical trials of preventative treatments," The Lancet said in a statement.
"These findings... raise new questions about the earliest brain changes involved in the predisposition to Alzheimer's and the extent to which they could be targeted by future prevention therapies," research leader Eric Reiman from the Banner Alzheimer's Institute in Arizona said.
Scientists still do not know quite what to make of the plaques and tangles that German doctor Alois Alzheimer first spotted in the brain of a dementia patient who died in 1906.
They disagree on the respective roles of beta amyloid plaque build-ups and of a protein called tau which forms tangles inside the brain cells.
Most test therapies have targeted beta amyloids, but some now suggest it is actually tau killing the brain cells.
According to Fox, the new study questioned existing models of Alzheimer's Disease "on several fronts".
Among other things, "neurodegeneration would seem to be occurring in advance of evidence of plaque deposition", widely thought to cause the brain damage.
Fox said the results should be treated with caution as the trial sample was small and the outcome may not apply to the much more common sporadic, late-onset form of Alzheimer's.
Alzheimer's Disease International (ADI) projects the number of people with dementia will rise from 35.6 million in 2010 to 65.7 million by 2030 and 115.4 million by 2050.
Friday, November 02, 2012
Physical activity may reduce dementia in oldest seniors
From EMAX Health:
A regular exercise program has many benefits. A new study has found that regular physical exercise may ward off dementia in oldest seniors. Researchers affiliated with the Department of Neurology, University of California, Irvine (UCI) published their findings online on October 22 in the journal Archives of Neurology.
Take home message:
Read the entire article here.
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