Multiple sclerosis sufferer Tracey gets a helping paw from clever Kofi

8:36am Thursday 1st March 2012 in News by Sally Clifford

Tracey Robinson, who suffers from multiple sclerosis, with her specially-trained labrador Kofi

They say a dog is man’s best friend. Tracey Robinson’s beautiful black labrador, Kofi, is much more than that.

Kofi collects the post and can open and shut doors – little things Tracey often finds difficult in her daily struggle with multiple sclerosis.

Tracey was 25 when she was diagnosed with the debilitating condition which her mum, Shirley, also suffers from. Shirley was diagnosed in her 40s, and Tracey says being able to talk to her mum and share experiences helps them both.

Tracey’s initial instinct that something was wrong stems from an episode of double vision when she was 15. she had an operation to correct a squint and saw a neurologist, but it would be many years later before she was diagnosed with MS.

around 100,000 people in the UK have MS. it is normally diagnosed between the ages of 20 and 40.

MS is a complex condition with many symptoms which can include fatigue, dizziness and vision problems. Balance can be affected, along with the bladder. it can also cause stiffness and spasms.

While nursing, Tracey noticed her leg dragging after a shift and pins and needles in her hands, but she put it down to the effects of having done a long shift.

Dizzy spells and the loss of the use of her right side were symptoms she couldn’t ignore, and after being referred to another neurologist, Tracey was diagnosed with MS.

Her eldest child, Sam, now 25, who runs the family pub in East Bierley, was six months old at the time, but Tracey never let it stop her living her life and copes with it as best she can.

Her daughter Kate is now 20. Both have been to university and Tracey is proud of them and continues to give herself goals.

“I used to have goals in my head – ‘I have got to wait until they are both at school before I get really bad’, ‘I have to wait until they have both left home’ – and now I think, ‘I have to wait until they are married before I get really bad’. It’s moving goals on,” says Tracey.

Her mobility is severely affected. she has an electric wheelchair and a scooter to go out and she never goes out alone.

Tracey has a supportive network around her with friends and family and Kofi, of course.

he joined the family three years ago after Tracey’s husband, Nick, found out about the charity Dogs for the Disabled.

“You hear about dogs for the blind, but I’d never known about them,” says Tracey, referring to Dogs for the Disabled.

“Nick went into it and said the dogs could pick things up for you. Bending down can be really bad for me. if I knelt down to pick something up, I wouldn’t get back up again,” she explains.

Kofi is specially trained to help Tracey around the house, and he can open and shut doors for her.

“If I drop something like the remote control or the phone he will pick it up for me and he fetches the post when it comes,” says Tracey.

“He’s also company for me. I know he is there.”

Tracey tells how Kofi is constantly by her side. he waits while she gets showered and changed on a morning, making sure she is all right.

“He is a lovely dog. he is so gentle,” says Tracey.

Kofi has a special coat so people know he is a working dog. around Tracey’s home village he has become a mini-celebrity. “Everybody likes him,” says Tracey. “He is just somebody else to watch over me.”

since its inception in 1988, Dogs for the Disabled has trained more than 575 assistance dogs. There are currently more than 250 working partnerships and teams across the UK.

Assistance dogs are provided for adults and children. The charity also offers an autism assistance dog service for children with an autistic spectrum condition between the ages of three and ten.

at eight weeks old, the puppies are given to a puppy socialiser, a family who volunteers to look after the puppy for a year, getting it used to sights and sounds in preparation for it becoming a qualified assistance dog.

Opening and closing doors; helping a person dress and undress; barking to raise the alarm in an emergency; picking up items such as mobile telephones or dropped articles like keys or a bag; loading and emptying the washing machine; retrieving slippers, gloves or a remote control; switching lights on and off; fetching the post; pressing a pedestrian crossing button; reaching up to shop-counters with items such as a wallet and helping people to walk by providing a constant forward motion are just some of the tasks the dogs are trained to do.

but the cost of training an assistance dog is £18,000 and the charity receives no Government funding, relying on voluntary donations to fund its work.

since 2004, Dogs for the Disabled has had runners taking part in the Great North Run to support its cause and the charity is appealing for people to participate in this year’s run on Sunday, September 16, to help raise much-needed funds to enable it to improve the quality of many more lives.

To find out more, visit dogsforthedisabled.org/support-us and click on ‘Raise money for us’, e-mail , or call (01295) 252600.for more information about multiple sclerosis, visit mssociety.org.uk.

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there are few medical diagnoses more life changing than Parkinson’s disease. This neurodegenerative disorder is detected in some 70,000 people in the U.S. each year; Michael J. Fox and Muhammad Ali are best known for having Parkinson’s disease.

As a neurologist, I find it particularly tragic that most of these patients are referred late and do not find out they have Parkinson’s until they are already suffering from the severe tremors, walking difficulties, loss of smell and other physical manifestations of the disease.

Parkinson’s occurs when dopamine-producing cells, which control aspects of movement, diminish in the brain. we know that the disease starts working its damage long before physical symptoms show up. Parkinson’s can take as long as 12 years or more to develop, and the first mild symptoms are often mistaken as part of the normal aging process.

Because there are no simple tests to detect Parkinson’s in its early stages, it can take up to two to three years to accurately diagnose the disease. By the time someone has their first physical sign (tremor, rigidity or shuffling gait), 50 percent to 70 percent of the brain cells that produce dopamine, which controls movement, have already died.

Unfortunately, there is little that we physicians can offer patients at that point other than damage control. if we could intervene earlier on, we might be able to stave off or delay the progression of disease through neuroprotection.

In Pasadena, we have the first-FDA approved radiopharmaceutical imaging agent that can help physicians evaluate patients with suspected parkinsonian syndromes (PS) and related diseases. It is called DaTscan. Despite the unavailability of a simple blood test, tools like DaTscan can offer evidence that may help lessen diagnostic uncertainty and confusion for early-stage Parkinson’s patients and their families.

When DaTscan is combined with a single photon emission computed tomography (SPECT) brain scanner, it produces visual evidence of the amount of dopamine transporter cells, allowing physicians to determine whether occasional tremors are the result of Parkinson’s or some other cause.

DaTscan has been in available in Europe for more than 10 years; the FDA approved the imaging agent for use in the U.S. in January 2011; I scanned the first patient in Pasadena with it on Sept. 6. I believe that DaTscan will revolutionize both neuroimaging and the treatment of Parkinson’s as more and more hospitals and physicians learn about this method.

DaTscan can also detect Parkinson’s Disease by detecting early risk factors (red flags) alone or in combination, that may appear more than a decade before physical symptoms, such as , decreased or lost sense of smell or certain sleep disorders, but these uses are not yet FDA approved.

Just think how much we could slow down this difficult disease and improve lives of patients and their caregivers if we are able to act before the symptoms of Parkinson’s become debilitating and ensure that treatment recommendations are appropriate. I am certain that early detection is the future for Parkinson’s disease.

Dr. Jerome Lisk is a physician at Southern California Movement Disorder Specialists, 65 N. Madison Ave. Suite 410, Pasadena. 626-792-6683. socalmds.com

When Lewis Carroll sent Alice down the rabbit hole, she encountered a strange and twisted land with distortions of size and time. Some headache experts see something else — the possible ghosts of the author’s migraines, which can leave victims temporarily blinded, nauseated, hallucinatory, numb, unable to concentrate or seeking shelter from painful stings of light and sound.

People with migraines travel between two worlds: one in which they are having a migraine and one in which they are not. “I’m very brave generally,” Tweedledum tells Alice, “only today I happen to have a headache.” But even after the headache is gone, migraine sufferers live with the dread of its return.

For more than a century, researchers have been trying to step through the looking glass to find clues to the mystery of migraines, with little success. Treatments that can prevent or end migraine attacks exist only because drugs for something else were found, often by accident, to quiet the migraine’s neurological storm.

“All of the major things we use were not designed for migraine at all,” says Peter Goadsby, a neurologist at the University of California, San Francisco. “It’s not good enough that one of the commonest of medical problems has treatment developed by serendipity.”

A major barrier to relief, it turns out, has been that migraines, which affect 36 million people in the United States, have no known cause. But researchers now think that they are, at least, looking for the culprits in the right places.

“For almost 100 years, people believed it was a vascular disease,” says Rami Burstein, academic director of the Comprehensive Headache Center at Beth Israel Deaconess Medical Center in Boston. Blood vessels, it is now thought, are probably just aiding and abetting the crime. instead, the perpetrators are nerves inside the brain itself, which misfire and set off a disastrous sequence of events. Making things more complicated, migraine sufferers may differ in their thresholds of susceptibility and sets of triggers. “Migraine is for the most part a genetic disease,” Burstein says, “a problem with genes that regulate excitability of neurons in the cortex.”

Study results announced last year point to three genes that may be linked to migraines. along with other “migraine genes,” the findings seem to paint a picture of brain cells that remain too jumpy when they are supposed to be settled down. With each new discovery, migraine sufferers are brought closer to the day when they might finally be able to escape the hell in their heads.

Stemming the tide

Migraine researchers spent a long time focusing on blood vessels, partly because the notion seemed to make sense: The pain of a migraine throbs in sync with a person’s heartbeat, and triptans — the first class of drugs approved specifically for migraines — constrict blood vessels in the brain. Research suggested that vessels in the head set off a domino of neurological reactions after abnormally contracting, then dilating. Ironically, some of the shift away from the blood vessel theory arose from the study of triptans themselves.

Sumatriptan, the first of the triptans, was introduced for clinical use in the early 1990s. “It was a real milestone in the headache world,” Goadsby says. “But as people looked at sumatriptan, it became clear that it did more than just constrict blood vessels.” The drug also affected nerves, raising the possibility of a different explanation for its effectiveness. more recent evidence has poked holes directly in the blood vessel theory: a study in 2008 in the journal Brain found that blood vessel size during much of the headache is normal (though a more recent study with better resolution is more supportive of at least some vascular role in a migraine attack).

Goadsby was drawn to study migraines largely because one part of the vascular theory never made sense to him. The pain often strikes only one side of the head, and it isn’t necessarily the same side from episode to episode. “I never understood how something originating from the bloodstream would just affect one side of the head,” he said.

So Goadsby decided to use medical imaging as a window into the brains of people having a migraine attack. His curiosity had mostly to do with the brain stem, which controls many basic body functions, such as digestion and circulation — some of the same systems known to go haywire during a migraine attack. It seemed logical to him that a migraine had to originate in some central area since, other than the headache itself, the symptoms don’t tend to be lopsided.

“The brain stem has, in a small area, the ability to affect a large part of the brain,” Goadsby says. in experiments he began publishing in 2005, he used PET scans to identify three locations in the brain stem (corresponding to three distinct structures) that show greater than normal activity during a migraine attack. These parts of the brain usually act as a damper on nerve signals, he says. But when the structures allow too much input to pass through, nerve signals pour into the rest of the brain without control, Goadsby hypothesizes. That’s why normal sensations such as light, sound and even the pulsing of blood through the head become painful. he also believes that the malfunctioning of these areas of the brain stem give rise to one of the most peculiar aspects of a migraine — the aura.

An aura is a sensory disturbance that occurs in about one in four people with migraines. It commonly begins as a flickering of bright lights, like the flashes of an ambulance, in the corner of the visual field and gradually intensifies as it works its way across the line of sight. Some patients experience tingling, nausea and slurred speech during the aura, as well as blind spots once it subsides. An aura vanishes within an hour, and is replaced by a detonation of pain in the head.

Unbearable lightness

The origin of the aura has long been a topic of research fascination. An explanation now gaining consensus emerged in the 1940s from Brazilian biologist Aristides Leão while he worked on his dissertation at Harvard Medical School. after performing experiments in rabbits, Leão noted a marked change in electrical activity that started in one group of cells and rippled across the cortex, the outer layer of the brain. The hyper-excited nerves fire, and then appear to recalibrate, going temporarily silent. Leão called the phenomenon “cortical spreading depression.” Later researchers connected the phenomenon to a migraine aura, reasoning that the flickering light that patients see could occur as the cortical spreading depression crosses the visual center at the back of the brain.

The theory of cortical spreading depression was mostly confined to animal data, remaining at the margins of medical research for decades, until researchers could obtain brain scans of patients experiencing a migraine. One of the first of these images, published in 1994 in the New England Journal of Medicine, came about by chance. a young woman was in a scanner at UCLA for a study of cerebral blood flow when suddenly her migraine began. For about 15 minutes, researchers were able to document a wave of low blood flow (which they believe corresponded to nerve cells going temporarily inactive) spreading across the woman’s brain. a second study was led by Michael Moskowitz of Harvard Medical School. Moskowitz says that in the late 1990s he learned of an engineer who could induce his migraine auras with intense exercise. So Moskowitz and his team invited the man to campus, had him play basketball for 80 minutes and then whisked him off for an MRI.

In 2001 in the Proceedings of the Na-tional Academy of Sciences, Moskowitz’s team published the first MRIs of an aura from start to finish. in addition to the engineer, the researchers also took brain images of two campus employees who entered the scanner shortly after their auras had begun. as predicted, the images showed a wave of overactive (then underactive) neurons creeping across the cortex. “It’s not unlike what would happen if a stone were dropped in quiet pond,” Moskowitz says. The data suggest that the blood flow changes in the brain — the ones that led researchers in the wrong direction for decades — are more likely caused by the aura, and not vice versa. Active neurons grow hungry for fuel.

There is little debate about whether cortical spreading depression is a component of a migraine, but one central question is where it comes from, as well as its exact relationship with the pain. Goadsby believes the aura and pain arise from the brain stem, but others, like Moskowitz, say the activity changes observed in the brain stem are a result of a migraine, not the cause.

“The evidence that this kind of an event is triggered in any precise region of the brain is overstated,” Moskowitz says. instead of having origins in the brain stem, he suggests, the cortical spreading depression can arise in any part of the brain, an idea consistent with animal studies.

Moskowitz also does not agree that the changes that occur in the brain stem during a migraine open the floodgates on nerve signals, allowing normal sensations to become painful. instead, he points to laboratory experiments supporting the idea that the cortical spreading depression itself is responsible for the pain. Most of the brain does not have the capacity to feel pain; only the nerve endings in the dura mater, the organ’s tough outer covering, and related tissue are pain-sensitive. a headache happens because of the stimulation of these nerves, which fire as the wave of excitability makes its way across the cortex, Moskowitz believes. “Cortical spreading depression releases in a drastic way a group of chemicals that are normally sequestered in cells of the brain,” he says. when those chemicals — such as potassium, hydrogen ions and the neurotransmitter glutamate — get dumped, they may activate the pain fibers on the brain’s surface through a process that is still being worked out.

Skeptics of this idea point out that most people get migraines without an aura. Moskowitz’s belief is that cortical spreading depression occurs but does not affect the brain’s visual processing and thus remains undetected — a kind of hidden aura.

In truth, much about migraines is still unknown, says Burstein of Beth Israel. “Migraine is a complex disorder,” he says, involving abnormalities in both the cortex and the brain stem. where the pain comes from is still unclear, and perhaps the mechanisms behind chronic migraines (which occur more than 15 days a month) are different from those for less frequent ones. Migraines that strike regularly could originate from the cortex but over time could damage the cells of the brain stem. “This damage may reduce the ability of the brain stem to mitigate incoming signals,” he says.

And none of the research so far has clearly answered the biggest question: What’s the first thing that goes wrong? The list of potential migraine triggers reads like a catalog of daily life experiences: hunger, flashing lights, alcohol, strong smells, chocolate, cheese, too little sleep, too much sleep, stress, relaxation after stress, menstrual cycle changes, weather changes, and on and on. (And there may be no triggers at all; the changes in the brain that lead to an attack could cause someone to crave chocolate or feel stressed, or undergo other physiological shifts.)

“We don’t know why someone gets a migraine when they are exposed to a perfume in the elevator, when 10 other days they smelled the perfume and didn’t get it,” Burstein says. “Once it starts, we know a lot about it. what we don’t know is why and how.”

Tinderbox of nerves

While scientists debate the why and how of the trigger, genetic studies are getting at a separate question — who. Most researchers believe that genes contribute to a person’s susceptibility to the triggers. The headaches seem to run in families, and the risk is higher if you have an immediate family member with migraines.

Most migraine sufferers probably possess a constellation of genes, each one of which contributes a little to the susceptibility. But there is one kind of migraine, called familial hemiplegic migraine, that appears to have an even stronger genetic component.

An international team of researchers studying this kind of migraine described the first “migraine gene” in the journal Cell in 1996. The discovery came after neurologist Michel Ferrari of Leiden University Medical Center in the Netherlands happened to see two patients on the same day with familial hemiplegic migraine. (They turned out to be both from the same region of the country and were obliquely related.)

Since then, researchers have discovered a handful of genes that may contribute. By understanding the role of these genes, scientists could gain clues to the mechanism behind a migraine. So far, all signs point to nerve activation.

“They confirm that migraine is a disease of hyperexcitability in the brain,” says Ferrari.

Nerve cells work by transmitting electrical impulses. normally, the inside of a nerve cell is negatively charged (thanks to a lot of negatively charged chlorine ions) and the outside is positive (from positively charged sodium, calcium and potassium ions). when a nerve cell releases a signaling molecule called a neurotransmitter, channels on the cell next door open up and allow positive ions to rush in. The cell briefly depolarizes — the inside loses its negative charge — and then returns back to its normal state.

Genes that have been linked to migraine all have some role in the firing of nerve cells and this positive-negative ion swap. The gene mutation described in 1996 affected the calcium ion channel. Another DNA variation, described in 2010 in Nature Genetics, inhibits a cell’s ability to clear away the neurotransmitter glutamate after the nerve has fired, allowing it to accumulate. in June 2011, Ferrari and an international team of researchers described signs of three more rogue genes in Nature Genetics. These, too, are involved in the transmission of signals from cell to cell.

“The story seems to go in the same direction,” Ferrari says. in a migraine-susceptible brain “it’s easier to trigger neuronal activity.”

The idea is also supported by a study published last January in the journal Neurology. Researchers exposed patients suffering a migraine attack to light — a normal stimulus that becomes excruciating during the headache. PET scans of the patients revealed that the light caused the nerves in the occipital cortex of the brain to fire. But when the patients were not experiencing an attack, the light did not have an effect on that part of the brain. like a drought-stricken forest, the nerves may be easy to ignite, and easy to fuel once they do.

“The fact of the matter is there is plenty of evidence now that the brain of a migraine sufferer is never normal,” says David Dodick, a neurologist at the Mayo Clinic in Scottsdale, Ariz., and president of the American Headache Society. It now appears that a migraine brain exists on edge, quick to set off a headache when the right combination of circumstances comes along. “Networks are active when normally they shouldn’t be,” Dodick says. “The threshold for generating an attack is always just below the surface.” The rabbit hole is always near.

But maybe not forever. soon migraine sufferers may, like Alice, be able to wake up from the nightmare inside their heads — something Alice’s creator could never do.

Because its presentation may be episodic — symptoms can get better — it may be easy to blow it off unless it is severe, said Dr. Viktoria Kaplan, neurologist at LDS Hospital and Rocky Mountain MS Clinic. “I need new contacts.” “I slept wrong.”

And sometimes, because symptoms can go with other conditions as well, it’s hard for a doctor to tease out what’s happening to someone. That’s bad news, because research shows that those with MS “do much better on treatment,” Kaplan said.

Multiple sclerosis is the topic of Saturday’s Deseret News/Intermountain Healthcare Hotline. From 10 a.m. to noon, Kaplan and Clare Wright, direct services director for the National MS Society Utah, will take phoned-in questions on symptoms, treatments, available services and more. They’ll also answer questions posted on the Deseret News Facebook page, facebook.com/desnews.

Multiple sclerosis is poorly understood by the public and many doctors don’t know what to do with it, either. Some people confuse multiple sclerosis and muscular dystrophy, two very different disease, said Wright. Some worry that it’s contagious. When one is diagnosed, questions about how it will progress are understandable, but nonetheless hard to answer. it can be extremely unpredictable, although Kaplan said that “people who do better in the first year will do better down the road.” That’s why it’s so important to get a good diagnosis and start treatment.

It’s an autoimmune disease where one’s immune system attacks the myelin or lining of the nerves in the central nervous system, which includes the brain, the optic nerves and the spinal cord. Loss of myelin messes up the body’s nerve signalling system. Kaplan said most people are diagnosed between age 20 and 50, though there have been cases in children as young as 5 and new diagnosis in those as old as 75. Diagnosis itself hinges on finding white matter on imaging tests in more than one location and sufficient quantity to quality. It’s a disease that affects more women than men, but men are more likely to see symptoms progress.

It’s not usually a life-shortening disease, although complications can do that. but it is certainly life-altering.

Among the disease’s sorrows is the fact that it strikes most people at the stage of their life when they are most productive. “They are in their prime career wise,” Wright said.

WHEN PAULA OLNEY became anxious about a medical complication in the birth of her grandson last month, she sought reassurance from her husband, Dr. Richard Olney of Corte Madera.

Lou Gehrig’s disease — amyotrophic lateral sclerosis — has robbed Dr. Olney of virtually every voluntary muscle function, yet he remains a pillar of strength for his wife and their two adult children.

“He’s the one I go to to calm me down,” his wife said. “He can’t stand up, can’t walk, can’t talk, can’t chew. But he can think. despite his incapacitation, he still helps all of us with the major decisions we make in our lives.”

When he was diagnosed with the disease in 2004 at age 55, Olney’s illness garnered national attention because of a cruel irony. at the time, he was working as a neurologist and director of the University of California at San Francisco’s ALS Treatment and Research Center, which he founded in 1993.

“That’s why it was such a big news story,” his wife said. “It was like the brain surgeon himself getting a brain tumor.”

Strapped in a wheelchair and able to communicate only with the assistance of a computerized speech synthesizer, Dr. Olney’s strength is not immediately apparent. it manifests itself gradually as one watches him doggedly manipulate the synthesizer. he painstakingly constructs sentences by moving his gaze over a computer tablet and selecting, sometimes a word or phrase, but usually a single letter at a time.

“ALS is more common than most people think,” Olney said, using the machine. the halting voice that emerges is his own, prerecorded with the prescience that came from watching countless patients succumb to the deadly disease.

According to the National Institute of Neurological Disorders and Stroke, only about 20,000 to 30,000 people in the United States have ALS, even though an estimated 5,000 people in the country are diagnosed with the disease each year.

Dr. Catherine Lomen-Hoerth, who took over as director of UCSF’s ALS Treatment and Research Center after being trained by Olney, said the number of people with ALS is misleading because the disease is so lethal.

“If people lived longer with ALS, it would be as common as multiple sclerosis,” Lomen-Hoerth said. Multiple sclerosis affects more than 350,000 people in the United States and 2.5 million worldwide.

Most people who have ALS die from respiratory failure, usually within three to five years from the onset of symptoms. About 10 percent of ALS patients, however, survive for 10 or more years without use of a ventilator.

While a ventilator might extend his life for years, Olney has already decided against it.

There is no cure for ALS. in clinical trials, the only drug approved for treatment, riluzole, has prolonged survival by several months, mainly in patients who have difficulty swallowing. Scientists have so far been unable to determine what causes the disease, which in 90 to 95 percent of cases seems to occur at random with no clearly associated risk factors. About 5 to 10 percent of ALS cases appear to be inherited.

In the case of Olney, who has no known incidence of the disease in his family, symptoms progressed quickly at first.

“Richard’s an anomaly,” his wife said, “He lost his ability to walk, his voice and fine motor skills, like typing, all in about one year. Then he plateaued.”

Rather than dwell on what he can no longer do, Olney has stayed focused on what he can do, as well as anyone in the country. with the assistance of his son, Nicholas, who recently graduated from medical school, Olney is racing against the clock to complete a research paper on ALS using data he accumulated before he became ill.

The ticking clock almost stopped in March, when breathing problems landed Olney in UCSF’s intensive care unit for several days. Since then, he has been forced to take nourishment through a tube to avoid choking.

“Then he got this horrendous cold that lasted five weeks,” his wife said. “We know he’s living on borrowed time, and every day is important.”

Olney said there are two reasons he is determined to complete his research paper.

Firstly, he said, “I want to write a paper with Nick.” also, he said, “I think there are many forms of ALS, and this paper documents several different forms.”

Olney hopes that the paper will demonstrate that neurophysiological tests conducted in the early stages of ALS can be utilized to predict how quickly patients will lose muscle control.

Lomen-Hoerth said, “He’s a very smart man and he enjoys being active and being able to contribute to science. I think that keeps him going.”

In the early stages of his illness, Olney himself became a guinea pig in a UCSF clinical trial of a promising ALS drug. the drug, however, proved ineffective, and Olney resolved himself to his fate.

“Some people get wrapped up in all these alternative treatments,” said Nicholas Olney. “Dad quickly focused on making the most of every day.”

Oselinda Ames, one of Olney’s caregivers, met and married a former ALS patient of Olney’s, David Ames, after Ames traveled to Abadiania, Brazil, to visit a spiritual healer who calls himself John of God. the couple were later married and returned to the United States where Oselinda cared for Ames until his death.

“I’m happy to work with Rick because he reminds me a lot of David,” Ames said. “David enjoyed every single day.”

When he’s not working on his paper, Olney exchanges emails with other ALS patients, updates his Facebook page, watches movies, listens to books on audio tape and attends concerts and plays. his wife recently took him to see a new favorite of hers: Lady Gaga.

“He’s not angry and he’s not depressed,” she said. “Can you believe it?”

Lomen-Hoerth said many ALS patients cope with their disease surprisingly well.

“I’m continually amazed by my patients, and their incredible endurance,” Lomen-Hoerth said. “In general, ALS patients have a very low incidence of depression and tend to be quite hopeful. I think the lack of pain helps.”

Although Olney is not traditionally religious, he said spirituality is one source of his strength.

“I feel God’s presence especially in nature,” he said.

And while Olney said his greatest pleasure these days is spending time with family and friends, he also has his dreams.

He said, “I can run, walk, hike and jog in my dreams.”

Contact Richard Halstead via email at

lou gehrig’s disease facts

• Amyotrophic lateral sclerosis, or ALS, is a disease of the nerve cells in the brain and spinal cord that results in a progressive loss of voluntary muscle movement.• ALS affects approximately five out of every 100,000 people worldwide.• in at least 90 percent of cases there are no known risk factors. About 5 to 10 percent of ALS cases appear to be inherited.• ALS leaves the senses unaffected and only rarely affects bladder or bowel function, or a person’s ability to think.• There is no known cure for ALS, and sufferers rarely live beyond 10 years without aid of a ventilator.

Sources: National Institute of Neurological Disorders and Stroke, National Center for Biotechnology Information

It’s key that you acquire a mastery of the basics. Master the basic causes and mechanisms of Parkinson’s disease and you’ll better understand your therapy. you will also have the ability to better know what questions to ask,  and I daresay, become better at debunking the quacks. Do that and you’re on your own track to guiding your own care. Become more a  part of you own care team a bit more as a colleague with your neurologist and your other caregivers.Thus, it’s key to your treatment that you begin to understand the basic mechanisms and alleged causes of Parkinson’s disease.

Although the specific causes might vary quite a bit from person to person, the mechanism by which Parkinson’s manifests itself follows a fairly straightforward pathway. I will invoke  some of the previous diagrams I have used in other articles, which explain the mechanisms  by   which cell death in the substantia nigra  causes a dopamine deficiency resulting in  Parkinson’s symptoms.

The Substantia Nigra

The root of the cause  can be found in this rather small region of the deep brain sitting atop the brainstem. This is where dopamine-producing neurons die in Parkinson’s although the mechanisms by which cells die here are less clear.beyond genetics, there are many environmental toxins that increase the risk including herbicides, pesticides, organic solvents, heavy metals and manganese. Head trauma may also be another mechanism: anyone who has lost consciousness more than once is at least at double the risk for Parkinson’s.  Whatever the cause, brain-cell bodies within this substantia nigra region start dying off.  These cells of which there are about 10,000 on each side of the brain normally get stimulated by various mechanisms (intense emotion, sexual arousal, novel stimuli). That stimulation causes the activation of dopamine production  in those cell bodies.  Normally their very long extensions that reach to other brain areas, called “axons,” deliver dopamine to  the nearby basal ganglia regions (controls movement and part of the mechanism of drive and motivation) and hypothalamus (controls bodily cycles like sleep and autonomic functions like cardiovascular tone and body temperature) and other further–away areas like the frontal lobe of the cortex. Dopamine-producing cell death causes a deficiency of dopamine in these regions.  In one way or another, the normal mechanisms of function of each of these regions relies on a steady supply of dopamine.

Local deficiencies of dopamine cause the neural circuits in these regions  to misfire. these disrupted mechanisms  of neural regulation cause the various symptoms of Parkinson’s disease seen.   Disruption in the basal ganglia for instance, causes an abnormal pattern of movement control and feedback to the higher brain, a very delicate mechanism upon which crisp  initiation of movement and smooth control of  that movement in becomes disrupted.

This causes the classic triad of symptoms originally described by Dr. Parkinson 150 years ago.  Although he did not understand the mechanism, Dr. Parkinson noted that patients would present with three primary movement abnormalities that caused a  great deal of distress and disability for them in normal everyday function. the classic three findings were coarse tremor, rigidity, and slowness of movement, which we now know are caused by dopamine deficiency and the resulting abnormal regulation of those movements via a disrupted  pattern of function in the basal ganglia.

In fact the mechanism by which adequate dopamine fails to reach these regions where it’s needed causes every one of the described symptoms in Parkinson’s, even those that have nothing to do with movement.  One mechanism by which at least some of these “other” “non-–motor symptoms” arise,  originates via this malfunction of the basal ganglia region, which besides controlling movement,  also regulates motivation and drive behaviors.  Thus, malfunction here might also be the cause of diminished motivation seen in Parkinson’s,  and at least in-part, the cause of daytime sleepiness.

Other non-motor abnormalities  involve dopamine deficiency causing malfunction in the other  regions supplied with dopamine.  These dying neurons from the substantia nigra also supply dopamine to the hypothalamus, as mentioned above, whose malfunction causes disrupted sleep cycles and the loss of vascula stability which causes postularal dizziness.

Dopamine deficiency in other areas to be specified in later articles causes depression, memory impairment, and may even lead to dementia, common in late Parkinson’s.

The exact mechanism by which these substantia nigra dopamine neurons die has not been fully elucidated however somehow all roads seem to lead to the lethal accumulation of an abnormal protein called “alpha-synuclein” which causes early cell death. by the time movement symptoms start appearing, as many as 70-80 percent of these neurons have already died.

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You just walked out of your neurologist office after receiving the devastating news that you have Multiple Sclerosis. what now?

This is when you need to make some very big decision and some very important lifestyle changes. Most of us loose control at this stage, but I am going to try and give you choices you are now presented with, and exactly what you should and should not do. There is a couple of ways to make this all the more bearable for you, and could also help you in your life ahead. Note that, I say your life ahead, as this is not the end of your life but the beginning of a new chapter in your life. what you do from now on will determine the rest of your life. you are likely to go through the certain stage emotional feelings and thoughts that most of us go through after our diagnosis.

The first of these stages is denial and it happens to all of us, and certainly after the recovery of your first relapse. you are now over your relapse and you feel fine and you are likely to feel normal again. “I feel fine, the Doctors could be wrong I don’t have Ms”. In about 5% of the entire patients this is certainly true, but a good neurologist will not diagnose you after meeting the criteria for Multiple Sclerosis. In certain patient you do get what is known as Clinical Isolated Syndrome in other words you only have one attack in your entire life and the symptoms disappear for ever. this diagnosis will only be given if you do not meet all the criteria of Multiple Sclerosis and most case you do not present with a second attack. But in 95% of all cases the diagnosis of multiple sclerosis is definite and no matter how you try to deny it you still have Multiple Sclerosis. The first thing you should do is not to dwell on this point to long; because the sooner you accept you have Multiple sclerosis the better it will be for you.

The next step is to get all the info you can get on Multiple Sclerosis out there. Be careful in this selection of reading material on the subject. The internet is probably in my opinion the worst place to get first time information on Multiple Sclerosis. There are so many false promises and hopes being published on it, unless you can get it from a recognised organisation out there. The best place to get this information is at the local chapter of a Multiple Sclerosis society. they have been around for many years and have lot of credible information on Multiple Sclerosis. If there is not a chapter near you, write to one. they will be more than willing to send you the information. Read through all this material and digest it all. this info will guide you through the rest of your life. once you have informed yourself on the basic facts on multiple sclerosis it would be safe to get on the internet. Join a support page and get some friends on it. But be very careful of opportunist out there. Multiple sclerosis is a disease that is fear driven, and a lot falls in the trap of trying to find a miracle cure out there. 99% of these operators have one thing in common, and that is to get you in their trap and use their powers of persuasion to follow their so called cure. Guide yourself by recognised societies information, and for the better part avoid all the so called cures. do not let yourself be fooled into believing all that is on the internet. We live in an era with very modern and fast spreading information out there, and this is called the World Wide Web. it has it positive side, but it also has a very negative side to it. Avoid the pitfalls on the internet as this will lead you to false hope in most cases.

Now that you are informed comes the big decision; do I tell my family, friends and co-workers? this is a definite yes, because the support of them will help you a lot in your life. or in certain cases the lack of support will also determine what you do in your life. The same information that you have armed yourself with now comes in handy. use this information and pamphlets as a tool to educate others in your life. Spread the information to the important people in your life and rally them behind you. But do it in a constructive way, so that they don’t pity you as this is not what you need. you need to surround you with positive people and friends out there. you are not over the wall yet, and the more positive backing you get the better for you. But they also need to understand what to expect as to your physical abilities. this education is an ongoing process, because as your Multiple Sclerosis changes so will your physical abilities and certainly while you are in relapse you may require the help and understanding of these persons in your life. But this is also the point where you should not be stubborn and accept the help that is given to you. it will go a long way in your recovery process.

Now comes the important part, do not give up hope. There is a good Latin saying “Dum spiro, spero, “while I breath, I hope””. this is not the stage to crawl in a corner and give up. Giving up is the worst thing that you can do now. it is understandable to feel helpless while you have a relapse, but as soon as this relapse is over get back out there and live life again. Set goals for yourself to achieve, but now your limitations. do not set impossible goals to achieve. get constructive, get involved. If you do still work, try to remain there as long as possible, but also do not over exert yourself or put to much stress on yourself. Avoid stress whenever possible, as this is one of the worst enemies of Multiple Sclerosis. If you are not working get involved with volunteer work, but get your mind busy with something else, it will go a long way to helping you. take up a hobby, but the important part is remaining active as long as possible. a healthy mind supports a healthy body. Keep your mind active, get books read. But keep your mind active, stay positive as positive thoughts lead to positive life.

Change your lifestyle, this is very important. Forget about the past the future is now and that is what counts. Change your diet, follow a healthy eating plan. But going healthy does not mean to go to the extreme i.e. vegetarian etc. you do not need to make drastic changes, but avoid fatty food, and eat more so called heart healthy foods. Eat a normal balanced diet. But it does not mean you cannot reward yourself with some treats every now and then. you are still you and there is no need to stop eating out etc. But the key figure is moderation. a big question that is likely on everyone’s mind do I stop having alcohol. Again moderation applies here as well. Have a glass of wine or a drink or two, but be conservative.

In comes the next step; exercise. this is a very complicated issue as you can only do what your body allows you too. Avoid exercise that will raise your core temperature. Exercise in moderation, for the longer you muscle stays active the longer you will be active. a very important part is to get back into action after a relapse. The better your muscles are trained the better your ability will be to handle Multiple Sclerosis. I am not saying getting trained to run the new York marathon. There are exercises like yoga that can get you in just as good shape without exerting yourself. Yoga type exercise will keep your muscle toned and supple, and this helps a lot to avoid muscle wasting away and going into spasm. For those who can afford it get physical therapy. But the important part is train your body to deal with Multiple Sclerosis. If you can do small exercise while you are sitting and watching TV etc, if you have leg that spasm, stretch and to subtle exercise. put a tennis ball under your foot and roll it, it will help even for foot drop.

Listen to your body; it has a story to tell. Look for early warning signs of a flare up or relapse. know the early signs like numbness, painful eyes, facial pains etc. when you see the warning signs get treatment sooner rather than later. your primary physician or neurologist is trained to look for other early warning sign. go to them if you see a sign of a possible attack. The sooner you get treated the quicker you will recover. Avoid opportunistic infection like flue or any viral infection. Don’t let this go untreated as it could trigger an immune response. Avoid contact with sick persons if possible. For those mothers of young children, this is going to be extremely difficult. The motherly instinct will take over, and I think it is unavoidable as your child comes first. get vaccinated every year for flue and do so for your whole family, but check that the vaccine is safe to use in Multiple Sclerosis. Rest when your body tells you too. this is very important in multiple Sclerosis.

Inform yourself as to the treatments out there, as disease modifying drugs (DMD) can go a long way to help slow down your Multiple Sclerosis. For those that can’t afford it, find out from your local Ms Chapter or neurologist as to drug sponsored help programmes. certain countries do have them. get the right DMD, if one do not work inform your neurologist as there are other options. it is likely that your neurologist will not put you on a DMD before your second attack. this is just good practice and do not worry about it then. always inform your primary if you are on DMD as certain medicine does not react well in combination with DMD’s. also now keep a dairy of all new and strange symptoms as this will come in handy in the future. take this to the Doctor with each visit and keep it up to date. this is the most important part of your literature for the future. it is your Ms Biography, keep it up to date. it is now part of the rest of your life. Lastly listen to the doctors as to what you can and cannot do.

Now comes my last part of important information. having multiple sclerosis does not mean you should stop living, follow all the important guidelines and you can live a long productive life being it with a bit more difficulty. Never give up hope, there are important medical advances made in the field of Multiple Sclerosis, and in the near future the new line of treatments and medicine will go a long way to help our battle against Multiple Sclerosis. The next five years is going to be very exciting times for Multiple sclerosis and I believe we will see a cure in the very near future or a stop in progression at least.

Copyright ©2010. The Associated Press. Produced by NewsOK.com all rights reserved. this material may not be published, broadcast, rewritten, or redistributed.  

The new Multiple Sclerosis Center of Excellence opened Tuesday, built on a concept of combining bedside treatment with laboratory research.

The center is designed to treat thousands of patients in Oklahoma and the region who have symptoms that may include the inability to walk, blindness and paralysis. it is in the Oklahoma Medical Research Foundation’s new seven-floor research tower at 825 NE 13.

The MS center will be headed by Gabriel Pardo, M.D., a neurologist and neuro-ophthalmologist who has specialized in treating MS patients for more than a decade. he said the center will allow an opportunity for top-notch MS scientists and doctors to work together to fight the baffling disease of the central nervous system.

“We meet in the middle. I bring my ideas from the bedside; they bring ideas from the lab side to brainstorm together,” he said.

Patients will be seen in technologically advanced examination rooms.

They will be treated in a specially designed infusion suite, ophthalmological and dental areas, and a physical therapy area with equipment designed just for MS patients.

“This is history-making time in MS. this is when things are happening. We’re understanding a lot of things and coming up with better strategies. what better than to be part of history making?” Pardo said.

Patients also will be able to participate in clinical trials and perhaps have a hand in helping future generations of MS sufferers, Pardo said.

“Multiple sclerosis doesn’t just take a toll on the body, but it drastically impairs a patient’s lifestyle,” said OMRF President Dr. Stephen Prescott.

The disease interrupts the flow of information within the brain, and between the body and brain.

“We’re not only improving our research capabilities with the new center, but by gathering many of the facilities used by MS patients in one place, we hope to make treatment more convenient,” Prescott said.

Experts estimate at least 4,200 Oklahomans have multiple sclerosis.

“As we move toward finding a cure, Oklahomans will now have access to quality, integrated care from this dedicated team of MS specialists,” said Lucy Fraser, development director for the Oklahoma Chapter of the National MS Society.

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LOS ANGELES (WJZ) — It’s the video that’s all over the Internet. a reporter at a television station in Los Angeles suddenly begins speaking gibberish on air.

Jessica Kartalija explains her diagnosis is actually more common than you may realize.

Serene Branson is eager to get back to reporting the news, instead of being the story.

The Los Angeles reporter was doing a live shot after the Grammys when she began speaking gibberish.  the video went viral.

“I was terrified,” she said.  “I was scared and confused.  I didn’t know what was going on.”

Dr. Howard Moses is a neurologist at St. Joseph Medical Center. he says many who saw the footage thought the veteran reporter suffered a stroke.

“this sort of thing in a woman who seemingly had no risk factors for stroke, we call that complex migraine or complicated migraine. That’s a migraine associated with neurological signs and symptoms which simulate a stroke,” Moses said.

Branson told doctors she hadn’t been feeling well. during her live shot, her cheek and hand went numb–symptoms of a severe migraine that mimic a stroke.

“My vision was blurry,” Branson said. “I knew something wasn’t right, but I just thought I was tired.”

“She knew what she wanted to say, but couldn’t say it,” Moses said. “It came out gibberish.  the brain knew what it wanted to say but the mouth wouldn’t do it. Typical of something called aphasia.”

Doctors hope to use the video for research and to train medical students.

Branson says she hopes to return to the red carpet reporting for Oscar night.

A migraine can often resolve itself on its own. a patient only needs treatment if it happens over and over again.

Migraines are often hereditary. Branson’s mother had a similar episode when she was her daughter’s age.

For full details on this story, click here.

Didier Jambart, 51, of Nantes, France, is suing the British pharmaceutical company GlaxoSmithKline, claiming the drug he took to treat his Parkinson’s symptoms, Requip, turned him into a gambling and gay sex addict.

The married father of two said he blew through his family’s savings and even took to stealing to finance his online gambling habit, the French Press Agency reported. He also became addicted to gay sex and risky sexual encounters that led to him being raped, his lawyers said.

Parkinson’s disease destroys neurons deep within the brain that release the “feel-good” neurotransmitter dopamine. Requip belongs to a class of drugs called dopamine agonists that relieve motor symptoms, such as shaking, stiffness, slowness and trouble balancing, by activating dopamine receptors. but the drugs have side effects that, while rare, are serious.

“There are plenty of reports of people developing side effects from Parkinson’s drugs, such as hypersexuality, gambling and excessive shopping,” said Dr. David Standaert, professor and interim chairman of neurology and director of the Center for Neurodegeneration and Experimental Therapeutics at the University of Alabama at Birmingham. “It’s uncommon, but very dramatic when it happens.”

Up to 17 percent of people with Parkinson’s disease who take dopamine agonists exhibit an impulse control disorder, according to a 2010 study published in the Archives of Neurology.

“It can be devastating for those people,” said Dr. Mark Stacy, a neurologist at Duke University Medical Center, who first linked the drugs to gambling in 2000. “And I think that because of the embarassing nature of the complaint, it’s a bit amplified.”