More than 50 experts on the use of deep brainstimulation for treatment of tremors and other symptoms of Parkinson’s disease have reached general agreement on when the surgical procedure should be considered and which patients might reap most benefits, a new report says.
The report, published in the online edition of Archives of Neurology, says the best candidates for deep brain stimulation are those who can’t tolerate the side effects ofmedication and those who don’t suffer from significant active cognitive or psychiatric problems but who do suffer from tremors or motor skills control.
In a deep brain stimulation procedure, a neurosurgeon surgically implants a neurostimulator in the brain in the location where abnormal electrical nerve signals generate the tremors and other symptoms common in Parkinson’s patients. The neurostimulator generates electric stimulation to the area to block the signals.
The report also says that:
Deep brain stimulation surgery is best performed by an experienced team and neurosurgeon who have expertise in stereotactic neurosurgery — microsurgery deep within the brain that is based on a three-dimensional coordinate system using advanced neuroimaging.
Deep brain stimulation is effective when used in the two most commonly treated areas of the brain, called the subthalamic nuclei and the globus pallidus pars interna. But treatment in the subthalamic nuclei may cause increased depressionand other symptoms in some patients.
Surgical removal of the area of the brain that causes Parkinson’s disease is an effective alternative and should be considered as an alternative in some people.
Surgical complication rates vary, with infection being the mostly commonly reported side effect of deep brain stimulation.
Making an Informed Decision
“We know that very little accessible information is out there to help a Parkinson’s patient make an informed decision as to whether he or she would be a good candidate for deep brain stimulation,” says report lead author Jeff Bronstein, MD, PhD, a professor of neurology at University of California, Los Angeles, in a news release.
Surgical studies take a long time, and what’s known about deep brain stimulation is focused, limited, and often written by one group, reflecting their opinions and biases, he says.
Bronstein says the results of a meeting in April 2009 of the Parkinson’s experts are intended to clarify some issues about the use of deep brain stimulation.
The FDA approved deep brain stimulation as a treatment for Parkinson’s disease in 2002, and since then more than 70,000 people have undergone the procedure. The authors write than more than 30% of failures of deep brain stimulation have been due to “inappropriate indications for surgery.”
The report says long-term improvements have been shown for up to five years for a number of Parkinson’s disease symptoms.
The experts caution that Parkinson’s disease continues to progress after deep brain stimulation.
Tuesday, October 19, 2010
Sunday, October 10, 2010
Depression Treatment | Depression – Symptoms, Causes And Treatment Options
Depression is a complex of psychological and physical symptoms. Low mood level or sadness is often the most prominent symptom. The common property of these symptoms is a decreased activity level in parts of the brain.
THE SYMPTOMS OF DEPRESSION
Depression may give one or more of these symptoms:
-Low mood level or sadness.
-Lack of joy or interest in activities that were joyful before.
-Pessimism.
-Feel of guilt of something without any substantial reason to feel so.
-Inferiority thoughts.
-Irritability.
-Slowness in the thought process.
-Slowness in interpreting sensorial stimuli.
-Slowness of digestion or other internal physical processes, and symptoms caused by this slowness, for example inflated stomach, constipation or difficulties by urination.
-Slow physical reactions.
Depression can be a mild disease that only causes some annoyance in the daily life, but can also get very serious and make a person totally unable to work and unable to participate in social life. By depression of some severity, there is also a greater risk of suicide.
Depression can occur in all age classes. In teenagers lack of interest in school work, withdrawal from social life and difficult mood can be signs of depression.
THE PHYSIOLOGICAL CHANGES THAT PRODUCE THE SYMPTOMS
By depression there is a decreased amount of neurotransmitters in parts of the central nervous system, mainly deficiency of serotonin, but also to some extend of noradrenalin, acetylcholine, dopamine or gamma-amino-butyric acid (GABA), or the nerve cells do not react properly by stimulation from neurotransmitters. A neurotransmitter is a signal substance that transmits the nerve signal through the junctions between two nerve cells.
Serotonin and noradrenalin cause nerve cells to send impulses along to other nerve cells, and thus increase the activity in the brain. Deficiency of these substances causes slowness in parts of the brain, and that again causes the depressive symptoms.
The role of GABA is the opposite, namely to slow down some nerve impulses, mainly those causing anxiety and panic response. Lack of GABA causes higher anxiety and easier panic response. Yet, lack of this transmitter also seems to cause depressive symptoms. This is because a too high activity in some brain processes may slow down other processes.
There are many causes and subtypes of depression with different physiological mechanisms involved.
TYPES OF DEPRESSION
Depression is often divided into subtypes according to exhibited symptoms.
1. Mono-polar depression and dysthymic disorder
By mono-polar depression there are pure depressive symptoms. Mild cases of mono-polar disorder that do not affect a persons ability to work and to participate in social activities are often called dysthymic disorder.
2. Bipolar disorder (manic-depressive disease) and cyclothymic disorder
In this condition there are periods with symptoms of depression – the depressive phase, alternating with periods of elevated mood level with increased mental and physical activity – the manic phase. In the manic phase, the affected person also sleeps poorly and has concentration difficulties. A mild form of this disease is called cyclothymic disorder.
3. Manic disorder
This condition is characterized by abnormally elevated mood, by unrealistic optimism, by lack of sleep and by hyperactive behaviour. Many psychiatrists think that this disorder is simply the same disease as bipolar disorder where the depressive face has not yet occurred.
4. Depression with mainly physical symptoms
Sometimes the physical symptoms of depression are alone or dominant, as for example: Digestive problems, constipation, difficulties with urination, slow response to sensorial stimuli or slow physical reactions.
CAUSES OF DEPRESSION
Two or more factors can have an effect simultaneously to cause depression. Depression can be an independent disease, or a part of other disease. Depression is also divided into different subtypes according to cause.
1. Reactive depression
This disease is simply a result from psychological stress, physical struggle or mental straining without proper rest or sleep over a long time period. The straining will simply wear out the nervous system or deplete the organism from nutrient necessary for the nervous system to work properly.
2. Endogenous depression
When there has not been any period of stress, straining or lack of rest that can explain the condition, the condition is often called endogenous depression. Inheritance is thought to be a part of the cause.
3. Depression by physical disease
Depression or depressive symptoms may be a symptom of physical disease. This is perhaps the most common cause of depression. Generally there are three categories of diseases that give depression:
Diseases often associated with depression are: Heart disease, Parkinson’s disease, stroke, hypertension or Cushing’s syndrome.
Mononucleosis or flu may trigger depression that continues after the infection has gone.
By lack of thyroid hormones, hypothyroidism, the metabolism in the whole body is slowed down, including the production of neurotransmitters in the brain. Therefore depression is an important symptom of hypothyroidism.
4. Depressive symptoms as a consequence of unsound lifestyle
A general unsound lifestyle with too less exercise, too much of stimulants like alcohol, coffee or tea, too less of important nutrient and too much of sugar and fat may give depressive symptoms, as well as physical problems.
5. Postnatal depression
Women will often have a period of depression after pregnancy and berth of the baby Pregnancy and berth is physically and mentally exhausting, and may drain the body for nutrient. This in turn can cause depressive symptoms
.
6. Seasonal affective disorder
Depression can occur in cold and dark periods of the year and go away in warm and light periods. Light stimulates brain activity, and lack of light is a causative factor.
TREATMENT OF DEPRESSION
Serious or prolonged depression is often treated with anti-depressive medication. Medicines used against depression generally increase the level of neurotransmitters like serotonin in the central nervous system, or they mimic the neurotransmitters.
The medications mostly used today increase the serotonin concentration by decreasing the removal of serotonin from the space around nerve cells. Examples of this medication type are: Fluoxetine (Prozac), fluvoxamine (Luvox), paroxetine (Paxil), escitalopram (Lexapro, Celexa), sentraline (zoloft).
By bipolar disorder in the manic face, heavy tranquilizers (neuroleptica) are used to stop the manic symptoms. By bipolar disorder, lithium salts are sometimes used to stabilize the condition, and prevent new outbreak of depressive or manic faces.
Psychotherapy is sometimes used by depression, usually in combination with medication.
Sometimes serious depression is treated by applying electric shock through the head, electroconvulsive therapy. The shock induces epileptic eruption of nerve signals through the brain and this gives cramps throughout the body. The cramps are alleviated or stopped by applying anaesthesia before the electroshock. This form of treatment is controversial, since it can cause memory loss and is suspected of causing brain damage. The possibility of brain damage is however denied by most psychiatrists.
By seasonal depression, light therapy maybe useful.
Adjustment of lifestyle should always be considered by depression or depressive symptoms. Lifestyle measures can sometimes be enough to cure depressive symptoms before a serious depression develop. Lifestyle adjustments can be:
– To slow down a stressful life with too much work or activities.
– Enough rest and sleep.
– A good diet with enough of necessary nutrients.
– Some physical exercise.
– Meditation.
– Supplement of vitamins, minerals, antioxidants, lecithin, amino acids and essential fatty acids.
– Stimulants like coffee or tea may help against depressive feelings in moderate amount. However, if you are a heavy user of these stimulants, you should cut down on your consumption.
There exist nutritional products in the marked to help against depressive symptoms. These contain ingredients that the brain uses as building blocks for neurotransmitters, for example amino acids and lecithin. They also often contain vitamins and minerals that the brain uses as tools to produce neurotransmitters, especially vitamin B6.
Supplements may further contain herbal extracts that trigger higher brain activity much like anti-depressive medications, but may have fewer side effects.
By: Knut Holt
THE SYMPTOMS OF DEPRESSION
Depression may give one or more of these symptoms:
-Low mood level or sadness.
-Lack of joy or interest in activities that were joyful before.
-Pessimism.
-Feel of guilt of something without any substantial reason to feel so.
-Inferiority thoughts.
-Irritability.
-Slowness in the thought process.
-Slowness in interpreting sensorial stimuli.
-Slowness of digestion or other internal physical processes, and symptoms caused by this slowness, for example inflated stomach, constipation or difficulties by urination.
-Slow physical reactions.
Depression can be a mild disease that only causes some annoyance in the daily life, but can also get very serious and make a person totally unable to work and unable to participate in social life. By depression of some severity, there is also a greater risk of suicide.
Depression can occur in all age classes. In teenagers lack of interest in school work, withdrawal from social life and difficult mood can be signs of depression.
THE PHYSIOLOGICAL CHANGES THAT PRODUCE THE SYMPTOMS
By depression there is a decreased amount of neurotransmitters in parts of the central nervous system, mainly deficiency of serotonin, but also to some extend of noradrenalin, acetylcholine, dopamine or gamma-amino-butyric acid (GABA), or the nerve cells do not react properly by stimulation from neurotransmitters. A neurotransmitter is a signal substance that transmits the nerve signal through the junctions between two nerve cells.
Serotonin and noradrenalin cause nerve cells to send impulses along to other nerve cells, and thus increase the activity in the brain. Deficiency of these substances causes slowness in parts of the brain, and that again causes the depressive symptoms.
The role of GABA is the opposite, namely to slow down some nerve impulses, mainly those causing anxiety and panic response. Lack of GABA causes higher anxiety and easier panic response. Yet, lack of this transmitter also seems to cause depressive symptoms. This is because a too high activity in some brain processes may slow down other processes.
There are many causes and subtypes of depression with different physiological mechanisms involved.
TYPES OF DEPRESSION
Depression is often divided into subtypes according to exhibited symptoms.
1. Mono-polar depression and dysthymic disorder
By mono-polar depression there are pure depressive symptoms. Mild cases of mono-polar disorder that do not affect a persons ability to work and to participate in social activities are often called dysthymic disorder.
2. Bipolar disorder (manic-depressive disease) and cyclothymic disorder
In this condition there are periods with symptoms of depression – the depressive phase, alternating with periods of elevated mood level with increased mental and physical activity – the manic phase. In the manic phase, the affected person also sleeps poorly and has concentration difficulties. A mild form of this disease is called cyclothymic disorder.
3. Manic disorder
This condition is characterized by abnormally elevated mood, by unrealistic optimism, by lack of sleep and by hyperactive behaviour. Many psychiatrists think that this disorder is simply the same disease as bipolar disorder where the depressive face has not yet occurred.
4. Depression with mainly physical symptoms
Sometimes the physical symptoms of depression are alone or dominant, as for example: Digestive problems, constipation, difficulties with urination, slow response to sensorial stimuli or slow physical reactions.
CAUSES OF DEPRESSION
Two or more factors can have an effect simultaneously to cause depression. Depression can be an independent disease, or a part of other disease. Depression is also divided into different subtypes according to cause.
1. Reactive depression
This disease is simply a result from psychological stress, physical struggle or mental straining without proper rest or sleep over a long time period. The straining will simply wear out the nervous system or deplete the organism from nutrient necessary for the nervous system to work properly.
2. Endogenous depression
When there has not been any period of stress, straining or lack of rest that can explain the condition, the condition is often called endogenous depression. Inheritance is thought to be a part of the cause.
3. Depression by physical disease
Depression or depressive symptoms may be a symptom of physical disease. This is perhaps the most common cause of depression. Generally there are three categories of diseases that give depression:
Diseases often associated with depression are: Heart disease, Parkinson’s disease, stroke, hypertension or Cushing’s syndrome.
Mononucleosis or flu may trigger depression that continues after the infection has gone.
By lack of thyroid hormones, hypothyroidism, the metabolism in the whole body is slowed down, including the production of neurotransmitters in the brain. Therefore depression is an important symptom of hypothyroidism.
4. Depressive symptoms as a consequence of unsound lifestyle
A general unsound lifestyle with too less exercise, too much of stimulants like alcohol, coffee or tea, too less of important nutrient and too much of sugar and fat may give depressive symptoms, as well as physical problems.
5. Postnatal depression
Women will often have a period of depression after pregnancy and berth of the baby Pregnancy and berth is physically and mentally exhausting, and may drain the body for nutrient. This in turn can cause depressive symptoms
.
6. Seasonal affective disorder
Depression can occur in cold and dark periods of the year and go away in warm and light periods. Light stimulates brain activity, and lack of light is a causative factor.
TREATMENT OF DEPRESSION
Serious or prolonged depression is often treated with anti-depressive medication. Medicines used against depression generally increase the level of neurotransmitters like serotonin in the central nervous system, or they mimic the neurotransmitters.
The medications mostly used today increase the serotonin concentration by decreasing the removal of serotonin from the space around nerve cells. Examples of this medication type are: Fluoxetine (Prozac), fluvoxamine (Luvox), paroxetine (Paxil), escitalopram (Lexapro, Celexa), sentraline (zoloft).
By bipolar disorder in the manic face, heavy tranquilizers (neuroleptica) are used to stop the manic symptoms. By bipolar disorder, lithium salts are sometimes used to stabilize the condition, and prevent new outbreak of depressive or manic faces.
Psychotherapy is sometimes used by depression, usually in combination with medication.
Sometimes serious depression is treated by applying electric shock through the head, electroconvulsive therapy. The shock induces epileptic eruption of nerve signals through the brain and this gives cramps throughout the body. The cramps are alleviated or stopped by applying anaesthesia before the electroshock. This form of treatment is controversial, since it can cause memory loss and is suspected of causing brain damage. The possibility of brain damage is however denied by most psychiatrists.
By seasonal depression, light therapy maybe useful.
Adjustment of lifestyle should always be considered by depression or depressive symptoms. Lifestyle measures can sometimes be enough to cure depressive symptoms before a serious depression develop. Lifestyle adjustments can be:
– To slow down a stressful life with too much work or activities.
– Enough rest and sleep.
– A good diet with enough of necessary nutrients.
– Some physical exercise.
– Meditation.
– Supplement of vitamins, minerals, antioxidants, lecithin, amino acids and essential fatty acids.
– Stimulants like coffee or tea may help against depressive feelings in moderate amount. However, if you are a heavy user of these stimulants, you should cut down on your consumption.
There exist nutritional products in the marked to help against depressive symptoms. These contain ingredients that the brain uses as building blocks for neurotransmitters, for example amino acids and lecithin. They also often contain vitamins and minerals that the brain uses as tools to produce neurotransmitters, especially vitamin B6.
Supplements may further contain herbal extracts that trigger higher brain activity much like anti-depressive medications, but may have fewer side effects.
By: Knut Holt
Sunday, September 12, 2010
Researchers Explore Molecular Basis of Parkinson's Disease Using Yeast
Dr Tiago Fleming Outeiro describes how his group is slowly uncovering the molecular basis of Parkinson's disease by studying the associated human protein in yeast cells.
Parkinson's disease is a neurodegenerative disorder without any known cure that affects around 6 million people worldwide. The symptoms, which include rigidity, difficulty in initiating movements and resting tremors, are all related to the specific death of dopamine-producing neurons in the brain. These neurons characteristically contain protein deposits, known as Lewy bodies. A small protein called alpha-synuclein is the main component of these deposits.
Dr Outeiro explains how baker's yeast, Saccharomyces cerevisiae, is helping researchers learn how alpha-synuclein might lead to Parkinson's disease. "Yeast is a very simple but powerful model in which to study how alpha-synuclein actually works as, remarkably, many of the biochemical pathways involved are similar between yeast and humans," he said. "There is still a lot we don't know about the function of this protein, but we do know that even small increases in the level of alpha-synuclein in cells lead to cell death."
Dr Outeiro and colleagues screened a library of 115,000 small compounds to try and identify those that are able to block the toxic effects of alpha-synuclein. Several of these molecules have proved effective in preventing Parkinson's disease in worms and blocking alpha-synuclein toxicity in rat neurons. If developed further, they could form the basis of future Parkinson's disease treatments.
New treatments for neurodegenerative diseases are urgently needed. "With the ageing of the human population the number of people affected by Parkinson's disease will continue to increase. This means the disease will become an even greater problem for modern societies due to the tremendous socio-economic costs associated," Dr Outeiro said. "It's therefore imperative that treatments for such neurodegenerative diseases are developed. Our studies in yeast have enabled us make a step towards this."
Parkinson's disease is a neurodegenerative disorder without any known cure that affects around 6 million people worldwide. The symptoms, which include rigidity, difficulty in initiating movements and resting tremors, are all related to the specific death of dopamine-producing neurons in the brain. These neurons characteristically contain protein deposits, known as Lewy bodies. A small protein called alpha-synuclein is the main component of these deposits.
Dr Outeiro explains how baker's yeast, Saccharomyces cerevisiae, is helping researchers learn how alpha-synuclein might lead to Parkinson's disease. "Yeast is a very simple but powerful model in which to study how alpha-synuclein actually works as, remarkably, many of the biochemical pathways involved are similar between yeast and humans," he said. "There is still a lot we don't know about the function of this protein, but we do know that even small increases in the level of alpha-synuclein in cells lead to cell death."
Dr Outeiro and colleagues screened a library of 115,000 small compounds to try and identify those that are able to block the toxic effects of alpha-synuclein. Several of these molecules have proved effective in preventing Parkinson's disease in worms and blocking alpha-synuclein toxicity in rat neurons. If developed further, they could form the basis of future Parkinson's disease treatments.
New treatments for neurodegenerative diseases are urgently needed. "With the ageing of the human population the number of people affected by Parkinson's disease will continue to increase. This means the disease will become an even greater problem for modern societies due to the tremendous socio-economic costs associated," Dr Outeiro said. "It's therefore imperative that treatments for such neurodegenerative diseases are developed. Our studies in yeast have enabled us make a step towards this."
Sunday, September 5, 2010
How patients with dementia show improvement with music therapy
It’s been said that, “Music is a universal language”, and recent research with Dementia patients is proving that to be true; music can actually calm many patients and help to improve their memory!
Dementia causes many changes in the brain that can, in a sense, short-circuit the brain. Alzheimer’s and Dementia patients may begin to get lost in familiar surroundings, repeat questions, become fearful of their surroundings, suspicious of family members that they may not recognize. They may have trouble following directions and doing the simplest daily tasks. They can become disoriented about time, places and people around them. Simply bathing, brushing their teeth, using a fork or spoon or even swallowing are typically forgotten and patients will end up being fed, strictly with liquids through tubes. Eventually, daily care can require up to six or more caregivers per patient, which is why so many end up in nursing facilities, but life doesn’t have to be all misery for them.
With studies conducted in Belgium, Canada and the US, the findings are amazingly hopeful. We human beings seem to remember things that have emotional components. The parts of the brain, the Amygdala and our neurotransmitters, work together to help us recall the more emotional times that occur throughout our lives.
Petr Janata, a University of California, Associate Professor of Psychology, conducted brain activity experiments on a group of people who listened to music and found that the medial prefrontal cortex area of the brain stays healthier in Alzheimer’s patients longer than the other brain parts and has the capacity for emotions and other sensations.
According to, Concetta Tomaino, at the Institute for Music and Neurologic Function, at the Beth Abraham Health Services, in New York; we can recall audio very easily and the audio functions are often one of the last abilities that we lose. This seems to allow Alzheimer’s and Dementia patients to still have the capacity to sing songs of their youth, despite losing the capacity to recall many words, phrases and names. Documented research has shown that it can even extend to the more advanced cases of the disease.
Patients will often sing, hum and some even will begin to dance, despite the fact that minutes before they weren’t even speaking. Revisiting the music of earlier years can actually get these patients up and enjoying their day while even allowing them to have their memories stimulated; some patients recall the words to the songs even when they can’t recall their own family members’ names and faces. They were able to recall words and lyrics to many songs when hearing an audio recording than when they heard the lyrics spoken.
The music therapy often consists of CD’s being played, appropriate to the age range of the individuals or groups. Usually, the music that they either enjoyed as children, teens or young adults; sometimes, a discussion of many of the individual pieces and their association with movies or other shows can stimulate memories associated with better times or time spent with loved ones.
You can find CD’s, DVD’s and more at the local library that contain music familiar to the patients for whom you are caring. Familiar musicals, operas or Broadway show tunes can spark and open those mental trunks of long sealed away memories, giving many patients a memory boost and pleasure during their days.
Classical music has been proven, time and time again, to be soothing, so if you can play music for about an hour during the daytime or evening for those you care for, it will help to keep them calm and relaxed. Studies have shown that more than an hour can sometimes create agitation or irritability.
Playing an instrument, having a family sing-a-long can, as well and it allows some quality time with the family and friends that these patients wouldn’t otherwise be able to really enjoy.
These and other amazing studies are allowing many patients to stay calm, less agitated; it reduces anxiety and decreases wandering, may allow patients to improve some memory functions while enjoying their sing-a-long time reminiscing about the music that they grew up with. It can increase their socialization and decrease some depression which is of immense help to caregivers. Perhaps someday, music will help researchers to unlock the secrets to aiding these patients and their caregivers in having a more fulfilling life despite their disease.
by M. L. Kiser.
Dementia causes many changes in the brain that can, in a sense, short-circuit the brain. Alzheimer’s and Dementia patients may begin to get lost in familiar surroundings, repeat questions, become fearful of their surroundings, suspicious of family members that they may not recognize. They may have trouble following directions and doing the simplest daily tasks. They can become disoriented about time, places and people around them. Simply bathing, brushing their teeth, using a fork or spoon or even swallowing are typically forgotten and patients will end up being fed, strictly with liquids through tubes. Eventually, daily care can require up to six or more caregivers per patient, which is why so many end up in nursing facilities, but life doesn’t have to be all misery for them.
With studies conducted in Belgium, Canada and the US, the findings are amazingly hopeful. We human beings seem to remember things that have emotional components. The parts of the brain, the Amygdala and our neurotransmitters, work together to help us recall the more emotional times that occur throughout our lives.
Petr Janata, a University of California, Associate Professor of Psychology, conducted brain activity experiments on a group of people who listened to music and found that the medial prefrontal cortex area of the brain stays healthier in Alzheimer’s patients longer than the other brain parts and has the capacity for emotions and other sensations.
According to, Concetta Tomaino, at the Institute for Music and Neurologic Function, at the Beth Abraham Health Services, in New York; we can recall audio very easily and the audio functions are often one of the last abilities that we lose. This seems to allow Alzheimer’s and Dementia patients to still have the capacity to sing songs of their youth, despite losing the capacity to recall many words, phrases and names. Documented research has shown that it can even extend to the more advanced cases of the disease.
Patients will often sing, hum and some even will begin to dance, despite the fact that minutes before they weren’t even speaking. Revisiting the music of earlier years can actually get these patients up and enjoying their day while even allowing them to have their memories stimulated; some patients recall the words to the songs even when they can’t recall their own family members’ names and faces. They were able to recall words and lyrics to many songs when hearing an audio recording than when they heard the lyrics spoken.
The music therapy often consists of CD’s being played, appropriate to the age range of the individuals or groups. Usually, the music that they either enjoyed as children, teens or young adults; sometimes, a discussion of many of the individual pieces and their association with movies or other shows can stimulate memories associated with better times or time spent with loved ones.
You can find CD’s, DVD’s and more at the local library that contain music familiar to the patients for whom you are caring. Familiar musicals, operas or Broadway show tunes can spark and open those mental trunks of long sealed away memories, giving many patients a memory boost and pleasure during their days.
Classical music has been proven, time and time again, to be soothing, so if you can play music for about an hour during the daytime or evening for those you care for, it will help to keep them calm and relaxed. Studies have shown that more than an hour can sometimes create agitation or irritability.
Playing an instrument, having a family sing-a-long can, as well and it allows some quality time with the family and friends that these patients wouldn’t otherwise be able to really enjoy.
These and other amazing studies are allowing many patients to stay calm, less agitated; it reduces anxiety and decreases wandering, may allow patients to improve some memory functions while enjoying their sing-a-long time reminiscing about the music that they grew up with. It can increase their socialization and decrease some depression which is of immense help to caregivers. Perhaps someday, music will help researchers to unlock the secrets to aiding these patients and their caregivers in having a more fulfilling life despite their disease.
by M. L. Kiser.
Thursday, August 12, 2010
UC Parkinson's treatment shows promise
BY PEGGY O'FARRELL
Every morning, from about 8:30 to 10, Dan Truesdale froze up.
His muscles grew rigid, locked in place because of Parkinson's disease, until the medication finally kicked in, allowing to him get up, move around, live his life.
That changed last year when Truesdale, 47, became the first patient in Ohio to receive an experimental drug delivery system that gives his body a continual dose of the medication that lets him control his muscle movements.
His "frozen" muscles have thawed, Truesdale said.
"It's the best thing that's happened to me since I discovered I had Parkinson's," he said.
Researchers at the University of Cincinnati's Neuroscience Institute at University Hospital are recruiting more patients like Truesdale to test the system as part of a national phase 3 clinical trial.
Phase 3 trials are large-scale tests of new drugs or devices and the final step before federal health regulators decide to allow manufacturers to put new therapies on the market. Earlier phases test safety and effectiveness of new therapies on smaller scales.
Parkinson's disease is a chronic brain disorder in which brain cells that make the chemical dopamine die off. It usually strikes people over 50, and men are about 50 percent more likely to get it than women.
Without dopamine, adults lose control of muscle movements and balance. Symptoms get worse over time, said Alberto Espay, the neurologist heading up UC's arm of the trial, and Parkinson's patients may eventually lose the ability to speak, feed themselves, swallow or chew.
Replacing the lost dopamine helps patients regain muscle control, but standard treatments give dopamine in oral medications taken in several doses throughout the day.
That means the brain gets the dopamine it needs in interrupted allotments, so patients have periods throughout the day where they either can't move at all or they can't stop their bodies from moving involuntarily.
The drug delivery system Espay is testing aims to change that.
Abbott Pharmaceuticals' Levodopa-Carbidopa Intestinal Gel treatment system feeds the medication levodopa, which in the body becomes dopamine, into the upper intestine via a small tube surgically placed directly into the duodenum, or the very tip of the small intestine. The drug is fed through the tube from a cassette worn on the patient's body. A programmable pump lets the patient or doctor adjust the rate at which the medication is delivered.
"With this system, we're basically bathing the patient in dopamine at all times," Espay said.
Truesdale of Maineville used to be able to set his watch by his symptoms. The pump has changed all that. "I don't notice the passing of the hours because my symptoms have been reduced so drastically," he said.
He was diagnosed with Parkinson's in 2000, and has been on disability for the last four years. He recently began studying to become a minister.
The pump system is designed for patients like Truesdale with severe symptoms that are no longer controlled by standard medications, Espay said.
"People who've withdrawn from social and intellectual activities, they can resume them. We've seen people take up new activities after they've gone on the pump," he said.
Every morning, from about 8:30 to 10, Dan Truesdale froze up.
His muscles grew rigid, locked in place because of Parkinson's disease, until the medication finally kicked in, allowing to him get up, move around, live his life.
That changed last year when Truesdale, 47, became the first patient in Ohio to receive an experimental drug delivery system that gives his body a continual dose of the medication that lets him control his muscle movements.
His "frozen" muscles have thawed, Truesdale said.
"It's the best thing that's happened to me since I discovered I had Parkinson's," he said.
Researchers at the University of Cincinnati's Neuroscience Institute at University Hospital are recruiting more patients like Truesdale to test the system as part of a national phase 3 clinical trial.
Phase 3 trials are large-scale tests of new drugs or devices and the final step before federal health regulators decide to allow manufacturers to put new therapies on the market. Earlier phases test safety and effectiveness of new therapies on smaller scales.
Parkinson's disease is a chronic brain disorder in which brain cells that make the chemical dopamine die off. It usually strikes people over 50, and men are about 50 percent more likely to get it than women.
Without dopamine, adults lose control of muscle movements and balance. Symptoms get worse over time, said Alberto Espay, the neurologist heading up UC's arm of the trial, and Parkinson's patients may eventually lose the ability to speak, feed themselves, swallow or chew.
Replacing the lost dopamine helps patients regain muscle control, but standard treatments give dopamine in oral medications taken in several doses throughout the day.
That means the brain gets the dopamine it needs in interrupted allotments, so patients have periods throughout the day where they either can't move at all or they can't stop their bodies from moving involuntarily.
The drug delivery system Espay is testing aims to change that.
Abbott Pharmaceuticals' Levodopa-Carbidopa Intestinal Gel treatment system feeds the medication levodopa, which in the body becomes dopamine, into the upper intestine via a small tube surgically placed directly into the duodenum, or the very tip of the small intestine. The drug is fed through the tube from a cassette worn on the patient's body. A programmable pump lets the patient or doctor adjust the rate at which the medication is delivered.
"With this system, we're basically bathing the patient in dopamine at all times," Espay said.
Truesdale of Maineville used to be able to set his watch by his symptoms. The pump has changed all that. "I don't notice the passing of the hours because my symptoms have been reduced so drastically," he said.
He was diagnosed with Parkinson's in 2000, and has been on disability for the last four years. He recently began studying to become a minister.
The pump system is designed for patients like Truesdale with severe symptoms that are no longer controlled by standard medications, Espay said.
"People who've withdrawn from social and intellectual activities, they can resume them. We've seen people take up new activities after they've gone on the pump," he said.
Parkinson's Disease Placebo Response Increases with Expectations
Individuals with Parkinson's disease were more likely to have a neurochemical response to a placebo medication if they were told they had higher odds of receiving an active drug.
Chicago, IL - infoZine - "The promise of symptom improvement that is elicited by a placebo is a powerful modulator of brain neurochemistry," the authors write as background information to a report in the August issue of Archives of General Psychiatry, one of the JAMA/Archives journals. "Understanding the factors that modify the strength of the placebo effect is of major clinical as well as fundamental scientific significance." In patients with Parkinson's disease, the expectation of symptom improvement is associated with the release of the neurotransmitter dopamine, and the manipulation of this expectation has been shown to affect the motor performance of patients with the condition.
Sarah C. Lidstone, Ph.D., of Pacific Parkinson's Research Centre at Vancouver Coastal Health and the University of British Columbia, Vancouver, Canada, and colleagues studied 35 patients with mild to moderate Parkinson's disease undergoing treatment with the medication levodopa. On the first day of the study, a baseline positron emission tomographic (PET) scan was performed, participants were given levodopa and a second scan was performed one hour later to assess dopamine response. On the second day, patients were randomly assigned to one of four groups, during which they were told they had either a 25-percent, 50-percent, 75-percent or 100-percent chance of receiving active medication before the third scan; however, all patients were given placebo.
Patients who were told they had a 75-percent chance of receiving active medication demonstrated a significant release of dopamine in response to the placebo, whereas those in the other groups did not.
Patients' reactions to the active medication before the first scan was also correlated with their response to placebo. "Importantly, whereas prior medication experience (i.e., the dopaminergic response to levodopa) was the major determinant of dopamine release in the dorsal striatum, expectation of clinical improvement (i.e., the probability determined by group allocation) was additionally required to drive dopamine release in the ventral striatum," the authors write. Both areas have been shown to be involved with reward processing; in patients with a chronic debilitating illness who have responded to therapy in the past, expectation of therapeutic benefit in response to placebo has been likened to the expectation of receiving a reward.
"Our findings may have important implications for the design of clinical trials, as we have shown that both the probability of receiving active treatment—which varies in clinical trials depending on the study design and the information provided to the patient—as well as the treatment history of the patient influence dopamine system activity and consequently clinical outcome," the authors conclude. "While our finding of a biochemical placebo response restricted to a 75 percent likelihood of receiving active treatment may not generalize to diseases other than Parkinson's disease, it is extremely likely that both probability and prior experience have similarly profound effects in those conditions."
This study was funded by the Michael Smith Foundation for Health Research, the Canadian Institutes for Health Research and a TRIUMF Life Sciences Grant. Dr. Stoessl is supported by the Canada Research Chairs Program.
Chicago, IL - infoZine - "The promise of symptom improvement that is elicited by a placebo is a powerful modulator of brain neurochemistry," the authors write as background information to a report in the August issue of Archives of General Psychiatry, one of the JAMA/Archives journals. "Understanding the factors that modify the strength of the placebo effect is of major clinical as well as fundamental scientific significance." In patients with Parkinson's disease, the expectation of symptom improvement is associated with the release of the neurotransmitter dopamine, and the manipulation of this expectation has been shown to affect the motor performance of patients with the condition.
Sarah C. Lidstone, Ph.D., of Pacific Parkinson's Research Centre at Vancouver Coastal Health and the University of British Columbia, Vancouver, Canada, and colleagues studied 35 patients with mild to moderate Parkinson's disease undergoing treatment with the medication levodopa. On the first day of the study, a baseline positron emission tomographic (PET) scan was performed, participants were given levodopa and a second scan was performed one hour later to assess dopamine response. On the second day, patients were randomly assigned to one of four groups, during which they were told they had either a 25-percent, 50-percent, 75-percent or 100-percent chance of receiving active medication before the third scan; however, all patients were given placebo.
Patients who were told they had a 75-percent chance of receiving active medication demonstrated a significant release of dopamine in response to the placebo, whereas those in the other groups did not.
Patients' reactions to the active medication before the first scan was also correlated with their response to placebo. "Importantly, whereas prior medication experience (i.e., the dopaminergic response to levodopa) was the major determinant of dopamine release in the dorsal striatum, expectation of clinical improvement (i.e., the probability determined by group allocation) was additionally required to drive dopamine release in the ventral striatum," the authors write. Both areas have been shown to be involved with reward processing; in patients with a chronic debilitating illness who have responded to therapy in the past, expectation of therapeutic benefit in response to placebo has been likened to the expectation of receiving a reward.
"Our findings may have important implications for the design of clinical trials, as we have shown that both the probability of receiving active treatment—which varies in clinical trials depending on the study design and the information provided to the patient—as well as the treatment history of the patient influence dopamine system activity and consequently clinical outcome," the authors conclude. "While our finding of a biochemical placebo response restricted to a 75 percent likelihood of receiving active treatment may not generalize to diseases other than Parkinson's disease, it is extremely likely that both probability and prior experience have similarly profound effects in those conditions."
This study was funded by the Michael Smith Foundation for Health Research, the Canadian Institutes for Health Research and a TRIUMF Life Sciences Grant. Dr. Stoessl is supported by the Canada Research Chairs Program.
Saturday, July 24, 2010
UCSF Gene Therapy Method Allays Parkinson’s Symptoms
by Lauren Hammit
A novel technique created at UCSF to deliver a growth factor directly to brain cells has shown promising results in treating Parkinson’s symptoms and could enter human clinical trials as early as next year.
The technique is part of an experimental treatment called gene therapy, which is considered a hopeful medical advance for neurodegenerative diseases such as Parkinson’s. Gene therapy involves introducing genetic material into a cell to cause the expression of a particular protein that can replace a missing or defective protein responsible for disease.
The UCSF team demonstrated for the first time that the infusion system they designed successfully spread a targeted protein to critical regions in the primate brain. This resulted, on average, in a 50 percent improvement of symptoms that continued out to two years.
“The approach is among the first shown to be beneficial to animals after they have already developed signs of Parkinson’s,” said Krystof Bankiewicz, MD, PhD, Kinetics Foundation Chair in Translational Research and professor of Neurological Surgery at UCSF. “Our ultimate goal is to reverse this disease in patients, and we hope this method will enable doctors to do exactly that.”
Findings are published online and in the July 14, 2010, issue of the Journal of Neuroscience.
In addition to an improvement in Parkinson’s symptoms, the treated animals also maintained a higher density of neurons that produce the brain chemical dopamine – the same neurons that disappear in Parkinson’s disease. Live imaging of the brain by positron emission tomography (PET) scanning, which has been used to gauge treatment effects in clinical studies of Parkinson’s, showed that those neurons remained active.
“The scans enabled us to see where the protein went – and just as hoped, it had been taken up by neurons and transported along nerve fibers to where it was needed, the substantia nigra.” Bankiewicz said. Parkinson’s disease attacks the substantia nigra, which is a part of the brain that controls movement.
A clinical trial is planned to test the safety of the method, according to the National Institutes of Neurological Disorders and Stroke, which funded this research. In a workup for the trial, the National Institutes of Health Rapid Access to Interventional Development (NIH RAID) program is supporting additional toxicity studies, as well as the production of clinical grade virus.
A novel technique created at UCSF to deliver a growth factor directly to brain cells has shown promising results in treating Parkinson’s symptoms and could enter human clinical trials as early as next year.
The technique is part of an experimental treatment called gene therapy, which is considered a hopeful medical advance for neurodegenerative diseases such as Parkinson’s. Gene therapy involves introducing genetic material into a cell to cause the expression of a particular protein that can replace a missing or defective protein responsible for disease.
The UCSF team demonstrated for the first time that the infusion system they designed successfully spread a targeted protein to critical regions in the primate brain. This resulted, on average, in a 50 percent improvement of symptoms that continued out to two years.
“The approach is among the first shown to be beneficial to animals after they have already developed signs of Parkinson’s,” said Krystof Bankiewicz, MD, PhD, Kinetics Foundation Chair in Translational Research and professor of Neurological Surgery at UCSF. “Our ultimate goal is to reverse this disease in patients, and we hope this method will enable doctors to do exactly that.”
Findings are published online and in the July 14, 2010, issue of the Journal of Neuroscience.
In addition to an improvement in Parkinson’s symptoms, the treated animals also maintained a higher density of neurons that produce the brain chemical dopamine – the same neurons that disappear in Parkinson’s disease. Live imaging of the brain by positron emission tomography (PET) scanning, which has been used to gauge treatment effects in clinical studies of Parkinson’s, showed that those neurons remained active.
“The scans enabled us to see where the protein went – and just as hoped, it had been taken up by neurons and transported along nerve fibers to where it was needed, the substantia nigra.” Bankiewicz said. Parkinson’s disease attacks the substantia nigra, which is a part of the brain that controls movement.
A clinical trial is planned to test the safety of the method, according to the National Institutes of Neurological Disorders and Stroke, which funded this research. In a workup for the trial, the National Institutes of Health Rapid Access to Interventional Development (NIH RAID) program is supporting additional toxicity studies, as well as the production of clinical grade virus.
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