2013 MDS International Congress

SYDNEY, AUSTRALIA – An iPod-based program using music as reward and behavioral reinforcement can lead to significant improvements in stride length and walking speed, according to data presented at the international congress of Parkinson’s Disease and Movement Disorders.

The AmbuloSono system, developed by researchers from the University of Calgary (Alta.), uses an accelerometer to measure stride length and distance walked, and is tied to a music program that only switches on above a certain stride length. The iPod is housed in a pouch strapped above the knee and connected wirelessly to headphones.

"It uses music as a reward, so you have to walk larger steps in order to trigger the music to play, and when your step size becomes smaller, the music stops," said lead author Dr. Bin Hu of the Hotchkiss Brain Institute, University of Calgary.

In a pilot study of 42 patients with Parkinson’s disease, use of the device over a 320-day trial period was associated with significant improvements in stride length (10%-30%) and walking speed (10%-20%) over long distances. In that time, patients walked more than 3,500 km and listened to more than 700 hours of music.

Researchers also noted significant improvements in other functional domains, including arm swings, facial expression, long-term fear and anxiety of using an escalator, and activity avoidance due to depression/apathy.

"Our pilot study indicates that AmbuloSono may be a more efficient behavioral training paradigm than simple rhythmic auditory stimulation to induce functional improvements in multiple domains of motor and nonmotor functions in patients living with Parkinson’s disease," the researchers wrote.

Postural instability and gait disorders can be particularly challenging to treat in Parkinson’s patients, as they do not respond well to drugs and are associated with major functional disability, Dr. Hu said in an interview.

"This program is designed based on the mechanism of reward seeking and learning, so instead of triggering neuroregeneration, you trigger functional compensation," Dr. Hu said.

The music used in the program was chosen particularly for its saliency, to maximize the reward.

"Over time, it becomes automatic, so you essentially learn how to automatically control your walk again, but you need a reward in order to achieve that state because the brain is built in that way – when you engage in reward-seeking, the behavior becomes automatic," he said.

Dr. Hu said the improvements were sustained and patients’ gait problems were minimized to the point where their walk appeared to be relatively normal.

The study was supported by the Canadian Institutes of Health Research, Alberta Innovations Health Solutions, the Hotchkiss Brain Institute, the Parkinson’s Society of Alberta, Alberta Health Services, and the Foothills Movement Disorders Clinic. No other conflicts of interest were declared.

SYDNEY, AUSTRALIA – An iPod-based program using music as reward and behavioral reinforcement can lead to significant improvements in stride length and walking speed, according to data presented at the international congress of Parkinson’s Disease and Movement Disorders.

The AmbuloSono system, developed by researchers from the University of Calgary (Alta.), uses an accelerometer to measure stride length and distance walked, and is tied to a music program that only switches on above a certain stride length. The iPod is housed in a pouch strapped above the knee and connected wirelessly to headphones.

"It uses music as a reward, so you have to walk larger steps in order to trigger the music to play, and when your step size becomes smaller, the music stops," said lead author Dr. Bin Hu of the Hotchkiss Brain Institute, University of Calgary.

In a pilot study of 42 patients with Parkinson’s disease, use of the device over a 320-day trial period was associated with significant improvements in stride length (10%-30%) and walking speed (10%-20%) over long distances. In that time, patients walked more than 3,500 km and listened to more than 700 hours of music.

Researchers also noted significant improvements in other functional domains, including arm swings, facial expression, long-term fear and anxiety of using an escalator, and activity avoidance due to depression/apathy.

"Our pilot study indicates that AmbuloSono may be a more efficient behavioral training paradigm than simple rhythmic auditory stimulation to induce functional improvements in multiple domains of motor and nonmotor functions in patients living with Parkinson’s disease," the researchers wrote.

Postural instability and gait disorders can be particularly challenging to treat in Parkinson’s patients, as they do not respond well to drugs and are associated with major functional disability, Dr. Hu said in an interview.

"This program is designed based on the mechanism of reward seeking and learning, so instead of triggering neuroregeneration, you trigger functional compensation," Dr. Hu said.

The music used in the program was chosen particularly for its saliency, to maximize the reward.

"Over time, it becomes automatic, so you essentially learn how to automatically control your walk again, but you need a reward in order to achieve that state because the brain is built in that way – when you engage in reward-seeking, the behavior becomes automatic," he said.

Dr. Hu said the improvements were sustained and patients’ gait problems were minimized to the point where their walk appeared to be relatively normal.

The study was supported by the Canadian Institutes of Health Research, Alberta Innovations Health Solutions, the Hotchkiss Brain Institute, the Parkinson’s Society of Alberta, Alberta Health Services, and the Foothills Movement Disorders Clinic. No other conflicts of interest were declared.

SYDNEY, AUSTRALIA – An iPod-based program using music as reward and behavioral reinforcement can lead to significant improvements in stride length and walking speed, according to data presented at the international congress of Parkinson’s Disease and Movement Disorders.

The AmbuloSono system, developed by researchers from the University of Calgary (Alta.), uses an accelerometer to measure stride length and distance walked, and is tied to a music program that only switches on above a certain stride length. The iPod is housed in a pouch strapped above the knee and connected wirelessly to headphones.

"It uses music as a reward, so you have to walk larger steps in order to trigger the music to play, and when your step size becomes smaller, the music stops," said lead author Dr. Bin Hu of the Hotchkiss Brain Institute, University of Calgary.

In a pilot study of 42 patients with Parkinson’s disease, use of the device over a 320-day trial period was associated with significant improvements in stride length (10%-30%) and walking speed (10%-20%) over long distances. In that time, patients walked more than 3,500 km and listened to more than 700 hours of music.

Researchers also noted significant improvements in other functional domains, including arm swings, facial expression, long-term fear and anxiety of using an escalator, and activity avoidance due to depression/apathy.

"Our pilot study indicates that AmbuloSono may be a more efficient behavioral training paradigm than simple rhythmic auditory stimulation to induce functional improvements in multiple domains of motor and nonmotor functions in patients living with Parkinson’s disease," the researchers wrote.

Postural instability and gait disorders can be particularly challenging to treat in Parkinson’s patients, as they do not respond well to drugs and are associated with major functional disability, Dr. Hu said in an interview.

"This program is designed based on the mechanism of reward seeking and learning, so instead of triggering neuroregeneration, you trigger functional compensation," Dr. Hu said.

The music used in the program was chosen particularly for its saliency, to maximize the reward.

"Over time, it becomes automatic, so you essentially learn how to automatically control your walk again, but you need a reward in order to achieve that state because the brain is built in that way – when you engage in reward-seeking, the behavior becomes automatic," he said.

Dr. Hu said the improvements were sustained and patients’ gait problems were minimized to the point where their walk appeared to be relatively normal.

The study was supported by the Canadian Institutes of Health Research, Alberta Innovations Health Solutions, the Hotchkiss Brain Institute, the Parkinson’s Society of Alberta, Alberta Health Services, and the Foothills Movement Disorders Clinic. No other conflicts of interest were declared.

SYDNEY, AUSTRALIA – Dopaminergic therapy has seen its heyday, and the time has come to look to other neurotransmitter systems for effective treatments for the nonmotor symptoms of Parkinson’s disease, a leading pharmacologist said.

Delivering the C. David Marsden lecture at the international congress of Parkinson’s Disease and Movement Disorders, Peter Jenner, Ph.D., said that Parkinson’s disease needs to be looked at as a multisystem, multibiochemical disorder, and many of the problems associated with the disease originate in areas of the brain that do not use dopamine as a neurotransmitter.

"We’re locked into this dopamine time warp and I’m not sure there’s much to be gained by pushing forward with new dopaminergic therapies," said Dr. Jenner of the Institute of Pharmaceutical Science at King’s College London.

"We can make them last longer, we can deliver them in different ways, we could probably reduce people’s amount of off time, but in terms of a big step forward, I doubt we’re going to get that out of dopaminergic therapy," he said in an interview.

The problem is that dopaminergic therapy has been so effective in dealing with the motor symptoms of Parkinson’s disease that it has exposed inadequacies in the treatment of nonmotor symptoms such as depression, sensory changes, sleep disturbance, fatigue, and apathy.

"In previous eras, people with Parkinson’s disease had a shortened life expectancy because their motor system didn’t work, they got hospitalized, they got bronchopneumonia, and they died," Dr. Jenner said. "Now we keep them going longer, and now we see that dementia is a very significant problem in the majority of older patients with Parkinson’s disease, and we never saw this before because they died before they got to that point in the illness."

Dr. Jenner suggested that adenosine antagonists and anticholinergic therapies could have potential as alternatives to the dopaminergic focus of current treatments.

Adenosine antagonists have had mixed results, Dr. Jenner said, pointing to the repeated failure in phase III trials of the A2A receptor antagonist preladenant after promising results in phase II trials, while another A2A receptor antagonist istradefylline has been approved in Japan as an adjunct treatment for Parkinson’s disease.

Anticholinergic therapies such as orphenadrine, procyclidine, and trihexyphenidyl are still available and effective but are not often used because of their side effect profile. As this class of drugs was developed several decades ago, there are few modern clinical trials on them, Dr. Jenner said.

"Since they were discovered, we now know there are multiple subtypes of muscarinic receptors and nobody’s gone back to try and target the one that seems to be significant in the motor system," namely, the M4 receptor, he said.

Despite the current shortfall in effective treatments for nonmotor Parkinson’s symptoms, Dr. Jenner said he was optimistic that progress would soon be made because of the growing awareness of the burden of nonmotor symptoms.

"People are going to wake up to the fact that their clinics, their beds in hospitals, and the beds in nursing homes are full of people with Parkinson’s disease because of nonmotor symptoms, and nonmotor is the biggest cause of people having to go into residential care, and it’s the biggest determinant of disease outcome," he said.

Dr. Jenner said he did not have any relevant financial disclosures.

cnnews@frontlinemedcom.com

SYDNEY, AUSTRALIA – Dopaminergic therapy has seen its heyday, and the time has come to look to other neurotransmitter systems for effective treatments for the nonmotor symptoms of Parkinson’s disease, a leading pharmacologist said.

Delivering the C. David Marsden lecture at the international congress of Parkinson’s Disease and Movement Disorders, Peter Jenner, Ph.D., said that Parkinson’s disease needs to be looked at as a multisystem, multibiochemical disorder, and many of the problems associated with the disease originate in areas of the brain that do not use dopamine as a neurotransmitter.

"We’re locked into this dopamine time warp and I’m not sure there’s much to be gained by pushing forward with new dopaminergic therapies," said Dr. Jenner of the Institute of Pharmaceutical Science at King’s College London.

"We can make them last longer, we can deliver them in different ways, we could probably reduce people’s amount of off time, but in terms of a big step forward, I doubt we’re going to get that out of dopaminergic therapy," he said in an interview.

The problem is that dopaminergic therapy has been so effective in dealing with the motor symptoms of Parkinson’s disease that it has exposed inadequacies in the treatment of nonmotor symptoms such as depression, sensory changes, sleep disturbance, fatigue, and apathy.

"In previous eras, people with Parkinson’s disease had a shortened life expectancy because their motor system didn’t work, they got hospitalized, they got bronchopneumonia, and they died," Dr. Jenner said. "Now we keep them going longer, and now we see that dementia is a very significant problem in the majority of older patients with Parkinson’s disease, and we never saw this before because they died before they got to that point in the illness."

Dr. Jenner suggested that adenosine antagonists and anticholinergic therapies could have potential as alternatives to the dopaminergic focus of current treatments.

Adenosine antagonists have had mixed results, Dr. Jenner said, pointing to the repeated failure in phase III trials of the A2A receptor antagonist preladenant after promising results in phase II trials, while another A2A receptor antagonist istradefylline has been approved in Japan as an adjunct treatment for Parkinson’s disease.

Anticholinergic therapies such as orphenadrine, procyclidine, and trihexyphenidyl are still available and effective but are not often used because of their side effect profile. As this class of drugs was developed several decades ago, there are few modern clinical trials on them, Dr. Jenner said.

"Since they were discovered, we now know there are multiple subtypes of muscarinic receptors and nobody’s gone back to try and target the one that seems to be significant in the motor system," namely, the M4 receptor, he said.

Despite the current shortfall in effective treatments for nonmotor Parkinson’s symptoms, Dr. Jenner said he was optimistic that progress would soon be made because of the growing awareness of the burden of nonmotor symptoms.

"People are going to wake up to the fact that their clinics, their beds in hospitals, and the beds in nursing homes are full of people with Parkinson’s disease because of nonmotor symptoms, and nonmotor is the biggest cause of people having to go into residential care, and it’s the biggest determinant of disease outcome," he said.

Dr. Jenner said he did not have any relevant financial disclosures.

cnnews@frontlinemedcom.com

SYDNEY, AUSTRALIA – Dopaminergic therapy has seen its heyday, and the time has come to look to other neurotransmitter systems for effective treatments for the nonmotor symptoms of Parkinson’s disease, a leading pharmacologist said.

Delivering the C. David Marsden lecture at the international congress of Parkinson’s Disease and Movement Disorders, Peter Jenner, Ph.D., said that Parkinson’s disease needs to be looked at as a multisystem, multibiochemical disorder, and many of the problems associated with the disease originate in areas of the brain that do not use dopamine as a neurotransmitter.

"We’re locked into this dopamine time warp and I’m not sure there’s much to be gained by pushing forward with new dopaminergic therapies," said Dr. Jenner of the Institute of Pharmaceutical Science at King’s College London.

"We can make them last longer, we can deliver them in different ways, we could probably reduce people’s amount of off time, but in terms of a big step forward, I doubt we’re going to get that out of dopaminergic therapy," he said in an interview.

The problem is that dopaminergic therapy has been so effective in dealing with the motor symptoms of Parkinson’s disease that it has exposed inadequacies in the treatment of nonmotor symptoms such as depression, sensory changes, sleep disturbance, fatigue, and apathy.

"In previous eras, people with Parkinson’s disease had a shortened life expectancy because their motor system didn’t work, they got hospitalized, they got bronchopneumonia, and they died," Dr. Jenner said. "Now we keep them going longer, and now we see that dementia is a very significant problem in the majority of older patients with Parkinson’s disease, and we never saw this before because they died before they got to that point in the illness."

Dr. Jenner suggested that adenosine antagonists and anticholinergic therapies could have potential as alternatives to the dopaminergic focus of current treatments.

Adenosine antagonists have had mixed results, Dr. Jenner said, pointing to the repeated failure in phase III trials of the A2A receptor antagonist preladenant after promising results in phase II trials, while another A2A receptor antagonist istradefylline has been approved in Japan as an adjunct treatment for Parkinson’s disease.

Anticholinergic therapies such as orphenadrine, procyclidine, and trihexyphenidyl are still available and effective but are not often used because of their side effect profile. As this class of drugs was developed several decades ago, there are few modern clinical trials on them, Dr. Jenner said.

"Since they were discovered, we now know there are multiple subtypes of muscarinic receptors and nobody’s gone back to try and target the one that seems to be significant in the motor system," namely, the M4 receptor, he said.

Despite the current shortfall in effective treatments for nonmotor Parkinson’s symptoms, Dr. Jenner said he was optimistic that progress would soon be made because of the growing awareness of the burden of nonmotor symptoms.

"People are going to wake up to the fact that their clinics, their beds in hospitals, and the beds in nursing homes are full of people with Parkinson’s disease because of nonmotor symptoms, and nonmotor is the biggest cause of people having to go into residential care, and it’s the biggest determinant of disease outcome," he said.

Dr. Jenner said he did not have any relevant financial disclosures.

cnnews@frontlinemedcom.com

SYDNEY, AUSTRALIA – New classification guidelines define dystonia as a movement disorder and shift towards classifying dystonia along the twin axes of clinical characteristics and etiology.

Under the new guidelines from the Movement Disorder Society, dystonia is described as "a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both."

"Dystonic movements are typically patterned and twisting, and may be tremulous. Dystonia is often initiated or worsened by voluntary action and associated with overflow muscle activation," the guidelines state.

The guidelines, presented at the international congress of Parkinson’s Disease and Movement Disorders, also describe a new approach to classifying dystonias according to both their phenomenological appearance and etiology. The guidelines also were recently published online (Mov. Dis. 2013 May 6 [doi:10.1002/mds.25475]).

Dr. Mark Hallett, a member of the guidelines review committee, said that this change had come about because of the difficulties in trying to classify individual patients according to a system that assumed a one-to-one match between a particular phenotype and a specific disease entity or cause.

"The problem is that we have patients that have certain characteristics, and there can be many possible causes, while on the other hand, we have individual causes such as individual genetic abnormalities that can have many different phenotypes, many different clinical syndromes associated with them," said Dr. Hallett, chief of the human motor control section of the National Institute of Neurological Disorders and Stroke, Bethesda, Md.

"The way we’re going about this now is having a two-axis approach to the classification of different disorders. One axis is the phenomenological appearance and the other is the etiology, so any individual case would be described as one phenotype and one or more etiologies," he explained.

The first axis of clinical characteristics incorporates information such as age at onset, body distribution, and temporal pattern, while the second axis of etiology examines nervous system pathology and whether the dystonia is inherited, acquired, or idiopathic.

The shift has been driven by the rapid advances in understanding of dystonia, particularly genetic etiologies of the disorder. This understanding will help in therapeutic decision-making, but it will take some time for therapeutic advances to catch up, Dr. Hallett noted.

"At the moment, we’re almost always using relatively nonspecific therapy. Sometimes it is important to get the etiology, but I think our etiologic therapies are still relatively weak," he said in an interview.

The guidelines also move away from the former phenotypic classifications of "primary" and "secondary" dystonia toward the terminology of "isolated" and "combined" dystonia.

Isolated dystonia refers to a situation in which dystonia is the only motor feature, and combined dystonia refers to dystonia combined with other movement disorders such as myoclonus or Parkinsonism.

There were no relevant conflicts of interest or disclosures reported.

cnnews@frontlinemedcom.com

SYDNEY, AUSTRALIA – New classification guidelines define dystonia as a movement disorder and shift towards classifying dystonia along the twin axes of clinical characteristics and etiology.

Under the new guidelines from the Movement Disorder Society, dystonia is described as "a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both."

"Dystonic movements are typically patterned and twisting, and may be tremulous. Dystonia is often initiated or worsened by voluntary action and associated with overflow muscle activation," the guidelines state.

The guidelines, presented at the international congress of Parkinson’s Disease and Movement Disorders, also describe a new approach to classifying dystonias according to both their phenomenological appearance and etiology. The guidelines also were recently published online (Mov. Dis. 2013 May 6 [doi:10.1002/mds.25475]).

Dr. Mark Hallett, a member of the guidelines review committee, said that this change had come about because of the difficulties in trying to classify individual patients according to a system that assumed a one-to-one match between a particular phenotype and a specific disease entity or cause.

"The problem is that we have patients that have certain characteristics, and there can be many possible causes, while on the other hand, we have individual causes such as individual genetic abnormalities that can have many different phenotypes, many different clinical syndromes associated with them," said Dr. Hallett, chief of the human motor control section of the National Institute of Neurological Disorders and Stroke, Bethesda, Md.

"The way we’re going about this now is having a two-axis approach to the classification of different disorders. One axis is the phenomenological appearance and the other is the etiology, so any individual case would be described as one phenotype and one or more etiologies," he explained.

The first axis of clinical characteristics incorporates information such as age at onset, body distribution, and temporal pattern, while the second axis of etiology examines nervous system pathology and whether the dystonia is inherited, acquired, or idiopathic.

The shift has been driven by the rapid advances in understanding of dystonia, particularly genetic etiologies of the disorder. This understanding will help in therapeutic decision-making, but it will take some time for therapeutic advances to catch up, Dr. Hallett noted.

"At the moment, we’re almost always using relatively nonspecific therapy. Sometimes it is important to get the etiology, but I think our etiologic therapies are still relatively weak," he said in an interview.

The guidelines also move away from the former phenotypic classifications of "primary" and "secondary" dystonia toward the terminology of "isolated" and "combined" dystonia.

Isolated dystonia refers to a situation in which dystonia is the only motor feature, and combined dystonia refers to dystonia combined with other movement disorders such as myoclonus or Parkinsonism.

There were no relevant conflicts of interest or disclosures reported.

cnnews@frontlinemedcom.com

SYDNEY, AUSTRALIA – New classification guidelines define dystonia as a movement disorder and shift towards classifying dystonia along the twin axes of clinical characteristics and etiology.

Under the new guidelines from the Movement Disorder Society, dystonia is described as "a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both."

"Dystonic movements are typically patterned and twisting, and may be tremulous. Dystonia is often initiated or worsened by voluntary action and associated with overflow muscle activation," the guidelines state.

The guidelines, presented at the international congress of Parkinson’s Disease and Movement Disorders, also describe a new approach to classifying dystonias according to both their phenomenological appearance and etiology. The guidelines also were recently published online (Mov. Dis. 2013 May 6 [doi:10.1002/mds.25475]).

Dr. Mark Hallett, a member of the guidelines review committee, said that this change had come about because of the difficulties in trying to classify individual patients according to a system that assumed a one-to-one match between a particular phenotype and a specific disease entity or cause.

"The problem is that we have patients that have certain characteristics, and there can be many possible causes, while on the other hand, we have individual causes such as individual genetic abnormalities that can have many different phenotypes, many different clinical syndromes associated with them," said Dr. Hallett, chief of the human motor control section of the National Institute of Neurological Disorders and Stroke, Bethesda, Md.

"The way we’re going about this now is having a two-axis approach to the classification of different disorders. One axis is the phenomenological appearance and the other is the etiology, so any individual case would be described as one phenotype and one or more etiologies," he explained.

The first axis of clinical characteristics incorporates information such as age at onset, body distribution, and temporal pattern, while the second axis of etiology examines nervous system pathology and whether the dystonia is inherited, acquired, or idiopathic.

The shift has been driven by the rapid advances in understanding of dystonia, particularly genetic etiologies of the disorder. This understanding will help in therapeutic decision-making, but it will take some time for therapeutic advances to catch up, Dr. Hallett noted.

"At the moment, we’re almost always using relatively nonspecific therapy. Sometimes it is important to get the etiology, but I think our etiologic therapies are still relatively weak," he said in an interview.

The guidelines also move away from the former phenotypic classifications of "primary" and "secondary" dystonia toward the terminology of "isolated" and "combined" dystonia.

Isolated dystonia refers to a situation in which dystonia is the only motor feature, and combined dystonia refers to dystonia combined with other movement disorders such as myoclonus or Parkinsonism.

There were no relevant conflicts of interest or disclosures reported.

cnnews@frontlinemedcom.com

SYDNEY, AUSTRALIA – An exercise-based intervention carried out at home with minimal supervision led to a significant reduction in falls in patients with mild but not severe Parkinson’s disease.

"The approach we took was to target three risk factors that exercise could potentially improve, that is, loss of muscle strength, poor balance, and freezing of gait," said lead author Colleen Canning, Ph.D., team leader for Parkinson’s disease research in the faculty of health sciences at the University of Sydney.

"The exercise program that we developed involved those three elements and was designed so that the participants did most of the exercise at home," she said in a poster presented at the international congress of Parkinson’s Disease and Movement Disorders.

In the study, Dr. Canning and her associates randomized 231 individuals with Parkinson’s disease to receive usual care or to participate in an exercise regimen involving 40-60 minutes of exercise three times a week for 6 months (Mov. Dis. 2013;28 [Suppl. 1]:442).

The intervention involved a range of balance, stepping, and strengthening exercises using weighted vests, as well as cueing using a metronome to overcome freezing. Around 10% of the exercise sessions were supervised by a physiotherapist.

There was a statistically nonsignificant 27% reduction (incidence rate ratio [IRR] = 0.73; 95% confidence interval [CI], 0.45-1.17; P = .18) in the incidence of falls between the intervention and control group, Dr. Canning said.

However, a subgroup analysis based on disease severity revealed a significant 69% reduction in the risk of falls among patients with lower disease severity (IRR = 0.31; 95% CI, 0.15-0.62; P less than .001), while there was a nonsignificant increase in the risk of falls in the higher–disease severity subgroup.

At the same time, there were significant improvements favoring the intervention group as a whole in a range of mobility and psychological functions, including the Short Physical Performance Battery, sit to stand, fear of falling, affect, and health and well-being measures.

The researchers also presented data on adherence to the program, showing that participants completed a mean of 72% of the prescribed exercise sessions, although this was based on patient self-report.

Patients with shorter disease duration, less bodily pain, better standing balance, and better perceived well-being and health were more likely to adhere to the exercise regimen. Disease severity and past falls did not significantly predict adherence, Dr. Canning noted.

"Our results suggest that this particular program has the potential to be quite an effective method of reducing falls in people with lower disease severity," she said in an interview. "This is an important finding because that’s the group that often doesn’t get offered exercise because they don’t have major motor difficulties early on."

There were no relevant conflicts of interest declared.

SYDNEY, AUSTRALIA – An exercise-based intervention carried out at home with minimal supervision led to a significant reduction in falls in patients with mild but not severe Parkinson’s disease.

"The approach we took was to target three risk factors that exercise could potentially improve, that is, loss of muscle strength, poor balance, and freezing of gait," said lead author Colleen Canning, Ph.D., team leader for Parkinson’s disease research in the faculty of health sciences at the University of Sydney.

"The exercise program that we developed involved those three elements and was designed so that the participants did most of the exercise at home," she said in a poster presented at the international congress of Parkinson’s Disease and Movement Disorders.

In the study, Dr. Canning and her associates randomized 231 individuals with Parkinson’s disease to receive usual care or to participate in an exercise regimen involving 40-60 minutes of exercise three times a week for 6 months (Mov. Dis. 2013;28 [Suppl. 1]:442).

The intervention involved a range of balance, stepping, and strengthening exercises using weighted vests, as well as cueing using a metronome to overcome freezing. Around 10% of the exercise sessions were supervised by a physiotherapist.

There was a statistically nonsignificant 27% reduction (incidence rate ratio [IRR] = 0.73; 95% confidence interval [CI], 0.45-1.17; P = .18) in the incidence of falls between the intervention and control group, Dr. Canning said.

However, a subgroup analysis based on disease severity revealed a significant 69% reduction in the risk of falls among patients with lower disease severity (IRR = 0.31; 95% CI, 0.15-0.62; P less than .001), while there was a nonsignificant increase in the risk of falls in the higher–disease severity subgroup.

At the same time, there were significant improvements favoring the intervention group as a whole in a range of mobility and psychological functions, including the Short Physical Performance Battery, sit to stand, fear of falling, affect, and health and well-being measures.

The researchers also presented data on adherence to the program, showing that participants completed a mean of 72% of the prescribed exercise sessions, although this was based on patient self-report.

Patients with shorter disease duration, less bodily pain, better standing balance, and better perceived well-being and health were more likely to adhere to the exercise regimen. Disease severity and past falls did not significantly predict adherence, Dr. Canning noted.

"Our results suggest that this particular program has the potential to be quite an effective method of reducing falls in people with lower disease severity," she said in an interview. "This is an important finding because that’s the group that often doesn’t get offered exercise because they don’t have major motor difficulties early on."

There were no relevant conflicts of interest declared.

SYDNEY, AUSTRALIA – An exercise-based intervention carried out at home with minimal supervision led to a significant reduction in falls in patients with mild but not severe Parkinson’s disease.

"The approach we took was to target three risk factors that exercise could potentially improve, that is, loss of muscle strength, poor balance, and freezing of gait," said lead author Colleen Canning, Ph.D., team leader for Parkinson’s disease research in the faculty of health sciences at the University of Sydney.

"The exercise program that we developed involved those three elements and was designed so that the participants did most of the exercise at home," she said in a poster presented at the international congress of Parkinson’s Disease and Movement Disorders.

In the study, Dr. Canning and her associates randomized 231 individuals with Parkinson’s disease to receive usual care or to participate in an exercise regimen involving 40-60 minutes of exercise three times a week for 6 months (Mov. Dis. 2013;28 [Suppl. 1]:442).

The intervention involved a range of balance, stepping, and strengthening exercises using weighted vests, as well as cueing using a metronome to overcome freezing. Around 10% of the exercise sessions were supervised by a physiotherapist.

There was a statistically nonsignificant 27% reduction (incidence rate ratio [IRR] = 0.73; 95% confidence interval [CI], 0.45-1.17; P = .18) in the incidence of falls between the intervention and control group, Dr. Canning said.

However, a subgroup analysis based on disease severity revealed a significant 69% reduction in the risk of falls among patients with lower disease severity (IRR = 0.31; 95% CI, 0.15-0.62; P less than .001), while there was a nonsignificant increase in the risk of falls in the higher–disease severity subgroup.

At the same time, there were significant improvements favoring the intervention group as a whole in a range of mobility and psychological functions, including the Short Physical Performance Battery, sit to stand, fear of falling, affect, and health and well-being measures.

The researchers also presented data on adherence to the program, showing that participants completed a mean of 72% of the prescribed exercise sessions, although this was based on patient self-report.

Patients with shorter disease duration, less bodily pain, better standing balance, and better perceived well-being and health were more likely to adhere to the exercise regimen. Disease severity and past falls did not significantly predict adherence, Dr. Canning noted.

"Our results suggest that this particular program has the potential to be quite an effective method of reducing falls in people with lower disease severity," she said in an interview. "This is an important finding because that’s the group that often doesn’t get offered exercise because they don’t have major motor difficulties early on."

There were no relevant conflicts of interest declared.

SYDNEY, AUSTRALIA – Rasagiline is safe and efficacious as add-on therapy in patients with early Parkinson’s disease whose symptoms are not adequately controlled with dopamine agonist monotherapy, results from a randomized, double-blind placebo-controlled study suggest.

Data from the ANDANTE study showed that adding rasagiline (1 mg/day) to dopamine agonist therapy led to an additional mean 2.4-point reduction (P = .012; 95% CI, –4.3 to –0.5) in the Unified Parkinson's Disease Rating Scale (UPDRS) total score at 18 weeks, compared with placebo.

The 18-week phase IV study involved 328 patients with Parkinson’s disease whose symptoms were poorly controlled with dopamine agonist monotherapy.

Researchers also observed an additional mean 1.8-point improvement (P =.007; 95% CI, –3.1 to –0.5) in the UPDRS motor scores and a nonsignificant improvement in the activities of daily living (ADL) score, compared with placebo.

Lead author Dr. Robert Hauser, director of the University of South Florida’s Parkinson’s disease and movement disorder center in Tampa, said rasagiline – a selective, irreversible inhibitor of monoamine oxidase type B – is currently approved in the United States under the brand name Azilect as an adjunct to levodopa in patients with motor fluctuations, and as monotherapy earlier in the disease.

However, this study examined its use in patients whose symptoms were not being controlled by dopamine agonists but who had not yet started on levodopa.

"That was the question: ‘If patients are on a dopamine agonist and the disease is progressing and patients aren’t doing as well as you would like, is adding rasagiline an option? Is it helpful?’ " Dr. Hauser said in an interview at the international congress of Parkinson’s Disease and Movement Disorders.

Although the UPDRS total and motor score improvements were statistically significant, Dr. Hauser said that the clinical improvements were small and that perhaps rasagiline would be more effective if given even earlier in the disease as monotherapy.

"I think you get the best effect by starting it before the agonist," he said. "Still, if a patient comes to you on their agonist and they’re not doing well enough, it remains an option, but I think option No. 1 is get it going before the agonist."

There were no significant differences in adverse events or serious adverse events between the rasagiline and placebo groups, particularly with respect to sleepiness, sudden onset sleep, confusion, hallucinations, or orthostatic hypotension.

No impulse control disorders were observed, and six patients in the rasagiline group and five patients in the placebo group required rescue with levodopa during the study.

The study was supported by Teva Neuroscience (USA), Teva Pharmaceutical Industries (Israel), and H. Lundbeck (Denmark).

SYDNEY, AUSTRALIA – Rasagiline is safe and efficacious as add-on therapy in patients with early Parkinson’s disease whose symptoms are not adequately controlled with dopamine agonist monotherapy, results from a randomized, double-blind placebo-controlled study suggest.

Data from the ANDANTE study showed that adding rasagiline (1 mg/day) to dopamine agonist therapy led to an additional mean 2.4-point reduction (P = .012; 95% CI, –4.3 to –0.5) in the Unified Parkinson's Disease Rating Scale (UPDRS) total score at 18 weeks, compared with placebo.

The 18-week phase IV study involved 328 patients with Parkinson’s disease whose symptoms were poorly controlled with dopamine agonist monotherapy.

Researchers also observed an additional mean 1.8-point improvement (P =.007; 95% CI, –3.1 to –0.5) in the UPDRS motor scores and a nonsignificant improvement in the activities of daily living (ADL) score, compared with placebo.

Lead author Dr. Robert Hauser, director of the University of South Florida’s Parkinson’s disease and movement disorder center in Tampa, said rasagiline – a selective, irreversible inhibitor of monoamine oxidase type B – is currently approved in the United States under the brand name Azilect as an adjunct to levodopa in patients with motor fluctuations, and as monotherapy earlier in the disease.

However, this study examined its use in patients whose symptoms were not being controlled by dopamine agonists but who had not yet started on levodopa.

"That was the question: ‘If patients are on a dopamine agonist and the disease is progressing and patients aren’t doing as well as you would like, is adding rasagiline an option? Is it helpful?’ " Dr. Hauser said in an interview at the international congress of Parkinson’s Disease and Movement Disorders.

Although the UPDRS total and motor score improvements were statistically significant, Dr. Hauser said that the clinical improvements were small and that perhaps rasagiline would be more effective if given even earlier in the disease as monotherapy.

"I think you get the best effect by starting it before the agonist," he said. "Still, if a patient comes to you on their agonist and they’re not doing well enough, it remains an option, but I think option No. 1 is get it going before the agonist."

There were no significant differences in adverse events or serious adverse events between the rasagiline and placebo groups, particularly with respect to sleepiness, sudden onset sleep, confusion, hallucinations, or orthostatic hypotension.

No impulse control disorders were observed, and six patients in the rasagiline group and five patients in the placebo group required rescue with levodopa during the study.

The study was supported by Teva Neuroscience (USA), Teva Pharmaceutical Industries (Israel), and H. Lundbeck (Denmark).

SYDNEY, AUSTRALIA – Rasagiline is safe and efficacious as add-on therapy in patients with early Parkinson’s disease whose symptoms are not adequately controlled with dopamine agonist monotherapy, results from a randomized, double-blind placebo-controlled study suggest.

Data from the ANDANTE study showed that adding rasagiline (1 mg/day) to dopamine agonist therapy led to an additional mean 2.4-point reduction (P = .012; 95% CI, –4.3 to –0.5) in the Unified Parkinson's Disease Rating Scale (UPDRS) total score at 18 weeks, compared with placebo.

The 18-week phase IV study involved 328 patients with Parkinson’s disease whose symptoms were poorly controlled with dopamine agonist monotherapy.

Researchers also observed an additional mean 1.8-point improvement (P =.007; 95% CI, –3.1 to –0.5) in the UPDRS motor scores and a nonsignificant improvement in the activities of daily living (ADL) score, compared with placebo.

Lead author Dr. Robert Hauser, director of the University of South Florida’s Parkinson’s disease and movement disorder center in Tampa, said rasagiline – a selective, irreversible inhibitor of monoamine oxidase type B – is currently approved in the United States under the brand name Azilect as an adjunct to levodopa in patients with motor fluctuations, and as monotherapy earlier in the disease.

However, this study examined its use in patients whose symptoms were not being controlled by dopamine agonists but who had not yet started on levodopa.

"That was the question: ‘If patients are on a dopamine agonist and the disease is progressing and patients aren’t doing as well as you would like, is adding rasagiline an option? Is it helpful?’ " Dr. Hauser said in an interview at the international congress of Parkinson’s Disease and Movement Disorders.

Although the UPDRS total and motor score improvements were statistically significant, Dr. Hauser said that the clinical improvements were small and that perhaps rasagiline would be more effective if given even earlier in the disease as monotherapy.

"I think you get the best effect by starting it before the agonist," he said. "Still, if a patient comes to you on their agonist and they’re not doing well enough, it remains an option, but I think option No. 1 is get it going before the agonist."

There were no significant differences in adverse events or serious adverse events between the rasagiline and placebo groups, particularly with respect to sleepiness, sudden onset sleep, confusion, hallucinations, or orthostatic hypotension.

No impulse control disorders were observed, and six patients in the rasagiline group and five patients in the placebo group required rescue with levodopa during the study.

The study was supported by Teva Neuroscience (USA), Teva Pharmaceutical Industries (Israel), and H. Lundbeck (Denmark).

SYDNEY, AUSTRALIA – Nearly one-quarter of patients decreasing or stopping dopamine agonist therapy experience dopamine agonist withdrawal syndrome, and one third of those suffer severe symptoms, according to results from the EuroDaws study.

In the prospective, observational study of 51 patients with Parkinson’s disease who were withdrawn from dopamine agonist treatment, 24% (12 of 51) reported symptoms of dopamine agonist withdrawal syndrome (DAWS), and in 33% of those (4 of 12), the symptoms were classified as severe.

Previous retrospective studies had suggested a prevalence of 14%-18% for dopamine agonist withdrawal syndrome in clinical practice, however, study investigator Miriam Parry and her colleagues said this was the first prospective clinical study examining the frequency of the syndrome. Ms. Parry, a movement disorders nurse specialist from the University Hospital Lewisham, London, presented the study in a poster at the international congress of Parkinson’s Disease and Movement Disorders.

The researchers assessed patients regularly over a 1-month follow-up period, using a non–motor symptoms questionnaire.

The multicenter European study found the most common withdrawal symptom was anxiety, which presented in 91.7% of cases, followed by pain (50%), hyperhidrosis (41.7%), anhedonia (16.7%), apathy (8.3%), and limb paresthesia (8.3%).

"The third who developed the severe symptoms, patients become very anxious, they cannot perform their everyday activity of daily living, they won’t go out, they develop pain, sweating, apathy, and some become very, very depressed," Ms. Parry said in an interview.

The researchers suggested there was considerable potential for misdiagnosis of the withdrawal syndrome, which is similar to drug withdrawal for addictive drugs, and the symptoms could also be confused with non–motor fluctuations.

Ropinirole, pramipexole, and cabergoline were the three types of dopamine agonists implicated in the withdrawal syndrome, with patients being taken off these treatments because of the emergence of hallucinations or impulse control disorders.

"When we do decide to take them off the treatment, it has to be done in a very slow, gradual manner, and you really have to observe them," Ms. Parry said.

She said following the results, the researchers were also looking at ways to reduce the likelihood of withdrawal symptoms developing, such as slowly escalating the dose when patients are started on dopamine agonists but aiming for a much lower optimum dose of the drugs.

Ms. Parry said that while there were no particular red flags to indicate which patients were likely to develop the withdrawal syndrome, it did seem to occur in patients with preexisting tendencies to those symptoms, as if withdrawal was exacerbating those features.

"DAWS needs to be considered in day-to-day clinical practice and patients should be advised regarding this problem," the researchers wrote.

The study was supported by the U.K. National Institute for Health Research’s Mental Health Biomedical Research Centre and Dementia Biomedical Research Unit at South London and Maudsley NHS Foundation Trust and the Institute of Psychiatry, Kings College London. There were no financial conflicts of interest declared.

SYDNEY, AUSTRALIA – Nearly one-quarter of patients decreasing or stopping dopamine agonist therapy experience dopamine agonist withdrawal syndrome, and one third of those suffer severe symptoms, according to results from the EuroDaws study.

In the prospective, observational study of 51 patients with Parkinson’s disease who were withdrawn from dopamine agonist treatment, 24% (12 of 51) reported symptoms of dopamine agonist withdrawal syndrome (DAWS), and in 33% of those (4 of 12), the symptoms were classified as severe.

Previous retrospective studies had suggested a prevalence of 14%-18% for dopamine agonist withdrawal syndrome in clinical practice, however, study investigator Miriam Parry and her colleagues said this was the first prospective clinical study examining the frequency of the syndrome. Ms. Parry, a movement disorders nurse specialist from the University Hospital Lewisham, London, presented the study in a poster at the international congress of Parkinson’s Disease and Movement Disorders.

The researchers assessed patients regularly over a 1-month follow-up period, using a non–motor symptoms questionnaire.

The multicenter European study found the most common withdrawal symptom was anxiety, which presented in 91.7% of cases, followed by pain (50%), hyperhidrosis (41.7%), anhedonia (16.7%), apathy (8.3%), and limb paresthesia (8.3%).

"The third who developed the severe symptoms, patients become very anxious, they cannot perform their everyday activity of daily living, they won’t go out, they develop pain, sweating, apathy, and some become very, very depressed," Ms. Parry said in an interview.

The researchers suggested there was considerable potential for misdiagnosis of the withdrawal syndrome, which is similar to drug withdrawal for addictive drugs, and the symptoms could also be confused with non–motor fluctuations.

Ropinirole, pramipexole, and cabergoline were the three types of dopamine agonists implicated in the withdrawal syndrome, with patients being taken off these treatments because of the emergence of hallucinations or impulse control disorders.

"When we do decide to take them off the treatment, it has to be done in a very slow, gradual manner, and you really have to observe them," Ms. Parry said.

She said following the results, the researchers were also looking at ways to reduce the likelihood of withdrawal symptoms developing, such as slowly escalating the dose when patients are started on dopamine agonists but aiming for a much lower optimum dose of the drugs.

Ms. Parry said that while there were no particular red flags to indicate which patients were likely to develop the withdrawal syndrome, it did seem to occur in patients with preexisting tendencies to those symptoms, as if withdrawal was exacerbating those features.

"DAWS needs to be considered in day-to-day clinical practice and patients should be advised regarding this problem," the researchers wrote.

The study was supported by the U.K. National Institute for Health Research’s Mental Health Biomedical Research Centre and Dementia Biomedical Research Unit at South London and Maudsley NHS Foundation Trust and the Institute of Psychiatry, Kings College London. There were no financial conflicts of interest declared.

SYDNEY, AUSTRALIA – Nearly one-quarter of patients decreasing or stopping dopamine agonist therapy experience dopamine agonist withdrawal syndrome, and one third of those suffer severe symptoms, according to results from the EuroDaws study.

In the prospective, observational study of 51 patients with Parkinson’s disease who were withdrawn from dopamine agonist treatment, 24% (12 of 51) reported symptoms of dopamine agonist withdrawal syndrome (DAWS), and in 33% of those (4 of 12), the symptoms were classified as severe.

Previous retrospective studies had suggested a prevalence of 14%-18% for dopamine agonist withdrawal syndrome in clinical practice, however, study investigator Miriam Parry and her colleagues said this was the first prospective clinical study examining the frequency of the syndrome. Ms. Parry, a movement disorders nurse specialist from the University Hospital Lewisham, London, presented the study in a poster at the international congress of Parkinson’s Disease and Movement Disorders.

The researchers assessed patients regularly over a 1-month follow-up period, using a non–motor symptoms questionnaire.

The multicenter European study found the most common withdrawal symptom was anxiety, which presented in 91.7% of cases, followed by pain (50%), hyperhidrosis (41.7%), anhedonia (16.7%), apathy (8.3%), and limb paresthesia (8.3%).

"The third who developed the severe symptoms, patients become very anxious, they cannot perform their everyday activity of daily living, they won’t go out, they develop pain, sweating, apathy, and some become very, very depressed," Ms. Parry said in an interview.

The researchers suggested there was considerable potential for misdiagnosis of the withdrawal syndrome, which is similar to drug withdrawal for addictive drugs, and the symptoms could also be confused with non–motor fluctuations.

Ropinirole, pramipexole, and cabergoline were the three types of dopamine agonists implicated in the withdrawal syndrome, with patients being taken off these treatments because of the emergence of hallucinations or impulse control disorders.

"When we do decide to take them off the treatment, it has to be done in a very slow, gradual manner, and you really have to observe them," Ms. Parry said.

She said following the results, the researchers were also looking at ways to reduce the likelihood of withdrawal symptoms developing, such as slowly escalating the dose when patients are started on dopamine agonists but aiming for a much lower optimum dose of the drugs.

Ms. Parry said that while there were no particular red flags to indicate which patients were likely to develop the withdrawal syndrome, it did seem to occur in patients with preexisting tendencies to those symptoms, as if withdrawal was exacerbating those features.

"DAWS needs to be considered in day-to-day clinical practice and patients should be advised regarding this problem," the researchers wrote.

The study was supported by the U.K. National Institute for Health Research’s Mental Health Biomedical Research Centre and Dementia Biomedical Research Unit at South London and Maudsley NHS Foundation Trust and the Institute of Psychiatry, Kings College London. There were no financial conflicts of interest declared.

SYDNEY, AUSTRALIA – Friedreich’s ataxia patients may be at greater risk of osteopenia and osteoporotic fractures, according to a study showing significant decreases in bone mineral density at key sites such as the femoral neck.

Data presented in a poster at the international congress of Parkinson’s Disease and Movement Disorders also showed a correlation between Friedreich’s ataxia disease severity measures and bone mineral density measures.

Dr. Wolfgang Nachbauer of the department of neurology at Innsbruck (Austria) Medical University and his colleagues measured bone mineral density of the femur, lumbar vertebral column, radius, and ulna, using dual-energy x-ray absorptiometry in 20 patients with Friedreich’s ataxia. Mean age of the patients was 39.4 years.

They found 45% of patients (9 of 20) had osteoporosis at the femur, and 20% (4 of 20) had osteopenia at the same site, while bone mineral density measurements of the lumbar vertebral column showed osteopenia in 30% (6 of 20) and osteoporosis in 10% (2 of 20). Seven patients (35%) had osteopenia in the forearm.

Dr. Nachbauer said this was the first study exploring the incidence of osteopenia and osteoporosis in patients with this disorder.

"We observed clinically some pathological fractures within our Friedreich’s ataxia patients and together with the known action of the iron metabolism it made us think there could be an increased prevalence of osteoporosis and osteopenia with Friedreich’s ataxia," Dr. Nachbauer said in an interview.

Friedreich’s ataxia is a neurodegenerative disorder caused by a mutation in the frataxin gene, which codes for a protein involved in mitochondrial oxidative metabolism and iron homeostasis. Nonneurologic manifestations of Friedreich’s ataxia include scoliosis and foot deformities.

The study found that the most significant decreases in bone mineral density were at the femoral neck site, which is also a common site for hip fracture.

The researchers also examined the correlation between degree of bone mineral density loss and clinical indicators of disease severity in Friedreich’s ataxia. They found a significant, negative association between bone mineral density measurements at the femoral neck and scores on the Scale for the Assessment and Rating of Ataxia (SARA) and the length of GAA allele repeats in the frataxin gene – the defining feature of Friedreich’s ataxia.

"We also used the FRAX score, which is the score for the risk of pathological fractures within the next 10 years and also this score was increased in Friedreich’s ataxia patients," Dr. Nachbauer said.

While there were no significant interactions between potential confounders such as age and body mass index, the study found that wheelchair-bound patients had significantly lower bone density, compared with mobile patients.

The findings offer an opportunity for early intervention to address what may be a significant comorbidity associated with Friedreich’s ataxia.

"Densitometry on a routine basis should therefore be included in the management of [Friedreich’s ataxia] patients [as] initiation of medical therapy may prevent osteoporosis-related fractures," the researchers said.

No conflicts of interest associated with the study were declared.

SYDNEY, AUSTRALIA – Friedreich’s ataxia patients may be at greater risk of osteopenia and osteoporotic fractures, according to a study showing significant decreases in bone mineral density at key sites such as the femoral neck.

Data presented in a poster at the international congress of Parkinson’s Disease and Movement Disorders also showed a correlation between Friedreich’s ataxia disease severity measures and bone mineral density measures.

Dr. Wolfgang Nachbauer of the department of neurology at Innsbruck (Austria) Medical University and his colleagues measured bone mineral density of the femur, lumbar vertebral column, radius, and ulna, using dual-energy x-ray absorptiometry in 20 patients with Friedreich’s ataxia. Mean age of the patients was 39.4 years.

They found 45% of patients (9 of 20) had osteoporosis at the femur, and 20% (4 of 20) had osteopenia at the same site, while bone mineral density measurements of the lumbar vertebral column showed osteopenia in 30% (6 of 20) and osteoporosis in 10% (2 of 20). Seven patients (35%) had osteopenia in the forearm.

Dr. Nachbauer said this was the first study exploring the incidence of osteopenia and osteoporosis in patients with this disorder.

"We observed clinically some pathological fractures within our Friedreich’s ataxia patients and together with the known action of the iron metabolism it made us think there could be an increased prevalence of osteoporosis and osteopenia with Friedreich’s ataxia," Dr. Nachbauer said in an interview.

Friedreich’s ataxia is a neurodegenerative disorder caused by a mutation in the frataxin gene, which codes for a protein involved in mitochondrial oxidative metabolism and iron homeostasis. Nonneurologic manifestations of Friedreich’s ataxia include scoliosis and foot deformities.

The study found that the most significant decreases in bone mineral density were at the femoral neck site, which is also a common site for hip fracture.

The researchers also examined the correlation between degree of bone mineral density loss and clinical indicators of disease severity in Friedreich’s ataxia. They found a significant, negative association between bone mineral density measurements at the femoral neck and scores on the Scale for the Assessment and Rating of Ataxia (SARA) and the length of GAA allele repeats in the frataxin gene – the defining feature of Friedreich’s ataxia.

"We also used the FRAX score, which is the score for the risk of pathological fractures within the next 10 years and also this score was increased in Friedreich’s ataxia patients," Dr. Nachbauer said.

While there were no significant interactions between potential confounders such as age and body mass index, the study found that wheelchair-bound patients had significantly lower bone density, compared with mobile patients.

The findings offer an opportunity for early intervention to address what may be a significant comorbidity associated with Friedreich’s ataxia.

"Densitometry on a routine basis should therefore be included in the management of [Friedreich’s ataxia] patients [as] initiation of medical therapy may prevent osteoporosis-related fractures," the researchers said.

No conflicts of interest associated with the study were declared.

SYDNEY, AUSTRALIA – Friedreich’s ataxia patients may be at greater risk of osteopenia and osteoporotic fractures, according to a study showing significant decreases in bone mineral density at key sites such as the femoral neck.

Data presented in a poster at the international congress of Parkinson’s Disease and Movement Disorders also showed a correlation between Friedreich’s ataxia disease severity measures and bone mineral density measures.

Dr. Wolfgang Nachbauer of the department of neurology at Innsbruck (Austria) Medical University and his colleagues measured bone mineral density of the femur, lumbar vertebral column, radius, and ulna, using dual-energy x-ray absorptiometry in 20 patients with Friedreich’s ataxia. Mean age of the patients was 39.4 years.

They found 45% of patients (9 of 20) had osteoporosis at the femur, and 20% (4 of 20) had osteopenia at the same site, while bone mineral density measurements of the lumbar vertebral column showed osteopenia in 30% (6 of 20) and osteoporosis in 10% (2 of 20). Seven patients (35%) had osteopenia in the forearm.

Dr. Nachbauer said this was the first study exploring the incidence of osteopenia and osteoporosis in patients with this disorder.

"We observed clinically some pathological fractures within our Friedreich’s ataxia patients and together with the known action of the iron metabolism it made us think there could be an increased prevalence of osteoporosis and osteopenia with Friedreich’s ataxia," Dr. Nachbauer said in an interview.

Friedreich’s ataxia is a neurodegenerative disorder caused by a mutation in the frataxin gene, which codes for a protein involved in mitochondrial oxidative metabolism and iron homeostasis. Nonneurologic manifestations of Friedreich’s ataxia include scoliosis and foot deformities.

The study found that the most significant decreases in bone mineral density were at the femoral neck site, which is also a common site for hip fracture.

The researchers also examined the correlation between degree of bone mineral density loss and clinical indicators of disease severity in Friedreich’s ataxia. They found a significant, negative association between bone mineral density measurements at the femoral neck and scores on the Scale for the Assessment and Rating of Ataxia (SARA) and the length of GAA allele repeats in the frataxin gene – the defining feature of Friedreich’s ataxia.

"We also used the FRAX score, which is the score for the risk of pathological fractures within the next 10 years and also this score was increased in Friedreich’s ataxia patients," Dr. Nachbauer said.

While there were no significant interactions between potential confounders such as age and body mass index, the study found that wheelchair-bound patients had significantly lower bone density, compared with mobile patients.

The findings offer an opportunity for early intervention to address what may be a significant comorbidity associated with Friedreich’s ataxia.

"Densitometry on a routine basis should therefore be included in the management of [Friedreich’s ataxia] patients [as] initiation of medical therapy may prevent osteoporosis-related fractures," the researchers said.

No conflicts of interest associated with the study were declared.

SYDNEY, AUSTRALIA  – Patients with mild cognitive impairment in Parkinson’s disease often show memory impairment and problems with visuospatial function, attention, and executive function, according to a study attempting to characterize the condition.

A cohort study assessed 219 patients newly diagnosed with Parkinson’s disease but without dementia and 99 age-matched controls using new criteria for the diagnosis of mild cognitive impairment in Parkinson’s disease (PD-MCI).

The criteria, released last year by the Movement Disorder Society, include tests of global cognition, attention, memory, executive function, visuospatial function, and language (Mov. Disord. 2012;27:349-56).

Patients were classified as having level 1 MCI if they scored less than 26 out of 30 on the Montreal Cognitive Assessment (MoCA), and as level 2 MCI if they were impaired on two tests in one cognitive domain or one impaired test in two different domains at 1, 1.5, or 2 standard deviations (SD) below normative values.

According to data presented in the Junior Award session at the international congress of Parkinson’s Disease and Movement Disorders, 41.5% of participants met the criteria for level 1 PD-MCI, while 65.8% met level 2 criteria at 1 SD below normative values, 42.5% at 1.5 SD, and 22.4% at 2 SD below norm.

The study found that among participants at 1.5 SD below normative values, memory impairment was the most common deficit (15.1%), followed by visuospatial (13.2%), attention (12.3%), and then executive dysfunction (11%).

Language function did not appear to be particularly affected, although lead author Dr. Alison Yarnall, clinical research fellow at the Institute for Ageing and Health at Newcastle University, Newcastle upon Tyne, England, said this may be because the tests weren’t sensitive enough to detect it.

"[The participants] also tended to be older. They had greater Parkinson’s disease severity even though it was still earlier on in the disease. They were more depressed, and they tended to be people [who] had reduced educational levels," Dr. Yarnall said in an interview.

Cerebrospinal fluid samples were also taken from some patients, and researchers found a significant correlation between amyloid-beta 42 levels, MoCA scores, and pattern recognition memory.

There were also significant differences in amyloid-beta 42 and 40 levels between patients who were cognitively normal and those who were impaired.

While the frequency of patients meeting the criteria for MCI was higher than had been shown in previous studies, Dr. Yarnall suggested this may be a factor of using the new criteria for diagnosis of PD-MCI.

"This is really the first step toward identifying patients with PD-MCI because, prior to last year, we didn’t have any of these standardized criteria and most of the other studies that are published in it extrapolated from the Alzheimer’s literature," Dr. Yarnall said.

While there are no treatments currently licensed for treatment of PD-MCI, Dr. Yarnall said identifying this cohort of individuals with PD-MCI could provide an opportunity for future research and treatment. Characterizing these patients could also help with identifying Parkinson’s disease patients at greater risk of developing dementia.

The research is part of the ongoing ICICLE-PD prospective cohort study that aims to determine predictors for dementia in Parkinson’s. It is funded by Parkinson’s UK and supported by the National Institute for Health Research. There were no other relevant conflicts of interest declared.

SYDNEY, AUSTRALIA  – Patients with mild cognitive impairment in Parkinson’s disease often show memory impairment and problems with visuospatial function, attention, and executive function, according to a study attempting to characterize the condition.

A cohort study assessed 219 patients newly diagnosed with Parkinson’s disease but without dementia and 99 age-matched controls using new criteria for the diagnosis of mild cognitive impairment in Parkinson’s disease (PD-MCI).

The criteria, released last year by the Movement Disorder Society, include tests of global cognition, attention, memory, executive function, visuospatial function, and language (Mov. Disord. 2012;27:349-56).

Patients were classified as having level 1 MCI if they scored less than 26 out of 30 on the Montreal Cognitive Assessment (MoCA), and as level 2 MCI if they were impaired on two tests in one cognitive domain or one impaired test in two different domains at 1, 1.5, or 2 standard deviations (SD) below normative values.

According to data presented in the Junior Award session at the international congress of Parkinson’s Disease and Movement Disorders, 41.5% of participants met the criteria for level 1 PD-MCI, while 65.8% met level 2 criteria at 1 SD below normative values, 42.5% at 1.5 SD, and 22.4% at 2 SD below norm.

The study found that among participants at 1.5 SD below normative values, memory impairment was the most common deficit (15.1%), followed by visuospatial (13.2%), attention (12.3%), and then executive dysfunction (11%).

Language function did not appear to be particularly affected, although lead author Dr. Alison Yarnall, clinical research fellow at the Institute for Ageing and Health at Newcastle University, Newcastle upon Tyne, England, said this may be because the tests weren’t sensitive enough to detect it.

"[The participants] also tended to be older. They had greater Parkinson’s disease severity even though it was still earlier on in the disease. They were more depressed, and they tended to be people [who] had reduced educational levels," Dr. Yarnall said in an interview.

Cerebrospinal fluid samples were also taken from some patients, and researchers found a significant correlation between amyloid-beta 42 levels, MoCA scores, and pattern recognition memory.

There were also significant differences in amyloid-beta 42 and 40 levels between patients who were cognitively normal and those who were impaired.

While the frequency of patients meeting the criteria for MCI was higher than had been shown in previous studies, Dr. Yarnall suggested this may be a factor of using the new criteria for diagnosis of PD-MCI.

"This is really the first step toward identifying patients with PD-MCI because, prior to last year, we didn’t have any of these standardized criteria and most of the other studies that are published in it extrapolated from the Alzheimer’s literature," Dr. Yarnall said.

While there are no treatments currently licensed for treatment of PD-MCI, Dr. Yarnall said identifying this cohort of individuals with PD-MCI could provide an opportunity for future research and treatment. Characterizing these patients could also help with identifying Parkinson’s disease patients at greater risk of developing dementia.

The research is part of the ongoing ICICLE-PD prospective cohort study that aims to determine predictors for dementia in Parkinson’s. It is funded by Parkinson’s UK and supported by the National Institute for Health Research. There were no other relevant conflicts of interest declared.

SYDNEY, AUSTRALIA  – Patients with mild cognitive impairment in Parkinson’s disease often show memory impairment and problems with visuospatial function, attention, and executive function, according to a study attempting to characterize the condition.

A cohort study assessed 219 patients newly diagnosed with Parkinson’s disease but without dementia and 99 age-matched controls using new criteria for the diagnosis of mild cognitive impairment in Parkinson’s disease (PD-MCI).

The criteria, released last year by the Movement Disorder Society, include tests of global cognition, attention, memory, executive function, visuospatial function, and language (Mov. Disord. 2012;27:349-56).

Patients were classified as having level 1 MCI if they scored less than 26 out of 30 on the Montreal Cognitive Assessment (MoCA), and as level 2 MCI if they were impaired on two tests in one cognitive domain or one impaired test in two different domains at 1, 1.5, or 2 standard deviations (SD) below normative values.

According to data presented in the Junior Award session at the international congress of Parkinson’s Disease and Movement Disorders, 41.5% of participants met the criteria for level 1 PD-MCI, while 65.8% met level 2 criteria at 1 SD below normative values, 42.5% at 1.5 SD, and 22.4% at 2 SD below norm.

The study found that among participants at 1.5 SD below normative values, memory impairment was the most common deficit (15.1%), followed by visuospatial (13.2%), attention (12.3%), and then executive dysfunction (11%).

Language function did not appear to be particularly affected, although lead author Dr. Alison Yarnall, clinical research fellow at the Institute for Ageing and Health at Newcastle University, Newcastle upon Tyne, England, said this may be because the tests weren’t sensitive enough to detect it.

"[The participants] also tended to be older. They had greater Parkinson’s disease severity even though it was still earlier on in the disease. They were more depressed, and they tended to be people [who] had reduced educational levels," Dr. Yarnall said in an interview.

Cerebrospinal fluid samples were also taken from some patients, and researchers found a significant correlation between amyloid-beta 42 levels, MoCA scores, and pattern recognition memory.

There were also significant differences in amyloid-beta 42 and 40 levels between patients who were cognitively normal and those who were impaired.

While the frequency of patients meeting the criteria for MCI was higher than had been shown in previous studies, Dr. Yarnall suggested this may be a factor of using the new criteria for diagnosis of PD-MCI.

"This is really the first step toward identifying patients with PD-MCI because, prior to last year, we didn’t have any of these standardized criteria and most of the other studies that are published in it extrapolated from the Alzheimer’s literature," Dr. Yarnall said.

While there are no treatments currently licensed for treatment of PD-MCI, Dr. Yarnall said identifying this cohort of individuals with PD-MCI could provide an opportunity for future research and treatment. Characterizing these patients could also help with identifying Parkinson’s disease patients at greater risk of developing dementia.

The research is part of the ongoing ICICLE-PD prospective cohort study that aims to determine predictors for dementia in Parkinson’s. It is funded by Parkinson’s UK and supported by the National Institute for Health Research. There were no other relevant conflicts of interest declared.

SYDNEY, AUSTRALIA – Many Parkinson’s disease centers performing deep brain stimulation surgery are not using formal, standardized screening for impulse control disorders in pre- or postsurgical patients, according to a large survey of Parkinson Study Group centers.

Deep brain stimulation surgery is known to increase impulsivity, and standard practice is to identify and treat impulse control disorders in patients before surgery, according to lead author Dr. Nawaz Hack, a junior fellow in movement disorders at the University of Florida, Gainesville, and his colleagues.

"Surgery will improve their motor symptoms, but it may make their impulsivity worse, especially if you don’t screen and appropriately identify it," Dr. Hack said. "But if you catch it early through a standardized screening, you can address it."

The researchers surveyed 48 Parkinson Study Group centers, 97% of which performed deep brain stimulation surgery and 67% of which said they served a population of over 500 patients a year.

The results showed that only 23% of sites employed a formal battery of tests for impulsive and compulsive behavior and that 7% did not report screening for impulse control disorders.

Speaking at a poster session at the international congress of Parkinson’s Disease and Movement Disorders, Dr. Hack said that the majority of sites were employing a more ad-hoc approach to screening for impulse control disorders, using questions that were not necessarily standardized.

The survey found that 80% of responding centers used a neuropsychologist to screen for potential behavioral issues but only 32% used a psychiatrist, suggesting that most are focused on identifying the problem but do not necessarily have the facilities to manage and treat it.

There was also a wide variety of approaches taken to manage impulse control issues in presurgical patients.

Seventy-nine percent of patients with an impulse control disorder were treated with medication reduction, although there were 10 different strategies employed across centers, the survey’s authors reported.

"This is what happens in the centers that understand Parkinson’s disease – these are centers that are knowledgeable – so if we’re deficient there, what’s happening?" Dr. Hack said.

The concern was that patients whose impulsivity becomes exacerbated by surgery were more likely to be lost to follow up because of the potential financial consequences of their behavioral disorder.

"If you’re impulsive before, and you’re not treated or screened, you will be seriously impulsive after, so they’ll leave the operating room, they’ll go home, and they’ll start doing behaviors that are literally destroying their family, their lives, and their finances," Dr. Hack said.

However, he said that identifying patients with impulse control disorders could be difficult because patients were sometimes reluctant to volunteer information on behaviors that might indicate the presence of impulsivity, such as hypersexuality or problem gambling.

Nearly three-quarters of centers (72%) reported observing impulse control disorders among deep brain stimulation surgery patients, and 68% reported it in postoperative patients.

Most centers (79%) did not feel that the choice of brain target, whether subthalamic nucleus or globus pallidus, was influential in behavioral disorders.

Dr. Hack did not declare any financial conflicts of interest with the research.

SYDNEY, AUSTRALIA – Many Parkinson’s disease centers performing deep brain stimulation surgery are not using formal, standardized screening for impulse control disorders in pre- or postsurgical patients, according to a large survey of Parkinson Study Group centers.

Deep brain stimulation surgery is known to increase impulsivity, and standard practice is to identify and treat impulse control disorders in patients before surgery, according to lead author Dr. Nawaz Hack, a junior fellow in movement disorders at the University of Florida, Gainesville, and his colleagues.

"Surgery will improve their motor symptoms, but it may make their impulsivity worse, especially if you don’t screen and appropriately identify it," Dr. Hack said. "But if you catch it early through a standardized screening, you can address it."

The researchers surveyed 48 Parkinson Study Group centers, 97% of which performed deep brain stimulation surgery and 67% of which said they served a population of over 500 patients a year.

The results showed that only 23% of sites employed a formal battery of tests for impulsive and compulsive behavior and that 7% did not report screening for impulse control disorders.

Speaking at a poster session at the international congress of Parkinson’s Disease and Movement Disorders, Dr. Hack said that the majority of sites were employing a more ad-hoc approach to screening for impulse control disorders, using questions that were not necessarily standardized.

The survey found that 80% of responding centers used a neuropsychologist to screen for potential behavioral issues but only 32% used a psychiatrist, suggesting that most are focused on identifying the problem but do not necessarily have the facilities to manage and treat it.

There was also a wide variety of approaches taken to manage impulse control issues in presurgical patients.

Seventy-nine percent of patients with an impulse control disorder were treated with medication reduction, although there were 10 different strategies employed across centers, the survey’s authors reported.

"This is what happens in the centers that understand Parkinson’s disease – these are centers that are knowledgeable – so if we’re deficient there, what’s happening?" Dr. Hack said.

The concern was that patients whose impulsivity becomes exacerbated by surgery were more likely to be lost to follow up because of the potential financial consequences of their behavioral disorder.

"If you’re impulsive before, and you’re not treated or screened, you will be seriously impulsive after, so they’ll leave the operating room, they’ll go home, and they’ll start doing behaviors that are literally destroying their family, their lives, and their finances," Dr. Hack said.

However, he said that identifying patients with impulse control disorders could be difficult because patients were sometimes reluctant to volunteer information on behaviors that might indicate the presence of impulsivity, such as hypersexuality or problem gambling.

Nearly three-quarters of centers (72%) reported observing impulse control disorders among deep brain stimulation surgery patients, and 68% reported it in postoperative patients.

Most centers (79%) did not feel that the choice of brain target, whether subthalamic nucleus or globus pallidus, was influential in behavioral disorders.

Dr. Hack did not declare any financial conflicts of interest with the research.

SYDNEY, AUSTRALIA – Many Parkinson’s disease centers performing deep brain stimulation surgery are not using formal, standardized screening for impulse control disorders in pre- or postsurgical patients, according to a large survey of Parkinson Study Group centers.

Deep brain stimulation surgery is known to increase impulsivity, and standard practice is to identify and treat impulse control disorders in patients before surgery, according to lead author Dr. Nawaz Hack, a junior fellow in movement disorders at the University of Florida, Gainesville, and his colleagues.

"Surgery will improve their motor symptoms, but it may make their impulsivity worse, especially if you don’t screen and appropriately identify it," Dr. Hack said. "But if you catch it early through a standardized screening, you can address it."

The researchers surveyed 48 Parkinson Study Group centers, 97% of which performed deep brain stimulation surgery and 67% of which said they served a population of over 500 patients a year.

The results showed that only 23% of sites employed a formal battery of tests for impulsive and compulsive behavior and that 7% did not report screening for impulse control disorders.

Speaking at a poster session at the international congress of Parkinson’s Disease and Movement Disorders, Dr. Hack said that the majority of sites were employing a more ad-hoc approach to screening for impulse control disorders, using questions that were not necessarily standardized.

The survey found that 80% of responding centers used a neuropsychologist to screen for potential behavioral issues but only 32% used a psychiatrist, suggesting that most are focused on identifying the problem but do not necessarily have the facilities to manage and treat it.

There was also a wide variety of approaches taken to manage impulse control issues in presurgical patients.

Seventy-nine percent of patients with an impulse control disorder were treated with medication reduction, although there were 10 different strategies employed across centers, the survey’s authors reported.

"This is what happens in the centers that understand Parkinson’s disease – these are centers that are knowledgeable – so if we’re deficient there, what’s happening?" Dr. Hack said.

The concern was that patients whose impulsivity becomes exacerbated by surgery were more likely to be lost to follow up because of the potential financial consequences of their behavioral disorder.

"If you’re impulsive before, and you’re not treated or screened, you will be seriously impulsive after, so they’ll leave the operating room, they’ll go home, and they’ll start doing behaviors that are literally destroying their family, their lives, and their finances," Dr. Hack said.

However, he said that identifying patients with impulse control disorders could be difficult because patients were sometimes reluctant to volunteer information on behaviors that might indicate the presence of impulsivity, such as hypersexuality or problem gambling.

Nearly three-quarters of centers (72%) reported observing impulse control disorders among deep brain stimulation surgery patients, and 68% reported it in postoperative patients.

Most centers (79%) did not feel that the choice of brain target, whether subthalamic nucleus or globus pallidus, was influential in behavioral disorders.

Dr. Hack did not declare any financial conflicts of interest with the research.