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I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible. I have Parkinson's
diseases as well and thought it would be nice to have a place where
updated news is in one place. That is why I began this blog.
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Thank you.

Sunday, October 22, 2017

Aware in Care Kit

The Aware in Care kit can be requested at or by calling 1-800-4PD-INFO (473-4636).
Did you know that three out of four people with Parkinson’s disease do not receive their medications on time when staying in the hospital? People with Parkinson’s visit hospitals more often, and, combined with the great importance of the timing and dosing of Parkinson’s medications, face greater risks in the hospital.
This is why the National Parkinson Foundation (NPF) has launched the Aware in Careprogram, which aims to help people with Parkinson’s disease get the best care possible during a hospital stay.
To protect, prepare and empower people with Parkinson’s before, during and after a hospital visit, NPF has developed a free Aware in Care kit with tools and information to share with hospital staff during a planned or emergency hospital stay.
The kit is large enough to fit your Parkinson’s medications to take with you on your next trip to the hospital.

The kit includes:
Hospital Action Plan
Read about how to prepare for your next hospital visit—whether it is planned or an emergency.

Parkinson’s Disease ID Bracelet
Wear your bracelet at all times in case you are in an emergency situation and cannot communicate.

Medical Alert Card
Fill in your card with emergency contact information and place in your wallet.

Medication Form
Complete this form and keep copies in your kit for use at the hospital.

Parkinson’s Disease Fact Sheet
Share the facts about Parkinson’s with hospital staff and ask that a copy be placed in your chart.

I Have Parkinson’s Reminder Slips
Share vital information about Parkinson’s disease with every member of your care team in the hospital.

Use this magnet to display a copy of your Medication Form in your hospital.

Get the Kit. Know the Facts. Be Aware in Care.® 

NPF has partnered with Parkinson Alberta and Parkinson Society British Columbia to provide the Aware in Care kit to people with Parkinson's in Canada. If you live in Canada, contact Parkinson Alberta at 1-977-243-9992 or Parkinson Society British Columbia at 1-800-668-3330 to order a kit.

Hospital Dangers for Patients With Parkinson’s

 admin   October 21, 2017

It was supposed to be a short stay. In 2006, Roger Anderson was to undergo surgery to relieve a painfully compressed spinal disk. His wife, Karen, figured the staff at the hospital, in Portland, Ore., would understand how to care for someone with Parkinson’s disease.
It can be difficult. Parkinson’s patients like Mr. Anderson, for example, must take medications at precise intervals to replace the brain chemical dopamine, which is diminished by the disease. “You don’t have much of a window,” Mrs. Anderson said. “If you have to wait an hour, you have tremendous problems.” Without these medications, people may “freeze” and be unable to move, or develop uncontrolled movements called dyskinesia, and are prone to falls.
But the nurses at the Portland hospital didn’t seem to grasp those imperatives. “You’d have to wait half an hour or an hour, and that’s not how it works for Parkinson’s patients,” Mrs. Anderson said. Nor did hospital rules, at the time, permit her to simply give her husband the Sinemet pills on her own.
Surgery and anesthesia, the disrupted medications, an incision that subsequently became infected — all contributed to a tailspin that lasted nearly three months. Mr. Anderson developed delirium, rotated between rehab centers and hospitals, took a fall, lost 60 pounds. “People were telling me, ‘He’s never going to come home,’” Mrs. Anderson said.
He did recover, and at 69 is doing well, his wife said, though his disease has progressed. But his wasn’t an unusual story, neurologists say.
Any older person faces dangers in a hospital, but for people with Parkinson’s — largely a disease of older adults — they’ve proved particularly hazardous. “Patients were telling us these horrendous stories,” said Dr. Michael Okun, a University of Florida neurologist and national medical director of the National Parkinson Foundation. “Even in good hospitals. Even in my own hospital.”
People with Parkinson’s are hospitalized much more frequently than others their age, and their stays last longer. A common reason: “These patients aren’t getting their meds on time, and they’re not getting the right meds,” Dr. Okun said. Some need to take their dopamine-replacing drugs as often as every two hours, a schedule at odds with standard hospital regimens.
Worse, some commonly prescribed drugs — including Compazine and Phenergan for nausea, and Reglan to stimulate bowel function after surgery — actually block dopamine and worsen symptoms in patients with Parkinson’s. Then they are at risk for falls and fractures and for aspiration pneumonia.
Moreover, any infection can lead to delirium, because Parkinson’s patients have lowered cognitive reserve. But the drug Haldol, which hospitals frequently use to reduce confusion, is also a dopamine blocker. “Haldol is the worst drug you can give a Parkinson’s patient,” Dr. Okun said. Over all, “it can be a real mess.”
With proper treatment, most Parkinson’s patients can live long and good lives, “but stressing them with a fall or an infection or anesthesia can make them fall apart,” he said, turning supposed in-and-out hospitalizations into weeks of illness and decline. Not everyone is as lucky as Roger Anderson.
What will help, in the long run, is educating hospital staffs about Parkinson’s and changing the way they function. And yet — isn’t this a sad commentary? — “it’s slow going to effect change in the health care system, and in the meantime a lot of people are getting hurt,” Dr. Okun said.
So, unfair as it may be to put the onus on patients and families, the foundation is offering a free Aware in Care kit that includes a bracelet identifying the wearer as a Parkinson’s patient and fact sheets and reminder slips to hand out to doctors and nurses. “We want to arm people,” Dr. Okun said.
The Andersons have used the kit for subsequent hospitalizations and found it useful. And Mrs. Anderson reports that now, years after their three-month nightmare, hospitals actually encourage her to bring along her husband’s medications and to administer the pills herself as his schedule demands.
You might argue that the hospital is magnanimously allowing her to do the job its staff is supposed to do, but she’s fine with that. It beats the alternative.
The Aware in Care kit can be requested at or by calling 1-800-4PD-INFO (473-4636).

New wellness centre coming for Parkinson’s sufferers in Victoria


Jillian Carson, with boxing instructor Jason Heit: A pilot project that helped people with Parkinson's vent their anger and frustration, stave off depression and increase co-ordination through boxing-inspired workouts has proved to be particularly popular.   Photograph By Darren Stone

A $500,000 gift from an anonymous donor is helping a local not-for-profit society open a Victoria community centre to help people with Parkinson’s disease and other movement disorders.
Jillian Carson, chairwoman of the Pacific Wellness Project, said the donation means the organization formerly known as ParkinGo Wellness Society should be able to open its new 2,400-square-foot gym and community centre at Blanshard Street and Hillside Avenue by January.
It will be housed in part of a building formerly occupied by Jordan’s Furniture and will offer a multi-disciplinary approach to Parkinson’s management based on rigorous exercise using PWR! Moves, a physical fitness regime for individuals living with Parkinson’s disease.
Activities such as cycling, yoga, circuit training and Rock Steady Boxing, found to be beneficial to those with Parkinson’s, will be provided along with music, voice and dance programs.
“I was absolutely thrilled,” said Carson, a Victoria physiotherapist who founded the volunteer-driven organization after she was diagnosed with Parkinson’s disease in 2009 and had to give up her practice.
“Working on this has been a passion, and it gave me a chance to use my physiotherapy skills, but it’s the result of a lot of hard work by volunteers.”
The donation provided the financial stability required to enable the organization to meet growing demands, she said.
“I get phone calls and emails every day, and at this point we haven’t been able to handle anymore,” said Carson, 57, whose fitness programs are currently offered in a patchwork of locations in the region.
An estimated 1,200 people in the capital region have been diagnosed with Parkinson’s disease, a progressive nervous system disorder that impairs movement and balance.
A pilot project that helped people with Parkinson’s vent their anger and frustration, stave off depression and increase co-ordination through boxing-inspired workouts has proven particularly popular, Carson said.
Classes are held at the Island MMA Training Centre, 831 Fisgard St., and led by Jason Heit, a longtime amateur and professional boxer and martial arts competitor.
“It’s very important that people with Parkinson’s get high-intensity exercise about one hour in duration, multiple times during the week,” said Heit, the new facility’s head coach.
“It can be any activity, even dance. The thing about boxing is there’s so much choreography to the moves. They’re thinking the whole time. It’s not just punch the bag. We spend a lot of time on co-ordination, body mechanics and balance.”
Carson said the new facility will dramatically increase the number of people with Parkinson’s it can serve, as well as their caregivers and families.
“We are very much making this a community place for many people to come. We don’t want to exclude anybody,” she said.
Heit says he is amazed by the progress he has witnessed during the pilot project.
“It’s challenging not just physically, but mentally,” he said. “They’re learning about cognitive processing because it activates the brain as well, keeping them stimulated and thinking.”
The donation provides core funding to the PWP program for the next three years.

Antipsychotic Increase Could Harm Mentally Ill TD Patients

OCTOBER 21, 2017  Ellen Kurek

Charlotte Mentzel, MD, PhD

An international 18-year-long cohort study of a Caribbean island’s entire inpatient population with severe mental illness found that current treatment recommendations for tardive dyskinesia (TD) might be wrong for severely mentally ill Afro-Caribbeans.

Charlotte Mentzel, MD, PhD, a research fellow in the Department of Psychiatry and Psychology, Maastricht University Medical Centre, Netherlands, led the study team.

The study population consisted of all patients with severe mental illness treated at the only psychiatric hospital in the former Netherlands Antilles, the David R. Capriles Clinic in Groot Kwartier, Curacao. TD was very common in the population, Mentzel told MD Magazine.

Switching from a first-generation antipsychotic to a second-generation is usually suggested for treatment, but it did not have a significant clinical effect on TD severity in this study.

“Conversely, increasing the antipsychotic dose reduced TD severity in the long term — at least 2 to 3 years,” Mentzel said. “And starting first-generation antipsychotic treatment in unmedicated patients or switching from a second- to a first-generation antipsychotic both reduced TD severity by about half.”

Researchers also found that all antipsychotic medication reduced the severity of parkinsonism in the study population with this movement disorder, and starting an antipsychotic agent with a high affinity for dopamine 2 (D2) increased it.

Mentzel noted the study has some “unique features.”

“The follow-up period was extremely long, and the dropout rate was very low because patients rarely moved off the island,” Mentzel said. “These features made the results representative of real-life outcomes in patients with severe mental disorders.”

To enroll in the study, patients had to be at least 18 years old, with cumulative exposure to antipsychotics of at least 3 months. Any patient with a history of movement disorders was excluded, as was any patient who had a lobotomy or a primary diagnosis of dementia or mental retardation.

Movement disorders and medication use were assessed in study subjects 8 times (usually annually) from 1992 through 2009. The same 2 raters measured TD severity by using the Abnormal Involuntary Movement Scale and measured parkinsonism severity by using the Unified Parkinson’s Disease Rating Scale.

In addition, the team categorized the antipsychotics patients used as first- or second-generation. They also noted whether the drug had high or low D2 affinity. Logistic regression was used to determine the effect of switching mediation within each axis of categorization.

As a result, the study team found a significant association between reduced TD severity and starting or switching to a first-generation antipsychotic. A similar association was also found for starting or switching to an agent with a high D2 affinity. Moreover, the study team further found an association between adding a second-generation antipsychotic to existing treatment with a first-generation agent and reduced TD severity.

However, they could not recommend this strategy because it increases the rate of side effects such as parkinsonism, cognitive impairment, diabetes, and weight gain.

Based on these findings, the study team concluded that patients with serious mental illness do not respond to interventions recommended in treatment guidelines as expected. They also suggested that these patients might therefore require different treatment algorithms than those recommended for the general population with schizophrenia.

However, they warned against generalizing the results of the study to ethnic groups aside from Afro-Caribbeans. 

Friday, October 20, 2017

Tremor: Is it Essential Tremor or Tremor from Parkinson’s Disease?

By Editorial Team—October 20, 2017 

Tremor is one of the characteristic symptoms of Parkinson’s disease (PD), but it is also characteristic of essential tremor (ET), a neurological disorder that produces involuntary and rhythmic shaking. ET is approximately eight times more common than PD, and there are several other differences between the two conditions.1,2

Difference when the tremor occurs

In PD, the tremor is mostly seen at rest, when the body part is not being used, and may be referred to as “resting tremor.” In ET, the tremor occurs mostly during action or movement, such as when writing, eating, or holding a posture.2,3

Difference in frequency and magnitude of tremor

The tremor seen in ET is generally of a higher frequency (more repetitions over a length of time), although the frequency can decrease over time. In PD, the frequency of tremor is slower. The magnitude, or strength, of the tremor also differs: in PD the magnitude of tremor is high, whereas the tremor in ET can be variable throughout the day, ranging from very low to high magnitude.2,3

Difference in family history

In cases of PD, there is rarely a family history (estimated 10-20% of cases), but in ET, a family history of tremor is seen in more than 50% of cases.2,3

Difference in sides of the body affected

The tremor in PD usually starts on one side of the body and may develop on the other side as the disease progresses. In ET, the tremor usually affects both sides from the beginning of the condition.2

Differences in what improves tremor

People with PD who experience tremor usually experience improvement in their symptoms with levodopa therapy. People with ET may get relief from their tremor with primidone and propranolol. Also, the tremor from ET can be improved with alcohol consumption, whereas alcohol consumption has no effect on a tremor from PD.2

Differences in what parts of the body are affected

The hands are more often affected with tremor than the legs in people with PD, and the voice and head are almost never involved. In ET, the hands are also predominantly affected, but the tremor can also be present in the head and voice.2,3

Differences in other symptoms

In ET, tremor is the primary symptom. In PD, there are four primary symptoms, including tremor, rigiditybradykinesia (slowed movements), and balance issues.2,3

Differences in when it occurs

PD is most commonly diagnosed in people over the age of 60, although approximately 5-10% of people with PD are diagnosed younger than the age of 50. ET most often occurs during middle age, but it can occur at any age, even in childhood.3,4

Differences in handwriting

One of the symptoms of PD is micrographia, or very small handwriting. In ET, a person’s handwriting generally gets large and tremulous.3

Evaluation and diagnosis

Both ET and PD are movement disorders, and sometimes they can be mistaken for each other. However, there are many differences between the two conditions, and proper and early diagnosis is important for receiving the right treatment and support.

VIDEO: Directional deep brain stimulation: novel treatment options for all Parkinson’s patients



Author: SPONSOREDPublished: 4 October 2017

Watch deep brain stimulation (DBS) experts Professor Pollo, Professor Timmermann, Professor Visser-Vanderwalle and Professor Volkmann explain the benefits of novel directional DBS systems for improved symptom control and fewer side effects

Every human brain is unique and every course of Parkinson’s disease has its own characteristics. In deep brain stimulation (DBS) therapy, physicians aim to target a very specific part of the brain – the subthalamic nucleus – in order to mitigate Parkinson’s symptoms.
Up until now, conventional DBS systems only allowed for stimulation with ring electrodes. With these electrodes, stimulation took the form of a ring around the electrode in the lead that was implanted into the patient’s brain. This meant that while physicians tried to target a very specific area of the brain, they always ran the risk of stimulating its neighbouring regions – since they could not steer the stimulation precisely. Unintended and unwanted stimulation could cause side effects such as speech problems.
The latest generation of DBS devices allow physicians to precisely steer the stimulation to target one specific area of the brain – significantly reducing side effects from unwanted stimulation. Our directional DBS systems use novel lead designs with segmented electrodes that allow the activation of individual electrode contacts. In addition, the technology in the pulse generator that powers the leads – the Multiple Independent Current Control (MICC) technology – allows the physician to specify exactly the amount of current needed for every contact of the electrode.
Through activating specific electrode contacts, and defining the amount of stimulation for each contact, stimulation precision is significantly increased. It is similar to shining a light on a specific spot with a flashlight. With the new systems, physicians now have full control of the stimulation steering and an increased set of stimulation options.
About deep brain stimulation (DBS) therapy
DBS uses a stimulator that is implanted into the patient’s chest. The stimulator sends mild electrical impulses to specific areas of the brain via thin wires called leads. This stimulation may help improve day-to-day experiences for people living with movement disorders such as Parkinson’s disease, dystonia, or essential tremor.

This article is sponsored by Boston Scientific. The information in this article is given for information purposes only and does not represent an endorsement by the EPDA of any particular treatments, products or companies. This article is not a substitute for advice from your doctor, pharmacist or other healthcare professional. Parkinson’s Life makes no representations or warranties of any kind, express or implied, about the completeness or accuracy of information provided.


Like all relationships, partnerships between Parkinson’s patients and their loved ones depend on good communication and mutual trust. Here are some ways to help strengthen communication:
  • Set expectations. Family and friends can sometimes feel helpless or feel they can only do so much. Let them know that listening, and offering empathy and support, is often all you need. 
  • Be clear. Discuss your needs openly. Whether it’s about your emotions or your symptoms, being as clear and direct as possible can help.
  • Listen. Listening to others can be just as important. Your family and friends may be able to observe things you can’t and share them with you and your doctor.
  • Be respectful of their experience. You’re living with Parkinson’s, and so are your family and friends. Recognize that their lives have also changed and that they may need time to adjust.
  • Make your relationship about more than the disease. You are each more than Parkinson’s, and you had a life “before Parkinson’s.” Keep in touch with the love and mutual interests that sustained your relationship before the disease.
  • Learn to ask for help from family and friends. Many people want to help, but don’t know what to offer. They may be waiting for you to ask. So be specific about what you need from those around you and you may find they are happy to help and respond readily to your request. 
  • Use humor. Sound silly? Maybe, but humor helps people feel better about themselves and the situation they’re in. It can help make a tough conversation easier.

In the Pipeline-Parkinson's Disease: Why a Common Asthma Drug Could Be a Disease Modifier for Parkinson's Disease

 Robinson, Richard  Neurology Today: October 19, 2017
Volume 17 - Issue 20 - p 1,23–23 doi: 10.1097/01.NT.0000526677.81786.42

Researchers reported evidence suggesting that treatment with an asthma drug was associated with a steep decline in risk for development of Parkinson's disease in a population-wide prescription database from Norway. They offered molecular evidence that beta2-adrenoreceptors are linked to transcription of alpha-synuclein, and may therefore be a potential target for therapies.
The common asthma drug salbutamol (also called albuterol) reduces expression of alpha-synuclein, the protein at the core of Lewy bodies in Parkinson's disease (PD), and improves neuronal survival in several preclinical models. What's more, and potentially more important for the human disease, treatment with salbutamol was associated with a steep decline in risk for development of PD in a population-wide prescription database from Norway.
“These findings are exciting and potentially have important implications for neuroprotection in Parkinson's disease,” said Anthony E. Lang, MD, FAAN, professor of neurology and director of the Program in Parkinson's Disease at the University of Toronto, who was not involved in the study, which was published in the September 1 issue of Science.
Clearance of misfolded alpha-synuclein has been the focus of much work in PD, but until this paper, no group has reported a search for compounds that would reduce its production.
“We hypothesized that this would be the most direct solution,” said principal investigator Clemens R. Scherzer, MD, associate professor of neurology at Harvard Medical School and Brigham & Women's Hospital in Boston.
That such down-regulation might be possible was suggested by previous discoveries by Dr. Scherzer's group, when they identified multiple transcription factors that directly control the gene. “This suggested a gene-regulatory path for lowering alpha-synuclein and inspired our gene expression drug screen in the current work,” he said.


To conduct that screen, the researchers exposed neuroblastoma cells to more than one thousand compounds, including natural products and Food and Drug Administration (FDA)-approved drugs, looking for those that reduced production of alpha-synuclein. After a multi-stage replication process, four compounds emerged, three of which — salbutamol, clenbuterol, and metaproterenol — are beta2-adrenoreceptor agonists. All three are prescribed for asthma. Salbutamol and metaproterenol are approved by the FDA, while clenbuterol is not, but it is prescribed in Europe. Intriguingly, the fourth compound was riluzole, approved for treatment of amyotrophic lateral sclerosis.
Each of the three beta2-adrenoreceptor agonists reduced alpha-synuclein protein expression in a dose-dependent manner to about 75 percent of normal in the cell-based screen. In mice, 24 hours of treatment with clenbuterol lowered alpha-synuclein production in the substantia nigra. And in patient cells from individuals with an alpha-synuclein triplication, clenbuterol treatment also reduced protein production.
The team found molecular evidence suggesting that treatment with clenbuterol decreased histone acetylation at sites regulating transcription of the alpha-synuclein gene, a change that would be likely to reduce transcription factor access to the gene, which may account for the reduced production of the protein.
Further supporting a direct role for the beta2-adrenoreceptor in regulating alpha-synuclein production, the team found that knocking out the gene for the receptor, and thus preventing it from signaling at all, more than doubled alpha-synuclein levels in neurons.
“Thus, beta2-adrenoreceptors are linked to transcription of alpha-synuclein,” Dr. Scherzer said, and may therefore be a potential target for therapies.
To test that hypothesis in humans, he and his team turned to the Norwegian Prescription Database, which contains complete information on prescriptions for the 4.6 million residents of the country, beginning in 2004. Over six years of follow-up, the proportion of people not developing PD was highest among those who had received salbutamol for at least 180 days during follow-up (n=69,511), was intermediate among those who had received it for between 60 and 180 days (72,911), and was lowest among those receiving it for less than 60 days, or never. Taking all salbutamol users together, the rate ratio was 0.66, with a 95% confidence interval of 0.58 to 0.76.
One possible link between asthma treatment and reduced PD risk might be smoking, Dr. Scherzer said, which is a behavior known to both increase asthma and reduce the likelihood of developing PD. But if the observed risk reduction were explained by a link through smoking, one would expect other asthma drugs, such as inhaled corticosteroids, which don't act through the beta2-adrenergic receptor, to also be associated with reduced PD risk. This was not the case, he said, “so it is unlikely smoking can fully account for this association.”
Based on these findings, Dr. Scherzer said it was logical to begin thinking about a clinical trial of a beta2-adrenergic receptor agonist to determine if it can slow development of PD after diagnosis. However, he cautioned, “there is reason to rethink the paradigm of how clinical trials are traditionally designed and conducted for PD,” noting the consistent failure of treatments intended for disease modification in recent decades.
Dr. Scherzer turned up another surprising result in the population study, strengthening the conclusion that beta2-adrenergic receptor signaling influences development of PD. He found that exposure to propranolol, which blocks this receptor, markedly increased PD risk, with a rate ratio of 2.2 (95% CI 1.62 to 3.00). Back in the lab, his team showed that propranolol increased histone acetylation near the alpha-synuclein gene, increased protein production, and abrogated clenbuterol's ability to lower alpha-synuclein levels.
“Our data raise the concern that propranolol might increase the risk of Parkinson's disease, and that is worrisome,” Dr. Scherzer said. “At the same time, it's too early to draw firm conclusions for clinical practice. More research and replication in other populations is warranted to clarify this question.”


“This is a pretty well-investigated area, so the discovery of a receptor of this type that regulates alpha-synuclein is surprising,” said Steven Finkbeiner, MD, PhD, director of the Taube/Koret Center for Neurodegenerative Disease and Gladstone Institutes and professor in the departments of neurology and physiology at the University of California, San Francisco, who was not involved with the study.
“Although the effect in cell models is modest, it is possible that this might be sufficient to produce a meaningful effect on Parkinson's risk, based on what we know about the effects of gene duplication and triplication and non-coding variants,” Dr. Finkbeiner said. “And the rate ratio reduction to 0.66 in the treatment cohort compared to the untreated one is potentially quite remarkable.”
But there are important unanswered questions, Dr. Finkbeiner added. The proposed mechanism, through modification of histone acetylation, “suggests that the drug is probably regulating many genes. Is modest reduction in alpha-synuclein responsible for the effects or are other targets even more important?”
Dr. Lang of Toronto added: “The concept of screening compounds that reduce transcription of the alpha-synuclein gene is novel, and the preclinical science looks very strong. The finding that propranolol has an opposite effect is very interesting and complies with the hypothesis very nicely.”
But the real importance of the paper comes from the epidemiologic data, Dr. Lang said. “We have failed to develop effective treatments with our toxin models of PD, and now we have models that over-express alpha-synuclein, and there are likely to be a lot of failures from these as well.” The difference here is that the benefits seen in the preclinical work seem to also be operating in a large human population, he said, adding: “But that needs to be confirmed in other databases.”
The Norwegian data raise several important questions that will need to be addressed as well, he said. “The effect of salbutamol appears to be rapid and quite profound. If that's the case, why haven't we seen this in epidemiological studies before?”
Regarding the propranolol effect on PD risk, he noted that propranolol is also used in PD to treat postural and action tremor. “But we never see the other features of the disease get worse,” which might be expected if the drug can increase alpha-synuclein production strongly enough to dramatically increase PD risk. “Why aren't we seeing propranolol worsening pre-existing Parkinson's disease?”
“I think the basic science here is really compelling, and it moves us in a completely new direction,” Dr. Lang said. “But the epidemiology is really where most people will look before taking this into clinical trials. That would be one of the more important things to reproduce as quickly as possible.”

Parkinson’s Disease: Do You Know These Early Warning Signs?

October 20, 2017

Symptoms can occur long before tremors

Just one correction:  dopamine (not levodopa) is the natural chemical found in the brain that is lacking or not being produced in enough quantities in a Parkinson’s. Levodopa (the pill) gets converted to dopamine when it reaches the brain.
Most people recognize the later stages of Parkinson’s disease — tremors and a shuffling walk are the most common signs. But the condition is difficult to diagnose early on; doctors don’t pinpoint most cases until they’re well past the initial stages. So is there a way to spot signs and seek treatment earlier?
Yes, but you need to know what to look for.
The vague symptoms of Parkinson’s could point to many problems. That’s what makes early specific diagnosis difficult. And that’s what frustrates those who search for reasons behind your movement problems.
But, there are recognizable signs that could at least put you and your doctor on alert, says neurologist Hubert Fernandez, MD, Director of Cleveland Clinic’s Center for Neurological Restoration. And getting a neurologist involved earlier is the key, he says.
“It’s not uncommon for patients to see a rheumatologist or orthopedist for six months to a year for pain in the right shoulder or dragging the right leg. They might even get steroid injections that don’t work,” he says. “But, only a neurologist can diagnose Parkinson’s.”

Symptoms follow stages of the disease

Parkinson’s motor problems are quickly recognizable, Dr. Fernandez says. The tremors — rhythmic movement of lips, chin, hands and legs; rigidity; stiffness and slowness are hallmark signs. Balance and gait problems are also common.
But, Parkinson’s symptoms start long before these problems emerge. As a progressive disease, Parkinson’s destroys the brain’s nerves from the bottom up, he says.
Stage 1: Parkinson’s attacks the base of the brain stem — the medulla — initially. This may cause constipation and can cause people to lose their sense of smell. These symptoms could strike decades before you see your first tell-tale tremor, Dr. Fernandez says.
Stage 2: Nerve deterioration in the pons (the brain’s message center) is next. Damage at this stage may lead to depression and REM sleep disorder. A person may “act out” their dreams while they sleep, potentially hurting themselves or others.
Stage 3: The tremor and shuffle appear here because the disease is attacking the part of the brain largely responsible for movement.
Stage 4 and 5: These are the most advanced Parkinson’s stages. Dementia and hallucinations often occur at this point.

When should you consult a neurologist?

Of course, not everyone who experiences constipation or depression, or who loses the sense of smell is at risk for developing Parkinson’s disease, Dr. Fernandez says. But, if you have those problems along with any of these factors, make an appointment with a neurologist:
  • First-degree relative with Parkinson’s with onset before age 60
  • One of the four motor features: resting tremor, stiffness, slowness, gait/balance problems
  • Repeated head trauma
  • REM sleep disorder

4 things you should know about Parkinson’s

In addition to learning what symptoms to watch for, there are four things you should know, Dr. Fernandez says:
1. It’s a progressive disease. Parkinson’s disease worsens over time, but each patient progresses differently. Doctors will treat the symptoms to limit how much they impact your daily life.
2. The cause is largely unknown. In 95 percent of cases, doctors don’t know why patients develop Parkinson’s. Often, a combination of factors are involved, including genetic susceptibility and environmental factors (such as having multiple head injuries). Research shows that genetic mutations are responsible for the rest of cases.
“We don’t know what factors contribute to Parkinson’s,” he says. “And, we’re just beginning to uncover the susceptibility genes.”
3. Treatment is symptom-dependent. How bothersome your symptoms are will determine how aggressively your doctor treats your disease. If your symptoms don’t disrupt your daily functioning, he or she likely will postpone prescribing medication.
Dopamine, a chemical found naturally in the brain, is lacking or not produced in high enough quantities in people with Parkinson’s disease. Patients may take levodopa, a pill that is converted to dopamine when it reaches the brain. This helps manage Parkinson’s symptoms.
It is often prescribed with a second drug called carbidopa, which prevents the nausea that can be caused by levodopa alone.
Doctors also may use deep brain stimulation to treat you if you don’t get relief with levodopa, Dr. Fernandez says.
4. Stroke, infection or other neurological conditions can mimic Parkinson’s. Don’t make any assumptions about your condition before you see a neurologist or Parkinson’s expert for a proper diagnosis.
Ultimately, remember that your journey with Parkinson’s is unique — so work closely with your doctor, Dr. Fernandez says.
“It’s important to remember that everyone’s experience with Parkinson’s is different, and treating it is about targeting the symptoms,” he says. “The most important thing is getting a good evaluation by a neurologist or Parkinson’s expert to make sure you’re on the right path.”