Implant to Help Slow PARKINSON’S DISEASE

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Dr. Steven Gill has been researching the benefits of Glial-cell line Derived Neurotrophic Factor (GDNF)  in PARKINSON’S DISEASE for many years.

Together with his team of researchers from Frenchay Hospital in Bristol, United Kingdom, he had developed a new implant device to deliver GDNF directly to the affected area of the brain.

GDNF has been shown to be an especially potent factor for dopaminergic cell survival and for improving motor deficits such as those seen in PARKINSON’S DISEASE.

Finding ways to deliver GDNF to the affected areas in appropriate ways has been the challenge

The new device developed by this team consists of a small port surgically implanted behind the patient’s ear.

From this port, a system of tubes connects to the basal ganglia and regulated dose of GDNF can be pumped directly to the brain once a month.

To date, six patients have undergone this treatment and the team is now recruiting 36 more patients for a new trial.

If this treatment technology proves successful and safe, many other neurological diseases will be able to benefit from this technique.

Review by Marcia McCall




review by Marcia McCall

Highlights From the World Parkinson Congress 2013

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Memory and Mood Program Presented at the 2013 Parkinson’s World Conference

Sarah K. Lageman, Ph.D., from the Virginia Commonwealth University, Richmond, VA Speaking at the Montreal 2013 World Parkinson’s Conference, presented an abstract of a program she developed with her colleagues that helps people with PARKINSON’S DISEASE enhance their memory and improve their problem solving skills.  Cognitive impairment is one of the biggest obstacles to independent living faced by people with PARKINSON’S DISEASE.  In this small study, participants met once a week and learned practical techniques to help their memory, such as writing in a memory book and using a calendar along with problem solving steps. They also were part of a support group that was client centered where they could share their frustrations and techniques.  Although the numbers in this study are small, the improvements have been large.  “If a neurocognitive program can help keep people functioning better at least for a couple of years, that’s a benefit”, said Dr. Lageman.


Mood and Sociability Presented at the 2013 Parkinson’s World Conference

Susan Spear Bassett, Ph.D. from Johns Hopkins spoke at her poster presentation about depression and social involvement in PARKINSON’S DISEASE.  She and her colleagues conducted a study with 101 people with PARKINSON’S DISEASE who did not have dementia to examine the changes in social function caused by the disease.  They found that cognitive impairments along with depression contributed more to social withdrawal than the motor or movement symptoms of PARKINSON’S DISEASE.  Depression, loss of verbal skills and loss of fine motor skills all contributed to loss of social function, but management of depression did more to improve the quality of life and help social involvement.


Falls, Cognition and Gait Presented at the 2013 Parkinson’s World Conference

What are the factors that increase the likelihood that people newly diagnosed with PARKINSON’S DISEASE will fall frequently?   Lynn Rochester, Ph.D. and her team enrolled 94 newly diagnosed people with PARKINSON’S who had never fallen. and followed them for a year.  They wanted to know why some people fall more frequently than others.  Subjects were asked to keep a diary of their falls and underwent testing in several domains over the course of the study.  Findings showed that gait was of major importance.  Step time, speed, and distance of steps as well as the thinking about walking were major predictors of falling.  People who had fallen several times also had less confidence in their ability.  Measurement scales included the Unified Parkinson’s Disease Rating Scale, and the Postural Instability and Gait Disorder that is a sub-scale of the UPDRS, the Hoehn and Yahr Progression Scale, Strength ratings and several cognitive testing scales.  Work for this abstract was done at Newcastle University in Newcastle upon Tyne, England.


Parkinson Research Foundation’s Parkinson Place
Parkinson Place - Good Days Start Here
Parkinson Place started in September of 2012 has implemented many of the programs discussed at Montreal and more!  If you want to get a taste of what is going on at Parkinson Place please visit the website  The mission of the Parkinson Research Foundation is to assist in finding a cure for Parkinson’s disease and improving the lives of those living with the disease right now.  Parkinson Place is a Pilot project that has proved very successful creating a one stop shop for everything you need to live well with Parkinson’s.  Many support groups are now starting a “place” of their own using the format and videos from the site.  Come see why we are smiling at Parkinson Place!


All abstracts are from the World Parkinson Congress, Montreal, Quebec, Canada.

3.  Gaina, B. et al “motor, cognitive and affective characteristics of new fallers compared to non-fallers in an incident cohort of Parkinson’s disease” WPC 2013 Abstract 13:05

2.  Bassett, S. et al, “Impact of Parkinson’s disease on social role function: multifaceted disability” WPC 2013

1. Lageman, S. et al; “Initial Results of a randomized clinical trial comparing a neurocognitive intervention to supportive therapy in individuals with Parkinson’s disease” WPC 2013; Abstract 15:11


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Two new research studies focused on PARKINSON’S DISEASE and Depression were published recently.  One studies the increased risk of developing PARKINSON’S DISEASE after bouts of treatment resistant depression.  The second study was an analysis of several studies of antidepressant medications used in PARKINSON’S DISEASE.

Depression is a serious risk in people with PARKINSON’S DISEASE; some studies have shown that as many as 60% of people with PD are depressed..  The first study looked at 10 years of records and found correlations between age of onset of depression and development of PD.  In younger patients, depression did not always lead to PARKINSON’S DISEASE, however more senior patients were twice as likely to be diagnosed and seniors whose depression did not respond to treatment were found to be three times more likely to develop  PD.

While this study is not proof-positive that depression necessarily leads to PARKINSON’S DISEASE,  the correlation does bear serious weight for future research.  It may be that depression could be an early symptom or biomarker, like loss of the sense of smell; but since 60% of people with PARKINSON’S report feeling depressed,  it may simply be a symptom.  One limitation of this study was that the population studied did not provide any information about family history or other environmental factors.  These factors will need careful evaluation in future studies.

The second study examined the effects of common antidepressant  treatment in PARKINSON’S DISEASE.  They based their study on 11 clinical trials of treatment for depression in Parkinson’s disease held between 1986 and 2013.  These trials used medications that are standard treatment for depression in PD as well as standard treatments for PD that have shown efficacy for treating depression.  These medications included Tricyclic Antidepressants (TCAs),  Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin and Norepinephrine Reuptake Inhibitore (SNRIs) and Dopamine agonists, which have also been promoted as relieving depression in PD.

The research was very thorough, examining not only the effect on depression, but also on troublesome side effects, such as nausea, dry mouth, headache, dizziness, hallucinations, somnolence and excessive dyskinesias.  They also compared the rating scales used to evaluate depression.  Their basic findings were that dopamine agonists were no more effective than placebo in relieving depression, and sometimes had more serious side effects.  SSRIs and SNRIs  were used as a first choice to avoid the side effects of tricyclic antidepressants, such as dry mouth, dry eyes and constipation.

Ultimately, it was found that tricyclic antidepressants were more effective than SSRis or SNRIs, and were often very well tolerated, suggesting that tricyclic antidepressants might well be a better first choice for depression in PD.

The authors caution that this study has several serious limitations, such as the age of the participants and the stage of the disease.  Motor fluctuations and other co-morbidities and medications also need to be accounted for.  Larger studies are needed to clarify and confirm the data that this early study has begun.


  1. C.-C. Shen, S.-J. Tsai, C.-L. Perng, B. I.-T. Kuo, A. C. Yang.Risk of Parkinson disease after depression: A nationwide population-based studyNeurology, 2013; DOI:10.1212/WNL.0b013e3182a956ad


  1.  Liu J, Dong J, Wang L, Su Y, Yan P, et al. (2013) Comparative Efficacy and Acceptability of Antidepressants in Parkinson’s Disease: A Network Meta-Analysis. PLoS ONE 8(10): e76651. doi:10.1371/journal.pone.0076651



Alpha-synuclein Under Your Skin???

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Alpha-synuclein has been the subject of so many articles, it does seem to get “under your skin”, so to speak!  Now a research team from Beth Israel Deaconess Medical Center in Boston has found that the alpha-synuclein found just under the skin may be a potent biomarker for PARKINSON’S DISEASE.  Non-motor symptoms such as changes in body temperature, bowel habits, and skin coloration often occur long before other symptoms that lead to the diagnosis of PARKINSON’S DISEASE.  Finding a way to know who is at risk to develop PARKINSON’S DISEASE early in the process could enable earlier treatment and delay onset of the disease, or possibly lead to finding a cure.  This is the search for a biomarker, and it is the basis of many current studies.

Dr. Roy Freeman and his team are one group involved in this search.  Their research has focused on autonomic and peripheral nervous functions in PARKISON’S DISEASE, so they naturally looked at autonomic skin functions and reactions in this disease.  They surmised that a skin biopsy might provide information that could identify a biomarker for PARKINSON’S DISEASE.  In a small study funded by a grant from the National Institutes of Health (NIH) they examined 20 people with a diagnosis of PARKINSON’S DISEASE and 14 non-Parkinsonian controls.  They took skin biopsies from three different locations on their legs and found … alpha-synuclein.  Even higher levels of alpha-synuclein were found in the skin biopsies of people in more advanced stages of PARKINSON’S DISEASE.

The next steps in this study will be to measure alpha-synuclein in skin of people known to be at risk for PARKINSON’S DISEASE, and to see if depositions of alpha-synuclein in the skin can differentiate PARKINSON’S DISEASE from other neurodegenerative diseases.  A small skin biopsy is a safe and simple procedure that could be a big breakthrough as a biomarker to predict PARKINSON’S DISEASE.

Article by Marcia McCall

N. Wang, C.H.Gibbons, J. Lafo, R. Freeman. Synuclein in cutaneous autonomic nerves. Neurology, 2013; DOI 10.1212/WNL.0b013e3182a9f449  



Competitiveness and Impulsivity Heightened after DBS of Sub-Thalamic Nucleus

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A detailed and very interesting study published this week in the journal Brain is the work of several German and Canadian doctors who focused on personal and social implications of people with PARKINSON’S DISEASE who had undergone deep brain stimulation (DBS) of the sub-thalamic nucleus (STN).  While the DBS offers marked improvements in motor function that definitely improves the quality of life from a movement perspective, many of these people report serious struggles with social and work related problems.  Aspects of a behavioral and social nature are rarely studied in relation to DBS treatment.

The researchers noted that while DBS of sub-thalamic nucleus (STN) is beneficial for motor symptoms, the region stimulated also affects areas of decision making and impulsivity.  This may have the effect of making these people feel over confident and encourages risk-seeking behaviors.  Parkinson Disease sufferers may or may not be aware of this shift in their impulsivity but it may be the basis for some of their personal and work related issues. The researchers hypothesized that DBS-STN causes a pathological change in the way self estimation is perceived in competitive situations.

In order to analyze the self awareness of Parkinson’s disease patients who had had DBS of STN, they used an experiment from behavioral economics that consisted of addition of a long string of numbers.  Groups tested consisted of people with PARKINSON’S DISEASE who had received DBS of Sub-Thalamic Nucleus, people with PARKINSON’S DISEASE who had not received DBS of Sub-Thalamic Nucleus, and non-Parkinsonian controls.  There were four sets of numbers with varying rewards, paired as low risk/low reward, low risk/high reward, to high risk/high reward..  Further, as the subjects progressed from one set to the next, they were asked to estimate their accuracy, and then to choose whether to accept a nominal “prize” or to continue on to a “tournament”.  In all the sets, the controls had the highest accuracy and the DBS-STN the lowest.  As they progressed, the DBS-STN had higher predictions of their accuracy, even though past performance was negative.  26% of the DBS-STN consistently chose high risk/high reward even though based on past performance this was not to their benefit.

This study generated data on many areas of performance and behavior.  One area examined the risk taking behavior of the DBS of Sub-Thalamic Nucleus group compared to the non DBS group.  While very similar in symptoms and length of disease, the non DBS group was less inclined to risk taking behavior leading the researchers to surmise that perhaps there was an inherent bias toward risk taking behavior in the DBS-STN group that perhaps lead them to undergo the potentially risky, invasive DBS surgery in the first place.

In conclusion, the study authors suggest that while the DBS of Sub-Thalamic Nucleus subjects are impaired in their self-estimation, they may naturally have a preference for competitive situations, but that the DBS-STN has impaired the pathways used to evaluate both their decision making skills and the risks involved.  This may help explain some of the social difficulties this population experiences in their work, social and personal lives.


E. Florin, D. Muller, J. Pfeifer, M. T. Barbe, G. R. Fink, L. Timmermann; Subthalamic stimulation modulates seslf–estimation of patients with Parkinson’s disease and induced risk-seeking behavior; Brain (2013) doi: 10.1093/brain/awt241 pub 9/25/2013

Stem Cell Transplantation Shows Promise for PARKINSON’S DISEASE

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Many studies going back many years have investigated the possibility of creating neural stem cells in the lab and transplanting them to regions of the brain damaged by PARKINSON’S DISEASE.  Usually, these studies have been done using mouse models of PD and have involved heavy uses of immunosuppression.  Some studies have used cells obtained from the transplanted mouse itself, but results have rarely shown any benefit and are very difficult to duplicate.

Now, a researcher at Kyoto University’s Center for IPS Cell Research and Application in Japan has experimentally shown that cells derived from the subject’s own body produced almost no immune response when transplanted into the brains of monkeys and actually resulted in viable neural cells.  Doctors Jun Takahashi and Asuka Morizane are interested in promoting new neural pathways to restore dopaminergic cell function in the hope that this approach will help people with PARKINSON’S DISEASE.

When cells are obtained from the subject’s own body, they are called autologus.  Cells derived from other sources are called allergenic and evoke a very strong rejection response from the subject that receives them.  Autologus transplants are generally better tolerated especially in those with Parkinson’s disease.  This study used cells derived from the blood of the donor/subject and grew them into induced pluripotent stem cells (iPSC), which were then differentiated into dopaminergic neural cells.  These same cells were then transplanted back to the monkeys’ brain.  The monkeys were observed for three months and not given any immunosuppressant drugs.   No rejection response was seen and the cells became viable, functioning dopaminergic cells in their new location.

This is a radical approach that shows promise, however much more research will be necessary before it can be translated to human applications.


“A direct Comparison of Autologus and Allergenic Transplantation of iPSC-Derived Neural Cells in the Brain of a Nonhuman Primate” Stem Cell Reports, 2013.

Blood Bio-Marker Found for Cognitive Impairment in Parkinson’s Disease

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Blood Bio-Marker Found for Cognitive Impairment in Parkinson’s Disease  “There currently is no cure for PARKINSON’S, but the earlier we catch it–the better chance we have to fight it,” says Michelle Mielke, Ph.D.


Dr. Mielke is a researcher at the Mayo Clinic in Rochester, Minnesota.  She is studying blood based bio-markers for PARKINSON’S DISEASE, as a simpler, less expensive , less invasive technique for diagnosing this disease than brain scans or spinal taps which are sometimes used.  (A “blood bio-marker” test uses a protein in the blood or urine as a marker for what is going on inside the body. The best known biomarker test is a home pregnancy test which works on the same principle.*)

Her laboratory has found a specific but very rare genetic mutation that can lead to early onset PARKINSON’S DISEASE cognitive impairments.  This occurs in only 4 to 7 per cent of PARKINSON’S DISEASE patients. The mutation is called GBA and it is a marker of lipids in the blood.  This mutation causes lipids, ceramides and glucosylceramides to be incorrectly metabolized.  They found that people with PARKINSON’S DISEASE who have higher levels of lipids in their blood are more at risk for developing dementias or cognitive impairments.

Cognitive impairments in PARKIINSON’S DISEASE together with the other symptoms of PARKINSON’S DISEASE are very challenging for both the patients and their caregivers.  If a blood bio-marker such as this can help diagnose patients who are at greater risk earlier, it might lead to a treatment to slow the progression or reverse some of the damage.

About Dr. Mielke

The principal research interests of Michelle M. Mielke, Ph.D., are to further the understanding of the epidemiology of neurodegenerative diseases and psychiatric disorders.

A primary focus of Dr. Mielke’s research is the identification of biomarkers for the diagnosis, prediction and/or progression of Alzheimer’s disease, as well as other neurodegenerative and neuropsychiatric conditions.

Much of her work has emphasized both lipid markers — particularly sphingolipids (ceramides and sphingomyelins) — and neuroimaging markers.




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Medications for the Management of Parkinson’s Disease Part 2 – Agonists

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Medications for the Management of Parkinson’s disease Part 2 – Agonists


The second “miracle drug” for PARKINSON’S DISEASE  are the dopamine agonists.  Agonists work by making the receptor neurons think they are getting enough dopamine and by keeping available dopamine in the synapse between neurons a little longer.  In the early stages of PARKINSON’S DISEASE , use of agonists alone may be beneficial, but as the disease progresses, they are not as useful alone as they are together with carbi/levodopa.  Agonists can be helpful in managing fluctuations in symptoms from carbi/levodopa treatments.  There are side effects, and they can exacerbate the side effects of the other medications. Some of the more serious side effects have been with impulse control.  Problems such as gambling, impulsive shopping and hyper sexuality have been blamed on these medications.  Excessive sleepiness has also been reported.  It takes an experienced, PARKINSON’S DISEASE  trained neurologist to “fine tune” dosage and timing of all the PARKINSON’S DISEASE  medications.  Dosage of agonists should be started low and built up; if symptoms warrant a withdrawal from agonists, they must be decreased slowly.  The most common agonists are pramipexole (Mirapex) and ropinerole (Requip).  Long acting versions of both are also available as Mirapex ER and Requip XL.

Several other pharmaceutical products have become available for treatment of PARKINSON’S DISEASE .  While they are not the mainstream medications, they can be very, very useful in certain situations.  A fast dissolving form of carbi/levodopa is available for situations when it would take too long for a regular pill to be effective.  This is Parcopa, and it is now available as a generic.  Another “rescue drug” is apomorphine (Apokyn)  This is an injectable drug, and a patient or a caregiver has to be trained to give the injection.  This is a short acting drug, in the agonist class, but if someone suffers from sudden “off” periods, this can get them going again very quickly.  It does cause nausea, so anti-nausea agents must be taken at the same time.

The rotigotine transdermal patch (Neupro) was hailed as another “miracle” when it first came out.  It delivered a steady dose of medication which was easily and readily absorbed through the skin.  Patients were thrilled to wear a patch instead of taking a regimen of drugs.  And it was effective for many of them, but it had problems, particularlly with the adhesive and the FDA forced it to be recalled from the market for several years.  It is now back.  It is in the agonist class, and while it is very useful, it  too, has side effects, some of which can be quite serious.  Sensitivity to sulfites is one drawback, but among people with PARKINSON’S DISEASE  this is not a common issue.  Drowsiness, nausea and the other side effects noted for drugs in the agonist class apply to this one, too.  Skin irritations can develop from either the ingredients or the adhesive in the patch and care must be taken not to expose the patch to either heat or water.  It comes in various doses.

If PARKINSON’S DISEASE  were the only disease a person needed treatment for, it would still be a very complex matter.  But because PARKINSON’S DISEASE  usually starts later in life, there probably are some other medical issues to consider, complicating the situation even further.  Seeking the advice of a neurologist who is both trained and experienced in movement disorders and especially in PARKINSON’S DISEASE  is essential.  The attention of a caring and dedicated primary care physician is also a high priority, especially if multiple medications for multiple medical issues are involved.  A good primary care physician can treat infections which  cause a person with PARKINSON’S DISEASE  extra distress and disrupt the benefit of the PARKINSON’S DISEASE  meds as well as oversee all the combinations of medications a person is taking to avoid serious drug interactions.

Although there is no cure for Parkinson’s disease, the symptomatic treatments that are available today are able to improve the quality of life and reduce the symptoms better than at any time in the past.  Of course, research is ongoing, new drugs will come along and perhaps that elusive cure will be found.  Living one’s life to the fullest and living well with PARKINSON’S DISEASE  can be possible with the help of a good neurologist and modern medications.

Side Effects


For a full list please see the information at:

Applies to pramipexole: oral tablet, oral tablet extended release

Along with its needed effects, pramipexole (the active ingredient contained in Mirapex) may cause some unwanted effects. Although not all of these side effects may occur, if they do occur they may need medical attention.

Check with your doctor immediately if any of the following side effects occur while taking pramipexole:

More common

  • Dizziness, lightheadedness, or fainting, especially when standing up
  • drowsiness
  • hallucinations (seeing, hearing, or feeling things that are not there)
  • nausea
  • trouble with sleeping
  • twitching, twisting, or other unusual body movements
  • unusual tiredness or weakness

Some side effects of pramipexole may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine. Also, your health care professional may be able to tell you about ways to prevent or reduce some of these side effects. Check with your health care professional if any of the following side effects continue or are bothersome or if you have any questions about them:

More common

  • Constipation
  • dryness of the mouth
  • headache
  • heartburn, indigestion, or acid stomach

Less common

  • Abnormal dreams
  • decreased sexual drive or ability
  • general feeling of discomfort or illness
  • increased cough
  • increased sweating
  • itching
  • joint pain
  • loss of appetite
  • runny nose
  • skin problems, such as rash or itching weight loss


For complete information please see:

Get emergency medical help if you have any of these signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat. Call your doctor at once if you have any of these serious side effects:

  • feeling like you might pass out;
  • fever, stiff muscles, confusion, sweating, fast or uneven heartbeats (especially if you stop taking Requip or use a lower dose);
  • hallucinations;
  • tremors (uncontrolled shaking); or
  • tight feeling in your chest, trouble breathing.

Call your doctor promptly if you fall asleep during a daily activity, if you faint, or if you have hallucinations (hearing or seeing something that is not there). Your doctor may want you to stop taking Requip, or take a lower dose.

Less serious Requip side effects may occur, such as:

  • mild nausea, vomiting, stomach pain, or loss of appetite;
  • worsened RLS symptoms early in the morning;
  • diarrhea or constipation;
  • dry mouth, sweating;
  • headache;
  • dizziness, drowsiness;
  • sleep problems (insomnia); or
  • agitation or anxiety.

This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.

See also: Requip side effects (in more detail) 

Medications for the Management of Parkinson’s disease Part 1

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Carbidopa/Levodopa, that miracle drug for the treatment of Parkinson’s disease has only been in use a little over 60 years. In that time frame, research has accelerated, more knowledge of the brain has been revealed and more drugs have been added to the arsenal for fighting the symptoms of Parkinson’s disease. This article will look at the classes of drugs commonly used. It is not intended to replace the advice of your neurologist or physician. Parkinson’s disease is a very complex disease, and no two people with Parkinson’s manifest the symptoms in the same way. Treatments must be tailored to the individual, and only a Parkinson’s disease specialist can effectively determine what is best.

Before carbidopa/levodopa came on the scene, treatment often consisted of anticholinergic drugs. Anticholinergic drugs block the activity of the neurotransmitter acetylcholine which is involved in memory and control of movement; it has no affect on the dopamine systems in the brain. This class of drug is rarely used today because there are more effective ways to treat PARKINSON’S DISEASE now available. In some cases, particularly in people with severe dystonias that develop from periods when their usual medications fail to work, anticholinergic medications may help. One of the main side-effects of this class of drug is mental “fogginess”, problems with memory as well as dry mouth, constipation and blurred vision. The pharmacological name for this medication is trihexiphenidyl (Artane).

MAO-B or monoamine oxidase inhibitor B, is also used early in the treatment of PARKINSON’S DISEASE . It has only a rather limited effect on PARKINSON’S DISEASE symptoms, however, if used very early in the diagnosis, it can delay the need for carbidopa/levodopa medications. Sometimes it can be added later in the course of the disease to enhance the effect of levodopa. Basically, this drug works by breaking down the levodopa in the brain and making it more available to weakened neurons. It too has side effects; it may cause dizziness and low blood pressure, indigestion, nausea and headaches. Some of the drugs in this class may provide some neuroprotection, and studies are on-going, however there has not been any really conclusive evidence . Rasagiline (Azilect) and seligiline or deprenyl (Eldepryl or Zelapar) are the pharmaceutical and trade names for this medication.

Carbidopa/levodopa is the “gold standard” of treatment for symptoms of PARKINSON’S DISEASE . It has been around only since the 1960s, but has made a world of difference in patients’ lives. It is the most effective treatment available but it has also has generated a lot of discussion, both pro and con. There were concerns about extended levodopa replacement becoming toxic, however research has not found that to be true. Other issues revolved about the best time to introduce it into the treatment program. There have been arguments that beginning treatment with carbi/levodopa too early in the course of the disease will limit the length of time its benefits are effective without causing serious side effects. The other side thinks that delaying the introduction of carbi/levodopa lowers the quality of life of the patient and leaves them vulnerable to other aspects of the disease. Most neurologists favor an earlier start, but there are some modifying factors.

Carbidopa/levodopa is available in many different combinations. Dosing strategies have to be carefully worked out in collaboration with the neurologist in order to avoid serious side effects and to obtain maximum benefit. This is not a medication where one size fits all! It is possible that more than one form of this medication may be used at different times of the day, so people who are taking this need to be very aware of which pill is taken at what time; and timing is equally as important as the pill. The formulations come in different shapes and colors, but careful vigilance is still necessary. Perhaps the oversight of a caregiver can be enlisted.

The first “miracle” was carbidopa/levodopa, introduced as “Sinemet”. The small amount of carbidopa listed first in the fraction, was added to reduce the nausea that levodopa can cause. The medical terminology “sin = without” and “emesis = nausea” became the clever name for this drug. A bit later, scientists figured out a way to make a controlled release form of this medication, one that would dissolve slowly over time and eliminate taking so many shorter acting pills. This was called Sinemet-CR. Carbidopa/levodopa does have side effects such as low blood pressure, dizziness, dry mouth and sometimes nausea.

What are the Common Side Effects?
Sinenet (Carbidopa/Levidopa)

  • Nausea
  • Vomiting
  • Loss of appetite
  • Lightheadedness
  • Lowered blood pressure
  • Confusion
  • Dyskinesia (if used as a long-term therapy; between 3-5 years)
  • People who use levodopa longterm may experience dyskinesia at some point, usually three to five years after starting the medication.
  • The term dyskinesia describes involuntary, erratic, writhing movements of the face, arms, legs, and/or trunk, which usually occur one to two hours after a dose of levodopa has been absorbed into the bloodstream and is having its peak clinical effect.

Eating Proteins with Levodopa/Sinemet*

  • It is best to take Sinemet 30 to 60 minutes before eating a meal. This allows the Sinemet to be quickly absorbed before the food can interfere.
  • Take the Sinemet along with foods that don’t contain proteins.
  • Ginger tea is a good choice for many people, because it often “settles the stomach”.
  • A graham cracker or soda cracker along with the ginger tea may help too. These foods are very low in protein and should not interfere with the absorption of Sinemet.

COMT Inhibitors

In the mean time, science found that adding another medication to the regimen kept the dopamine active in the brain, prolonging its effect and preventing “wearing off”. This was the addition of a COMT inhibitor. COMT is Catechol-O-Methyl Transferase and it was pharmaceutically known as entacapone (Comtan) or tolcapone (Tasmar). Both prescriptions were given together. This medication, too, must be carefully monitored. Anyone taking Tolcapone (Tasmar) must have regular blood tests to check liver function. COMT can also increase the side effects of carbi/levodopa and hallucinations can occur as well as increased movements, called dyskinesias.

Then a brilliant idea from a pharmaceutical company:…Why not combine the two in one pill? And Stalevo was born; a combination of carbidopa, levodopa and entacapone in one tablet. This medication also comes in multiple strengths. It has the advantage that only one pill is necessary instead of two, simplifying the regimen, but for some people, side effects can limit its usefulness. There is also some consideration that the combination may contribute to prostate problems for men, but this is still under scientific investigation.

What are the Common Side Effects?

  • Dyskinesia
  • nausea
  • diarrhea
  • hyperkinesia (an abnormal amount of uncontrolled muscular action; spasm.)
  • abdominal pain
  • dizziness
  • harmless discoloration of urine
  • saliva and/ or sweat
  • hallucinations

Early Diagnosis of Parkinson’s by Handwriting Analysis

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“Micrographia” or small handwriting has been a signal symptom of Parkinson’s disease (PD) for many years.  Why the handwriting gets smaller and smaller is not well understood.  But now a group of occupational therapists working at University of Haifa and the Rambam Hospital have studied this phenomenon and found what is perhaps and early way to predict and diagnose Parkinson’s disease based on handwriting.

Professor Sara Rosenblum noted that many people who have Parkinson’s disease have often felt there were cognitive changes happening in their brains well before any motor symptoms were seen and they were aware of changes in their handwriting, sometimes years before there were motor symptoms.  Most studies have focused on the motor skills of hand writing and not on the cognitive changes.  Professor Rosenblum decided to look at the cognitive changes by asking the participants to sign their name and write several addresses, as if addressing an envelope, tasks that require cognitive skills.  She chose 40 subjects: 20 healthy and 20 with early stage PD that had no motor symptoms.

Using a plain piece of paper placed on an electronic tablet and a special, pressure sensitive pen, they were able to analyze the writing from several perspectives.  They could see how the subjects formed the letters, the length, height and width as well as how much pressure was applied and the time it took to write them.  They found some interesting differences.

The people with Parkinson’s disease wrote smaller letters, used less pressure and took longer to write them than the healthy group.  Of special note was the longer time the people with PD held the pen in the air before writing, which shows the amount of time their brain was contemplating the next writing action.  This suggests that there is a reduced or slower cognitive ability.

Further development of this research could lead to earlier detection of Parkinson’s disease .  It has the advantage that it could be done my a technologist other than the physician and if the changes are noted, the patient can then be referred to a physician for further evaluation and treatment.

Professor Rosenblum is presently collaborating with Dr. Ilana Schlessinger, the head of the Movement Disorders and Parkinson’s Disease at Rambam Hospital in Haifa, Israel..  They are using handwriting analysis to measure the degree of Parkinson’s patients improved functioning after undergoing deep brain stimulation.

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Sara Rosenblum, Margalit Samuel, Sharon Zlotnik, Ilana Erikh, Ilana Schlesinger. Handwriting as an objective tool for Parkinson’s disease diagnosisJournal of Neurology, 2013; DOI: 10.1007/s00415-013-6996-x.


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