Neurosciences | Parkinson's Disease | Questions & Answers | Penn Medicine

What could cause problems with the extensor halluces longus (EHL) muscle?

2013-12-18T10:19:00.003-05:00

Question: I am 47 years old and was diagnosed with early stage Parksinons’s Diseaese four years ago. I am on a relatively low dose of Stalevo®. Initially, my coordination was only affected in my left arm and hand. Shortly after, I noticed an intermittent leg driven gait asymmetry. Post-diagnosis I have had several lumbar disk surgeries. After years of concentrating and reading about this gait disturbance I have narrowed down the main problem (I think). During off periods, I experience hypomobility and weakness of one foot extensor hallucis longus function that is not associated with any dystonia and DEFINITELY improves with medications. Has this been described to you before? Do you think there is an element of true neuropathy? Also, is there anything you can think of to improve extensor halluces longus (EHL) strength? When I do exercises for my toes/feet/ankle do you think I should concentrate on "on" or "off" periods?

Answer: Although I cannot find evidence or recall any patients with specific problems with the extensor hallucis longus (EHL) muscle—the muscle that points the big toe upwards--self-perceived weakness is actually quite common in Parkinson’s Disease. One recent study of 113 PD patients found that 43.8% reported weakness. On clinical examination, all of these individuals who reported weakness had normal muscle strength. This phenomenon—patients reporting weakness but having normal strength on neurological testing—is quite common in our clinical experience, as well. What explains this disconnect?

Try to think about it this way: every part of the body senses things in a different way, and the brain interprets those signals in a very particular way. For example, the eye is limited to sensing things in light & color, and the brain interprets all of that information into what we call vision. But what happens if a fly ball catches you in the face? You ‘see stars’, right? The eye can’t really sense pain… it can only sense things in the way it’s allowed to… through light and color. So the shock of that fly ball gets interpreted by the brain as a sudden burst of light and color.

Similarly, the brain is used to interpreting information from the muscles as strength and movement. If one’s leg isn’t moving the way it usually moves, the brain interprets it as being weak. In reality, that leg might be stiff or just moving much slower than we’d like, but the brain will still ‘tell us’ that it’s weak. For many people who complain of self-perceived weakness, it is often underlying rigidity or bradykinesia of the muscles (particularly when the feeling is responsive to medications) that is tricking the brain into thinking it’s weak. Without examining you, of course, it is impossible to be 100% certain or to exclude neuropathy. However, weakness from neuropathy would not improve with PD medications. In terms of specific things to do, I would see a physical therapist specially trained in Parkinson’s Disease to find the precise exercises that help relieve the feeling of weakness. Hope this helps!

For more information about Penn’s Parkinson’s Disease and Movements Disorders Center, or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

Are paresthesias common in Parkinson’s Disease?

2013-12-18T10:17:00.003-05:00

Question: I have had Parkinson’s Disease for 27 years and was diagnosed with deep brain stimulation (DBS) 12 years ago. Are paresthesias common in PD, which tend to be particularly intense during the wearing-off and off medication periods? Is there a relationship between the amount of daily Sinemet® taken and the symptoms (itching, burning, tickling)?

Answer: Paresthesias—abnormal sensations that can include tingling, coldness, muscle tightening, pins & needles, or numbness—are a common non-motor symptom in PD, occurring in anywhere between 30-69% of patients. These often occur as an “off” phenomenon, as you mentioned, meaning that this symptom emerges as the medications are wearing off or are completely out of your system. Although motor fluctuations have been studied in relation to the amount of dopaminergic medication taken, non-motor fluctuations like paresthesias have only recently been recognized, so the relationship between medication doses/strength is still poorly understood. However, sensory symptoms that are associated with off periods may respond to increases of dopaminergic medications or to medication adjustments to try to achieve more ‘on’ time during the day. Talk with your neurologist about these symptoms and their timing, and you should be able to come up with a plan together. Great question!

For more information about Penn’s Parkinson’s Disease and Movements Disorders Center, or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

What could be the cause of dyskinesias?

2013-10-22T10:10:00.005-04:00

Question: I’ve read conflicting descriptions of how/when the dyskinesias that most PD patients eventually deal with are caused: (a) length of time on levodopa, (b) size of levodopa dose (in response to disease progression), (c) any stimulus to the nervous system (even the dopamine agonists). Could you please explain the details, what is the best current thinking on the causes (and delaying the start time) of dyskinesias?

Answer: Dyskinesias are the involuntary movements of the face, arms, legs, and/or trunk that can occur 1-2 hours after a dose of levodopa has been absorbed in the bloodstream. Dyskinesias require two things to ever develop: Parkinson’s disease plus levodopa. Either of those alone are not enough to cause dyskinesias.

Development of dyskinesias appears to be related to length of time on levodopa, dose of levodopa, and characteristics of the patient. In a 1996 study by Blanchet and colleagues that followed 100 people with PD treated with levodopa for varying amounts of time, 56% of patients developed dyskinesia after an average of 2.9 years. Those who developed dyskinesias were more likely to be on higher doses of levodopa and to be younger at the time of PD onset than those who did not develop dyskinesias. When thinking about those results, it’s very important to recognize that medication regimens have changed dramatically since that study. People in that study—many of whom started treatment in the early 1970s!—were treated in an era where high-dose levodopa-only therapy was the go-to choice for Parkinson’s disease. This change in practice is reflected in a study by Kumar and colleagues from 2005 in which 50% of people with PD onset between 40-59 years of age developed dyskinesias by 5 years into the disease (not 3). For PD patients with age at onset of 60-69 years, the 5-year risk of dyskinesias was 26%, and for people with onset at age 70 or later, the risk was 16%.

The STRIDE-PD study (Olanow et al, 2012) looked specifically at the relationship of levodopa dose to dyskinesia development and found a clear difference with people taking <400mg of levodopa daily at far lower risk of dyskinesias, and a steady increase in the risk as the dose increased to 400-600mg, or >600mg.

The biologic explanation for the development of dyskinesias is found in the continuous dopaminergic stimulation theory. Normally, our dopamine-producing brain cells (neurons) make and release a small steady stream of dopamine throughout the day, fueling our motor control systems. In the early stages of PD, that stream gets progressively smaller, but the neurons have a backup system: there are several molecules that help the neuron recycle the dopamine they just released, getting more ‘bang for the buck’ out of the dopamine they make. As PD progresses and that stream becomes even smaller and insufficient to help the motor systems function normally, we need to replace the dopamine itself (with levodopa), mimic the effects of dopamine (with a dopamine agonist), or make the recycling mechanisms work even harder (with rasagiline, selegiline, or entacapone).

No matter how the drugs are given, they cannot completely mimic the slow, steady release of normal dopamine. An additional risk factor for the development of dyskinesias is the degree of difference between the normal steady streams versus a very choppy, intermittent, unevenly spaced stream of dopamine. This is why doses of levodopa should be spaced equally apart during waking hours—to get as close to normal as possible—and why there has been a strong push to develop more long-lasting, steady-release forms of levodopa. Stay tuned!

For more information about Penn's Parkinon's Disease and Movements Disorders Center, or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

What are the pros and cons of immediate release vs. controlled release generic Sinemet® for early-stage Parkinson’s disease?

2013-10-22T10:07:00.003-04:00

Question: Could you please discuss the pros and cons of immediate release vs. controlled release generic Sinemet®, especially in relatively early-stage disease? Different articles have said one or the other is preferable but the evidence is sketchy. I thought controlled release was preferable (the "continuous dopaminergic stimulation hypothesis", constant is better than pulsatile, etc.), but I just read an article saying immediate release is better in early-stage disease?

Answer: Early on in Parkinson’s disease, most movement disorder specialists prefer to use immediate release carbidopa-levodopa (generic Sinemet®) instead of extended-release for several reasons. First, although the extended-release (ER) is marketed as lasting longer, the actual difference in practice is not very significant for most people, particularly in early-stage disease. Immediate-release (IR) carbidopa-levodopa starts to take effect in as little as 30 minutes, but ER only starts to kick in after about 2 hours. Also, only 70-75% of the levodopa in the ER form is absorbed; the rest passes through the intestines and is excreted. This all leads to the IR form causing a quicker “on” state compared to ER.

Although the ER form stays in your bloodstream for slightly longer than IR, the difference is not noticeable in most people, particularly early on. This is because early in Parkinson’s disease, your brain is still producing some dopamine on its own and can store some of the dopamine that it converts from levodopa. So even though levodopa is no longer detectable in your bloodstream several hours after taking the IR form, your brain has taken it up into storage and can use it steadily for several more hours.

The most common situation where ER is used would be when patients wake up frequently in the middle of the night to use the bathroom and experience “off” symptoms during that time that limit their ability to get out of bed and walk to the bathroom and back. If severe stiffness or slowness are occurring in the middle of the night and the person needs to be more mobile, a dose of ER at bedtime makes sense, since it will start to kick in a few hours later and last nearly until the morning.

For more information about Penn's Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

How do MTHFR mutations and Parkinson’s disease relate?

2013-06-05T08:42:00.005-04:00

Question: Are you testing for MTHFR mutation and appropriate treatment as it relates to Parkinson's disease symptoms?

Answer: The simple answer is no, we are not currently testing for mutations in the MTHFR gene because it would not change treatment plans for Parkinson’s Disease (PD) at this time. The best scientific evidence supports selecting a medication regimen based on the individual patient’s symptoms and limitations, keeping in mind any other medical conditions. Expert guidelines do not suggest checking these mutations or altering our treatment plan.

The more complicated answer needs to be put in context. MTHFR, or methylenetetrahydrofolate, is a protein necessary for survival. It helps metabolize other proteins, basically recycling other important molecules that would otherwise build up in our bodies. The genes that code for MTHFR vary between different people. Some genes code for a less efficient MTHFR, which means that some of the proteins that should get recycled are able to build up instead. One of the critical proteins that build up is homocysteine. At very high levels, homocysteine has been associated with vascular disease, such as coronary artery disease, heart attacks and strokes. So, people with certain mutations in the MTHFR protein have slightly, to moderately higher levels of homocysteine. In most people, this is NOT enough to cause disease.

Scientists have learned that people who have PD and are taking levodopa have slightly higher levels of homocysteine, too. The MTHFR gene mutations do not cause PD. These mutations are just as common in people who have PD as in people who do not. But one particular mutation (677) seems to affect the way that levodopa is processed, so that people with that mutation who are on levodopa have higher homocysteine levels than people who are not on levodopa. Studies looking at the risk of this higher homocysteine level have NOT shown any differences in these patients in terms of motor symptoms or cognitive symptoms related to PD.

Basically, the slightly higher homocysteine levels in the blood do not change PD symptoms and do not elevate a person’s risk of vascular disease enough to avoid this very effective medication in people who need it. Studies have shown—and clinical experience with thousands of patients seen in our center supports—that improving daily function with PD medications has a huge, positive effect on quality of life and survival.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center , or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

What neurologists specialize in Parkinson’s Disease only?

2013-06-05T08:40:00.003-04:00

Question: What neurologists specialize in Parkinson Disease only?

Answer: Many general neurologists take care of patients with Parkinson's Disease (PD) very frequently and are quite comfortable managing the condition. General neurologists have completed four years of medical school, one or more years of internal medicine residency, and three years of neurology residency. Neurologists who want to further sub-specialize in PD and similar conditions may complete 1-2 additional years of fellowship training in the field of Movement Disorders. During this time, neurologists learn the "ins and outs" of treating PD by seeing patients alongside experts in the field. Most fellowship programs are located at academic institutions with a history of excellence in Parkinson's Disease care and research. After completing a fellowship, that physician is considered a Movement Disorders specialist.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center , or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

Is taking melatonin beneficial to patients with Parkinson’s Disease?

2013-05-09T14:22:00.004-04:00

Question: Research literature suggests both that melatonin is bad for Parkinson’s Disease (melatonin antagonists e.g., light therapy, may be useful) and also that melatonin is good for Parkinson’s Disease (melatonin supplementation may be a useful therapy). Obviously, this is all still early research with very small test patient numbers, but could you please take a stab at explaining for the layman and the implications if any, especially if one or the other approach might do harm?

Answer: The data on this issue is very limited, consisting of multiple studies on animal models of Parkinson’s Disease with a few very small randomized clinical trials in people with PD. In 2011, the Movement Disorders Society published a thorough review of the scientific evidence for the treatment of non-motor manifestations of PD, including sleep disturbances. They concluded that there was insufficient evidence to recommend melatonin for insomnia (at low doses like 3-5mg per night, or at high doses of 50mg per night). It was noted, however, that the low doses did not cause significant side effects. While there are some case reports of melatonin worsening motor symptoms, this is quite rare. More importantly, it is important to recognize that there are many ways in which sleep can be disturbed in PD, and melatonin might be useful for certain disturbances (like REM Behavior Disorder), but not others (like insomnia).

According to Dr. Lama Chahine, a movement disorders and sleep disorders specialist, light therapy in general is considered part of routine care for specific circadian rhythm disorders, including delayed and advanced sleep phase syndrome—conditions in which a person’s internal clock is either set much later or much earlier in the day than usual. Light therapy acts in part by shifting the timing of melatonin release. This has not been studied well in PD but in the right context, light therapy would be appropriate. There is also good evidence for light therapy in depression, although again, light therapy for PD and depression has not been well studied. In summary, both melatonin and light therapy may be quite useful in the right context for certain symptoms, but neither is recognized as being clearly protective or detrimental for PD in general.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center , or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

What are the best remedies for dry mouth?

2013-04-10T10:20:00.003-04:00

Question: I have PD and take Mirapex®, three pills, three times a day since September and Azilect®, one pill, once a day for a year. I have developed severe dry mouth over the past month and understand that my medications may be the cause. How do I treat the dry mouth?

Answer: Dry mouth, also called xerostomia, is a common side effect of many medications used in the treatment of Parkinson’s Disease (PD). Other risk factors for dry mouth include older age, mouth breathing, diabetes, anxiety, and many medications for non-PD conditions. Dry mouth is not just a matter of discomfort or annoyance; in addition to causing dry lips, tongue, and gums, dry mouth can also lead to gum disease, dental cavities, and tooth loss. Thank you for bringing up this important symptom!

Simple strategies for coping with dry mouth include increasing fluid intake, including water or decaffeinated beverages. Sometimes it’s difficult to motivate ourselves to drink lots of plain water, so adding sugarless flavor mixes or flavor drops (like Crystal Light, Mio, Dasani®, or store-brand flavorings) can help make water more enjoyable. Rinsing with cold water or salt water can ease dry mouth, as can sucking on ice chips or sugarless hard candies. Sour candies in particular can increase saliva production to ease dry mouth, so look for sugarless lemon drops and similarly tart treats. Sugarless gum is another great remedy.

If these strategies are not enough, there are many over-the-counter artificial saliva products available in liquid, spray, lozenge, and gel forms (Aquoral®, Biotene®, Caphosol®, NeutraSal®, Entertainer’s Secret, Mouth Kote®, Numoisyn™, Oasis®, Saliva Sure™). These can be used as needed for dry mouth; read the instructions on each product for the maximum daily dose recommended.

Most importantly, frequent dental care is crucial! See your dentist at least twice each year for a check-up to identify problems early.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

Are there reasons not to try neurostimulation with early stage PD?

2013-03-19T09:00:00.002-04:00

Question: Can you discuss neurostimulation, both DBS and extradural motor cortex (EMCS)? New articles appeared recently suggesting that EMCS is effective, safe, with little if any downside. If so, what are the reasons not to try it? Then, can you elaborate on the New England Journal of Medicine (NEJM) article on the EARLYSTIM trial? If I read correctly, DBS improves motor symptoms and major secondary outcomes significantly better than medical therapy alone for earlier stage PD. There is no significant difference in serious adverse events and the bottom line is in favor for carefully chosen young patients. For patients with primarily motor symptoms, the appeal of relief without starting the clock on levodopa is obvious. All thoughts or recommendations are welcome, including additional references.

Answer: Extradural motor cortex stimulation (EMCS) involves placing a strip of electrodes over the outside layer of the brain in order to deliver continuous electrical stimulation to one of the areas controlling movement. The larger studies published thus far include very heterogeneous groups of patients, making any general conclusions impossible. The studies have included not just Parkinson’s disease but also atypical parkinsonian conditions. They have studied different locations and methods of electrode placement, and different stimulation settings. The most recent study from the journal of Neurosurgery, July 2012, involved only nine subjects with moderate to severe PD, who had had the disease for nine to 28 years. Therefore, while this may be a useful option in the future, it requires far more rigorous study—with uniform type and location of electrode placement, uniform stimulation programming, and well-defined, similar types of patients--before suggesting its widespread use. Studies would need to look at the performance of this surgery in people with early PD specifically before it would be accepted as a therapeutic option. It is also important to remember that this is still a type of brain surgery, with all of the potential risks of a surgical procedure.

In the recently published EARLYSTIM trial, 251 patients with PD were randomly assigned to receive either bilateral deep brain stimulation (DBS) plus medication therapy, or medication therapy alone. While the results showed significant improvements in quality of life and disability for the group receiving surgery, there are some important points to note. On average, the participants had had PD for about 7.5 years. To be eligible for this trial, participants had to be under the age of 60, have had fluctuations or dyskinesia, and have an improvement in their motor symptoms of at least 50 percent when on dopaminergic medications (either levodopa or a dopamine agonist).

Aside from the age limit and strict criteria for disease duration, the last point is the most important. Deep brain stimulation can be very effective for the management of PD, however, it can be expected to relieve symptoms only as well as the patient’s best response to dopaminergic medication. Some individuals with PD or atypical parkinsonism may not respond very well or at all to dopaminergic drugs, and if those patients went straight to DBS, they would receive all of the risks of surgery without any benefits. For many people with PD, careful adjustment of their medications can lead to many years of good symptom control with minimal disability. In those cases, the risks of surgery may outweigh the benefits. If a patient has had years of good response to medications but then starts to develop motor complications (on and off periods or dyskinesias) DBS can be considered in order to achieve the same benefits of the medications “at their best”, while minimizing some of the side effects. In summary, levodopa is still the most effective medication that we have for the control of PD symptoms. It is also the most helpful way to predict who will benefit from surgery.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

Is it beneficial to delay taking levodopa?

2013-03-18T09:00:00.002-04:00

Question: Is there a clear answer or even a consensus on whether to try to delay levodopa as long as possible? Will the first exposure “challenge” or diagnostic dose start the clock toward dyskinesias? The literature seems contradictive/unclear, even argumentative. Some say there are “proven” benefits especially if you start in early UPDRS stages, maybe even neuroprotective dyskinesias due to disease progression (increasing amount of levodopa needed) not an effect of levodopa itself. Others say it produces both motor and mental complications eventually. Even the challenge dose starts the clock, eventually decreases dopamine receptor sensitivity, worsens disease, and say don’t start until you really need it.

Answer: Therapy is indicated when a patient is bothered by PD symptoms, and there is good evidence from the ELLDOPA trial, published in the New England Journal of Medicine, 2004 that levodopa is not toxic and may slow the progression of symptoms. It is also widely accepted that levodopa remains the most effective drug available for the relief of motor symptoms in PD, along with having the lowest risk of short-term side effects. It is not, however, approved as a neuroprotective agent. In other words, the underlying pathology of PD continues to progress at the same rate, even though the outward signs and symptoms of the disease seem to be progressing slower. We also know that by starting medications and improving symptoms, we improve quality of life, and reduce morbidity and mortality. It is also possible that by starting therapy early, we preserve the brain’s ability to use compensatory mechanisms, which would be lost by delaying the start of medications.

On the downside, motor complications such as dyskinesias and wearing-off can occur in up to 90 percent of patients with PD who have taken levodopa for five to ten years. However, we do not know whether there is a threshold in terms of dose or frequency that increases this risk. Many of the studies that found such high rates of motor complications were conducted before the majority of other PD drugs were available. Instead of using just high doses of levodopa, the accepted practice is to use more than one medicine at low doses in order to reap the benefits of both while avoiding both short- and long-term side effects.

According to “The Scientific and Clinical Basis for the Treatment of Parkinson Disease”, published by the journal Neurology in 2009, “the general view of experts is that there is not sufficient evidence to consider levodopa toxic in PD, and that levodopa should not be withheld unless further information to the contrary becomes available. Rather, we advocate that levodopa should be used in patients with PD when it is deemed necessary, taking into account the efficacy and (side effect) profile of the drug in relation to the individual patient.”

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

What can I take to eliminate the side effects of my PD medication?

2013-03-14T13:43:00.002-04:00

Question: I take Azilect® 1 mg in the morning and Mirapex® ER two and one half at bedtime for my Parkinson’s. I get frequent freezing of my left leg that has increased in the past 2 months. Is there any medication to eliminate freezing? If there is a medication, are there any side effects that may occur from the medication?

Answer: Freezing—the experience of not being able to move one or both legs either immediately on starting to walk or in the middle of walking—is a common problem for many people with Parkinson’s Disease (PD). Like all questions about medication management, though, the right answer depends on the individual person and requires discussion with your doctor.

In general, the treatment of freezing depends on when and how often it is occurring, whether the freezing is related to ‘on’ and ‘off’ times or not, what medications you are already taking, the response you have had to those medications, and any other medical problems or medications in the mix. Sometimes we are able to increase the dose of the dopaminergic drug (like Mirapex®, Requip®, Sinemet®, or Stalevo®) to improve freezing. If the freezing is happening at a particular time of day, the doses of medications might need to be taken earlier or later in the day, or the dose might need to be split up during the day.

For example, if you take an extended-release preparation at bedtime, the medicine is in your system for about 24 hours, but may run out or have less effect towards the end of that 24-hour period. So, if freezing was happening in the afternoon and evening right before the pill was taken, one approach might be to change from a once-a-day pill to an equivalent total dose of immediate-release medication divided up into two or more doses throughout the day. In other words, instead of 3mg Mirapex® ER at bedtime, your doctor might suggest taking regular Mirapex® 1mg three times each day. The extended-release medications cannot be cut or split, though. Your doctor would need to prescribe the regular, NOT extended-release form of the drug.

For other people, this type of change might not be effective against their freezing, and it might require the addition of another medicine at low doses. There is no medicine that is 100 percent effective for treating freezing. Just like no two people with Parkinson’s are alike, there is no “cookie-cutter” approach to medication adjustments for different symptoms. Be sure to discuss this with your neurologist to find the best treatment for you.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

How can I prolong my wearing off time from my PD medications?

2013-01-28T11:20:00.003-05:00

Question: I am presently on Requip® XL 4 mg daily, Sinemet® 25/100 three to four times a day, and Azilect® 1 mg at night. I am having more wearing off time and am wondering what my next step might be. Would it be to take Stalevo® and would that be in addition to what I am taking or would I wean off Requip®?

Answer: Wearing-off is a type of motor fluctuation that can often occur in people with Parkinson’s disease on carbidopa/levodopa (Sinemet®), and symptoms can include the recurrence of tremor, stiffness, or slowness that was well-controlled for the first few hours after taking each dose. Wearing-off can also include non-motor symptoms, such as feelings of anxiety or depression that arise only towards the end of each dose and improve once the medication kicks in. Other motor fluctuations include dyskinesias—extra, involuntary movements such as fidgeting or restlessness—that can happen right as the medication is reaching the peak levels in a person’s bloodstream or right as the medicine is wearing off, and involuntary twisting or turning of a body part (dystonia).

There are many ways to manage wearing-off phenomena and motor fluctuations. However, as for all medication management questions, the right answer depends on the individual PD symptoms, other medical problems, and other medications. Stalevo® is the brand name for a combination pill made up of carbidopa, levodopa, and entacapone. Entacapone has no effect on PD symptoms when taken by itself. It helps with wearing-off by blocking the breakdown of levodopa. This increases the time that each levodopa dose lasts. On average, adding entacapone extends a person’s ‘on’-time by about 0.8 to 1.4 hours each day.

Because carbidopa/levodopa doses may need to be adjusted when starting entacapone, some physicians prefer to add entacapone as a separate pill with each carbidopa/levodopa dose. Then, when wearing-off is minimized and symptoms are better controlled, your physician may recommend changing from carbidopa/levodopa and entacapone to the combination pill carbidopa/levodopa/entacapone—Stalevo®. Stalevo® is available in many different dose combinations.

Other options for managing wearing-off might include increasing the number of carbidopa/levodopa doses each day, adding tolcapone (a medication related to entacapone), or adjusting extended-release dopamine agonists (e.g. Requip® XL). Again, there are many available options. The right option for you is best determined by a conversation with your doctor.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

Are there any PD support groups in the Lower Merion area?

2013-01-07T13:52:00.003-05:00

Question: I am trying to assist a friend who has just found out that she has Parkinson's disease. Are there any support groups in the Lower Merion area for her to attend?

Answer: Thanks for being a great advocate for your friend! The nearest support group is the Bryn Mawr PD Support Group that meets weekly on Tuesdays at 2 pm at Bryn Mawr Presbyterian Church on Montgomery Avenue. Please contact Debi Weinberg 610-649-1260, Dolly Johnson 610-647-1486, or Suzanne Reichwein 215-829-7273 for more information.

There are support groups throughout greater Philadelphia, New Jersey, and Delaware. There are also groups specifically for newly-diagnosed and early-onset individuals with PD, people with Parkinson's-Plus syndromes, and groups for caregivers. For further information about these additional groups, please contact Suzanne Reichwein 215-829-7273.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

Wishing everyone a very healthy and happy New Year from the Parkinson's Disease & Movement Disorders Clinic!

What medication is appropriate for my tremble?

2012-12-10T11:13:00.003-05:00

Question: I have been taking Sinemet® for several months and I still have a tremble from my head to my feet, but mostly in my shoulder. I tried a drug called Mysoline® and it worked but I could not tolerate it. What medication should I try next?

Answer: This is an important question, but one that is impossible to answer from a distance. Tremors come from many different conditions, including Parkinson’s Disease (PD), Essential Tremor (ET), and other causes. Sinemet® (carbidopa-levodopa) is a medicine commonly used for PD; it acts by giving back the neurotransmitter chemical dopamine which is lost over time in people with PD. Mysoline® (primidone) is commonly used for ET— a familial disease that primarily involves tremor of the hands, head, and/or voice without the stiffness, slowness, or tremor at rest that is seen with PD.

Sometimes, patients have tremors that are difficult to categorize as PD or ET. Often, the answer is only revealed with time when the patient either develops additional symptoms of PD or has a worsening tremor of the hands that is clearly consistent with ET. It is important to think about when your tremor is most bothersome and what things make it better or worse. It would be best to see your neurologist so that your examination can be repeated and the proper diagnosis—and best treatment—can be determined.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

Will green coffee extract interfere with my PD medication?

2012-12-10T10:58:00.005-05:00

Question: I have PD and take Azilect® and Mirapex®. I would like to take a supplement called green coffee extract which is supposed to help with weight loss. Will it interfere with my PD meds?

Answer: Green coffee extract (GCE) is a combination of chemicals present in green (raw) coffee. On average, GCE causes about a five-pound weight loss in research study participants compared to participants given a placebo. It is important to recognize that because it is a supplement, there is minimal oversight of the actual contents in many GCE products available. The Food and Drug Administration, which monitors the production and claims made by companies that produce and market medications, has no oversight for the production of supplements.

With the little information that has been published about GCE, I find no mention of any interactions with Azilect® (rasagiline) or Mirapex® (pramipexole). This supplement is so new that it is actually not listed in the main interaction reference used by most physicians! So, as with most supplements, proceed with caution and buy the product from a reputable store. Watch for side effects and tell your doctors that you are taking a GCE supplement.

Most importantly, while GCE may help with weight loss, the best-studied and most effective strategies are still a healthy, balanced diet and regular exercise. If you can incorporate regular exercise into your daily routine (start gently and try to work up to at least 30 minutes per day, 5 days per week), not only will your waistline see the benefits, but your PD symptoms may, too!

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please call 800-789-PENN (7366) or request an appointment online.

How helpful is a voice amplifier for PD patients?

2012-11-06T15:03:00.005-05:00

Question: My wife was diagnosed with Parkinson's disease seven to eight years ago. Recently, it has been very difficult to understand her because her voice is becoming weaker and it is too low to hear what she is saying. I am very interested in voice amplifiers, which are devices that I have seen listed in many different books. Can you recommend a few of these devices?

Answer: There are many aspects of a person’s speech that can be affected by PD—people can develop hoarseness or a very soft voice. Often, family and friends will notice the voice changes more than the person with PD. Those with low voices may be asked to speak up or repeat themselves, especially on the phone. Other individuals develop slurred speech, or dysarthria—this can often be accompanied by difficulty swallowing and episodes of coughing or choking during meals.

A critical first step is evaluation by a speech-language pathologist (SLP), who is a trained health care professional specializing in the evaluation and treatment of people with speech, voice, swallowing, and language problems. We are fortunate to have terrific SLP staff at the Dan Aaron Center who are experts in PD-related speech disorders. An intervention that has been widely studied and supported by positive results is PD-specific speech therapy, such as the Lee Silverman Voice Treatment. This can have a dramatic impact on the loudness of a person’s voice.

When speech therapy is not enough, voice amplifiers can be used. However, these will only make a person’s voice louder; they will not improve the quality of a voice. Different types of amplifiers are available and a speech pathologist can help match the right device to each individual. Examples of companies that make these devices, and more information on speech problems in PD, can be found at: http://www.parkinsonswny.com/Speaking-Effectively.pdf

Before purchasing a device, discuss the voice problems with a movement disorders specialist and a speech pathologist to find the ideal solution tailored to your wife’s needs. Merisa Palovcak MS CCC-SLP/L, is available for appointments at Penn Therapy and Fitness at Pennsylvania Hospital. To schedule a consultation with Merisa Palovcak or another Penn speech-language pathologist, please call 800-789-PENN (7366) or request an appointment online.

What medications for frequent urination are compatible with PD?

2012-10-15T16:45:00.005-04:00

Question: My father has PD. He's been treated with Levodopa-Carbidopa and Clonazepam. He has trouble sleeping due to a frequent need to urinate (almost every hour). He was given Darifenacin but his neurologist recommended stopping this medication because it interferes with his PD treatment, and it wasn't really helping. Is there another medication that he could take for his sleep disorder/frequent urination that is compatible with his PD medication? Are these symptoms related to PD?

Answer: PD often causes changes in urinary habits, including increased frequency of urination during the day and night, as well as a sense of urinary urgency—that “gotta go right now!” feeling. At least 35 to 40 percent of people with PD have urinary disturbances, most often including increased nighttime urination (nocturia). This is usually due to overactive bladder muscles (detrusor hyperactivity). However, it is important to rule out other common, treatable causes of urinary tract symptoms especially since they occur more often as people age. In men, this may include referral to a primary care physician or urologist to evaluate for prostate enlargement or urinary tract infections. In women, this may start with referral to a primary care physician or gynecologist. If these evaluations do not find another cause, there are several other medicines besides Darifenacin that can be tried.

Like many aspects of Parkinson’s, though, the management of urinary problems must be tailored to the individual patient. Specific medication recommendations vary depending on a person’s age, mental status, other medical problems, and other medications.

Decreasing the amount of fluid that a person drinks in the several hours before bedtime can cut down on some of the nighttime urination. In preparation for your next doctor’s visit, it can be helpful to keep a diary of urinary symptoms including how often you are waking up each night, any urgency or accidents during the day, and how much fluid you are drinking and when. This will help your doctor choose the best approach for you.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please contact 800-789-PENN (7366) or request an appointment online.

Can I use an electric razor after DBS surgery?

2012-10-15T16:43:00.009-04:00

Question: I have recently undergone a DBS surgery. Can I use an electric shaver since I have heard that the electromagnetic fields it produces can be harmful after surgery?

Answer: Great question! The short answer is yes, you can use an electric razor after you have had Deep Brain Stimulation (DBS). Although DBS is an electronic device that can be affected by very powerful electrical or electromagnetic fields—such as power lines, electric substations, airport/security screening devices, and electric steel furnaces—normal household appliances including electric razors, hairdryers, workshop tools, and microwaves should not cause a problem. Scientific literature and the DBS manufacturers confirm this.

Furthermore, in the rare case that you use an electric razor and then notice a change in your Parkinsonian symptoms, you should use your magnetic programmer to check your DBS settings. If a change has occurred or if the device turned off, you can turn it back on and/or reset the device to your regular settings. Keep in mind that DBS is treating the symptoms of Parkinson’s, not the underlying disease process. So, in the very rare event that your settings were to change—because of a trip through airport security or your proximity to a powerful electrical field—remember that the change is easily corrected, will not cause permanent harm, and should be discussed with your doctor.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please contact 800-789-PENN (7366) or request an appointment online.

Is there a connection between glaucoma and Parkinson’s Disease?

2012-10-15T16:43:00.008-04:00

Question: I am a 65 year-old male who was diagnosed with PD one year ago. Yesterday I was diagnosed with the beginning stage of glaucoma. Is there a connection between glaucoma and PD, or PD medications?

Answer: Glaucoma is a condition causing gradual loss of peripheral vision and eventually central vision due to the loss of the nerve cells in the retina. Both PD and glaucoma are relatively common conditions, each occurring in about 2 percent of people over the age of 60. The major risk factors for developing glaucoma include older age, African-American race, a family history of glaucoma, and elevated pressures within the eye. Having near-sightedness (myopia), cardiovascular disease, high blood pressure, diabetes, or hypothyroidism can also increase your risk of glaucoma. Certain drugs—including anticholinergic medicines like benztropine and trihexyphenidyl, COMT inhibitors like entacapone, tolcapone, and components of combination pills like Stalevo®—have the potential to worsen glaucoma.

Two very small studies (Yenice et al., 2008, Bayer et al., 2002) have suggested a possible connection between PD and glaucoma, but at the moment, this is far from being proven. We know that the retinal nerve cells in glaucoma show a similar pattern of injury as some injured nerve cells in PD (a process of cell death called apoptosis). So far, that is the only link between PD and glaucoma, other than the medications above.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please contact 800-789-PENN (7366) or request an appointment online.

How does deep brain stimulation (DBS) work?

2012-04-09T16:43:00.006-04:00

Alice Chen-Plotkin, MD, assistant professor of neurology, explains deep brain stimulation (DBS) as a therapeutic option for Parkinson's disease and describes how it works.

Question: What is deep brain stimulation (DBS)? How does it work?

Dr. Chen-Plotkin responds: A deep brain stimulator (DBS) is an electronic device implanted by a neurosurgeon into the brain. It can be controlled externally to send electrical impulses at a particular strength (amplitude) and frequency to the electrodes implanted in the brain.

For patients with Parkinson's disease, the most common placement for the electrodes is in a deep area of the brain called the subthalamic nucleus, or STN. Because of how the brain is wired, signals from the STN tend to decrease the overall message for the body to be able to move smoothly and easily. By stimulating the STN in a particular way, doctors are able to "cancel" the signal to depress movements. This often helps Parkinson's patients with their bradykinesia (slow movements or less movement) as well as other symptoms.

Clinicians stimulate the STN with a regular train of electric impulses, although they can increase/decrease the amplitude of the impulses and increase/decrease the frequency of the impulses. Sometimes, changing the settings on the stimulator (amplitude or frequency) can optimize the performance for DBS in controlling PD symptoms. It is important to note, however, that DBS, like levodopa, treats the symptoms of PD, not the underlying process of neurodegeneration. So, over time, as more and more neurons die, it may become harder and harder to manage PD symptoms, even with DBS adjustments.

What is the Connection Between Music and Movement in PD Patients?

2012-02-23T11:11:00.004-05:00

Alice Chen-Plotkin, MD, assistant professor of neurology, explains why certain triggers seem to help PD patients move during a “freeze.”

Question: I am 62 years old and have had Parkinson's for 14 years. I was a professional dancer/choreographer for 30 years. These past two years, I've been taking dance classes and performing again on occasion. I am taking small doses of levodopa (Parcopa®) plus small doses of Requip® about eight to 10 times a day. I am generally stable with minimum down time and a type A personality.

While I'm waiting for the medicine to work, I cannot walk. However, if I put on music, I can execute and perform dance steps. For example, if I focus on my hips and do a mambo or cha cha step with my feet, I can move forward. Is there a connection between movement and music in how the brain works?

Dr. Chen-Plotkin responds: It is not uncommon for PD patients to find that certain "triggers" can help them move, even in the midst of a freeze. I wish I could answer this in a more precise way! However, all I can say is that your experience is not uncommon. Many PD patients notice that by executing a particular motor program -- in your case, dance steps you know very well -- they can somehow "bypass" the freezing associated with Parkinson's disease.

Our best understanding has to do with how the brain may be wired. The main areas that malfunction in Parkinson's disease are the substantia nigra dopaminergic neurons, which then project to the basal ganglia of the brain. This basal ganglia system then seems to send a signal to the thalamus (a kind of deep-seated control center of the brain) to increase movement. It is possible that with some memorized activities with which you are very familiar, you are somehow bypassing this basal ganglia circuit.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please contact 800-789-PENN (7366) or request an appointment online.

Can Supplements Provide “Neuroprotection” for PD Patients?

2012-02-14T13:53:00.005-05:00

Alice Chen-Plotkin, MD, assistant professor of neurology, discusses neuroprotective” benefits for patients with Parkinson's disease.

Question: I am 65 years old and was diagnosed with PD about a year ago. I am looking for neuroprotective supplements that I can take with my PD medication. Specifically, is there any evidence that B12 or fish oil help or harm neuroprotection?

Dr. Chen-Plotkin responds: Frequently, the question comes up of how one might "protect" one's brain against further neurodegeneration, or slow the process down.

Unfortunately, there is not much evidence the various vitamins of dietary supplements (such as B12 or fish oil) provide neuroprotection from Parkinson's disease. There is a small amount of evidence that the medication rasagiline (also called Azilect®) may have a little neuroprotective benefit early in the disease. It's not a huge benefit, and the evidence is not irrefutable, but it is there.

In addition, there is evidence that exercise may be helpful (and certainly is not harmful) in protecting against further neurodegeneration. I recommend consulting with your physician.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please contact 800-789-PENN (7366) or request an appointment online.

Can PD medications cause a bitter taste in the mouth?

2012-01-06T13:37:00.003-05:00

Alice Chen-Plotkin, MD, assistant professor of neurology, talks about taste and loss of appetite for patients with Parkinson's disease.

Question: My dad takes generic Sinemet® (carbidopa/levodopa) 25/100 mg for PD. He is experiencing severe bitter taste in his mouth that has lasted over one year. He is losing weight (15 pounds in two months) because he can't tolerate the taste of food. Can the medication be causing the bitter taste? Would taking the brand-name medication alleviate the problem?

Dr. Chen-Plotkin responds: It would be pretty unusual for carbidopa/levodopa to be causing a bitter taste in the mouth -- I don't think I have ever had a patient with this particular side effect. It's possible, however, that your father has altered taste sensation from the Parkinson's disease itself.

One of the parts of the brain affected earliest by the process that causes PD is smell. Thus, many PD patients suffer from some difficulty with smelling. Luckily, most people barely notice this. However, sometimes the difficulty with one's sense of smell (olfaction) manifests as things tasting “funny.” This is because one's sense of smell is closely related to what is experienced as taste.

Alternatively, the medication may be causing some nausea which your father experiences as altered taste and loss of appetite. If this is the case, most of the time it is due to the levodopa part of the medication being broken down outside of the brain, where it is converted and used. The carbidopa part of the medication usually prevents this from happening but for some people, the ratio of 25 parts carbidopa to 100 parts levodopa is not quite enough and a higher dose of just the carbidopa part of the medication may be helpful.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please contact 800-789-PENN (7366) or request an appointment online.

Do panic attacks prevent me from having deep brain stimulation (DBS)?

2011-12-21T16:28:00.006-05:00

Alice Chen-Plotkin, MD, assistant professor of neurology, answers a representative question about deep brain stimulation (DBS) as a neurosurgical option for some Parkinson's disease patients.

Question: I have had Parkinson’s disease for about eight years. My doctor says I am not a candidate for deep brain stimulation (DBS) because I have had panic attacks in past. Should I get a second opinion?

Dr. Chen-Plotkin responds: Anxiety, depression and panic attacks by themselves are not contraindications for DBS. In general, when I am trying to decide whether or not to refer someone for DBS, I consider a couple of things.

• Does the patient have contraindications – are there reasons that he or she might have bad outcomes? The major contraindications are general medical problems that might make brain surgery risky and cognitive impairment (problems with thinking). DBS requires tunneling electrodes through the brain. By necessity, the procedures must shear some neuronal processes. Sometimes, patients can have a marked increase in cognitive impairment after the surgery.

• Does the patient stand to benefit from the surgery? A simple way to think about DBS is that it is an electrical method for achieving the same results that some PD medications provide. As a result of DBS, most PD patients are able to decrease the amount of dopamine they take. With this decrease in dopamine, they often experience a substantial decrease in the medication side effects (like dyskinesia). So, for those people who constantly fluctuate between being "off" and having dyskinesia, DBS may be a good option.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please contact 800-789-PENN (7366)or request an appointment online.

What is the difference between tremor caused by anxiety and tremor from Parkinson’s disease?

2011-12-16T10:46:00.005-05:00

Alice Chen-Plotkin, MD, assistant professor of neurology, answers a representative question about what makes a tremor “parkinsonian.”

Question: I am 65 years old. I have had generalized anxiety for nearly 10 years. I developed left hand tremor about three months ago and it is getting worse with time. This occurred along with a C-spine problem (neck and left shoulder pain). Otherwise, I am in pretty good health. I started taking Lexapro® and receiving physical therapy. It seems the Lexapro® and physical therapy make the tremor much better for awhile, but it's not completely gone.

Are there differences between anxiety tremor and PD tremor? And is there a possibility that nerve root pressure (radial neuropathy) can cause hand tremor? I've seen two different neurologists. One said it's PD, the other one is undecided.

Dr. Chen-Plotkin responds: There are many causes of tremor, only one of which is Parkinson's disease. Under conditions of stress and anxiety, many people exhibit physiological tremor, which is totally normal.

That said, certain characteristics are more typical of a tremor due to Parkinson's disease (PD). First, the PD tremor is usually most prominent at rest -- when you are not doing anything with your hand or when it's lying in your lap. Second, the PD tremor tends to be slower than an anxiety-provoked tremor. If you were to measure its frequency, you might find that the PD tremor is at about 5 Hz — roughly the same speed a dog shakes off water. Third, the PD tremor is often lateralized, meaning more prominent or possibly only seen in one hand, rather than being equally visible in both hands. These are not hard-and-fast rules, but rather clues to what might be more typical for PD.

At the end of the day, I suggest a few possible practical courses of action:

1. Ask the undecided neurologist what the possibilities in his/her mind are.

2. If you are still not sure what is going on, you can always see a movement disorders specialist. I would suspect that most can tell you with a fair amount of certainty whether or not the tremor looks parkinsonian.

3. If the tremor is becoming a major problem in your life and there is a suspicion that it is due to PD, you could consider trying PD medications for it. If it responds, that's a pretty good sign that it's due to PD.

For more information about Penn’s Parkinson's Disease and Movement Disorders Center, or to schedule an appointment with a specialist, please contact 800-789-PENN (7366). You can also request an appointment online.