QUESTIONS AND ANSWERS:
How do you make a diagnosis of Parkinson's Disease?
Parkinson's Disease is diagnosed by the presence of bradykinesia (slowness of movement) associated with at least one of the following three signs: resting tremor, cogwheel rigidity, and/or gait disturbance (shuffling, balance impairment). There is a gradual loss of the brain's ability to produce a neurotransmitter chemical called dopamine. Medications designed to treat Parkinson's Disease enhance dopamine neurotransmission by either acting as the fuel to make more dopamine or to simulate the actual dopamine chemical itself.
What is the difference between typical and atypical Parkinson's Disease?
Atypical Parkinson's Disease (Parkinson's plus syndromes) are characterized by a rapid progression, lack of response to medications, and a severe balance impairment from the very beginning of the disease. These syndromes go under different names.They are characterized by a lack of the ability of the brain to receive dopamine in addition to the lack of the brain to produce dopamine. Syndromes include: Striatonigral Degeneration, Progressive Supranuclear Palsy, Olivopontocerebellar atrophy, Shy-Drager Disease and Corticodentatonigral degeneration. These patients have a rapid progression of balance impairment and are typically not able to walk unaided after 4-6 years.
Is there any way of slowing the progression of Parkinson's Disease?
There is no proven way of slowing the progression although Azilect may have a disease modifying effect at the 1 mg a day dose and dopamine agonists may help to keep the areas of the brain that receive dopamine healthy for longer periods of time. I start patients with early-onset PD on Azilect and then add a dopamine agonist in an attempt to delay progression. Staying active mentally and physically with the aid of exercise aimed at strengthening the legs seem to keep patients walk better. Other medications under investigation include/have included Co-enzyme Q10 and NADH.
Do Parkinson's Disease patients have dementia?
Dementia is defined as having cognitive impairments that are severe enough to effect the ability of a patient to function with activities of daily living and/or working. Most patients do not have dementia until very late in the disease if at all. There is a form of Parkinson's Disease called Diffuse Lewy Body Disease, in which dementia is the presenting symptom. These patients are very sensitive to the medications used to treat the physical symptoms of Parkinson's Disease and frequently develop hallucinations and confusion from low doses of L-Dopa. Medications approved for the treatment of Alzheimer's Disease often help the attention, concentration and memory deficits. Medications that prevent hallucinations like Seroquel enable the use of enough L-Dopa to treat the patient's rigidity and slowness.
Do people die of Parkinson's Disease?
No. Not of Parkinson's Disease itself. Patients die as a consequence of the balance impairment associated with Parkinson's Disease. They fall. In addition, patients may develop infections (usually infections of the urinary and respiratory systems). Patients with dementia have a worst prognosis than patients who are cognitively intact.
Is it important to take the medications on time?
Yes. Very important. Patients must alter their lifestyles in order to gain the ability to predict when they will be able to best function. They should wake up and go to sleep the same time every day. They must eat the same times every day. Medications should be taken at least one half hour before meals and/or one hour after meals if three meals a day are taken. The proteins in food interfere with the absorption of L-DOPA; the lunch meal can make or break the ability of the medications to work in the afternoon and should consist of low protein.
What is the difference between tremor and dyskinesia?
Tremor is manifested by an oscillating repetitive movement. A tremor at rest is a symptom of Parkinson's Disease. Dyskinesias are writhing and twisting movements. Patients with duskinesia may sway while standing. Dyskinesias are due to the medications used to treat Parkinson's Disease.
Is constipation common?
Yes. Patients must eat lots of fruits and vegetables, salads and cereals and drink as much fluids as they can. Colace and Senekot taken every day can help. An oral laxative may help if a bowel movement does not occur after one day. Glycerin suppositories or enemas may be helpful if no bowel movement occurs after 2 days. If no bowel movement occurs after 3 days, fecal disimpaction from the rectum is often necessary followed by an enema.
Are alterations in blood pressure common?
Yes. Patients may develop low blood pressure upon standing. This could be due to medications or the Parkinson's Disease itself. Alternatively, these same patients may develop high blood pressure during the night when lying down. Treatments for low blood pressure include avoiding medications that lower blood pressure, fludrocortisone (Florinef) and midodrine (ProAmatine). Treatments for high blood pressure include raising the head of the bed using blocks placed under the headboard legs. Some patients may have significant alterations of blood pressure all day long. In this case, treating the low blood pressure that occurs upon standing and preventing feinting is most important.
Are urination problems common?
Yes. The urinary bladder may be overactive, especially at night when patients produce more urine because of the increase in blood pressure in the torso which is communicated to the kidneys as more blood volume. Patients may need to void several times during the night and this can lead to falls because of poor lighting and balance.
What happens as Parkinson's Disease progresses?
The balance impairment and/or cognitive impairments usually worsen. This often happens over decades. Most patients do very well for a long time if they see their specialist at least three times a year., sooner if alterations in drug schedules are made or if problems develop. Mt patients see me about every three months.
Is L-DOPA harmful? Should patients wait as long as possible before starting L-DOPA?
There are two facts that have been scientifically proven : 1) that patients who take L-DOPA do better than patients who do not take L-DOPA over time and 2) that patients who take L-DOPA alone develop on/off fluctuations after 5-10 years of treatment which would not have occurred if those patients were maintained on dopamine agonists and/or Azilect although they may have been more disabled without the addition of L-DOPA. The moral of this story? Use dopamine agonists and Azilect early and bring the doses of the dopamine agonist up to the maximal amount the patient can tolerate but do NOT hold off on using L-DOPA if needed to maintain a patient in as near a normal condition as possible. HOWEVER, use the least amount of L-DOPA that you need and have most of this L-DOPA be controlled release with amplification by MAO-B (Azilect) and COMT inhibitors (Comtan) . For example- a 52 year old female with PD for two years who is still trying to work is seen by me and is obviously very slow with moderate PD. She is taking Requip 3mg/day but is very sedated. I start her on Sinemet CR 25/100 twice a day and amplify it with Azilect. She looks great. Requip may need to be lowered if sedation persists.
My belief is to get people better and then keep them better. This is how I fight Parkinson's Disease.
L-DOPA therapy has never been proven to be harmful. Patients do not develop a tolerance to L-DOPA as they would with narcotics. It is my belief based on clinical experience with thousands of patients over the last 28 years that it is the duration of disease and not the duration of therapy which leads to an increased sensitivity to L-DOPA. I believe in treating the symptoms of Parkinson's Disease aggressively in order to get patients as better as possible and then to make adjustments using whatever means necessary to keep them better.
What happens when patients become sensitive to L-DOPA?
Patients experience a "wearing off" of the beneficial effects of L-DOPA 3-4 hours after a dose after several years of having Parkinson's Disease. This is usually easily corrected. After 10-13 years of Parkinson's Disease, patients begin to experience times when the medication works too much and times when the medications work too little. They eventually can become brittle in response to the medications. These "wearing off" and "on/off" fluctuations can develop within months of starting L-DOPA therapy in patients who have had Parkinson's Disease for 10 or more years. Don't take a "wait and see" attitude! Early treament with the right medications will have an effect on you years and years from now!
How do you treat patients who develop "wearing off" and "on/off" fluctuations?
Decrease the amount of immediate release Sinemet, add CR Sinemet and a COMT-inhibitor (Comtan) or MAO-B inhibitor (selegiline or Azilect) and use dopamine agonists. Decreasing the interval between doses also helps. The rotigitine patch will be of great help because it provides a continuous release of medication.
What is Sinemet?
Sinemet is the most commonly prescribed medication used to treat patients with Parkinson's Disease. It is a combination of L-DOPA and carbidopa. The L-DOPA is the fuel for the brain to make dopamine. The carbidopa is an enzyme inhibitor (dopa-decarboxylase inhibitor) which allows the L-DOPA to get into the brain better thus alleviating the nausea associated with L-DOPA administration. The Sinemet dose has 2 numbers: the first is the amount of carbidopa; the second number is the amount of L-DOPA. Thus 25/100 means 25mg of carbidopa and 100mg of L-DOPA. It is important to note that there are two carbidopa-levodopa preparations that have the same ratio:25/100. One is immediate release and the other is a controlled/extended release preparation.
What is the difference between L-DOPA and a dopamine agonist?
L-DOPA is the fuel which the brain uses to make dopamine. A dopamine agonist acts like dopamine and directly stimulates the areas of the brain which normally receive dopamine. Dopamine agonists therefore bypass the degenerating neurons which are affected in Parkinson's Disease. One analogy I like to use is to compare the area of the brain which lacks dopamine to a farmfield. Imagine a plot of land which has 100 plants spaced apart equally. Now imagine that there is one sprinkler to every ten plants. If 80% of the hoses to the sprinklers is cut off only 20% of the plants will receive the proper hydration and will live. What can you do to save the remaining plants? You could pump more water out of the remaining sprinklers which is what L-DOPA administration does- it pumps more dopamine out of the remaining neurons. Dopamine agonists act like rain on the farmfield to keep all the plants alive. Dopamine agonists directly stimulate the caudate nucleus and putamen keeping these areas of the brain healthy. They do not force the remaining neurons (which are stressed and dysfunctional already) to make more dopamine. I believe that the use of dopamine agonists prevents the progression of dementia and balance impairment in patients with Parkinson's Disease.
What are the side effects of medications used to treat Parkinson's Disease?
Too much medication may cause psychosis and dyskinesia. The dopamine agonists derived from ergotamine (pergolide and bromocriptine) may rarely cause heart valve problems, fluid around the lungs, and circulation problems. The non-ergot derived dopamine agonists (Mirapex and Requip) can cause sleep attacks and obsessionalisms. There is a potential interaction between the MAOB inhibitors and sudafed (a common allergy medication). For a complete list of side effects patients should contact their physicians.
What is done to treat psychosis induced by the medications used to treat Parkinson's Disease?
The medications must be changed. In some cases certain medications must be discontinued. Anti-psychotic medications such as Seroquel in low doses may allow the physician to treat the psychosis without lowering the medications needed to help movement.
What is the pacemaker surgery?
This is an operation in which a jamming electrode (pacemaker) is inserted into a part of the brain called the subthalamic nucleus. This part of the brain becomes overactive as a consequence of low dopamine. The major benefit of the surgery is to stabilize the clinical "on/off" fluctuations in response to the medications used to treat Parkinson's Disease.
Who is a candidate for the subthalamic nucleus deep brain stimulator (pacemaker) surgery?
Any patient who manifests severe "on/off" fluctuations despite aggressive medical therapy. Candidates are often very sensitive to small amounts of L-DOPA so that even a slight increase from 1/4 to 1/2 tablet causes wild involuntary movements followed by deep and prolonged periods of slowness ("off") periods. It is important that patients see a neurologist specially trained in treating Parkinson's Disease before deciding to have this surgery.
What are the risks of subthalamic deep brain stimulation (pacemaker) surgery?
It is best to discuss the risks with the surgeon. There is a small risk of bleeding. The major risk is that patients with moderate cognitive impairments may have a worsening of concentration and attention following this procedure.
Does the pacemaker surgery stop the progression of Parkinson's Disease?
No. This has never been proven. Patients may continue to fluctuate in response to the surgery. There are no guarantees that the surgery will help.
What nutritional supplements do I recommend? CoQ10 (1200 mg/day), NADH (20 mg/day), Vitamin D3, creatine and selenium as well as B vitamins and folic acid.CEREFOLIN WITH NAC is a great source of B complex vitamins and N Acetyl Cystine which can now be sent directly to the Brand Direct Health Pharmacy for cost savings. Their phone number is 866-331-6440. Patients with Parkinosn's Disease, in my experience, feel better when taking this prescription strength vitamin complex.
Is chelation helpful? Only if it is proven that you have high levels of metals in your body.
Is Azilect and selegiline interchangeable? Do not let your pharmacy take you off Azilect and put you on selegiline. They are two different drugs. Selegiline is not the generic version of Azilect (rasagiline). Only Azilect at 1 mg/day has been demonstrated to have a strong trend towards disease progression modification.