I am a board-certified neurologist with subspecialty training in Movement Disorders and a PhD in Behavioral Neuroscience. My neurology residency was at Boston University (1984-87) where I also received my PhD and my Movement Disorders fellowship was at Columbia-Presbyterian (1987-89).

I am also a specialist in the diagnosis and treatment of dystonia. Dystonic cramps may occur in patients with Parkinson's disease but there are patients who have a disorder called adult onset focal idiopathic dystonia who do not have Parkinson's Disease. Adult-onset focal dystonia usually affects the head and neck and patients usually present with head turning or tilting (spasmodic torticollis) or excessive blinking (blepharospasm). I consider myself one of the most experienced chemodenervation specialists; I have been using BOTOX (R) for the treatment of dystonia since 1987. The experience of the injector makes all the difference in the world to the outcome of those injections.
The Treatment of Parkinson's Disease is an art- Not every neurologist and to be quite honest, not even every Movement Disorders specialist has as much expertise in this art as I do.I HAVE BEEN DOING THIS SINCE 1984! COME SEE ME WHAT ARE YOU WAITING FOR!!! You must realize: There are 8 types of Carbidopa-Levodopa preparations (Sinemet 10/100, 25/100, 25/250, Sinemet CR 50/200 and CR 25/100, Parcopa 10/100, 25/100 and 25/250), several Carbidopa-Levodopa-Comtan preparations (Stalevo 50, 75, 100, 125, 150 and 200), 2 dopamine agonists (Mirapex and Requip), 3 MAO-B (selegiline oral tablets-Eldepryl and selegiline dissolving wafers-Zelapar and rasagiline-Azilect and sufinamide Xadago) and 2 COMT inhibitors (Comtan and Tasmar). There also exist three anticholinergics (artane, cogentin, akineton)and amantidine and medications used to treat other neurological conditions (Proamatine, Florinef, antidepressants, antiepileptics like Zonisamide, Aricept, Namenda, Exelon and Seroquel) which are very important in the treatment of Parkinson's disease. THESE MEDICATIONS WORK DIFFERENTLY IN DIFFERENT PATIENTS AND YOU MUST SEE ME IF YOU WANT TO HAVE THE BENEFIT OF MY 28 YEARS OF EXPERIENCE. I have been treating patients with Parkinson's Disease since 1984. I have the ability to not only use the available medications in a specially and personally designed way FOR YOU but also to enroll you in trials with medications that will not even be on the market for 3-5 years. For example, my patients who were enrolled in the rotigotine dopamine agonist time-release patch had been receiving and benefiting from this therapy from 2004; the rotigotine patch was not available in the United States until mid- 2007. YOU DO NOT NEED TO CHANGE YOUR CURRENT NEUROLOGIST-GIVE ME 3 WEEKS TO ADJUST YOUR MEDICATIONS AND SEE THE DIFFERENCE IN YOUR PHYSICAL AND MENTAL FUNCTIONING. Learn more about me by searching my name on google and see my publications on the EntrzPubMed below. You may also see my profile on the NYU web site and click on find a doctor.
Call 212-983-1370 for Manhattan appointments (40th and Lexington) and for appointments in New Rochelle (838 Pelhamdale Avenue), or Long Island (Westbury).
My patients have the ability to contact me on my cell phone in an emergency AND to make an appointment to see me THAT DAY if needed. You will NEVER find this level of availablility in any Movement Disorders specialist with my level of expertise.
Nuplazid is now available! It is a medication designed to treat hallucinations, delusions, paranoia and other psychotic symtoms that may occur in patients (usually with dementia)  that are taking medications to treat their physical symptoms of Parkinson's Disease. Nuplazid is a game changer. It is the first antipsychotic that does NOT block dopamine receptors. It only alters the function of a few subsets of serotonin receptors. Therefore, it would not be expected to cause sedation or cause the Parkinson's Disease symptoms to worsen. It could potentially block the side effect of these medications patients need to move, enabling us to increase those medications in order to help those patients. 

RYTARY is a new form of controlled release Carbidopa-Levodopa that has become available as of the Spring or 2015. The RYTARY 195 is roughly equivalent to the Sinemet CR 25/100. RYTARY is superior to either the controlled release or immediate release Sinemet preparations on the market because it is much better quality controlled and it works as fast as the immediate release but lasts as long as the controlled release generic preparations currently available. 


Horizant is a medication that can help control restless leg syndrome (RLS) , especially if it exists in Parkinson's Disease patients. It is a long acting form of gabapentin (gabapentin enacarbil) that is absorbed throughout the small and large intesting giving smooth levels of relief all night and day unlike gabapentin which is only absorbed in the proximal small intesting by a saturable amino acid transport mechanism and has to be dosed three times a day. Horizant for RLS needs to be dosed only once a day which is just after dinner. RLS is a condition where patients experience severe uncomfortable sensations in their legs, worsened during periods of inactivity especially at night and made better by movement. Some conditions like iron deficiency can mimic RLS and need to be ruled out. Horizant is indicated for primary moderate to severe RLS. 

DUOPA is a form of L-DOPA paste that can be infused by a pump into the small intestine. Sounds crazy? To have a tube placed in your small intestine with an L-DOPA pump? It's not. If it were me, and I was looking at having two electrodes implanted in MY brain (subthalamic deep brain stimulators) for impossible to control with medication "on-off" fluctuations, I would seriously consider trying this out. It is safer than brain surgery. If it doesn't work, you pull the tube out. OK, now how about those patients who need the DBS surgery but have dementia and the surgeons do not want to operate on because the dementia might get worst? The DUOPA is the treatment of choice for this group of Parkinson's disease patients: horrible "on-off" fluctuators on every available medication with dementia and hallucinations. And DUOPA is covered by most insurances. 

Droxidopa is now available for patients with orthostatic hypotention that have failed Florinef and Midodrine and the reduction of medications used to treat Parkinson's Disease that can lower blood pressure. 


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.



Update on Gene Therapy: 

In gene therapy, a virus is used as a vector to deliver a protein. The majority of the viral genome is removed and the RNA of the desired protein is inserted into the viral vector . Once the RNA is delivered to the target neuron by "infecting" that neuron, the RNA it is converted from RNA to DNA by reverse transcriptase and the new DNA material will now code for the production in that neuron of the new protein. The varying factors are what proteins to inject and where to inject them as well as which virus is used . Other issues are what happens to the virus and protein after it is made and/or injected, how long will the new protein be expressed, what is the safety of the entire procedure and does it work. The three types of proteins which have been used are 1) those which make dopamine (AADC, tyrosine hydroxylase and GTP cyclohydrolase) inserted into the striatum and substantia nigra, 2) proteins to inhibit the overactive neuronal activity in the subthalamic nucleus (just like deep brain stimulation/jamming surgery) and 3) neurotrophic substances (GDNF, neurturin) which help the neurons to survve, sprout and make new connections which are inserted into the striatum.  The AAV (adeno-associated virus vector) virus is generally regarded as the standard viral vector because it does not cause disease in humans or produce inflammation, is defective for replication, does not integrate into chromosome, and has persistent (more than 4 years) of expression.  In addition to the delivery viral vector, there is thought to be a need for a regulator vector which could turn on or off the production of the gene product especially in case of uncontrolled growth or toxicity but the use of these regulator viral vectors has not been tested in humans and may itself cause side effects. Clinical trials with all of these proteins has shown benefit in a small number of patients but there has never been a double blind scientifically controlled study that has proven efficacy and long term safety. Potential problems with gene therapy are 1) unregulated growth of virus, 2) unregulated expression of gene and protein, 3) possible immune reactions including rejection, 4) benefits not yet confirmed in doule blind trials and 5) there is a real risk of unanticipated side effectssuch as off medication dyskinesia, tumors or cancer (insertional mutagenesis).

Update on Dopamine Cell Transplantation for PD:

Transplantation therapies offer the potential to replace degenerating dopamine neurons and to restore physiologic dopaminergic innervation to the striatum. Fetal substantial nigral transplantation has been shown to survive, reinnervate the striatum, manufacture and release dopamine and reverses animal models of parkinsonism. However, the conclusions of the Colorado/Columbia Transplant study which used a double blinded study design did not successfully demonstrate the efficacy of this therapy. Moreover, more than 50% of the patients receiving transplantation developed off medication dyskinesia (dyskinesia which persists for more than 12 hours off medication) which was so severe that some patients needed to get the deep brain stimulation surgery. These off medication dyskinesia were asymmetric and primarily affected the legs. In one of the most interesting developments, it has been reported that in a few patients that have had fetal transplantation and who have died from other causes, it has been found that the transplanted neurons themselves have developed PD-like changes (Lewy bodies) implying that the new fetal tissue has developed PD.  This is still being investigated (possible environmental influence (prions??) on these implanted cells or there were changes induced by the transplantation process itself). The conclusions on dopamine cell based transplantation therapies is that 1) all the double blinded trials have failed to show efficacy 2) off medication dyskinesias have been reported in more than 50% of patients 3) the dopamine transplants are not likely to benefit the non dopaminergic features of PD, 4) the implanted cells themselves seem to demonstrate PD pathology and may not function normally and it can be therefore concluded that the future of dopamine cell based transplantation therapy is questionable at this time.

Non-fetal cell transplantation offers a much more viable alternative to a fetal cell source. Although President Obama has allowed federal funding for experimentation on existing fetal cell lines the Dickey-Wicker amendment prevents the creation or destruction of human embryos. As above described, fetal mesencephalon does not seem to work anyway. More attractive is to derive cells from the patients themselves. For example, skin cells from PD patients could be reprogrammed into pluripotential stem cells that maintain their embryonic properties after potentially cancer causing genes are deleted and re-grown into dopamine producing neurons. The use of tissue from the patient lessens the risk of rejection although that never was an important factor in fetal transplantation.

The problem with cell transplantation is that there may be an increased risk of malignancy (brain cancer) in patients receiving such therapies. I have seen firsthand a patient who received autologous adrenal medullary tissue in 1988 (adrenal medulla tissue produces catecholamines like dopamine and can be taken from the patient's own body) who developed fatal cerebral malignancy.


Attempts are underway to try to decrease the production of this compound which is the major component of Lewy bodies or to increase the removal of this compound from neurons.



Goals are to protect neurons from dying and interfere with the pathological mechanisms that lead to neuronal dysfunction. Most studies on neuroprotection rely on animal models of PD. Neurotoxins that kill dopaminergic neurons are 6 hydroxydopamine, MPTP and compounds such as rotenone and paraquat. These neurotoxins produce motor symptoms, are useful to develop and test symptomatic treatments, have effects which are similar to observations seen in the brains of patients with PD and are widely used to test neuroprotective therapies. Advantages of using these neurotoxins in animals are that they reproduce the loss of dopaminergic neurons. The limitations are that the relationship to PD mechanisms is uncertain. PD affects many systems: motor (bradykinesia, rigidity, and tremor), postural imbalance, olfactory loss, cognitive decline, depression/anxiety, sleep disturbances, hypotension and constipation.

Gene defects implicated in familial PD include alpha synuclein mutations, Parkin, gene multiplication, PINK-1, GJ-1 and LRRK2 dardarin. Some of these mutations can be produced in animals. The neurotoxin models of neuroprotection view the primary pathology as a loss of dopamine neurons. The genetic models view the pathology as starting outside the substantia nigra by virtue of genetic mutations some of which are relevant to sporadic cases of PD which form the majority of cases of PD that are seen. Neuroprotection has been elusive. The question remains that this may be a virtue of problems with the models both environmental and genetic that are used in causing PD models in animals. The three most important characteristics of an animal model of PD are relevence, relevance and relevance. A good model would be based on disease mechanisms and be able to predict clinical efficacy.

Alpha synuclein overexpression may provide a clear link between mutation-linked mechanisms and sporadic PD. One alpha synuclein overexpressor (ASO) is thy 1-asyn which causes an increase in the production of alpha synuclein. This genetic mutation does seem to mimic in mice many of the non-motor symptoms of PD mentioned above which are seen in humans. Therefore, this is one model being looked at to test neuroprotection in PD. One other mutation is called DJ-1 in which deficiencies produce mitochondrial dysfunction by virtue of the lack of protection against oxidative stress. However, "knock out" mice with this genetic deficiency of DJ-1 DO NOT manifest a loss of dopamine neurons unless a second hit, ie a toxic environmental event occurs. For example, if these knock out mice with DJ-1 mutations are fed a diet low in selenium they will develop PD. This underscores one of the problems with neuroprotection models: Genetic and environmental influences are BOTH necessary in causing PD and it is almost impossible to develop a system of delaying neuroprotection without having a true animal model of PD.

Nevertheless, numerous attempts have been made to try to delay the progression of PD. In the DATATOP study it was suggested that selegiline delayed progression but it was not known at the time that selegiline had a symptomatic effect on treating PD and that a wash out of three months was needed before the drug effects truly wore off. Here the endpoint was the need to take L-DOPA and motor progression was also examined. Numerous other drugs have been tested and so far have not been demostrated to slow down disease progression (L-DOPA, CoQ10, neurotrophic factors, dopamine agonists, amantidine, Neuroimmunophilin A, riluzole, vitamin c and others).

Imaging studies have also been used to try to measure dopamine decline in the brain. Radioactive tracers such as 18fluro-dopa PET scans and beta-CIT scans can measure dopamine production and its decline. In many cases the clinical outcomes suggest neuroprotection but the imaging studies do not. This may be due to pharmacological modulation of RTI (radioactive tracer imaging) binding sites or disease progression related to non dopamine systems.

The delayed start design has been developed as a new technique to measure progression trying to dissect symptomatic versus disease modifying effects. In the ADAGIO study patient groups were rasagiline 1 mg/day, placebo and then delayed start rasagiline 1 mg/day, placebo and then delayed start rasagiline 2 mg/day or rasagiline 2 mg a day. Patients had placebo or active drug for 36 weeks and then the delayed start occured and patients were studied for another 36 weeks. The key finding was a small divergence in the curves measuring progression of disease during the first 36 weeks in the patients taking rasagiline 1 mg not 2 mg as compared to placebo. This divergence was not as strong once the rasagiline was started and disease progression was measured in either group; in other words the disease progressed faster in patients on placebo than rasagiline during the first 36 weeks but equally in patients who had initially been on placebo or rasagiline from the beginning in the second 36 weeks. Suffice it to say- these were not highly significant results but there was a suggestion of disease modification in early PD with 1 mg/day rasagiline. Why 2 mg/day of rasagiline did not give as good a benefit as 1 mg/day rasagiline is not known. The study may have been over powered with a too short trial period and patients enrolled with too mild symptoms. Nevertheless, patients followed for up to six years on 1mg a day of Azilect do seem to have less Parkinson's disease signs and symptoms than patients on placebo or with a delay in the start of Azilect therapy.  I believe that Azilect at 1mg a day does delay disease progression and I try to give it to all of my patients.

The PROUD study looking at whether Mirapex (pramipexole) might delay progression employed 535 subjects over 15 months and used 1.5 mg/day of Mirapex (not a high dose of drug since up to 4.5 mg/day is used in clinical practice). There was no difference noted between early and delayed start patients or in RTI (beta CIT SPECT scans) implying no disease progression prevention at that dose of Mirapex during that length of time. Higher doses and longer durations might have been necessary. As you will read below my bias is towards a neuroprotective effect of dopamine agonists but again, it depends as to how you measure progression (is it of cognitive decline or number of falls due to balance impairment?).

There are numerous trials underway to find some better way of measuring disease protection through the use of unbiased biomarkers. We still do not have a great way of measuring disease progression. In the NET-PD FS1 and FS2 study creatine, minocycline, CoQ10, neuroimmunophillan ligand A and placebo are being investigated to compare these patients to the placebo treated patients of the DATATOP study which is now considered a historical control because those patients have now been followed for many years. Creatine has been shown to be of some benefit.

In the SURE-PD study uric acid is being studied as patients with PD have been found to have low uric acid levels. Inosine treatment is being given to raise the uric acid levels and the safety and efficacy of this treatment is being studied.

REQUIP XL AND MIRAPEX ER (controlled release dopamine agonists)

REQUIP-XL: The conversion from Requip immediate release to the extended release tablet is approximately 1mg to 1mg so that patients taking 12 mg per day (3 doses of 3mg) of immediate release Requip can be placed on one tablet of 12 mg Requip XL. Patients on other dopamine agonists can be converted to Requip XL in order to acheive a smoother control of Parkinson's Disease symptoms.

The maximum suggested dose of Requip XL is 24 mg/day. New dopamine agonist patients can start on 2mg/day and gradually increase the dose by 2mg/day/week. A dose of around 8-12mg/day is the expected therapeutic dose. An effective dose of Requip XL can therefore be attained in one month in a new patient.

The maximal time to onset of peak levels of Requip XL is 3-4 hours and the medication lasts all day and gradually wears off 24 hours after the initial dose is taken in the morning. I have recently found that giving 2/3 of the total daily dose in the morning and 1/3 of the dose in the later afternoon may acheive even better action of this medication. The most common side effect of Requip XL is sedation. Patients converted from generic ropinerole to brand ropinerole (Requip XL) almost always do better because the immediate release ropinerole and the brand Mirapex only work for 6-8 hours after a dose is taken which worsens the effect of the up and down fluctuations in L-Dopa levels which occurs when a patient is also taking L-Dopa. In addition to working better (smoother) the Requip XL has less side effects than the generic immediate release ropinerole. In patients already on high dose (greater than 2 mg a day) of Mirapex I have not found any advantage to converting to Requip XL.

Mirapex ER:  became available March, 2010. This medication works smoother than the immediate release Mirapex and patients are able to function more consistently during the day with less on/off fluctuations and wearing off. The conversion from Mirapex to Mirapex ER is mg for mg; patients on Mirapex 1.5 mg three times a day can take one Mirapex ER 4.5 mg extended release tablet a day.

NOTE: the generic "equivalents" to Requip XL and Mirapex ER are not equivalent!!!! Ropinerole and Pramipexole are the generic names of Requip and Mirapex. They are NOT controlled release and they do NOT provide the same and improved symptom control acheived with the brand controlled release Requip XL and Mirapex ER. Insist of the brand controlled release preparations! The controlled release dopamine agonists (Requip XL and Mirapex ER) provide patients with less "off" times, less dyskinesia (due to the ability to use lower doses of L-Dopa) and better sleep comfort, less dystonic cramps and an overall better feeling of well-being (clinical global impression) than do the immediate release generic preparations. If possible, it is better to use the controlled release dopamine agonist preparations.

Neupro was removed from the market in July, 2008 because of the presence the tendency in some patches for the drug to crystallize within the patch leading to erratic aborption and delivery across the skin. In some cases this could have led to too much or too little drug being absorbed across the skin during the 24 hours of usage. Neupro was reintroduced in 2012 and does not crystalize any longer. Neupro is an excellent dopamine agonist because of the delivery system (transdermal) and the fact that it is a better mimicker of dopamine because it stimulates all five dopamine receptors. The D1, D4 and D5 receptors are located in the frontal lobes and hippocampus and are important in learning and memory. The D2 receptors are in the striatum (caudate nucleus and putamen) and are important in Parkinson's Disease. The D3 receptors are located in the limbic system.


Permax has been taken off the market-. You will not be able to refill your prescriptions if you have been taking this medication. DO NOT STOP THIS MEDICATION SUDDENLY IF AT ALL POSSIBLE!! You may experience an abrupt worsening of your symptoms of Parkinson's Disease.   To convert to Mirapex- use a 1:1 conversion ratio so that .25mg of Permax is converted to .25mg of Mirapex and so on. To convert to Requip use a 1:5  ratio so that 1 mg of Permax is converted to 5 mg of Requip and so on.  The loss of pergolide was very detrimental to the treatment of PD because this dopamine agonist worked differently than Requip, Mirapex and Neupro in stimulating the dopamine receptors in the striatum supplied by the nigrostriatal pathway (D1 and D2) 3-4 times as strongly as the dopamine receptors in the limbic system. What this meant was that patients with dementia who were prone to the side effects of Requip and Mirapex (obsessions, hallucinations, paranoia) and patients who could not take Requip or Mirapex because of sedation were able to take pergolide in order to improve mobility. I believe that the medication should have been left on the market in the US for patients who had failed treatment with the other dopamine agonists with the caveat that echocardiograms could have been checked periodically. Permax provided more D2 than D3 dopamine receptor activation and had less of the side effects of Requip and Mirapex. It was stronger at helping the motor symptoms of Parkinson's Disease.

Dopamine agonists are direct stimulators of the areas in the brain (caudate nucleus and putamen collectively known as the striatum) that need dopamine. This class of medications works like dopamine itself. They bypass the degenerating dopamine producing neurons which are weak and forced to make more dopamine by the administration of L-Dopa.

Although no medications have ever been proven to delay the progression of Parkinson's disease, there has been evidence that dopamine agonists by virtue of continuing dopamine receptor stimulation in the areas of the brain that need dopamine (striatum) may reduce decline in striatal beta CIT uptake as compared to L-Dopa on SPECT scans and in putaminal dopamine storage as compared to L-Dopa on PET scans. This has never been firmly established because there remained a possibility that the drugs themselves may have interacted with the radioligands and contaminated the results. However, this theme of dopamine agonists delaying progression continues to appear in the literature. For example, cabergoline (an ergot derived dopamine agonist available outside of the US) may increase glutathione production, decrease free radical production, increase mitochondrial membrane potential and ameliorate cell death in A53T mutated alpha synuclein and paraquat exposed cells.
If you do not take a dopamine agonist you are condemned to develop fluctuations in response to L-Dopa which will worsen until you are either in an "off" state when L-Dopa barely relieves the stiffness, tremors and slowness or in an "on" state contaminated by writhing, twisting involuntary dyskinesias. The problem is that all of the dopamine agonists on the market have side effects. There is no perfect dopamine agonist which would mimic perfectly the action of dopamine. This should be the goal of drug development: to develop the perfect dopamine agonist which would take away the need for giving L-Dopa. Unfortunately, there are no new dopamine agonists being studied at this time. If Neupro, Mirapex ER and Requip XL are not tolerated you will have to get Permax from outside of the United States or try Parlodel (bromocriptine) or Dostinex (cabergoline) which in my experience do not work as well as the above four. However, ANY dopamine agonist is better than NO dopamine agonist.

VIRAL VECTOR GENETIC ENGINEERING ALLOWS THE SUBTHALAMIC NUCLEUS TO MANUFACTURE AN INHIBITORY NEUROTRANSMITTER (GABA)  THEREFORE INHIBITING THIS OVERACTIVE CIRCUIT ALLOWING THE MOTOR SYMPTOMS OF PARKINSON'S DISEASE TO DIMINISH. It has been known since the mid 1990s that inhibiting the output of either the globus pallidus or subthalamic nucleus would decrease the symptoms of PD. The deep brain stimulator is nothing more than a jamming electrode which when placed in the subthalamic nucleus interrupts this overactive circuit. The new technique which accomplishes the same outcome is to implant a virus which carries the genetic material which will allow the neurons to make and release an inhibitory neurotransmitter. The virus infects the neurons and implants the genetic sequence. This is the first double-blinded evidence that use of a viral vector to genetically engineer neurons does work. Problems are the increased risk of cancer which has been seen in patients undergoing transplantation of tissue, a possible lack of control over which cells are infected and how much new chemical is made, and what the long term beneficial or detrimantal effects might be. Also- this technique does not have any effect on the degenerating substantia nigra or the caudate nucleus and putamen which are at the heart of the brain damage seen in patients with Parkinson's disease. The motor symptoms seem to be lessened but there is not expected to be any alteration in the progressive mental decline which can occur in patients with PD. Also - this may have no effect on altering disease progression. Nevertheless, it is a very exciting development and holds much promise!


Families that have a large number of affected relatives with parkinsonism are continually being studied as to any genetic abnormalities which may lead to nervous system degeneration. You can keep informed of this progress by logging onto and typing in Parkinson's Disease. Google also has a medical section in which you can have new articles emailed to you on a daily basis.

The neurons of the substantia nigra seem to be very sensitive to the formation of free radicals. Free radicals are formed when dopamine is broken down in the neuron. Free radicals are made because of a complex l deficiency in the mitochondria and this production of free radicles is greatly increased in the presence of abnormally high levels of dopamine. This sensitivity is increased by the presence of iron and reduced glutathione. The free radicals cause  the accumulation of alpha synuclein which cannot be "tagged" properly by ubiquitin for degradation. The alpha synuclein accumulates and eventually forms the structure called the Lewy body which is seen in the dead substantia nigra neurons.

There is a genetic influence, especially in patients who manifest Parkinson's Disease below the age of 50 years old. Alpha synuclein is present on chromosome 4. A mutation of Alanine for Threonine at the 53rd mRNA sequence for synuclein produces an abnormal form of synuclein which is more prone to clump. Alpha synuclein expression is increased under conditions of neuronal stress as might occur with toxin exposure of lack of oxygen. As a consequence of abnormal synuclein, dopamine transport within the neuron and attachment to the neuron membrane for release to the areas where dopamine is needed is abnormally affected allowing toxic concentrations of dopamine to build up within the cell which poisons the cell at the mitochondrial level partially because of the production of free radicles.

The parkin gene is present on chromosome 6. Parkin attaches ubiquitin to the alpha synuclein which allows it to be degraded. Abnormalities of Parkin are found in 20-40% of young onset patients with PD.

Another genetic defect may relate to a LRRK2 expression. This DNA sequence and the proteins it controls may play a role in dopamine expression and is under investigation which includes drugs which may alter its function.

What is 23 and me? This is an organization which can provide help in getting screened for genetic forms of Parkinson's Disease. Should you get this done? PROs- if you find out that you have a selective genetic disorder you can pay attention to research that deals with these different parts of the disease process. For example, let's say you have a PINK 1 defect which affects the mitochondria. You might then want to do everything possible to boost mitochondrial function through the use of anti-oxidants, Azilect, NADH, CoQ10 etc. Let's say you have an alpha synnuclein defect. You may want to pay more attention to research that is aimed at preventing the misfolding of these proteins. Cons- it might not be good to tell someone who does not have PD that they may develop it when they get older because there is nothing we can do to prevent PD from happening and it could have devastating effects on the paersons life. Genetic testing is a personal decision. Talk to your doctors and family before getting it.


DOES PERMAX CAUSE HEART VALVE ABNORMALITIES?: There exists concern that use of ergot derived dopamine agonists (Permax and Parlodel) may cause cardiac valve abnormalities. The only article writtten on this matter presented three patients out of the 10's of thousands that have been treated but a recent abstract presented at the American Academy of Neurology also rose some questions. It would be prudent to avoid the use of Permax or Parlodel in patients with heart disease and to check by auscultation all patients at each visit if they are on these medications. In addition, ultrasound should be performed if patients present with the signs or symptoms of cardiac dysfunction. Having said this - I have been using Permax since 1984 and I have NEVER seen a case of any significant heart problems caused by Permax in thousands of patients.

NEUROTROPHIC FACTORS: There is increased interest in the use of BDNF (brain derived neurotrophic factor) to try to induce the sprouting of remaining neurons and treat the symptoms of PD. I am worried that this procedure if effective will place too much stress on the remaining neurons and could cause an acceleration in disease progression after a 2-3 year interval of clinical improvement. I am also concerned regarding malignancy production.The Amgen trials have been halted in the United States because of the potential of danger to patients as has been seen in animals receiving the drug. This has lead to a great debate regarding the ethics of stopping the investigation of a drug even if it may help a patient because of the potential for litigation against the company sponsering the research.

STEM CELL AND OTHER TRANSPLANTS: Unless there is some control over the amount of dopamine production these procedures will not work in any consistent fashion. Every area of the brain is connected to every other area - this provides a delicate balance and intense communication is essential to normal brain functioning. You cannot expect to dump brain cells into an area that needs them and expect they will produce just the right amount of dopamine. In fetal tissue trials, 1/3 of the patients have no response because too little dopamine is produced, 1/3 have just the right response and are improved, and 1/3 have too much dopamine production and are psychotic and/or dyskinetic. More work is needed on this and genetic engineering of brain tissue before these procedures can be deemed safe and effective. The future is in understanding the mechanism of disease and treating the cause of Parkinson's disease at a molecular level!

More insight into the benefits of subthalamic nucleus (STN) deep brain stimulation: This procedure is not experimental and does provide a consistent and measured improvement in the symptoms of PD. It should be reserved, however, only in those patients with severe fluctuations in response to medications despite the more aggressive and careful medical management. Patients may have cognitive and psychological impairments after STN DBS. This may have t do with the approach to the STN or the exact part of the STN where the electrode penetrates. Other targets such as the globus pallidus are again being studied. The pathways interconnecting the globus pallidus with the STN may be the best sites for deep brain stimulation.

DOES LEVODOPA SLOW OR HASTEN THE RATE OF PROGRESSION IN PD?     patients (361) with early PD NOT requiring symptomatic therapy were broken down into 4 treatment groups: 1/2 25/100 carbidopa/levodopa three times a day (tid), 25/100 tid, 50/200 extended release tid, and placebo. Doses were increased over 9 weeks and maintained until week 40 at which time the medications were halted. Patients were examined and beta-CIT SPECT scans were taken 2 weeks after treatments were halted. The SPECT scans measure the health of the areas of the brain which accept dopamine (the striatum) . RESULTS: patients did better when they took levodopa in terms of their symptoms and quality of life. There was a slight decrease in the health of the striatum in patients on levodopa which was bearely statistically significant and greatest with the ER and 1/2 25/100 group and least with the 25/100 group. COMMENTS: Of course the patients did better on levodopa. The SPECT scans were inconclusive. Longer followups are needed and are underway to make any conclusions. Why is this study important? Because it challanges the notion that levodopa is toxic through it's stress on the remaining neurons by forcing them to make more dopamine and thereby increasing the production of free radicals. What is interesting to me is the fact that the ER levodopa/carbidopa group had the most striatal interference and the 25/100 group the least striatal interference which is the opposite of what I would think would be true given the smoother release of levodopa in the ER form. No real conclusions can be drawn from this study at this time given the short followup in these patients. In general, the more dopamine agonist you can take and the least levodopa you can get away with seems to be the way to slow the progression of PD. In addition - another abstract demonstrated that dihydroxyphenylacetaldehyde (dopal) is the toxic metabolite of dopamine which causes selective dopamine loss in the substantia nigra. Free hydroxy radicals generated by dopal could trigger the aggregation of alpha-synnuclein to its toxic state leading to the formation of Lewy bodies.

Apomorphine injections help decrease the severity and duration of "off" periods (of course but who wants to inject themselves with apomorphine and it is better to maximize therapies which decrease the duration and severity of the "offs"). There are many studies regarding the continued efficacy and lack of serious side effects in patients receiving bilateral STN deep brain stimulation. Two patients who got worst after receiving 8 human embryo midbrain tansplantation were studied and found to have increased dyskinesia because of erratic dopaminergic innervation (transplantation, stem cells, altering the genetic ability of the brain to make dopamine- all these therapies are experimental. Unless you have absolute control over what is being placed into or altered in your brain it is too dangerous. Too much dopamine production leads to dyskinesia and psychosis.)


HEAD TRAUMA IS ASSOCIATED WITH AN INCREASED RISK OF GETTING PD. This has important legal implications. If you developed PD soon (less than a year) after a significant head injury with no family history of PD and you are less than 50 years old, this may be one of the mechanisms for etiology. Also - if you have PD and sustain a head injury and worsen - this may also be important in disease progression.

My Story: How I became interested in Parkinson's Disease and my experiences in treating patients with Parkinson's Disease

My first exposure to Parkinson's disease was as an undergraduate at the State University of New York at Stony Brook. During the third summer at college, I had the fortune of enrolling in a course in Psychology as a pre-requisite for medical school. Dr. Ted Lidsky was the course director and Paul Weinhold, a PhD student, was his associate. They were physiological psychologists who were mapping out the pathways of the areas of the brain which were damaged in patients with Parkinson's disease: the basal ganglia. I became intensely interested in neuroscience and in addition to presenting research at the Society for Neuroscience meeting in Toronto that year (1978), I spent the entire last year of college taking courses in Neuroscience such as electrical and chemical brain stimulation and it's laboratory where we studied the effects of various lesions on the brains of rats. I knew that I wanted to be a Parkinson's disease specialist before getting into medical school. I also knew that I wanted to study the relationship between the brain and the mind, between movement and psychology, between the body and the spirit. This quest eventually led to my subspecializing in Movement Disorders and getting a PhD in Neuropsychology.

After that last year of college, I was not certain if I wanted to go directly to medical school or to get my PhD. I enrolled in the Neuroscience PhD program in the University of California in San Diego and spent one year studying graduate level neuroscience. After that year, I decided that I would best able to help people if I became a physician and a neurologist and I enrolled in the University of Osteopathic Medicine and Health Sciences (now called Des Moines University) in 1979. I spent the entire first summer of medical school with the biggest neurosurgical group in Des Moines, Drs. Bakody, Jones and Winston. I spent the next summer with the biggest Neurology group in town, Drs. Stein and Friedgood. My elective was in Neurology at Hahneman University.

I selected Boston University for my Neurology residency in 1984 because Dr. Robert Feldman specialized in Parkinson's disease and had an inpatient Parkinson'd disease unit at Boston University Hospital. In addition, the Jamaica Plain Veteran's Hospital in Boston was (and is) a major center for behavioral neurology with pioneers in neuropsychology such as Drs. Norman Geshwin, Edith Miller, Harold Goodglass, Mick Alexander, and Martin Albert.  I spent three years at Boston University and starting in the second year of my residency, Dr. Feldman offered me the ability to get my PhD. I took graduate level courses in Neuropsychology such as Aphasia, Neuropsychological Testing principles and practice and after driving back and forth to Worcester every day for three months I had my pilot study approved- I was going to study the effects of MPTP (which had been found to produce Parkinson's disease in people who had mistakenly injected it into themselves thinking it was demerol) on a C57 black mouse AND see if I could reverse the damage to the brain using neurotrophic gangliosides. My PhD research and the defense of the dissertation was very difficult but I did it. I realized that a PhD was much more difficult to get than a medical degree because the process is entirely unstructured and dependent on the students ability to think totally independently. I received my PhD in Behavioral Neuroscience from Boston University during my fellowship at Columbia in 1989.

I was accepted into Fellowship training at Columbia Presbyterian in 1987 under the supervision of Dr. Stan Fahn. Dr. Fahn was and still is one of the most important influences on the entire field of Movement Disorders and from 1987 to 1989 I studied in detail all varieties of Movement Disorders. Cell transplantation as a therapy for patients with Parkinson's disease was a hot topic back then as well as now and I headed the research on adrenal medulla transplantation and traveled to Mexico City to meet a surgeon, Dr. Madrazo, who was performing these surgeries and had just started fetal mesencephalon implantation.

I then had the biggest break in my career when I overheard on the escalator from Dr. Lieberman at a national conference that he was leaving NYU for a position in Arizona where he remains (Barrow Neurological Institute).  Dr. Abraham Lieberman had the biggest Parkinson's disease practice in New York City and within two months of the completion of my fellowing in September of 1989, I was single handedly running this practice. Dr. Michael Dogali and Dr. Joseph Ransahoff were interested in a surgeon, Dr. Lauri Laitinen, who had rediscovered a procedure whereby making a discrete lesion in the globus pallidus, patients with Parkinson's disease were able to reduce their contralateral bradykinesia and dyskinesia. Dr. Laitinen had rediscovered the work of Dr. Lars Leksell who had performed this surgery in Sweden in the 1960's before the discovery of L-Dopa but which had been abandoned in lieu of the successful use of L-Dopa to treat Parkinson's disease. Just around that same time, Dr. Mahlon DeLong had worked out the circuitry of the overactive discharges which emanate from the globus pallidus and subthalamic nucleus; these electrical dischages exist as a consequence of low dopamine and the rush was on to find a surgical procedure to correct this overactive circuit. Our target was to make discrete lesions in the globus pallidus internal segment as Dr. Leksell and Laitinen had done. I remember my presentation at the American Academy of Neurology in 1991 at which time I was the first neurologist in decades to even mention surgical therapy for Parkinson's disease. We continued to study pallidotomy for several years but when it was found that bilateral lesions had more side effects than additional benefit, the target was changed to the subthalamic nucleus and the lesion effect was acheived with an indwelling electrical jamming device known as the deep brain stimulator. The subthalamic nucleus deep brain stimulation surgery remains the best treatment for severe brittle on/off fluctuator patients with Parkinson's disease.

I was invited to write for the American Parkinson's Disease Association questions and answer column in their national newsletter and to head the APDA centers in Mahnattan and Long Island. I owe this to Dr. Paul Maestrone and Mario Esposito. 

Through the help of Adele Smithers, I established a Parkinson's Disease treatment center at the New York College of Osteopathic Medicine in 1995 where we have a computerized gait analysis laboratory.

I have continued to perform clinical trials and was a part of the team which developed Botox (1987), pergolide (1984-9), rasagiline (2002) , pramipexole (1996) , zydis eldepryl (2003)and the rotigitine patch (2006). There were many other trials with compunds which were not brought to market for various reasons even though some of them (in particular an excellent D1/D2 dopamine agonist with the strength of and without the ergot side effects of pergolide called sumanirole whose development was terminated by Pfizer after the purchase of Pharmacia).

I have been treating patients with Parkinson's disease since 1984. I was born in 1956. I have lived and breathed this disorder for almost half of my life and have been studying this disease since I was 22 years old.

I am frustrated in many ways by the lack of progress in the treatment of this disease. It seems that we are in a worst condition now with medical therapy than we were even a year ago (when we had Permax and Neupro). We need to find out what causes Parkinson's disease; although there are numerous genetic abnormalities which have been identified it remains a distinct possibility that every patient has a different genetic and environmental causation. We still have no way of slowing progression. The progression of Parkinson's disease is almost impossible to measure and although medications like MAO-B inhibitors (selegiline and rasagiline) and dopamine agonists (pramipexole and ropinerole) should theoretically delay progression there is to this day no drug which is indicated for that purpose. I am frustrated by pendulum swings in recommendations for using l-dopa early to not using it early to using it early again; I have always believed that my duty is to make patients better and then keep them better with whatever medications and surgical procedures are available. It seems to me that our measurements of movement and on/off fluctuations remain primative and computerized gait analysis and blink rate monitoring (which I am working on) might offer a better means towards this goal.

I pray that I can continue to find better ways to fight this horrible disease and that I have the strength to continue to get patients better and keep them from getting worst.

Dr. Enrico Fazzini