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 botulinum toxin 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! You must realize: There are 12 types of Carbidopa-Levodopa preparations, several Carbidopa-Levodopa-Entacapone preparations, 2 dopamine agonists, 3 MAO-B and 2 COMT inhibitors. There also exist three anticholinergics and medications used to treat other neurological conditions, antidepressants 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. YOU DO NOT NEED TO CHANGE YOUR CURRENT NEUROLOGIST-GIVE ME 3 WEEKS TO ADJUST YOUR MEDICATIONS. 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.
A NEW MEDICATION IS NOW AVAILABLE IN THE UNITED STATES FOR THE TREATMENT OF PARKINSON'S DISEASE!!! This adenosine A2A receptor antagonist is the first medication treatment that calms down the overactive pathway which emanates from the globus pallidus (indirect pathway). Dopamine normally inhibits this pathway. As a consequence of decreased dopamine, this pathway becomes overactive and blocks movement. This medication is indicated as add on therapy to L-DOPA.


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 MAO-B inhinitors may have a disease modifying effect 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 MAO-B inhibitors 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 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 as well as taking medications to raise blood pressure . 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 MAO-B inhibitors although they may have been more disabled without the addition of L-DOPA. The moral of this story? Use dopamine agonists and MAO-B inhibitors 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 (and COMT inhibitors . 

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 Carbidopa-Levodopa, add CR Carbidpa-Levodopa and a COMT-inhibitor or MAO-B inhibitor  and use dopamine agonists. Decreasing the interval between doses also helps. The dopamine agonist patch will be of great help because it provides a continuous release of medication.

What is Carbidopa/L-Dopa?

Carbidopa/L-Dopais 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 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 may rarely cause heart valve problems, fluid around the lungs, and circulation problems. The non-ergot derived dopamine agonists can cause sleep attacks and obsessionalisms. 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.


Is chelation helpful? Only if it is proven that you have high levels of metals in your body.




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. 

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 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. 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 and dopamine agonists 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