Wednesday, August 23, 2017

9th Annual PD Patients and Caregivers Conference

Thank you for your patience, we now have 4 of the 5 speakers from the 2017 conference posted, as well as the question and answer session.  One speaker will be added at a later date. 

Thank you again to everyone who attended, we are excited about the new outreach possibilities that we will have in 2018, and also hope that we can continue this annual educational conference.



Thursday, June 1, 2017

Moving Day 2017

Thank you to everyone who came out for the Moving Day San Francisco, on May 7 at Justin Herman Plaza!  We were so excited to see so many new walkers and hope that everyone enjoyed themselves.

Reminder: Moving Day-San Jose is this Saturday, June 3, at Evergreen Valley College, in San Jose.  Link to the event is here:

Please come out and support the Parkinson's Foundation and keep moving!


Friday, March 24, 2017

9th Annual PD Conference Saturday, May 20, 2017- 12:00-4:30

We will be hosting another great PD patient and caregiver conference on May 20, at the Mission Bay Conference Center.  Tickets and more information for this popular annual event can be found here:

Please be aware that this event sells out, so buy your tickets now.

The information and agenda for the conference are below:

Saturday, May 20, 2017

UCSF Mission Bay Campus
William J. Rutter Center – Robertson Auditorium
1675 Owens Street, 2nd Floor
San Francisco, CA 94158

11:00 – 12:00

12:00 – 12:10
Welcome & Introductions
Michael Aminoff, MD, DSc, FRCP
Distinguished Professor of Neurology & Director of UCSF Parkinson’s Disease Clinic and Research Center

12:10 – 12:45
Robert Edwards, MD
Professor, Department of Neurology
“Investigating the Causes of Parkinson's Disease”

12:45 – 1:20
Chad Christine, MD
Professor, Department of Neurology
“Nutritional Status in Parkinson’s Disease”

1:20 – 1:55
Maya Katz, MD
Assistant Professor, Department of Neurology
“Care of Patients with Advanced Parkinson's Disease”

1:55 – 2:30
Break & Light Refreshments
2:30 – 3:05

Joey Laus, CCC-SLP, MS
Speech Pathologist, Department of Otolaryngology and Head and Neck Surgery
“Management of Communication and Swallowing Disorders in People with Parkinson's Disease”

3:05 – 3:40
Catherine D. Printz, PT, DPT, NCS
Assistant Clinical Professor, Department of Physical Therapy and Rehabilitation Science
“Exercise Strategies to Combat the Symptoms of Parkinson's Disease”

3:40 – 4:15

Friday, October 7, 2016

Physical Therapy for PD

Exercise should be part of the daily routine of a patient with Parkinson’s disease (PD). Exercise and regular activity improve mobility, dexterity, and balance, and may even slow the progression of PD. Exercise, especially outdoors, also helps to alleviate depression, which is a common accompaniment of parkinsonism. Finally, there is a growing belief in the medical community that regular exercise improves or preserves cognitive function. For most PD patients, it is not necessary to consult with their primary care provider (PCP) before starting a low-impact exercise regimen, such as taking a daily walk for 30 minutes. However, for a PD patient with heart or pulmonary disease, in particular, it is important for the PCP to determine what exercise can be done safely.

For a more focused program, patients may want to consult with a physical therapist on specific exercises that can be done to keep muscles, joints, and limbs in an optimal state. Neurologic Clinical Specialists (NCS) are physical therapists who specialize in movement disorders, such as PD. However, a patient should not delay starting a program in order to meet with an NCS, as all physical therapists are trained movement professionals and will be able to assist in creating an exercise plan.

A physical therapy (PT) program ideally should focus on improving posture and balance and on maintaining dexterity and functional ability in the limbs. Such programs can be tailored to emphasize exercises that may reduce the risks of falling. It is common for patients with PD to have disturbances of gait, and certain exercises can help to maintain good strides, improve arm swing, and counter freezing episodes.

PD motor symptoms are usually asymmetric, affecting one side of the body more than the other. Some patients with PD show a reticence to use their affected side. Seeking to hide their tremor, they will attempt to stay the tremor by clasping hands or sitting on the tremulous hand. Others, knowing that one hand is slower and clumsier, will favor the “better” hand for most activities. Patients with PD who have predominantly lower limb symptoms often reduce the amount of walking they do, or rely increasingly on a cane or walker. If an assistive device is necessary to protect the patient from repeated falls, it should be employed —however, the danger in neglecting an affected limb is that the less the limb is used, the less usable it becomes. Patients must actively strive to do more with affected limbs. “Forced” use of an affected limb leads to neural adaptation. In other words, the limb becomes more responsive because the neural pathways that control it are activated more fully. Neural adaptation has been shown to occur in patients who have undergone forced use rehabilitative strategies after a stroke.

In the daily routine of a patient with PD, time should be spent on improving range of motion, task performance, and coordination, particularly of the more symptomatic limb. For the hands, practice precise repetitive movements: drumming or tapping the fingers, turning the palm up and down, throwing, catching, and squeezing a ball, putting small objects in small containers, using a finger to quickly touch mobile and stationary objects, and so on. Exercises to practice with the legs include: marching and stepping in place while occasionally changing directions, and toe tapping. When walking, keep the head up, the shoulders back, and swing the arms purposefully. The point is to challenge the limbs to be as active as possible.

After a PT program has been outlined and followed for a while, periodic re-evaluation by the physical therapist will help to confirm that the program is providing some benefit. PD is a disease that tends to worsen over time, and exercise programs may need to be adjusted with disease progression.

Keeping the mind limber is also important. Learning-based exercises can help maintain multi-tasking capabilities, which may —in turn— have a positive effect on work and inter-personal interactions. Solving puzzles, playing board games, and exploring new hobbies are all things that PD patients can do to challenge the mind and keep it nimble. Other activities like dance, tai chi, and yoga are especially beneficial, pairing relatively low-impact movement with learning, memory, and repetition. In addition, these activities provide pleasure and increase opportunities to socialize. Physical therapy offers the opportunity to collaborate with a movement professional to create a regimen that is unique to the patient, and will help the patient keep the body and mind durable, flexible, and resilient.

Monday, April 11, 2016

Bay Area NPF 2016 Moving Day, 2 dates!

In case you haven't heard, the National Parkinson Foundation is having its second annual Moving Day® in San Francisco (May1) and Silicon Valley (June 4) and we would love to see you there!

UCSF is a National Parkinson Foundation Center of Excellence and the UCSF Parkinson’s Disease and Movement Disorders Clinic (Parnassus Campus) and the UCSF Movement Disorder and Neuromodulation Center (Mt Zion Campus) are working with the NPF to produce another successful event.  We are currently establishing the UCSF PD Center walking team and hope you will be inspired to create your own team and join with the hundreds of other people walking and celebrating together!

Moving Day® is a fun and inspiring fundraising event that will unite families, friends, and communities in the fight against Parkinson’s disease. More than just a walk, Moving Day highlights NPF’s belief in a better life until we have a cure for PD.  It focuses on “movement” and exercise as a symbol of hope and progress because of its essential role in treating the disease.   The funds raised by this event help support NPF programs vital to the advancement of PD research and outreach at the national and local level.  Last year, support from the NPF helped to expand our community outreach in San Francisco.

REGISTER TODAY for either:  San Francisco - Sunday, May 1, 2016 or Silicon Valley (San Jose) – Saturday, June 4, 2016.  You can find additional information at

Moving Day® features a unique Movement Pavilion, with stations such as yoga, Pilates, Tai Chi, PWR, LSVT Big, boxing, and dance — all proven to help manage the symptoms of Parkinson’s disease. The walks also feature a Resource Pavilion, which will include local medical and paramedical professionals like neurologists, physical therapists, social workers, and other community resources for patients and caregivers.  Included in the festivities are family-friendly walk routes of 1, 2, or 3 miles, a kids’ area, music, entertainment and much more. 

Thank you for your support and if you have any questions concerning Moving Day®, please reach out to walk coordinator, Colleen Fischer at 925-421-6737 or email her at

Hope you can make it out for a day of movement and exercise and support for the fight against PD.

Aaron (Team Captain, UCSF PDCRC)

Monday, April 4, 2016

The History of Levodopa

Levodopa is the “gold standard” for the medical treatment of the motor symptoms of Parkinson’s disease (PD) [1].  How levodopa was discovered and the process by which it was found to have anti-parkinsonian effects is an interesting scientific story.

Levodopa is the precursor to the neurotransmitter dopamine, i.e., it is converted to dopamine in the body.  A neurotransmitter is a chemical that “transmits” information from one neuron (nerve cell) to another [2].   Dopamine is involved in the ability to move, form memories and learn, experience pleasure, sleep, and keep stable emotional states.   It was first synthesized in 1911, by Casimir Funk in London [3].  At the same time, an Italian pharmacologist, Torquato Torquati, isolated and crystallized levodopa from the seeds of a broad bean plant (Vicia faba), while researching naturally occurring compounds in plants [4].  

In 1913, Swiss biochemist Marcus Guggenheim discovered that the compound that Torquati had produced was levodopa [3, 4].  Guggenheim used himself as a test subject and ingested 2.5 g of levodopa (the equivalent of taking 25 Sinemet 25/100 pills at once) and recorded his body’s reaction.  He became nauseous and began to vomit, which he assumed incorrectly was due to an irritation of the mucus membrane layer of his stomach [5]. 

Four years after Guggenheim’s work with levodopa, Swiss dermatologist Bruno Bloch correctly postulated that levodopa was the parent compound—a chemical composite from which derivatives can be created—of melanin [3].  Melanin is responsible for determining skin and hair color, i.e., their pigmentation [6].   This discovery showed that levodopa occurred naturally in human skin cells.

For many years it was not realized that levodopa had any useful biological functions.  In the early 1940s, however, it was found that the body converted levodopa into dopamine and in the 1950s dopamine was also found to occur naturally in the body [7].  Swedish scientist Arvid Carlsson discovered that dopamine was a neurotransmitter in the brain [8] and established a scientific method for measuring dopamine levels in brain tissue [9].  Subsequent analysis showed that the basal ganglia, an area of the brain essential for movement, normally contained high levels of dopamine [10]. By giving animals a drug called reserpine—which reduces the levels of dopamine—Carlsson induced a loss of spontaneous movements [11]. In 2000, he was awarded the Nobel Prize in Physiology or Medicine for his work.

In 1959 two Austrian doctors, Ehringer and Hornykiewicz, measured dopamine levels in the brains of deceased patients. Using 17 human control brains, they compared dopamine levels to those in the brains of 2 patients with Huntington’s disease, 6 patients with movement disorders of unknown origin, and 6 brains of patients with PD. Compared to the controls and the patients with other neurodegenerative diseases, only the brains of the 6 PD patients showed severe dopamine loss [12]. 

A treatment hypothesis was soon formed: PD patients suffer from a loss of dopamine; therefore, the introduction of dopamine to the body should have a beneficial effect.  Certain substances, including dopamine, are unable to penetrate from the blood into the brain. Accordingly, levodopa —which does penetrate this blood-brain barrier —was used instead as the therapeutic agent.  In 1961, two independent medical studies found that levodopa led to significantly improved motor function of PD patients [13, 14].  Seven years later, neurologist George Cotzias outlined a high-dose levodopa treatment for PD patients that is still in use today [15, 16].

While levodopa can cross the blood-brain barrier, researchers discovered that the majority of levodopa administered was being metabolized by the body before it reached the brain.  The inclusion of the compound carbidopa to the levodopa inhibited this extra-cerebral breakdown of levodopa, so that more levodopa was able to get into the brain.  An added benefit of slowing the extra-cerebral breakdown of levodopa was a significant reduction in the nausea experienced by patients.  Consequently, patients were able to take much smaller doses of levodopa with the same (or more) therapeutic benefit. 

In 1972 a combination carbidopa/levodopa treatment was approved in the United States under the trade name Sinemet© (a Latin combination of Sin-“without” and Emet-“vomiting”) in four different dose strengths, 10/100, 25/100, 25/250 and 50/250.  Madopar© was created for distribution in Europe and other countries, using a combination of levodopa and benserazide (a compound with the same inhibitory capability as carbidopa).  Over forty years have passed since symptomatic levodopa treatment was introduced for PD, and to this day it remains the most widely used course of treatment for combatting the motor symptoms of PD.

  1. Aminoff MJ. Parkinson's disease. Neurol Clin. 2001;19(1):119-28, vi.
  2. National Institute of Health. Brain Basics. Available at Accessed on March 23, 2016
  3. Hornykiewicz O. L-Dopa: A historical perspective. In: Yoshimi Misu, Yoshio Goshima, eds. Neurobiology of DOPA as a Neurotransmitter. Boca Raton, FL: CRC Press; 2005: 3-16
  4. Hauser RA. Levodopa: past, present, and future. Eur Neurol. 2009;62(1):1-8.
  5. Hornykiewicz O. A brief history of levodopa. J Neurol. 2010;257(Suppl 2):S249-52.
  6. Mandal, A. What is Melanin? Accessed 12/17/2015
  7. Carlsson A, Lindqvist M, Magnusson T, Waldeck B. On the presence of 3-hydroxytyramine in brain. Science. 1958;127(3296):471.
  8. Carlsson A. The occurrence, distribution, and physiological role of catecholamines in the nervous system. Pharmacol Rev. 1959;11(2, Part 2):490-3.
  9. Carlsson A, Waldeck B. A fluorimetric method for the determination of dopamine (3-hydroxytyramine). Acta Physiol Scand. 1958;44(3-4):293-8.
  10. Lees AJ, Tolosa E, Olanow CW. Four pioneers of L-dopa treatment: Arvid Carlsson, Oleh Hornykiewicz, George Cotzias, and Melvin Yahr. Mov Disord. 2015;30(1):19-36.
  11. Carlsson A. A half century of neurotransmitter research: impact on neurology and psychiatry. In: Hans Jornvall, ed. Nobel Lectures in Physiology or Medicine 1996-2000. River Edge, NJ: World Scientific; 2003: 303-322.
  12. Ehringer H, Hornykiewicz O. [Distribution of noradrenaline and dopamine (3-hydroxytyramine) in the human brain and their behavior in diseases of the extrapyramidal system]. Klin Wochenschr. 1960;38:1236-9.
  13. Birkmayer W, Hornykiewicz O. [The L-3,4-dioxyphenylalanine (DOPA)-effect in Parkinson-akinesia.]. Wien Klin Wochenschr. 1961;73:787-788.
  14. Barbeau A, Sourkes TL, Murphy GF. Les catécholamines dans la maladie de Parkinson. In: de Ajuriaguerra J (ed) Monoamines et système nerveux central. Georg & Cie SA; Geneva: 1962: 247–262
  15. Cotzias GC, Van woert MH, Schiffer LM. Aromatic amino acids and modification of parkinsonism. N Engl J Med. 1967;276(7):374-9.
  16. Cotzias GC, Papavasiliou PS, Gellene R. Modification of Parkinsonism--chronic treatment with L-dopa. N Engl J Med. 1969;280(7):337-45.

Thursday, December 17, 2015

The Importance of Remaining Independent

In any discussion of the symptoms of Parkinson disease (PD), the loss of personal independence is often an important issue.  Parkinson’s disease is a progressive disorder affecting mobility, dexterity, and balance.  Activities of daily life—such as buttoning a shirt collar or fastening a bra strap — become more difficult as the disease advances.  People with PD are often embarrassed and frustrated by their increased dependence on a spouse or caregiver.  Caregivers also report more depression, anger, and apathy in patients as they come to need more help and become more limited in their activities and capabilities.

Frustration is understandable.  The best course of action for PD patients combating their limitations is for them to complete daily activities for themselves.  Even if this takes more time, it helps patients retain dexterity and a sense of normality.  For the caregivers, this means going against their instinct to help.  Although helping may seem a kindness to caregivers and people with PD, assisting patients with daily tasks is a slippery slope.  Aiding someone with PD to button a cuff or lace a shoe on one occasion makes it more likely that they will seek help the next time.  Eventually patients becomes more reliant on the caregivers, less able to complete the task unassisted, and more frustrated by his or her own increasing limitations. 

Encouraging patients to complete tasks for themselves reinforces the central objective of their management, namely, the conservation of personal independence.  Clear communication between patients and caregivers on the importance of remaining independent is necessary.  This helps to avoid the impression that caregivers who decline to help with daily tasks are uncaring or hostile and thus to avoid the development of tension between patients and caregivers.  

People with PD should attempt to do everything themselves, even if it takes longer, is getting more difficult, and causes irritation.  For difficult daily activities, it may help to think of the tasks as a component of physical therapy (in addition to regular exercise and any therapy that has been prescribed).  The importance of accomplishing daily tasks independently despite the physical limitations of PD cannot be overemphasized.

Caregivers must remain supportive but not “enablers” of dependency.  Caregivers must let PD patients accomplish daily tasks on their own as much as is possible.  Allowing more preparation time may be helpful when planning an activity.

People with PD must commit to completing all daily activities unaided for as long as possible.  When it comes to personal independence and a disease like PD, truly, if you don’t use it, you lose it.