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Frequently asked questions

Parkinson’s disease (Parkinson’s) is a progressive neurological disorder that is considered to be one of the most common neurological conditions.  In Parkinson’s, certain specific nerve cells are lost, leading to the typical major symptoms of tremor, stiffness of muscles and slowness of movement.  Every person with Parkinson’s experiences individual symptoms.  For example, not everyone has tremor; and for some, rigidity is the major symptom.  With modern medication, symptoms can be increasingly well controlled. Parkinson’s is caused by the destruction of nerve cells in the brain that produce the neurotransmitter dopamine.  A similar destruction occurs naturally with ageing, but in Parkinson’s the process is much faster.

Parkinson’s is named after the London doctor, James Parkinson (1755–1824), who identified the symptoms typical of the disease in his publication “An Essay on the Shaking Palsy”.

The causes of Parkinson’s are as yet unknown.  Some poisons, for example mould toxins and synthetic drugs, can give rise to Parkinson’s.  Additionally there are some genes that can trigger Parkinson’s if they become damaged.  Extensive brain damage can cause Parkinson’s symptoms.

Some products seem to be protective, including green tea, Q10, tomatoes, caffeine and nicotine.  In addition to the multiple antioxidants recommended for high risk populations, additional antioxidants include natural b-carotene, d-a-tocopheryl succinate, vitamin C, coenzyme Q10, NADH, N-acetylcysteine, Zinc and selenium.

Parkinson’s affects one in 100 people over the age of 60, with the average age of onset being 60.  It can also affect younger people.  Young-onset Parkinson’s (onset at age 40 or younger) is estimated to occur in five to 10% of people with Parkinson’s.

Parkinson’s affects both men and women in almost equal numbers.  It shows no social, ethnic, economic or geographic boundaries.  Of all the neurodegenerative disorders it is second to Alzheimer’s disease in the number of cases, with up to 1.2 million people living with the condition in the five largest EU countries.  While Parkinson’s usually develops after the age of 65, 15% of those diagnosed are under 50.

Parkinson’s is a disease that is characterised by four major features:

  • rest tremor of a limb (shaking with the limb at rest)
  • slowness of movement (bradykinesia)
  • rigidity (stiffness, increased resistance to passive movement) of the limbs or trunk
  • poor balance (postural instability).


When at least two of these symptoms are present, and especially if they are more evident on one side than the other, a diagnosis of Parkinson’s is made, unless there are atypical features that suggest an alternative diagnosis.  People may first realise something is wrong when they develop a tremor in a limb; movements are slowed and activities take longer to perform, or they experience stiffness and have balance problems.  Initially, symptoms are a variable combination of tremor, bradykinesia, rigidity and postural instability.  Symptoms typically begin on one side of the body and spread over time to the other side.

Changes occur in facial expression so that there is a certain facial fixity (blank expression showing little emotion) or a staring appearance (due to reduced frequency of blinking).  Complaints of a frozen shoulder or foot drag on the affected side are not uncommon.  As symptoms appear gradually, older people may attribute these changes to ageing.  The tremor is often thought to be “shakiness”, bradykinesia is regarded as normal “slowing down”, and stiffness is attributed to arthritis.  The stooped posture, common to Parkinson’s, may be attributed to age or osteoporosis.  Both younger and older people may experience initial symptoms for a year or more before seeking medical evaluation.

Initially the symptoms are mild, usually on one side of the body.  Rest tremor is a major characteristic of Parkinson’s, and the most common presenting symptom, but some people never develop it.


Tremor may be the least disabling symptom, but is often the most embarrassing to the people affected.  They may keep their affected hand in their pocket, behind their back or hold something to control the tremor, which may be more psychologically distressing than any physical limitation that it imposes.  Over time, initial symptoms become worse.  A mild tremor becomes more bothersome and more noticeable. Difficulties may develop with cutting food or handling utensils with the affected limb.

Slowness of movement

Slowness of movement (bradykinesia) becomes a significant problem and the most disabling symptom.  Slowness may interfere with daily routines; getting dressed, shaving or showering may take much of the day.  Mobility is impaired and difficulty develops in getting into or out of a chair or a car, or turning over in bed. Walking is slower and there is a stooped posture, with the head and shoulders hanging forward.  The voice becomes soft and monotonous.  A disturbance of balance may lead to falls.  Handwriting becomes small (micrographia) and illegible.  Automatic movements, such as arm swing when walking, are reduced.


Rigidity in Parkinson’s is a stiffness of the muscles.  To test for rigidity, the examining doctor moves the relaxed body part slowly and gently and tests for any resistance to movement.

Poor balance

The ability to maintain posture and balance may be affected in people with Parkinson’s.  This can lead to poor balance (postural instability) and unsteadiness when walking, turning or standing, or when performing actions such as rising from a chair or bending over.  Any of these unsteady movements may lead to a fall, which is a major cause of injury in people with Parkinson’s.

There are many practical devices, such as handrails, walking sticks and walking frames, that can help with stability and can prevent falls.  A physiotherapist will be able to identify the right walking device for each person.

Symptoms may originally be restricted to one limb, but will typically spread over time to the other limb on the same side.  They eventually progress to the other side of the body.  Generally this progression is gradual, but the rate of progression varies.  As symptoms progress, it is important for people to talk with their physicians so that optimal treatment can be established.  The goal of treatment is not to abolish symptoms, but rather to help the person manage them, function independently and make the appropriate adjustments to a chronic illness.  The illness will not go away, but management of its symptoms can be successful in reducing disability.

People are aware of the progressive nature of the illness and this may become a source of much anxiety.  It is not uncommon for them to over-monitor themselves and their symptoms, compare themselves to other people with Parkinson’s whom they may meet (length of diagnosis, level of symptoms, etc.) and avoid situations such as support groups, where they may see others who are worse off than they are.  Concern about the progression of the disease and the ability to continue working is frequently voiced.

Symptoms are caused by the breakdown of certain dopamine-containing nerve cells in the brain.  Dopamine is one of many neurotransmitters, i.e. a substance needed for communication between nerve cells.  Dopamine is produced by nerve cells seated deep in the centre of the brain.  The brain is always using dopamine to control nerve signals, which in turn control the body’s movements.  Dopamine, like other neurotransmitters, is constantly produced and used up (destroyed).  In Parkinson’s, the production of dopamine is impaired while its use and destruction remains.  This causes a dopamine deficit, whereby the body’s movement control is impaired.

No, Parkinson’s is not usually hereditary although there are a few families reportedly having a hereditary form of the disease.  Even in identical twin studies, most of the data suggests that something else is inducing this disease.  It is likely that there are several genes that predispose the individual to getting Parkinson’s, as well as environmental factors.

Mental health in Parkinson’s can be affected.  Existing documentation shows that the medication used to treat Parkinson's or the disease progression can cause:

  • depression
  • hallucinations
  • anxiety
  • panic disorders
  • obsessive-compulsive and addictive behaviours
  • cognitive impairment
  • confusion and psychosis with paranoid delusion that leads to hospital admission.

No.  People do not die from Parkinson’s, rather they die with Parkinson’s.  Complications, for example pneumonia caused by aspiration in connection with difficulty swallowing, can lead to death.  Parkinson’s by itself does not directly cause people to die.  With the treatment that is now available, life expectancy for someone with Parkinson’s is fairly normal and none of the medication that are used have any serious side effects that could cause death. 

However, occasionally in people who are seriously disabled (usually those who have had Parkinson’s for many years), their general physical and mental condition can either cause or exacerbate other illnesses and so contribute to the final cause of death.

The process of making a Parkinson’s diagnosis can be difficult.  There is no X-ray or blood test that can confirm Parkinson’s.  A physician arrives at the diagnosis only after a thorough examination.  Blood tests and brain scans known as magnetic resonance imaging (MRI) may be performed to rule out other conditions that have similar symptoms.  People suspected of having Parkinson’s should consider seeking the care of a neurologist who specialises in Parkinson’s. Poor differential diagnosis is a major problem in the management of Parkinson’s.

People who get Parkinson’s will most likely need medication for the rest of their lives.  Continuous medication is one of the cornerstones of treatment. Today, the symptoms of the disease can be very effectively relieved.

Through medication, the dopamine deficiency in the brain is controlled.  In the early stages of the disease, a single drug or a combination of different drugs can be used.  Medical treatment is started in low doses and increased gradually.  Furthermore, medication is always individual and can vary greatly between people.  After some time, the medication can also cause side effects.  Therefore, medical treatment of people with Parkinson’s requires follow-up by a physician with a good knowledge of the condition.

Neurologist professor Stocchi believes treatment should be started as early as possible and continued throughout the course of the disease.  By slowing down the progression of the disease, people with Parkinson’s can maintain a good quality of life for longer.


The cornerstone of Parkinson’s medication is levodopa. Levodopa, or L-dopa, is a so-called amino acid that exists naturally in the body and also in tiny amounts in some vegetables.  The name is an abbreviation of dihydroxy-L-phenylalanine.  Levodopa medications are: Madopar, Madopar depot, Madopar Quick, Madopar Quick Mite, Sinemet, Sinemet depot and Stalevo, and, during later stages of the disease, the pump-based medication levodopa/carbidopa.  Levodopa is very effective against Parkinson’s symptoms.  It is the precursor of dopamine, but levodopa is used instead because dopamine cannot pass directly into the brain.  Medication is started with low doses that are increased gradually until the best possible symptom relief is obtained for the individual.  Levodopa begins to have an effect after a few weeks’ use, but sometimes it can take up to several months to achieve the maximum benefit. 

The uptake and transportation of levodopa into the blood can be obstructed by the amino acids of proteins in food.  In order to achieve the best possible result, levodopa should therefore be taken approximately 30 minutes before eating food containing proteins, e.g. meat, fish, cheese, milk, egg etc. Levodopa is absorbed in the upper small intestine and therefore is also dependent on gastric emptying.

Dopamine agonists

These substances cross into the brain and mimic the effects of dopamine in the dopamine receptors.  Cabaser (cabergoline), Parlodel (bromocriptine), Requip (ropinirole), Mirapexin (pramipexole) and apomorphine (pen and pump administration) are dopamine agonists.  In addition, one dopamine agonist, Neupro (rotigotine), is now available in patch form to apply to the skin.  Dopamine agonists can be used alone or in combination with levodopa.  They often provide good relief of symptoms, especially tremor. Dopamine agonists also seem to have some antidepressive effect.

Dopamine enhancers


Levodopa has a relatively short duration of action.  Therefore, additional medication can be used that smooth out and prolong its effect.  Both inside and outside the brain, enzymes break down dopamine to substances that are of no use in Parkinson’s treatment.

One such enzyme is catechol-O methyl transferase (COMT).  If this enzyme is blocked, the levodopa dose will last longer and the fluctuations of the brain’s dopamine levels during the day will be reduced.  At present, two COMT inhibitors are available: Comtess (entacapone) and on-licence Tasmar (tolcapone).  These medications have symptom-relieving effects only in combination with levodopa, not by themselves.  Both should therefore be taken in combination with levodopa medication.

Another enzyme, monoamine oxidase type B (MAO-B) breaks down dopamine in the brain.  Inhibitors of this enzyme, e.g. Eldepryl (selegiline) and Selegiline (selegiline), increase the dopamine level and provide symptom relief, but not as effectively as levodopa or dopamine agonists.  Eldepryl also has a certain antidepressive effect.  Some research data indicates that the progression of Parkinson’s could be slowed by Eldepryl, which is usually taken once every morning together with food.  The most recent dopamine booster is Azilect (rasagiline).

Symmetrel (amantadine) can be used as initial treatment, primarily in older people or to improve the effect of levodopa.  Amantadine is actually a medication used against viral disease, but it can be effective in Parkinson’s by increasing the release of dopamine from cells that still produce it.

We now know that motor complications are not so much a reflection of the inherent properties of levodopa, but rather are related to the way in which they are administered.

Evidence from preclinical and clinical studies indicates that pulsatile stimulation of striatal dopamine receptors is a key factor in the development of levodopa-associated motor complications.  Therefore, in the de novo person, it is believed that providing a more continuous dopaminergic stimulation from the start of anti-Parkinson therapy may prevent priming for motor fluctuations and dyskinesia.

Chronic levodopa treatment in people with Parkinson’s frequently results in the development of motor complications, including dyskinesia and motor fluctuations.  These complications are associated with discontinuous stimulation of dopamine receptors induced by intermittent oral doses of levodopa.

In the more advanced person with Parkinson’s who already is experiencing motor complications, it is believed that providing a more continuous stimulation may reverse the development of motor complications, enabling the person to enjoy more stable benefits from therapy.

According to neurologist Professor Per Odin, continuous dopaminergic stimulation (CDS) is a treatment strategy hypothesised to avoid or reduce the motor complications of longterm levodopa therapy, motor fluctuations, and dyskinesia. CDS achieves this by preventing or reversing sensitisation induced by pulsatile dopaminergic stimulation.  The CDS hypothesis is itself based on several hypotheses.  First, tonic dopaminergic stimulation is physiological.  Second, sensitisation is undesirable and should be reversed.  Third, reduction of “off” time and dyskinesia can be induced simultaneously.  Finally, clinical studies substantiate the CDS hypothesis.

The infusion pump is a very good way in advanced, or even moderate Parkinson’s, to help people obtain a smoother plasma response and more continuous stimulation at the post-synaptic receptor site.
The plasma profile induced by the infusion is always higher than with oral treatment, but the trough levels during the day are much less.

The pharmacokinetic studies suggest that the key to CDS may be the elimination of trough levels, rather than delivering a constant concentration of a drug.  High concentrations of levodopa may not be a problem if low trough levels are avoided.

Surgery can ease the symptoms of Parkinson’s, but it is not a cure.  Because of the risks associated with brain surgery, it is usually not considered unless all appropriate medications have been tried but prove to be unsuccessful.  When considering surgery, it is important to see both a neurologist and a brain surgeon who specialise in the treatment of Parkinson’s.

Deep brain stimulation (DBS) is one of a group of treatments involving surgical implantation of a medical device called a brain pacemaker, which sends electrical impulses to specific parts of the brain.  This surgical procedure is used to treat severe essential tremor and tremor, rigidity and bradykinesia (slow movement) associated with Parkinson’s, as well as primary dystonia and other conditions.

Generally, bowel movements in individuals with Parkinson’s are weaker and slower.  The stomach may empty less frequently.  Levodopa, which is absorbed in the upper small intestine, is dependent both on stomach emptying and on the absence of competing amino acids in the form of protein-rich food in the stomach.  It is therefore advisable to take medication, especially levodopa medication, approximately 30 minutes before a meal.  Some patients prefer to eat the more protein-rich foodstuffs in the evenings.  However, the most important aspect is a nutritious, varied and well-composed diet with plenty of fibre.  It may be a good idea to consult a dietician to get advice.

Exercise and mental training are good for people with Parkinson’s.  It is important to break their isolation, for example to engage them in the work and activities of a society.  It is also advantageous to cultivate ‘healthy’ interests.

It is also important that a person with Parkinson’s keeps as busy as they can.  They must keep as active both physically and mentally as they are able.

Some advice:
  • ‘never allow anyone to do something for me that I am able to do for myself.’  The reason for this is simple.  The longer you force yourself to do everything you can, the longer you will be able to do them
  • get involved and try to help someone every day.  This keeps you busy, so that you are not concentrating on your own problems
  • understand that things take longer to do.  Be patient with yourself and others.

During the last 25 years, the medical treatment of Parkinson’s has developed rapidly; drug research is continuously ongoing in different parts of the world.  At the moment, several new Parkinson’s medications are under development and being tested for future use.

New surgical methods and gene therapies are also under development.  The possibilities for treating Parkinson’s will therefore become increasingly better with time.

The European Parkinson's Disease Association (EPDA) is a non-political, non-religious, and non-profit making organisation concerned with the health and welfare of people living with Parkinson's disease and their families and carers.

Founded in June 1992 in Munich, with a membership of nine European Parkinson's patient organisations, the EPDA currently has a membership of 45 organisations across Europe, see www.epda.eu.com/members.

The EPDA provides an important forum for partnership. By encouraging constructive dialogue between international patient and neurological organisations and the pharmaceutical industry, they are able to develop research projects into quality of life issues, and conferences for multidisciplinary teams and people with Parkinson’s of all ages.

Mission statement

To ease the lives of people with Parkinson's disease and their families and carers by promoting a constructive dialogue between science and society, and by encouraging and supporting the development of national PD organisations.


The EPDA aims to ensure the best possible quality of life for people with Parkinson's, their carers and families. This can be achieved by:
  • providing and continually updating medical and caring best practice to all involved in their management;
  • making this information readily available to facilitate dialogue and sharing of successful activities across member organisations;
  • providing targeted educational tools, and acting as a voice for Parkinson’s in Europe with key decision makers.

Further information

Read more about the organisation and its work programme, activities, events, projects, publications, news and Parkinson’s information by visiting the EPDA website: www.epda.eu.com.

National organisations carry out numerous activities.  They create awareness of the disease, break the isolation of their members, arrange different activities and provide information.  Some carry out surveys and influence decision makers.  A substantial part of the work involves giving help and support.

For more information about the national organisations, visit EPDA’s website:

  • Mohammed Ali (1942–), Amerikaanse bokser.
  • Paus Johannes Paulus II (1920–2005), eerste symptomen vastgesteld begin 1991.
  • Michael J. Fox (1961–), film- en televisiester die op 26 november 1998, na zeven jaar ziekte, toegaf Parkinson te hebben.
  • Janet Reno (1938–), voormalige Amerikaanse minister van justitie, van Deense afkomst, kondigde in november 1995 aan dat ze Parkinson had.
  • Billy Graham (1918–), evangelist, heeft sinds 1992 Parkinson en beëindigde zijn evangelische kruistochten in 2000.
  • Salvador Dali (1904–1989), Spaanse surrealistische schilder, woonde sinds 1940 vooral in de VS.
  • Deborah Kerr (1921–2007), Britse filmactrice die in 1993 een Oscar kreeg en bij wie in haar laatste jaren Parkinson werd vastgesteld.

Visit these websites for more information: