Parkinson's disease.

Parkinson's is a progressive neurological condition affecting movements such as walking, talking, and writing. It is named after Dr James Parkinson (1755-1824), the London doctor who first identified Parkinson's as a specific condition.
Parkinson's occurs as result of a loss of nerve cells in the part of the brain known as the substantia nigra. These cells are responsible for producing a chemical known as dopamine, which allows messages to be sent to the parts of the brain that co-ordinate movement. With the depletion of dopamine-producing cells, these parts of the brain are unable to function normally.'s-disease-to-be-fought-through-new-education-programme/376/2807


The main symptoms of Parkinson's can also be symptoms of other disorders. Conditions that produce these symptoms are known collectively as parkinsonism. Parkinson's is the most common form of parkinsonism and is often referred to as "idiopathic Parkinson's disease" (this means of unknown cause). Other, less common, forms of parkinsonism include:

multiple system atrophy (MSA)

Multiple system atrophy (MSA) is a rare, degenerative neurological disorder. MSA is associated with the degeneration of nerve cells in specific areas of the brain. This cell degeneration causes problems with movement, balance and autonomic functions of the body such as bladder control. The cause of MSA is unknown and no specific risk factors have been identified.[1] Around 55% of cases occur in men, with typical age of onset in the late 50s to early 60s.[2]

The overall prevalence of MSA is estimated at 4.6 cases per 100,000 people.

MSA is characterized by a combination of the following:

Progressive damage to the autonomic nervous system, commonly leading to low blood pressure when standing (postural hypotension), incontinence, difficulty urinating (dysuria), and/or abnormal breathing during sleep
Muscle rigidity +/ tremor and slow movement (Parkinsonism)
Poor coordination / unsteady walking (ataxia)
When autonomic failure predominates, the term Shy-Drager syndrome is often used, although this term is no longer current, given the recent terminology changes which are explained below.

The most common first sign of MSA is the appearance of an "akinetic-rigid syndrome" (i.e. slowness of initation of movement resembling Parkinson's disease) found in 62% at first presentation. Other common signs at onset include problems with balance (found in 22%), followed by genito-urinary problems (9%). For men, the first sign can be erectile dysfunction (unable to achieve or sustain an erection). Both men and women often experience problems with their bladders including urgency, frequency, incomplete bladder emptying or an inability to pass urine (retention). About 1 in 5 MSA patients will suffer a fall in their first year of disease.

As the disease progresses three groups of symptoms predominate. These are:

parkinsonism (slow, stiff movement, writing becomes small and spidery)
cerebellar dysfunction (difficulty coordinating movement and balance)
autonomic dysfunction (impaired automatic body functions) including:
— postural or orthostatic hypotension, resulting in dizziness or fainting upon standing up
— urinary incontinence
— impotence
— constipation
— dry mouth and skin
— trouble regulating body temperature due to abnormal sweating
— abnormal breathing during sleep
Not all patients experience all of these symptoms.

MSA usually progresses more quickly than Parkinson's disease.There is no remission from the disease. The remaining lifespan after the onset of symptoms is on average about 9 years. Almost 80% of patients are disabled within 5 years of onset of the motor symptoms, and only 20% survive past 12 years. Rate of progression differs in every case and speed of decline may vary widely in individual patients.

There is no discovered cure for MSA, so treatment involves treating the symptoms.

Management by rehabilitation professionals (physiotherapists, occupational therapists, speech therapists, and others) for problems with walking/movement, daily tasks, and speech problems is essential. Also social workers can help with coping with disability and access to health care services, both for the person with MSA as well as his/her family caregivers.

Ongoing care from a neurologist specialized in "movement disorders" is recommended as the complex symptoms of MSA are often not familiar to less-specialized health care professionals.

One particularly serious problem, the drop in blood pressure upon standing up (with risk of fainting thus injury from falling) often responds to fludrocortisone, a synthetic mineralocorticoid. Another common drug treatment is midodrine (an alpha-agonist.) Non-drug treatments include "head-up tilt" (elevating the head of the whole bed by about 10 degrees), salt tablets, generous intake of fluids, and pressure (elastic) stockings. Avoidance of triggers of low blood pressure (e.g. hot weather, alcohol, dehydration) are crucial.

Hospice/homecare services can be very useful as disability progresses.

Levdopa (L-Dopa) (a drug used in the treatment of Parkinson's disease)fails to improve the parkinsonian symptoms of most MSA patients. A recent trial reported that only 1.5% of MSA patients experienced a >50% improvement when taking levodopa, and even this was a transient effect lasting less than one year. Poor response to L-Dopa has been suggested as a possible element in the differential diagnosis of MSA from Parkinson's disease.

A recent study conducted in Europe failed to find an effect for the drug riluzole in treating MSA or PSP.

In some cases, a diagnosis of MSA can only be confirmed post-mortem. When brain tissue of a person with MSA is examined under a microscope, structures called glial cytoplasmic inclusion bodies are visible. The presence of these inclusions (also known as Papp-Lantos bodies) in the movement, balance and automatic control centres of the brain are the defining histopathologic hallmark of MSA. Recent studies have shown that major fillamentous component of glial and neuronal cytoplasmic inclusions is alpha-synuclein

Other terms have been used to refer to this disorder, based on the predominant systems presented. These terms and their distinctions have been dropped in recent (1996 onwards) medical usage[9] and replaced with MSA subtype naming, but are helpful to understanding the older literature about this disease:

progressive supranuclear palsy (PSP)

What is progressive supranuclear palsy?

Progressive supranuclear palsy (PSP) is a rare brain disorder that causes serious and permanent problems with control of gait and balance. The most obvious sign of the disease is an inability to aim the eyes properly, which occurs because of lesions in the area of the brain that coordinates eye movements. Some patients describe this effect as a blurring. PSP patients often show alterations of mood and behavior, including depression and apathy as well as progressive mild dementia.

The disorder's long name indicates that the disease begins slowly and continues to get worse (progressive), and causes weakness (palsy) by damaging certain parts of the brain above pea-sized structures called nuclei that control eye movements (supranuclear).

PSP was first described as a distinct disorder in 1964, when three scientists published a paper that distinguished the condition from Parkinson's disease. It is sometimes referred to as Steele-Richardson-Olszewski syndrome, reflecting the combined names of the scientists who defined the disorder. Although PSP gets progressively worse, no one dies from PSP itself.

Who gets PSP?

Approximately 20,000 Americans - or one in every 100,000 people over the age of 60 - have PSP, making it much less common than Parkinson's disease, which affects more than 500,000 Americans. Patients are usually middle-aged or elderly, and men are affected more often than women. PSP is often difficult to diagnose because its symptoms can be very much like those of other, more common movement disorders, and because some of the most characteristic symptoms may develop late or not at all.

What are the symptoms?

The most frequent first symptom of PSP is a loss of balance while walking. Patients may have unexplained falls or a stiffness and awkwardness in gait. Sometimes the falls are described by the person experiencing them as attacks of dizziness. This often prompts suspicion of an inner ear problem.

Other common early symptoms are changes in personality such as a loss of interest in ordinary pleasurable activities or increased irritability, cantankerousness, and forgetfulness. Patients may suddenly laugh or cry for no apparent reason, they may be apathetic, or they may have occasional angry outbursts, also for no apparent reason. It must be emphasized that the pattern of signs and symptoms can be quite different from person to person.

As the disease progresses, most patients will begin to develop a blurring of vision and problems controlling eye movement. In fact, eye problems usually offer the first definitive clue that PSP is the proper diagnosis. PSP patients have trouble voluntarily shifting their gaze downward, and also can have trouble controlling their eyelids. This can lead to involuntary closing of the eyes, prolonged or infrequent blinking, or difficulty in opening the eyes.

Another common visual problem is an inability to maintain eye contact during a conversation. This can give the mistaken impression that the patient is hostile or uninterested.

Speech usually becomes slurred and swallowing solid foods or liquids can be difficult. In rare cases, some patients will notice shaking of the hands.

What causes PSP?

We know that the symptoms of PSP are caused by a gradual deterioration of brain cells in a few tiny but important places at the base of the brain, in the region called the brainstem. One of these areas, the substantia nigra, is also affected in Parkinson's disease, and damage to this region of the brain accounts in part for the motor symptoms that PSP and Parkinson's have in common.

Scientists do not know what causes these brain cells to degenerate. There is no evidence that PSP is contagious, and genetic factors have not been implicated in most patients. No ethnic or racial groups have been affected more often than any others, and PSP is no more likely to occur in some geographic areas than in others.

There are, however, several theories about PSP's cause. One possibility is that an unconventional virus-like agent infects the body and takes years or decades to start producing visible effects. Creutzfeldt-Jakob disease is one disease known to be caused by such an agent. Another possibility is that random genetic mutations, of the kind that occur in all of us all the time, happen to occur in particular cells or certain genes, in just the right combination to injure these cells. A third possibility is that there is exposure to some unknown chemical in the food, air, or water which slowly damages certain vulnerable areas of the brain. This theory stems from a clue found on the Pacific island of Guam, where a common neurological disease occurring only there and on a few neighboring islands shares some of the characteristics of PSP, Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (Lou Gehrig's disease). Its cause is thought to be a dietary factor or toxic substance found only in that area.

Another possible cause of PSP is cellular damage caused by free radicals, reactive molecules produced continuously by all cells during normal metabolism. Although the body has built-in mechanisms for clearing free radicals from the system, scientists suspect that, under certain circumstances, free radicals can react with and damage other molecules. A great deal of research is directed at understanding the role of free radical damage in human diseases.

How is PSP diagnosed?

Initial complaints in PSP are typically vague and an early diagnosis is always difficult. The primary complaints fall into these categories: 1) symptoms of disequilibrium, such as unsteady walking or abrupt and unexplained falls without loss of consciousness; 2) visual complaints, including blurred vision, difficulties in looking up or down, double vision, light sensitivity, burning eyes, or other eye trouble; 3) slurred speech; and 4) various mental complaints such as slowness of thought, impaired memory, personality changes, and changes in mood.

PSP is often misdiagnosed because some of its symptoms are very much like those of Parkinson's disease, Alzheimer's disease, and more rare neurodegenerative disorders, such as Creutzfeldt-Jakob disease. In fact, PSP is most often misdiagnosed as Parkinson's disease early in the course of the illness. Memory problems and personality changes may also lead a physician to mistake PSP for depression, or even attribute symptoms to some form of dementia. The key to diagnosing PSP is identifying early gait instability and difficulty moving the eyes, the hallmark of the disease, as well as ruling out other similar disorders, some of which are treatable.

How is PSP different from Parkinson's disease?

Both PSP and Parkinson's disease cause stiffness, movement difficulties, and clumsiness. However, patients with PSP usually stand straight or occasionally even tilt their heads backward (and tend to fall backward), while those with Parkinson's disease usually bend forward. Problems with speech and swallowing are much more common and severe in PSP than in Parkinson's disease, and tend to show up earlier in the course of the disease. Eye movements are abnormal in PSP but close to normal in Parkinson's disease. Both diseases share other features: onset in late middle age, bradykinesia (slow movement), and rigidity of muscles. Tremor, almost universal in Parkinson's patients, is rare in PSP. Although Parkinson's patients markedly benefit from the drug levodopa, patients with PSP respond poorly and only transiently to this drug.

What is the prognosis?

PSP gets progressively worse but is not itself directly life-threatening. It does, however, predispose patients to serious complications such as pneumonia secondary to difficulty in swallowing (dysphagia). The most common complications are choking and pneumonia, head injury, and fractures caused by falls. The most common cause of death is pneumonia. With good attention to medical and nutritional needs, it is possible for most PSP patients to live a decade or more after the first symptoms of the disease.

Is there any treatment?

There is currently no effective treatment for PSP, although scientists are searching for better ways to manage the disease. In some patients the slowness, stiffness, and balance problems of PSP may respond to antiparkinsonian agents such as levodopa, or levodopa combined with anticholinergic agents or amantadine, but the effect is usually temporary. The speech, vision, and swallowing difficulties usually do not respond to any drug treatment.

Another group of drugs that has been of some modest success in PSP are antidepressant medications. The most commonly used of these drugs are fluoxetine (Prozac), amitriptyline (Elavil), and imipramine (Tofranil). The anti-PSP benefit of these drugs seems not to be related to their ability to relieve depression.

Non-drug treatment for PSP can take many forms. Patients frequently use weighted walking aids because of their tendency to fall backward. Bifocals or special glasses called prisms are sometimes prescribed for PSP patients to remedy the difficulty of looking down. Formal physical therapy is of no proven benefit in PSP, but certain exercises can be done to keep the joints limber.

A surgical procedure that may be necessary when there are swallowing disturbances is a gastrostomy. A gastrostomy (or a jejunostomy) is a minimally invasive procedure which is performed when the patient has difficulty swallowing or when severe choking is a definite risk. This surgery involves the placement of a tube through the skin of the abdomen into the stomach (intestine) for feeding purposes. Pallidotomy and other surgical procedures used in Parkinson's patients have not been proven effective in PSP.

What research is being done?

Studies to improve the diagnosis of PSP have recently been conducted at the National Institute of Neurological Disorders and Stroke (NINDS). Experiments to find the cause or causes of PSP are currently under way.

In addition, there is a great deal of ongoing research on Parkinson's and Alzheimer's diseases at the National Institutes of Health and at university medical centers throughout the country. Better understanding of those common related disorders will go a long way toward solving the problem of PSP, just as studying PSP may help shed light on Parkinson's and Alzheimer's diseases.

Where can I get more information?

For more information on neurological disorders or research programs funded by the National Institute of Neurological Disorders and Stroke, contact the Institute's Brain Resources and Information Network (BRAIN) at:

P.O. Box 5801
Bethesda, MD 20824
(800) 352-9424

If you have one of these rarer conditions, the Parkinson's Disease Society can provide you with support and may be able to put you in touch with specific organisations that support people with these conditions.

Perception is an intangible part of every being. It cannot be explained, defined, or nailed down the way that most scientists would like. In some ways, perception can be taught-a person's circumstance and background would cause him or her to perceive a situation in a particular way. In other ways, perception is unpredictable and ever changing. Even here, attempting to describe the indescribable, there are flaws in the last two sentences because they are based on the writer's perceptions of perception. It is too subjective for a "scientific" definition. What does it mean for a person suffering from bradykinesia? If the individual understands the condition, she will realize that the perceptions she has are not always correct. She may perceive herself to be making a fist, or spreading her fingers, but in fact she may not have accomplished this. (1) A blind and deaf person may have perceptions about the world around her. Most likely, her only correct perceptions are those perceptions about herself such as: "I am moving my arm," or "I am swinging my legs." The external stimuli are ineffective in this person, whereas a person with bradykinesia can only react completely and at a normal speed to external stimuli. Because of damage to signal pathways, the internal stimuli are ineffectively activated. (1)

Bradykinesia is a Greek term that means "slow movement", and it is one of the constituents of Parkinson's disease (2), although it is also associated with other diseases. For patients suffering from Parkinson's disease, it is usually the most tiring and frustrating of the associated conditions. Small muscle movement is one of the first affected areas of the body. Therefore, a common test is to ask the patient to tap her finger. Normal individuals tap their fingers at 4 or 5 Hz, someone afflicted with bradykinesia can usually manage only up to 1 Hz.(3) There is no cure for bradykinesia. Certain surgeries may help decrease the condition. Hope remains for the future while researchers continue to explore different possibilities, examining causes and treatments that will lead to a cure and to more clues about Parkinson's disease, Huntington's disease, and other conditions with which bradykinesia is associated. (4)

Not only does bradykinesia affect the speed of movement, the person's ability to complete a motion suffers. While walking, the arms no longer swing, but remain lax at the person's sides. (2) If a person suffering from bradykinesia is asked to make a fist without looking, he or she can tell that their movements are slow. The individual does not, however, realize that she never makes a complete fist. The fingers may be only slightly bent. Slowness of movement, by itself, is not bradykinesia. It can be associated with depression, stroke, or any kind of brain injury. The motion may be slow, but it is complete. The shuffling stride of a Parkinsonian and the monotonous voice are examples of bradykinesia-not only is the person moving the feet and legs slowly, they are unable to make a full stride. (1) Bradykinesia is a motion disorder and a perception disorder. A therapy treating both aspects has yet to be found.

Most cases of bradykinesia do not affect the entire body, but it is possible for the whole body to be afflicted. In severe cases, patients have a noticeable, unnatural stillness. While seated, they make no movements the way normal individuals move, such as crossing and uncrossing legs, crossing and uncrossing arms, shifting the angle of their head, or tapping their fingers. Bradykinesia in the face can lead to what is called "mask face" because of the constant lack of expression. Loss of voice volume and lack of intonation are common occurrences in those with bradykinesia.(4)

Since the most obvious symptoms of bradykinesia can apply to other diseases, and there are several causes for the condition, it is important that all bases are checked, including a thorough family history, drug use, and any pre-existing conditions must be considered. MRI generally rules out stroke and tumor. Sometimes a lumbar puncture is taken to measure the presence of metabolites and neurotransmitters in order to rule out metabolic disorders such as dopa-responsive dystonia. Drugs such as calcium-channel blockers, neuroleptics, and serotonin-reuptake inhibitors can be causes of bradykinesia. (4) Other causes include dementia, depression, dementia, drug-induced parkinsonism, and repeated head trauma.(5)

The problem of bradykinesia lies in the internal connections and stimuli within the nervous system. It is not a behavior that can be overcome with training. When there is an interruption of the signal pathway in the nervous system, the brain has an amazing ability to reroute the signal, creating a new pathway. The new pathway, however, does not accomplish effectively the task of carrying the signal. It takes a much longer time, and thus the translation of the signal into motion is much slower than before. Bradykinesia is reduced in patients who undergo therapies that attempt to restore the signal pathway by dealing with the interruption.(2) Even during such treatments, however, the patient may experience what is called the "freezing phenomenon" in Parkinson's disease. The entire body becomes frozen, and the person is literally trapped within her own body, unable to help herself. Although the specifics are not known, it is suspected that the freezing comes when there is a dopamine deficiency in a specific portion of the nervous system called the substantia nigra. Since people who suffer from bradykinesia respond better to external stimuli than internal stimuli, triggering an internal stimulus with an external one can end the "freezing phenomenon" control over their bodies.(6)

One of the identifiable chemical imbalances in people suffering from Parkinson's disease is the depletion of dopamine levels within specific regions of the brain. The treatment, therefore, is L-dopa, a precursor of dopamine, which is designed to convert to dopamine within the brain, compensating for the dopamine losses.(4) This type of medication does much to slow the progression of the disease, but it has little affect on bradykinesia. Surgeries are also used to alleviate the symptoms of Parkinson's disease. The two main surgeries performed are the thalamotomy and the pallidotomy. Of these, only the pallidotomy affects bradykinesia. The surgery involves placing a heat lesion, in the globus pallidus internus, that is commissioned to correct the abnormal amount of discharged nerve cells located in that area of the brain. This treatment was in existence before the introduction of L-dopa in the 1960s. L-dopa became overwhelmingly popular, but because of occasional drastic side effects, not all Parkinson's disease patients can take the medication. Furthermore, there seemed to be little long-term success of L-dopa. Despite this, it continues to be one of the main treatments for Parkinson's disease.(7)

As long as there is creativity and variation of perception, research will continue to explore and probe further into the hows and whys of diseases such as Parkinson's. While research on the larger diseases continues, new information on the symptomatic conditions will surface and help to explain the large and small pictures. Presently, much research is taking place. Neurotrophic proteins are being researched as ways to protect nerve cells from deteriorating. Neuroprotective agents such as naturally occurring enzymes are being investigated in their relationship to the deactivation of so-called free radicals. Explorations continue in neural tissue transplantation and genetic engineering.(8) The possibilities that research suggests are exciting. It holds the promise that future generations will only dig deeper, learn more, and question more. Bradykinesia is part of every day life for some. Others have never heard of it. Perhaps someday research will reveal something exciting that may lead to more information that will lead to effective treatment and better understanding of the functions within the brain

Parkinson's Disease and Sleep

Parkinson's disease is a disorder of the central nervous system that causes a loss of cells in the part of the brain that controls movement. People with Parkinson’s disease experience a range of symptoms, including tremor (shaking), rigidity (stiffness), slowness of movement, and problems with balance and coordination. They may also have memory problems, depression, and sleep complaints. Parkinson's disease is both chronic and progressive, meaning that once it occurs it does not go away and symptoms generally get worse over time; the rate or speed of progression is different from person to person.

Parkinson’s disease can be idiopathic, meaning that it occurs with no known cause. In this case it probably develops by some interaction between a person's genes and their environment. It can also be secondary, occurring as a result of another disease, exposure to certain drugs, or as a result of repeated head trauma. According to the Parkinson's Disease Foundation, between 15 and 25 percent of people with Parkinson's have a relative with the disease, suggesting that for some people it may be inherited. Age is also a risk factor, with older people being more likely to develop Parkinson’s disease than younger people, according to the National Institute of Neurological Disorders and Stroke at the National Institutes of Health. Exposure to toxins may also play a role but the nature of that role is not well understood.

Sleep problems may be an early sign of Parkinson’s disease, even before motor symptoms have begun. Some of the common sleep problems for Parkinson’s patients include:

Excessive daytime sleepiness
Sleep attacks (a sudden involuntary episode of sleep)
REM sleep behavior disorder (acting out dreams during sleep)
Periodic leg movement disorder (PLMD)
Restless legs syndrome (RLS)
Sleep apnea
Nocturia (frequent nighttime urination)
A recent study by UCLA researchers found an association between Parkinson's disease and narcolepsy, a disorder caused by the brain's inability to regulate sleep/wake cycles normally. The study revealed that patients with Parkinson's disease and those with narcolepsy both display a loss of orexin/hypocretin (Hcrt) cells in the brain and that loss of Hcrt cells is correlated with severity of PD. However, there is no reason to believe that narcolepsy patients are at increased risk of developing Parkinson's disease. According to study author Jerry Siegel, PhD, professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA, the cause of the hypocretin cell loss in Parkinson's is likely to be quite different from the cause of this cell loss in narcolepsy.

There may also be a connection between REM sleep behavior disorder (dream–enacting behaviors during sleep) and the subsequent development of Parkinson’s disease. In one study, researchers found that up to 75% of patients with REM behavior disorder went on to develop a Parkinsonian disorder, presumably Parkinson’s disease. In addition, people with Parkinson’s disease are at higher risk for restless legs syndrome (RLS) and periodic leg movement disorder, two conditions that may seriously disrupt sleep. However, there is no evidence that RLS or PLMD are risk factors for Parkinson’s disease.

In addition to sleep problems, people with Parkinson's disease often experience sleepiness during the daytime. In fact, one study found daytime sleepiness in 76% of Parkinson’s patients. These sleep-related symptoms can have a major impact on quality of life for Parkinson’s patients and treatment for these problems should be integrated with their therapeutic regimens.

Because of the mystery surrounding the origin of Parkinson’s disease, a great deal of research has been done on this problem. We know that the symptoms of Parkinson’s are primarily the result of the gradual loss of dopaminergic cells (neurons that release dopamine, a neurotransmitter that activates dopamine receptors) in the brain. Some Parkinson’s research has focused on the relationship between Parkinson’s and both the timing and duration of sleep. For example, a 12-year study by researchers at the National Institute of Environmental Health Sciences of the U.S. National Institutes of Health found that among nearly one million nurses, working the night shift was associated with a lower risk of Parkinson’s disease. They also found that long sleep (sleeping 9 hours or more) was associated with a higher risk.

People with Parkinson’s disease have a shortened life expectancy and may find it difficult to maintain their quality of life. Striving to maintain healthy sleep habits can help Parkinson’s patients with both the physical and psychological symptoms of their disease.

The hallmark symptoms of Parkinson's disease are tremor, rigidity, slow movements and problems maintaining balance. Other symptoms may include difficulty walking, talking, eating, or carrying out other simple tasks. Parkinson’s patients also suffer incontinence, constipation, and sexual dysfunction and are at higher risk for developing depression, anxiety, memory, and emotional problems.

Because Parkinson's disease is associated with "sleep attacks," patients may be suddenly overcome with drowsiness and fall asleep – regardless of what they are doing. This is particularly dangerous for those patients who are still driving, operating equipment (even kitchen and lawn equipment or other tools) or caring for dependents.

Not everyone with Parkinson's disease develops all or even most of the symptoms described above. The rate at which the disease progresses is also variable, with some people experiencing a rapid worsening of symptoms shortly after being diagnosed and others spending many years with only mild symptoms.

With Parkinson’s disease, there is a gradual loss of dopaminergic cells in the brain. There is no treatment for slowing or reversing this process, but there are drugs used to treat the symptoms that result. These drug therapies can dramatically improve quality of life for Parkinson's patients. Here are some of the most common types:

Dopaminergic agents – a class of drugs made from the neurotransmitter dopamine; these are the most effective therapies for Parkinson's patients, improving all of the motor symptoms. Some dopaminergic medications may cause sleepiness.
COMT inhibitors – block an enzyme that breaks down dopamine; decreases "off time" in Parkinson's patients, which is a period of impaired movement.
MAO-B inhibitors – prolong the action of dopamine in the brain to improve symptoms; may cause insomnia.
Anti-cholinergics – restore the balance between acetylcholine and dopamine, thus improving tremor and rigidity.
Amantadine – an antiviral drug that improves tremor, rigidity, and movement control.
Following diagnosis and the start of treatment, Parkinson's patients may experience a reduction of symptoms. This is called a "honeymoon." After a few years, the honeymoon ends and symptoms intensify, especially the motor symptoms.

People with Parkinson’s disease often have excessive daytime sleepiness. They also fall into REM sleep more quickly than the average person, according to their brain activity. These are both symptoms of narcolepsy and although there is no evidence that narcolepsy is a risk factor for Parkinson’s disease or vice versa, sleep-related symptoms in patients with Parkinson’s may be successfully treated with drugs that are used for narcolepsy, including stimulants for daytime sleepiness and sleeping medication for nighttime sleep. Bothersome dream-enacting behaviors often respond favorably to clonazepam, a sedative medication.

As Parkinson’s disease progresses and symptoms get worse, sleep problems may become more serious. For example, pain and uncontrollable movements may cause severe insomnia. Nighttime symptoms may be improved by taking Parkinson’s medication later in the day or by taking hypnotic sleep aides.

Insomnia may also be caused by certain medications used to treat Parkinson’s symptoms. In that case, taking medication earlier in the day may improve sleep. Keep in mind that any change in medication – including the addition of sleep aides or the timing of administration - should be prescribed by a physician. Sleep aides you can buy without a prescription usually contain diphenhydramine, an anti-histamine, which blocks absorption of dopamine.

Daytime sleepiness may also increase as Parkinson’s disease progresses. Using stimulant or alerting medications during the day may prevent sleep attacks and help patients avoid excessive napping, which may contribute to insomnia. In addition to drug therapies, behavioral techniques should be used for sleep and sleepiness problems in Parkinson’s patients.

Coping with Parkinson’s disease isn’t easy and will depend on the type and severity of the symptoms. However, there are certain things you can do to minimize symptoms, including taking medication as prescribed and getting healthy sleep. Here are some sleep tips for Parkinson’s patients:

Keep a regular sleep schedule, going to bed and getting up at the same time each day.
Take sedating medication late enough in the day so that you don’t get an increase in symptoms as you are trying to sleep.
Use satin sheets and pajamas to help with getting in and out of bed.
Minimize beverages before bedtime to help avoid nocturia (frequent nighttime urination).
Get exercise and exposure to light early in the day.
If the Parkinson’s disease is not advanced then behavioral therapies may be useful to try. Behavioral techniques may include changing attitudes about sleep, learning new sleep habits, and sticking to a regular sleep schedule.

Parkinson’s patients are encouraged to spend time outdoors and to exercise each day, preferably in the morning or shortly after waking. Light therapy may also help normalize the sleep/wake cycles of Parkinson’s patients, especially those who may be unable to spend time outdoors.

In general, the quality of life for patients with Parkinson’s disease may be optimized with support and recognizing the opportunities to make lifestyle adjustments. That is why support groups for patients, family members and caregivers can be important. They introduce the participants to caring and supportive individuals and you can learn what decisions others have made and what works best. This can help avoid getting "stuck" at one stage and can help to take advantage of a useful idea. Support groups may be in your local community or you may be able to participate in information exchanges online. Visit the National Parkinson Foundation support group information page to find support resources in your area.


Levodopa (Madopar and Sinemet)

Levodopa has been used to treat the symptoms of Parkinson's since the 1960s. It is a natural amino acid that the brain converts into dopamine and so it replaces the missing chemical.

The commonly prescribed forms of levodopa are:

Madopar (co-beneldopa)
Sinemet (co-careldopa)

Both contain an extra substance that prevents levodopa being changed to dopamine before it reaches the brain. Madopar contains levodopa plus benserazide and Sinemet contains levodopa plus carbidopa.

People with Parkinson's are usually started on a low dose and this is gradually increased until they and their GP/consultant feel that there has been a satisfactory response.

There are a number of forms of Madopar and Sinemet containing different amounts of the drugs.

Dispersible Madopar

Madopar has a dispersible form that may be swallowed whole or dissolved in water. Absorption of the dispersible form is quicker and can be used to 'kick start' people with Parkinson's. It can also be used in cases where control of the Parkinson's is difficult with standard levodopa. People who have difficulty swallowing tablets or capsules may also find this beneficial.

Once dispersed, the preparation leaves a chalky residue at the bottom of the glass that does not contain the drug.

Madopar capsules should NOT be broken.

Controlled release (CR) preparations of Madopar and Sinemet

Controlled release preparations are recognised by the letters CR after the drug name. The drug is released over a four- to six-hour period and may result in less fluctuation of levodopa levels in the blood. When changing from standard to controlled release preparations up to 30 percent more levodopa can be needed.

With controlled release preparations the time between doses can sometimes be prolonged by 30-50 percent. They may be used when a person with Parkinson's is experiencing 'wearing-off' of the dose of standard levodopa. They can also be taken before going to bed to reduce stiffness and immobility during the night.

Advantages of levodopa

Most people can tolerate Sinemet or Madopar and experience considerable long-term improvement, especially in stiffness and slowness of movement.

Disadvantages of levodopa

In the early days of taking these tablets some feelings of sickness and nausea are common. However, in most people, they are usually mild and pass as the body adjusts to the drug.

A small percentage of people cannot tolerate these drugs at all because of severe sickness, or other side effects such as confusion, hallucinations, mood swings or psychological changes.

In the longer term, the response to these drugs can become less reliable, and people may experience increasing periods when the effect of the most recent dose wears off before the next one is due or has begun to work (end-of-dose deterioration). Unwanted involuntary movements (dyskinesias) may appear, and there may be sudden switches from being 'on' and able to move to being 'off' and immobile.

These longer-term effects can sometimes be improved by altering the type or amount of Sinemet or Madopar, or the frequency with which the drug is taken. If this is not satisfactory, other types of drug can be combined with levodopa

Dopamine agonists

How they work

Dopamine agonists are a class of drug that mimic the effects of the brain chemical dopamine. These agonists stimulate nerve cells and produce similar effects to the natural dopamine found in our brains.


Commonly prescribed dopamine agonists are:

pramipexole dihydrochloride (Mirapexin®)
ropinirole hydrochloride (Requip®)
pergolide mesilate (Celance®)
bromocriptine mesylate (Parlodel®)
cabergoline (Cabaser®, Dostinex®)
rotigotine (Neupro®)
apomorphine hydrochloride (APO-go®)

Why they are used

Dopamine agonists may be used alone or in combination with levodopa to relieve the motor symptoms of Parkinson's.

People who are newly diagnosed with Parkinson's may be prescribed a dopamine agonist alone. This occurs frequently when the person is younger than 60 years of age.

Agonists can also be given in combination with levodopa therapy. This often occurs in people with more advanced Parkinson's, whose response to levodopa begins to fluctuate, and whose motor symptoms are not well-controlled.

Taking levodopa for a long time often leads to motor complications that are difficult to manage. Therefore, by commencing treatment with a dopamine agonist instead of levodopa, the onset of levodopa-related motor problems can be postponed.

How they are taken

A variety of dopamine agonists are currently available. These differ in what form they are delivered, how long their effects last, and potential side effects.

Most agonists are taken by mouth as tablets or capsules for up to several times a day. There is also a patch for rotigotine that is applied once daily onto the skin. Apomorphine is available as a single injection or as a continuous infusion under the skin.


The effects of dopamine agonists tend to last longer than levodopa. People on agonists are less prone to side effects such as dyskinesias (uncontrolled movements) and 'on/off' fluctuations.

Agonists are delivered in a range of different forms including: tablets/capsules; skin patch; injection and continuous supply under the skin.


When agonists are used alone, they can be less effective than levodopa at controlling the motor symptoms of Parkinson's.

Dopamine agonists need to be carefully introduced to minimise their side effects. Agonists are therefore started at a low dose and increased gradually until the best benefits are achieved.

Side effects

Common side effects of dopamine agonists include:

nausea and vomiting
drowsiness and sudden 'attacks' of sleepiness
dizziness or fainting due to low blood pressure
hallucinations and confusion
existing dyskinesias may become more troublesome

Compulsive behaviour

There is growing evidence that suggests a link between certain dopamine agonists and compulsive behaviour.

Compulsive behaviour is when a person is unable to resist an impulse or temptation such as gambling, shopping, eating and sex. This behaviour performed repetitively, excessively or obsessively may cause harm to the individual or others.

Studies have shown that compulsive behaviour is an uncommon side effect. It is currently estimated that up to 14% of people with Parkinson's taking dopamine agonists experience some form of compulsive behaviour to varying degrees
There is also the possibility that some people may become addicted to their dopamine agonists. These people take increasing doses despite experiencing side effects.

Heart valve and lung problems

Recent studies have shown that people taking pergolide (Celance®) or cabergoline (Cabaser®, Dostinex®) have a higher risk of heart valve and lung problems than people taking other dopamine agonists.

Both pergolide and cabergoline are part of a sub-class of drugs called ergolines. These drugs cause a condition called fibrosis in various organs of the body. Fibrosis is the hardening of tissues that can make the organs not work properly.

In 2007, the US Food and Drug Administration (FDA) announced that manufacturers of pergolide would voluntarily withdraw these drugs from the market due to concerns over its effect on heart valves. Pergolide is still available in the UK, however, the use of the drug is restricted and people are carefully monitored for adverse side effects.


Apomorphine is a dopamine agonist that is administered by (subcutaneous) injection under the skin. When sudden fluctuations in symptoms occur, in spite of all efforts to adjust medication, injections of apomorphine may be used - almost like a 'rescue remedy' - between doses of a person's usual tablets.

Many people self-inject intermittently with a syringe or a ready-loaded disposable APO-go pen. In some cases, a more continuous supply of apomorphine is required which is administered via a pump. This portable, battery-driven syringe pump works by the insertion of a needle under the skin. It can be injected into the outside thigh, or into the stomach (below the navel).


It acts very quickly and reliably so that people who need to be active at specific times can continue with their normal activities.

It can bring great relief to people who are experiencing extreme variations in mobility and prolonged 'off' periods.


Apomorphine can only help those people with Parkinson's who show a response to Sinemet® or Madopar®. It can cause nausea and therefore another drug called domperidone (Motilium®), which acts specifically against nausea and sickness, has to be taken in addition, at least while apomorphine is being introduced.

COMT inhibitors

COMT inhibitors work by blocking an enzyme called Catechol-O­methyl Transferase (COMT) that breaks down levodopa. As a result they slow the destruction of levodopa in the body. COMT inhibitors are therefore used with levodopa to prolong the duration of action.

These are:

Entacapone (Comtess)

Taken with each levodopa dose and tolcapone three times a day. Both drugs should be effective from the first dose with noticeable benefits from the first or second day.

Tolcapone (Tasmar)

Recently reintroduced in March 2005. It was withdrawn from the UK in 1998 on the recommendation of the European Medical Agency, due to an association with rare but potentially fatal liver failure.

Stalevo (levodopa/carbidopa/entacapone)

Introduced in November 2003, is a combination drug to treat Parkinson's, and contains levodopa, carbidopa and entacapone in one tablet.

To avoid any potential risks, only physicians experienced in the management of advanced Parkinson's will be able to prescribe the drug and patients must undergo regular medical checks and undergo blood tests to check liver function.


When used with levodopa, COMT inhibitors can reduce the daily 'off' time and increase the 'on' time. In many cases, the levodopa dose and dosing frequency can also be reduced.


Due to how these drugs work, there may be an increase in the side effects caused by levodopa, notably dyskinesias, nausea and vomiting. Where these side effects increase after starting the drug, people should raise the issue with their GP/consultant, as reducing the levodopa dose can often help. Be aware that other drugs (for Parkinson's or other conditions) can affect the action of COMT inhibitors, although the combination of apomorphine and entacapone needs careful supervision.

Other reported side effects of COMT inhibitors include abdominal pain, loose stools and diarrhoea. Also urine can become discoloured; this is simply due to the substances in the drug and is harmless.

MAO-B inhibitors

These are:

selegiline (Eldepryl/Zelapar)
rasagiline (Azilect).

Selegiline works by blocking the enzyme monoaomine oxidase type B (MAO-B), which breaks down dopamine in the brain. It is used to make the dose of Sinemet or Madopar last longer or reduce the amount required.

Sometimes a GP/consultant may treat those newly diagnosed with Parkinson's with selegiline on its own as it may improve the symptoms, delay the need for levodopa, and possibly delay the onset of fluctuations in the effectiveness of drugs.

Early research suggested that selegiline might slow down the progression of Parkinson's. Other research has suggested that it might increase mortality. There is no conclusive evidence to support these claims.


By itself, selegiline has very few side effects. Because Zelapar is absorbed better, a smaller dose is needed.

In trials, rasagiline has shown the ability to reduce 'off' time and improve motor function in patients with motor fluctuations related to levodopa.


When selegiline is taken together with Sinemet and Madopar, levodopa side effects such as dyskinesias, hallucinations or vivid dreaming may sometimes occur or worsen. To compensate for this, the dose of levodopa may be reduced.

When selegiline is given on its own it can cause blood pressure to drop. Selegiline acts as a mild stimulant, so is often prescribed as a single dose to be taken in the morning rather than in the evening when it might interfere with sleep.

When people have taken rasagiline on its own (without levodopa), the most commonly reported side effects have been:

aching joints
flu-like symptoms

When taken with levodopa, the most common reports were of uncontrolled movements and accidental falls. These effects may be due to the increase in dopamine caused by rasagiline, so always report such problems to your doctor.

It should not be taken together with, or within 5 weeks of receiving, Fluoxetine (Prozac) or Fluvoxamine (Faverin).

Rasagiline works by slowing the breakdown of dopamine in the brain, keeping it 'available' for longer. It can be taken early in Parkinson's disease on its own (as 'monotherapy') to help boost dopamine still being produced by the brain, and/or later in the disease, to boost the effect of levodopa (as' adjunct therapy').

Glutamate Antagonist

Amantadine (Symmetrel)

This drug works in a different way from those already discussed. It does several things, but its main beneficial effect may be to promote the release of dopamine and to allow it to stay longer at its site of action.

Amantadine can be prescribed alone, but can also be taken in combination with other anti-parkinsonian drugs. Amantadine is available in capsules and as a syrup.

Relatively few newly diagnosed people with Parkinson's are prescribed amantadine.


It has relatively few side effects. In some patients it reduces drug-induced dyskinesias without worsening the Parkinsonian symptoms. It may have a stimulatory effect and can help some people with tiredness.


It usually has only a mild effect, helps only a minority of people and its effectiveness may be short-lived. It may cause swelling of the ankles or a mottled appearance on the skin of the lower leg, as well as causing confusion.


Anticholinergics are older drugs, less commonly prescribed these days, that can have a mild effect on the symptoms of Parkinson's by blocking the action of the chemical messenger acetylcholine.

These are:

trihexyphenidyl (Broflex, Artane, Agitane)
benztropine (Cogentin)
orphenadrine (Disipal)
procyclidine (Kemadrin, Arpicolin).

Anticholinergics are often prescribed alone, especially in the early stages before levodopa is necessary, although they are also used in conjunction with levodopa or amantadine. Trihexyphenidyl, orphenadrine and procyclidine are available in liquid form.


They can be useful for younger people in the early stages of Parkinson's when symptoms are mild. They tend to improve tremor more than slowness and stiffness. Anticholinergics may also be used to reduce saliva production when drooling is a problem and to damp down bladder contractions that can cause a strong, frequent urge to urinate.


Confusion, a dry mouth, constipation and blurring of vision can occur. They are not usually prescribed to older people with Parkinson's because there is an increased risk of confusion as well as memory loss, and in men, urinary hesitancy. Also, anticholinergics may interfere with levodopa absorption in the small bowel. This can reduce the effectiveness of Sinemet or Madopar.

Compulsive behaviour

There are several categories of drugs for the treatment of Parkinson's and it is thought that there may be a connection between some dopamine agonists (one class of drugs that can be used to treat Parkinson's) and the incidence of compulsive behaviour.

However, clinical studies have shown this to be an uncommon side effect, currently estimated to occur in up to 14% of people taking dopamine agonists to varying degrees. Some studies have suggested that other types of anti-Parkinson's medication can produce similar effects.

What is compulsive behaviour?

Compulsive disorders are associated with a person's inability to resist a temptation or impulse that may ultimately cause harm to themselves or others. In a lot of cases, this behaviour may be out of character for the person. These can be expressed in a number of ways and here are just a few examples:

Pathological (addictive) gambling
Compulsive (binge) eating
Compulsive shopping
Punding or 'compulsive hobbyism'
Addiction to anti-Parkinson's medication

What can be done to help?

It is important to realise that this behaviour, which is known as Impulse Control Disorder (ICD), is abnormal and a person experiencing it should seek help from a Parkinson's nurse, neurologist or hospital physician urgently.

As the person themselves may not realise that there is a problem, it is key that carers and family members note any abnormal behaviour and discuss it with the appropriate professional at the earliest possible stage.

Treatment strategies

Treatment strategies can involve reducing the dose of Parkinson's medication, undertaking psychotherapy and also considering whether other types of medication should be introduced.

The PDS does not advise anyone to stop taking their Parkinson's drugs without seeking the advice of their health professional. Changes to a Parkinson's medication regimen should only be made with the advice of a Parkinson's specialist.

As well as discussing medication concerns with a Parkinson's nurse, neurologist or hospital physician, appropriate action should be taken immediately to limit the impact of these compulsive behaviours. For example, you may need to seek financial advice if compulsive gambling has led to financial difficulties, or speak to a relationship counsellor if your relationships are being affected by your libido.