what is tremor and parkinson

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What is tremor?

Tremor is an unintentional, somewhat rhythmic, muscle movement involving to-and-fro

movements (oscillations) of one or more parts of the body. It is the most common of allinvoluntary movements and can affect the hands, arms, head, face, vocal cords, trunk, and legs.

Most tremors occur in the hands. In some people, tremor is a symptom of another neurologicaldisorder. The most common form of tremor, however, occurs in otherwise healthy people.Although tremor is not life-threatening, it can be embarrassing to some people and make it

harder to perform daily tasks.

What causes tremor?

Tremor is generally caused by problems in parts of the brain that control muscles throughout the body or in particular areas, such as the hands. Neurological disorders or conditions that can

produce tremor include multiple sclerosis, stroke, traumatic brain injury, and neurodegenerativediseases that damage or destroy parts of the brainstem or the cerebellum. Other causes include

the use of some drugs (such as amphetamines, corticosteroids, and drugs used for certain psychiatric disorders), alcohol abuse or withdrawal, mercury poisoning, overactive thyroid, or

liver failure. Some forms of tremor are inherited and run in families, while others have no knowncause.

What are the characteristics of tremor?

Characteristics may include a rhythmic shaking in the hands, arms, head, legs, or trunk; shaky

voice; difficulty writing or drawing; or problems holding and controlling utensils, such as a fork.Some tremors may be triggered by or become exaggerated during times of stress or strong

emotion, when the individual is physically exhausted, or during certain postures or movements.

Tremor may occur at any age but is most common in middle-aged and older persons. It may be

occasional, temporary, or occur intermittently. Tremor affects men and women equally.

A useful way to understand and describe tremors is to define them according to the followingtypes. Resting or static tremor occurs when the muscle is relaxed and the limb is fully

supported against gravity, such as when the hands are lying on the lap. It may be seen as ashaking of the limb, even when the person is at rest. This type of tremor is often seen in patients

with Parkinson's disease. An action tremor occurs during any type of movement of an affected body part. There are several subclassifications of action tremor. Postural tremor occurs when

the person maintains a position against gravity, such as holding the arms outstretched. Kinetic (or

intention) tremor occurs during purposeful voluntary movement, such as touching a finger toone's nose during a medical exam. Task-specific tremor appears when performing highlyskilled, goal-oriented tasks such as handwriting or speaking. Isometric tremor occurs during a

voluntary muscle contraction that is not accompanied by any movement.

What are the different categories of tremor?



Psychogenic tremor (also called hysterical tremor) can occur at rest or during postural or kineticmovement. The characteristics of this kind of tremor may vary but generally include sudden

onset and remission, increased incidence with stress, change in tremor direction and/or body partaffected, and greatly decreased or disappearing tremor activity when the patient is distracted.

Many patients with psychogenic tremor have a conversion disorder (defined as a psychological

disorder that produces physical symptoms) or another psychiatric disease.

Orthostatic tremor is characterized by rhythmic muscle contractions that occur in the legs and

trunk immediately after standing. Cramps are felt in the thighs and legs and the patient shakesuncontrollably when asked to stand in one spot. No other clinical signs or symptoms are present

and the shaking ceases when the patient sits or is lifted off the ground. Orthostatic tremor mayalso occur in patients who have essential tremor.

Physiologic tremor occurs in every normal individual and has no clinical significance. It is

rarely visible to the eye and may be heightened by strong emotion (such as anxiety or fear), physical exhaustion, hypoglycemia, hyperthyroidism, heavy metal poisoning, stimulants, alcohol

withdrawal, or fever. It can be seen in all voluntary muscle groups and can be detected byextending the arms and placing a piece of paper on of the hands. Enhanced physiologic tremor is

a strengthening of physiologic tremor to more visible levels. It is generally not caused by aneurological disease but by reaction to certain drugs, alcohol withdrawal, or medical conditions

including an overactive thyroid and hypoglycemia. It is usually reversible once the cause iscorrected.

Tremor can result from other conditions as well. Alcoholism, excessive alcohol consumption, or alcohol withdrawal can kill certain nerve cells, resulting in tremor, especially in the hand.

(Conversely, small amounts of alcohol may help to decrease familial and essential tremor, butthe mechanism behind this is unknown. Doctors may use small amounts of alcohol to aid in the

diagnosis of certain forms of tremor but not as a regular treatment for the condition.) Tremor in peripheral neuropathy may occur when the nerves that supply the body's muscles are traumatized

by injury, disease, abnormality in the central nervous system, or as the result of systemicillnesses. Peripheral neuropathy can affect the whole body or certain areas, such as the hands,

and may be progressive. Resulting sensory loss may be seen as a tremor or ataxia (inability tocoordinate voluntary muscle movement) of the affected limbs and problems with gait and

balance. Clinical characteristics may be similar to those seen in patients with essential tremor.

How is tremor diagnosed?

During a physical exam a doctor can determine whether the tremor occurs primarily during

action or at rest. The doctor will also check for tremor symmetry, any sensory loss, weakness or muscle atrophy, or decreased reflexes. A detailed family history may indicate if the tremor isinherited. Blood or urine tests can detect thyroid malfunction, other metabolic causes, and

abnormal levels of certain chemicals that can cause tremor. These tests may also help to identifycontributing causes, such as drug interaction, chronic alcoholism, or another condition or disease.

Diagnostic imaging using computerized tomography or magnetic resonance imaging may helpdetermine if the tremor is the result of a structural defect or degeneration of the brain.



The doctor will perform a neurological exam to assess nerve function and motor and sensoryskills. The tests are designed to determine any functional limitations, such as difficulty with

handwriting or the ability to hold a utensil or cup. The patient may be asked to place a finger onthe tip of her or his nose, draw a spiral, or perform other tasks or exercises.

The doctor may order an electromyogram to diagnose muscle or nerve problems. This testmeasures involuntary muscle activity and muscle response to nerve stimulation.

Are there any treatments?

There is no cure for most tremors. The appropriate treatment depends on accurate diagnosis of the cause.

Some tremors respond to treatment of the underlying condition. For example, in some cases of psychogenic tremor, treating the patient's underlying psychological problem may cause the

tremor to disappear.

Symptomatic drug therapy is available for several forms of tremor. Drug treatment for parkinsonian tremor involves levodopa and/or dopamine-like drugs such as pergolide mesylate,

bromocriptine mesylate, and ropinirole. Other drugs used to lessen parkinsonian tremor includeamantadine hydrochloride and anticholinergic drugs.

Essential tremor may be treated with propranolol or other beta blockers (such as nadolol) and

primidone, an anticonvulsant drug.

Cerebellar tremor typically does not respond to medical treatment. Patients with rubral tremor

may receive some relief using levodopa or anticholinergic drugs.

Dystonic tremor may respond to clonazepam, anticholinergic drugs, and intramuscular injectionsof botulinum toxin. Botulinum toxin is also prescribed to treat voice and head tremors and

several movement disorders.

Clonazepam and primidone may be prescribed for primary orthostatic tremor.

Enhanced physiologic tremor is usually reversible once the cause is corrected. If symptomatic

treatment is needed, beta blockers can be used.

Eliminating tremor "triggers" such as caffeine and other stimulants from the diet is often

recommended.

Physical therapy may help to reduce tremor and improve coordination and muscle control for

some patients. A physical therapist will evaluate the patient for tremor positioning, musclecontrol, muscle strength, and functional skills. Teaching the patient to brace the affected limb

during the tremor or to hold an affected arm close to the body is sometimes useful in gainingmotion control. Coordination and balancing exercises may help some patients. Some therapists



recommend the use of weights, splints, other adaptive equipment, and special plates and utensilsfor eating.

Surgical intervention such as thalamotomy and deep brain stimulation may ease certain tremors.

These surgeries are usually performed only when the tremor is severe and does not respond to

drugs.

Thalamotomy, involving the creation of lesions in the brain region called the thalamus, is quite

effective in treating patients with essential, cerebellar, or parkinsonian tremor. This in-hospital procedure is performed under local anesthesia, with the patient awake. After the patient's head is

secured in a metal frame, the surgeon maps the patient's brain to locate the thalamus. A smallhole is drilled through the skull and a temperature-controlled electrode is inserted into the

thalamus. A low-frequency current is passed through the electrode to activate the tremor and toconfirm proper placement. Once the site has been confirmed, the electrode is heated to create a

temporary lesion. Testing is done to examine speech, language, coordination, and tremor activation, if any. If no problems occur, the probe is again heated to create a 3-mm permanent

lesion. The probe, when cooled to body temperature, is withdrawn and the skull hole is covered.The lesion causes the tremor to permanently disappear without disrupting sensory or motor

control.

Deep brain stimulation (DBS) uses implantable electrodes to send high-frequency electrical

signals to the thalamus. The electrodes are implanted as described above. The patient uses ahand-held magnet to turn on and turn off a pulse generator that is surgically implanted under the

skin. The electrical stimulation temporarily disables the tremor and can be "reversed," if necessary, by turning off the implanted electrode. Batteries in the generator last about 5 years

and can be replaced surgically. DBS is currently used to treat parkinsonian tremor and essentialtremor.

The most common side effects of tremor surgery include dysarthria (problems with motor

control of speech), temporary or permanent cognitive impairment (including visual and learningdifficulties), and problems with balance.

What research is being done?

The National Institute of Neurological Disorders and Stroke, a unit of the National Institutes of

Health (NIH) within the U.S. Department of Health and Human Services, is the nation's leadingfederal funder of research on disorders of the brain and nervous system. The NINDS sponsors

research on tremor both at its facilities at the NIH and through grants to medical centers.

Scientists at the NINDS are evaluating the effectiveness of 1-octanol, a substance similar to

alcohol but less intoxicating, for treating essential tremor. Results of two previous NIH studieshave shown this agent to be promising as a potential new treatment.

Other NINDS-funded grantees are studying two antidepressant medications, paroxetine and

venlafaxine, to see if they can help control depression in Parkinson's disease and affect motor symptoms such as tremor, stiffness, slowness, and loss of balance.



An additional NINDS study will examine how dextromethorphan, a drug that alters reflexes of the larynx (voice box), might reduce voice symptoms in people with voice disorders, including

vocal tremor. This study will compare the effects of dextromethorphan, lorazepam (atranquilizer), and a placebo in patients with four types of voice disorders.

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 andInformation Network (BRAIN) at:

BRAIN

P.O. Box 5801Bethesda, MD 20824

(800) 352-9424http://www.ninds.nih.gov

Information also is available from the following organizations:

International Essential Tremor FoundationP.O. Box 14005

Lenexa, KS [email protected]

http://www.essentialtremor.org Tel: 913-341-3880 888-387-3667

Fax: 913-341-1296

WE MOVE (Worldwide Education & Awareness for Movement Disorders)204 West 84th Street

New York, NY [email protected]

http://www.wemove.org Tel: 212-875-8312 866-546-3136

Fax: 212-875-8389

Tremor Action Network

P.O. Box 5013Pleasanton, CA 94566-5013

[email protected] http://www.tremoraction.org

Tel: 510-681-6565 925-462-0111Fax: 925-369-0485

National Ataxia Foundation (NAF)

2600 Fernbrook Lane North Suite 119 br> Minneapolis, MN [email protected]



http://www.ataxia.org Tel: 763-553-0020

Fax: 763-553-0167

SOURCE: National Institutes of Health (www.nih.gov)

What is Parkinson's disease?

Parkinson's disease is the second most common neurodegenerative disorder and the mostcommon movement disorder. It is characterized by progressive loss of muscle control, which

leads to trembling of the limbs and head while at rest, stiffness, slowness, and impaired balance.As symptoms worsen, it may become difficult to walk, talk, and complete simple tasks.

The progression of Parkinson's disease and the degree of impairment vary from individual toindividual. Many people with Parkinson's disease live long productive lives, whereas others

become disabled much more quickly. Premature death is usually due to complications such as

falling-related injuries or pneumonia.

In the United States, about 1 million people are affected by Parkinson's disease and worldwide

about 5 million. Most individuals who develop Parkinson's disease are 60 years of age or older.Parkinson's disease occurs in approximately 1% of individuals aged 60 years and in about 4% of

those aged 80 years. Since overall life expectancy is rising, the number of individuals withParkinson's disease will increase in the future. Adult-onset Parkinson's disease is most common,

but early-onset Parkinson's disease (onset between 21-40 years), and juvenile-onset Parkinson'sdisease (onset before age 21) also exist.

Descriptions of Parkinson's disease date back as far as 5000 BC. Around that time, an ancient

Indian civilization called the disorder Kampavata and treated it with the seeds of a plantcontaining therapeutic levels of what is today known as levodopa. Parkinson's disease was

named after the British doctor James Parkinson, who in 1817 first described the disorder in greatdetail as "shaking palsy."

What causes Parkinson's disease?

A substance called dopamine acts as a messenger between two brain areas - the substantia nigraand the corpus striatum - to produce smooth, controlled movements. Most of the movement-

related symptoms of Parkinson's disease are caused by a lack of dopamine due to the loss of dopamine-producing cells in the substantia nigra. When the amount of dopamine is too low,

communication between the substantia nigra and corpus striatum becomes ineffective, andmovement becomes impaired; the greater the loss of dopamine, the worse the movement-related

symptoms. Other cells in the brain also degenerate to some degree and may contribute to non-movement related symptoms of Parkinson's disease.

Although it is well known that lack of dopamine causes the motor symptoms of Parkinson's

disease, it is not clear why the dopamine-producing brain cells deteriorate. Genetic and pathological studies have revealed that various dysfunctional cellular processes, inflammation,



and stress can all contribute to cell damage. In addition, abnormal clumps called Lewy bodies,which contain the protein alpha-synuclein, are found in many brain cells of individuals with

Parkinson's disease. The function of these clumps in regards to Parkinson's disease is notunderstood. In general, scientists suspect that dopamine loss is due to a combination of genetic

and environmental factors.

Parkinson's Disease (cont.)

In this Article

y What is Parkinson's disease?

y What causes Parkinson's disease?

y What genes are linked to Parkinson's disease?

y Who is at risk for Parkinson's disease?

y What are the symptoms of Parkinson's disease?

y What other conditions resemble Parkinson's disease?

y How is Parkinson's disease diagnosed?

y What is the treatment for Parkinson's disease?

y How can people learn to cope with Parkinson's disease?

y Can Parkinson's disease be prevented?

y What is the prognosis for Parkinson's disease?

y Parkinson's Disease At A Glance

y Parkinson's Disease Glossary

y Parkinson's Disease Index

y Find a local Neurologist in your town

What genes are linked to Parkinson's disease?

In most individuals, Parkinson's disease is idiopathic, which means that it arises sporadicallywith no known cause. However, about 15% of individuals have family members with Parkinson's

disease. By studying families with hereditary Parkinson's disease, scientists have identifiedseveral genes that are associated with the disorder. Studying these genes helps understand the

cause of Parkinson's disease and may lead to new therapies. So far, five genes have beenidentified that are definitively associated with Parkinson's disease.

1. SNCA (synuclein, alpha non A4 component of amyloid precursor): SNCA makes the protein

alpha-synuclein. In brain cells of individuals with Parkinson's disease, this protein aggregates in

clumps called Lewy bodies. Mutations in the SNCA gene are found in early-onset Parkinson's

disease.

2. PARK2 (Parkinson's disease autosomal recessive, juvenile 2): The PARK2 gene makes the protein

parkin. Mutations of the PARK2 gene are mostly found in individuals with juvenile Parkinson's

disease. Parkin normally helps cells break down and recycle proteins.



3. PARK7 (Parkinson's disease autosomal recessive, early onset 7): PARK7 mutations are found in

early-onset Parkinson's disease. The PARK7 gene makes the DJ-1 protein, which may protect

cells from oxidative stress.

4. PINK1 (PTEN-induced putative kinase 1): Mutations of this gene are found in early-onset

Parkinson's disease. The exact function of the protein made by PINK1 is not known, but it may

protect structures within the cell called mitochondria from stress.

5. LRRK2 (leucine-rich repeat kinase 2): LRRK2 makes the protein dardarin. Mutations in the LRRK2

gene have been linked to late-onset Parkinson's disease.

Several other chromosome regions and the genes GBA (glucosidase beta acid), SNCAIP(synuclein alpha interacting protein), and UCHL1 (ubiquitin carboxyl-terminal esterase L1) may

also be linked to Parkinson's disease.

Who is at risk for Parkinson's disease?

y Age is the largest risk factor for the development and progression of Parkinson's disease. Most

people who develop Parkinson's disease are older than 60 years years of age.

y Men are affected about 1.5 to 2 times more often than women.

y A small number of individuals are at increased risk because of a family history of the disorder.

y Head trauma, illness, or exposure to environmental toxins such as pesticides and herbicides may

be a risk factor.


In this Article




y Who is at risk for Parkinson's disease?

y What are the symptoms of Parkinson's disease?













What are the symptoms of Parkinson's disease?

The primary symptoms of Parkinson's disease are all related to voluntary and involuntary motor

function and usually start on one side of the body. Symptoms are mild at first and will progressover time. Some individuals are more affected than others. Studies have shown that by the time

that primary symptoms appear, individuals with Parkinson's disease will have lost 60% to 80%or more of the dopamine-producing cells in the brain. Characteristic motor symptoms include thefollowing:

y Tremors: Trembling in fingers, hands, arms, feet, legs, jaw, or head. Tremors most often occur

while the individual is resting, but not while involved in a task. Tremors may worsen when an

individual is excited, tired, or stressed.

y Rigidity: Stiffness of the limbs and trunk, which may increase during movement. Rigidity may

produce muscle aches and pain. Loss of fine hand movements can lead to cramped handwriting

(micrographia) and may make eating difficult.

y Bradykinesia: Slowness of voluntary movement. Over time, it may become difficult to initiate

movement and to complete movement. Bradykinesia together with stiffness can also affect the

facial muscles and result in an expressionless, "mask-like" appearance.

y Postural instability: Impaired or lost reflexes can make it difficult to adjust posture to maintain

balance. Postural instability may lead to falls.

y Parkinsonian gait: Individuals with more progressive Parkinson's disease develop a distinctive

shuffling walk with a stooped position and a diminished or absent arm swing. It may become

difficult to start walking and to make turns. Individuals may freeze in mid-stride and appear to

fall forward while walking.

Secondary symptoms of Parkinson's disease

While the main symptoms of Parkinson's disease are movement-related, progressive loss of muscle control and continued damage to the brain can lead to secondary symptoms. These vary

in severity, and not every individual will experience all of them. Some of the secondarysymptoms include:

y anxiety, insecurity, and stress

y confusion, memory loss, and dementia (more common in elderly individuals)

y constipation

y depression

y difficulty swallowing and excessive salivation

y diminished sense of smell



y increased sweating

y male erectile dysfunction

y skin problems

y slowed, quieter speech, and monotone voice

y urinary frequency/urgency


In this Article




y Who is at risk for Parkinson's disease? y What are the symptoms of Parkinson's disease?











What other conditions resemble Parkinson's disease?

In its early stages, Parkinson's disease can resemble a number of other conditions with

Parkinson-like symptoms known as Parkinsonism. These conditions include multiple systematrophy, progressive supranuclear palsy, corticobasal degeneration, Lewy body dementia, stroke,

encephalitis (inflammation of the brain), and head trauma. Alzheimer's disease and primarylateral sclerosis can also be mistaken for Parkinson's disease. Other similar conditions include

essential tremor , dystonic tremor, vascular Parkinsonism, and drug-induced Parkinsonism.

How is Parkinson's disease diagnosed?

An early and accurate diagnosis of Parkinson's disease is important in developing good treatment

strategies to maintain a high quality of life for as long as possible. However, there is no test todiagnose Parkinson's disease with certainty (except after the individual has passed away). A

diagnosis of Parkinson's disease - especially in the early phase - can be challenging due to



similarities to related movement disorders and other conditions with Parkinson-like symptoms.Individuals may sometimes be misdiagnosed as having another disorder, and sometimes

individuals with Parkinson-like symptoms may be inaccurately diagnosed as having Parkinson'sdisease. It is therefore important to re-evaluate individuals in the early phase on a regular basis to

rule out other conditions that may be responsible for the symptoms.

A neurologist who specializes in movement disorders will be able to make the most accuratediagnosis. An initial assessment is made based on medical history, a neurological exam, and the

symptoms present. For the medical history, it is important to know whether other familymembers have Parkinson's disease, what types of medication have been or are being taken, and

whether there was exposure to toxins or repeated head trauma in the past. A neurological exammay include an evaluation of coordination, walking, and fine motor tasks involving the hands.

Several guidelines have been published to assist in the diagnosis of Parkinson's disease. These

include the Hoehn and Yahr scale and the Unified Parkinson's Disease Rating Scale. Tests areused to measure mental capacity, behavior, mood, daily living activities, and motor function.

They can be very helpful in the initial diagnosis, to rule out other disorders, as well as inmonitoring the progression of the disease to make therapeutic adjustments. Brain scans and other

laboratory tests are also sometimes carried out, mostly to detect other disorders resemblingParkinson's disease.

The diagnosis of Parkinson's disease is more likely if:

1. at least two of the three major symptoms are present (tremor at rest, muscle rigidity, and

slowness);

2. the onset of symptoms started on one side of the body;

3. symptoms are not due to secondary causes such as medication or strokes in the area controllingmovement; and

4. symptoms are significantly improved with levodopa (see below).

What is the treatment for Parkinson's disease?

There is currently no treatment to cure Parkinson's disease. Several therapies are available todelay the onset of motor symptoms and to ameliorate motor symptoms. All of these therapies are

designed to increase the amount of dopamine in the brain either by replacing dopamine,mimicking dopamine, or prolonging the effect of dopamine by inhibiting its breakdown. Studies

have shown that early therapy in the non-motor stage can delay the onset of motor symptoms,thereby extending quality of life.

The most effective therapy for Parkinson's disease is levodopa (Sinemet), which is converted to

dopamine in the brain. However, because long-term treatment with levodopa can lead tounpleasant side effects (a shortened response to each dose, painful cramps, and involuntary

movements), its use is often delayed until motor impairment is more severe. Levodopa isfrequently prescribed together with carbidopa (Sinemet), which prevents levodopa from being



broken down before it reaches the brain. Co-treatment with carbidopa allows for a lower levodopa dose, thereby reducing side effects.

In earlier stages of Parkinson's disease, substances that mimic the action of dopamine (dopamine

agonists), and substances that reduce the breakdown of dopamine (monoamine oxidase type B

(MAO-B) inhibitors) can be very efficacious in relieving motor symptoms. Unpleasant sideeffects of these preparations are quite common, including swelling caused by fluid accumulationin body tissues, drowsiness, constipation, dizziness, hallucinations, and nausea.

For some individuals with advanced, virtually unmanageable motor symptoms, surgery may be

an option. In deep brain stimulation (DBS), the surgeon implants electrodes to stimulate areas of the brain involved in movement. In another type of surgery, specific areas in the brain that cause

Parkinson's symptoms are destroyed.

An alternative approach currently being explored is the use of dopamine-producing cells derived

from stem cells. While stem cell therapy has great potential, more research is required before

such cells can become of therapeutic value in the treatment of Parkinson's disease.

In addition to medication and surgery, general lifestyle changes (rest and exercise), physical

therapy, occupational therapy, and speech therapy may be beneficial.

How can people learn to cope with Parkinson's disease?

Although Parkinson's disease progresses slowly, it will eventually affect every aspect of life -from social engagements, work, to basic routines. Accepting the gradual loss of independence

can be difficult. Being well informed about the disease can reduce anxiety about what lies ahead.Many support groups offer valuable information for individuals with Parkinson's disease and

their families on how to cope with the disorder. Local groups can provide emotional support aswell as advice on where to find experienced doctors, therapists, and related information. It is also

very important to stay in close contact with health care providers to monitor the progression of the disease and to adjust therapies to maintain the highest quality of living.

Can Parkinson's disease be prevented?

Scientists currently believe that Parkinson's disease is triggered through a complex combinationof genetic susceptibility and exposure to environmental factors such as toxins, illness, and

trauma. Since the exact causes are not known, Parkinson's disease is at present not preventable.

What is the prognosis of Parkinson's disease?

The severity of Parkinson's disease symptoms vary greatly from individual to individual and it isnot possible to predict how quickly the disorder will progress. Parkinson's disease itself is not a

fatal disease, and the average life expectancy is similar to that of people without the disease.Secondary complications, such as pneumonia, falling-related injuries, and choking can lead to

death. There are many treatment options that can reduce some of the symptoms and can prolongthe quality of life of an individual with Parkinson's disease.



Parkinson's disease at a glance

y Parkinson's disease is a neurodegenerative disorder which leads to progressive deterioration of

motor function due to loss of dopamine-producing brain cells.

y Primary symptoms include tremor, stiffness, slowness, impaired balance, and later on a shuffling

gait.

y Some secondary symptoms include anxiety, depression, and dementia.

y Most individuals with Parkinson's disease are diagnosed when they are 60 years old or older, but

early-onset Parkinson's disease also occurs.

y With proper treatment, most individuals with Parkinson's disease can lead long, productive lives

for many years after diagnosis.

REFERENCES:

Arenas, E. Towards stem cell replacement therapies for Parkinson's disease. Biochemical and Biophysical Research Communications, 2010; vol 396: pp 152-156.

Chen, J.C. Parkinson's Disease: Health-Related Quality of Life, Economic Cost, and

Implications of Early Treatment American Journal of Managing Care, 2010; vol 16: pp S87-S93.

Fricker-Gates, R.A. and Gates, M.A. Stem cell-derived dopamine neurons for repair in

Parkinson's disease. Regenerative Medicine, March 2010; vol 5(2): pp267-78.

Hauser, R.A., Early Pharmacologic Treatment in Parkinson's Disease. American Journal of Managing Care, 2010; vol 16: pp S100-S107.

Pahwa, R. and Lyons, K.E. diagnosis of Parkinson's disease: recommendations from diagnostic

clinical guidelines. American Journal of Managing Care, 2010; vol 16: pp S194-S99.

Last Editorial Review: 8/23/2010

what is tremor and parkinson

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