What is Parkinson's disease?

Parkinson’s disease is a neurodegenerative disorder of unknown cause that affects nearly 1.5 million people in the United States. While there is no test that can clearly identify the disease, there are a variety of tests, such as brain scans, that can help doctors decide if a patient has true Parkinson’s disease or some other disorder that resembles it.

Parkinson’s disease belongs to a group of conditions called motor-system disorders. Parkinson’s and related disorders are the result of the loss of dopamine producing brain cells. Dopamine is a chemical messenger responsible for transmitting signals within the brain. Parkinson’s disease occurs when certain nerve cells, or neurons, die or become impaired. Normally, these neurons produce dopamine. Loss of dopamine causes the nerve cells to fire out of control, leaving patients unable to direct or control their movement in a normal manner.

The four primary symptoms of Parkinson’s are tremor or trembling in hands, arms, legs, jaw, and face; rigidity or stiffness of the limbs and trunk; bradykinesia, or slowness of movement; and postural instability or impaired balance and coordination. Patients may also have difficulty walking, talking, or completing other simple tasks. The disease is both chronic and progressive. Parkinson’s is not usually inherited. Early symptoms are subtle and occur gradually.

Parkinson’s disease was first formally described in “An Essay on the Shaking Palsy,” published in 1817 by a London physician named James Parkinson, but it has probably existed for many thousands of years. Its symptoms and potential therapies were mentioned in the Ayurveda, the system of medicine practiced in India as early as 5000 BC, and in the first Chinese medical text, Nei Jing, which appeared 2500 years ago.

What is Alzheimer Disease? How is the dementia of Alzheimer different from the Dementia of Parkinson? (called Lewy Body Dementia)

Copyrighted by Abraham Lieberman MD 18 Jul 05, Revised 3 March 07

Dementia is a progressive loss of the ability to remember, think, reason,  pay attention, behave appropriately, use and understand language.  Dementia can be caused by alcohol, drug abuse, head injury, AIDS, syphilis, liver failure, multiple strokes (vascular dementia), normal pressure hydrocephalus, pernicious anemia (vitamin B12 deficiency), thyroid disease, uremia (kidney failure), and Wernicke’s – Korsakoff psychosis (vitamin B1 thiamine deficiency) and Parkinson disease (called Lewy Body Dementia).  In the elderly,  65 years +, about 10 % of patients with dementia will have a cause such as  alcohol, drug abuse, head injury, syphilis, multiple strokes, normal pressure hydrocephalus, vitamin B12 deficiency, thyroid disease, uremia, or thiamine deficiency.

In 90 % of patients with dementia, while they are alive, Alzheimer disease (AD) will be diagnosed. Subsequent studies including post-mortem examination usually reveal 40 % have AD, 20% have PD Dementia or Lewy Body Dementia (LBD), 25% have a combination of AD and PD, and 5% have Fronto-temporal Dementia (FTD). In life it may be difficult to distinguish one of these dementias from another. As there is NO specific treatment for any of these dementias, distinguishing one from another is, at this time, not critical: in terms of leading to a specific treatment.

At post-mortem examination dementia is associated with a degeneration of, or shrinkage of brain tissue: atrophy. In AD and LBD the atrophy begins in the nucleus basalis, in the frontal lobe, and the hippocampus, part of the temporal lobe, and spreads to the rest of the brain. In AD, loss of brain cells, neurons, is accompanied by:

Amyloid plaques: deposits of a protein, amyloid, around blood vessels and outside nerve cells. Using conventional stains for cells, amyloid appears as a pinkish, amorphous (shapeless) deposit. The exact function of amyloid is not known. It is believed to be one of the components (parts) of the “cement” that holds the cell together. If the amyloid is defective (as it is in AD), it is as though the cement of the cell is defective and the cell, or the walls of the cell, or the surrounding blood vessels collapses.

Neuro-fibrillary tangles: twisted nerve fibers on which are deposited a protein, Tau. The exact function of tau is not known. It is believed to be an integral part of the microtubules: thousands of “tunnel-like” structures that move molecules from one part of the cell to another. In AD it is as though the “steel” used to reinforce an underground tunnel, corrodes and collapses.

In LBD, loss of neurons, is accompanied by:

Lewy bodies inside neurons.

About one-third of LBD patients begin with PD.

In Fronto Temporal Dementia, atrophy is confined to the frontal and temporal lobes. Loss of neurons is accompanied by:

Neuro-fibrillary tangles (like AD).

Pick bodies inside neurons. Not all FTD patients have Pick bodies.

No amyloid plaques (unlike AD)

About one-third of FTD patients develop Progressive Supranuclear Palsy (PSP) or Corticobasal Degeneration (CBD). The relationship of FTD to PSP and CBD is similar to that between LBD and PD.

The greatest risk factor for AD, LBD, and FTD is growing old. From 1950 to 2005, life-span increased from 65 to 77 years, while AD and PD increased more. Over age 75, about 10% of people have AD or PD, and over age 85, about 20

AD is the most common dementia. Of 100 people diagnosed with dementia, 65% will have AD. In 40% AD is the only finding. In 25% AD is accompanied by another cause of dementia: LBD, strokes. Alzheimer disease was described by Alois Alzheimer in 1906 who noted the shrunken brain, the early and marked involvement of the hippocampus, and the neurofibrillary tangles and amyloid plaques: hallmarks of the disease.

Ronald Reagan (1911 – 2004, age 93) 40th President of the United States had AD

Barry Goldwater (1909 – 1998, age 89), US Senator from Arizona, Republican Candidate for President, had AD.

Charlton Heston (1923 – , age 82), actor has AD.

Rita Hayworth (1918 – 1987, age 79), actress had AD.

Winston Churchill (1874 – 1965, age 91), world statesman had multiple strokes, may have had AD.

About 5 million Americans have AD. About 10 million, have a decreased ability to remember or think (called minimal cognitive impairment) which may, in time, progress to AD or LBD. It’s estimated there will be 20 million people with AD and LBD by 2050. The cost of caring for a patient with AD or LBD is as high as $50,000 per year. AD, next to cancer and heart disease is the leading cause of death in America. The cause of death in AD and LBD, as in PD, is pneumonia. Death is not caused directly by AD or LBD but AD and LBD are debilitating. The debilitation, the weakness and weariness, not the AD or LBD, lowers the patient’s resistance and makes him or her more vulnerable to pneumonia and other infections. Diseases such as PD, PSP, and CBD, are one of the great challenges facing our aging population for what will we gain by living longer, if ever more of us develop AD or PD?

Unlike PD, which affects 55 men for every 45 women, AD affects women more than men. In part, estrogen may be protective and when this affect is withdrawn, at menopause, the brain may be more vulnerable to AD. In part, women live longer than men, and thus, more women are at risk for AD.

In 10% of AD patients, there’s a family history (versus 15% in PD). And in some of these patients AD appears below age 60. In 90% of AD patients there’s no family history. Genetics play a role, but one over-shadowed by other, unknown causes.

In most patients AD begins insidiously, subtly. You can’t remember whether you left the door locked—or not. You can’t remember the directions to your daughter’s house. You can’t remember the directions to your own house. You can’t remember your social security number or phone number. You can’t remember your grandchildren’s name, or your daughter’s name—or your wife’s name.

You can’t remember how to start your car: Do you release the brakes and then turn on the ignition? Or do you turn on the ignition and then release the brakes? And which way do you turn the ignition key: clockwise? Counter-clockwise? Right to left or left to right? You can’t remember how to use the telephone: Which end of the phone do you speak into? Do you wait for a “tone” and then push the buttons or do you push the buttons before you hear the “tone?” You can’t remember how to make change? The man gave you $1.00 do you give him back 3 quarters, two nickels and a dime, or two dimes and a nickel? Not remembering how to perform commonly learned skills: starting a car, using the telephone, making change, is called apraxia. You are able to perform each component of the act: you can put the key into the ignition, you can turn the key, you can release the brake, but you can’t get the sequence right.

You don’t know the day of the month: Is it the 21st or 22nd or 23rd ? You don’t know the day of the week: Is it Wednesday or Thursday or Friday? Not knowing the day of the month or week—isn’t bad, after-all you’re retired, you don’t work, one day is like the next. You don’t know the month: Is it June or July or October? Not knowing the month isn’t bad, after all you live in Florida and one month is like another. You don’t know the year: Is it 2004 or 2005 or 1929? It can’t be 1918 because that’s when you were born. And didn’t something happen in 1918? The War ended, but which one: World War II, or World War I, or the Korean War? In addition to difficulty with knowing the time, called disorientation for time, there’s denial, believing there’s nothing wrong. Or there’s neglect, not realizing there’s something wrong.

You don’t know the state or the city you’re in: Are you in Florida or New York? Are you in Miami or Manhattan? You can’t remember how to go from your house to your daughter’s house. You can’t remember how to go from your neighbor’s house to your house—which is next door! You go outside and you turn right? Or left? Disorientation for space is more troubling than disorientation for time. People get lost! Disorientation for time may not be the beginning of dementia. Disorientation for space, getting lost in your own neighborhood or your own house—may be the beginning of dementia. AD and LBD can begin with disorientation in time followed by disorientation in space.

You can’t remember what you call the “thing” you write with: is it a pickle? Or a pretzel? Or a pencil? You know the “thing” with an eraser on the top. You can’t understand what you read in the paper. It’s as though you are reading a foreign language. Difficulty in using and understanding language is called aphasia. Difficulty in expressing your thoughts into language is called expressive aphasia. Difficulty in understanding other people’s thoughts as expressed in language, your native language, is called receptive aphasia. Language is centered in the left, called the dominant, hemisphere. FTD and AD can begin with aphasia.

You lack the desire to do things, things you did in the past. Such a lack of desire, called apathy, may be part of depression, or it may be part of dementia. People who suffer from dementia may be apathetic, but may not be depressed: they don’t cry, they’re not guilt-stricken, they’re not ashamed, and they don’t respond to counseling, or “pep-talks” or anti-depressant drugs. AD and LBD can begin with apathy.

You take no pleasure in doing things, things you enjoyed in the past. Such a lack of pleasure, called anhedonia, may be part of depression, or it may be part of dementia.

You lack the energy to do things. Such a lack of energy, called anergia, may be part of depression. It may be part of Parkinson disease, or heart disease, or lung disease, or kidney disease, or diabetes, or thyroid disease, or a vitamin deficiency, or it may be part of dementia.

Your moods, formerly stable, change rapidly: you’re anxious for no reason. Then you’re calm. Then you’re anxious. You’re “down,” depressed, then you’re “up”, overjoyed – and nothing’s happened, nothing’s changed.

You panic easily.

You’re confused, disoriented, irritable at night, when it’s dark: “sun-downing.” AD and LBD can begin with “sun-downing.”

You’re confused, disoriented, you don’t what day it is or where you are when you wake up in the morning—in your own bed in your own home—and you hadn’t had any alcohol to drink the night before and you hadn’t taken a sleeping pill the night before.

You become angry, agitated, screaming, shouting, striking-out or no reason.

You feel detached, unreal, that you’re on a strange planet, in a strange universe. Psychosis, caused by drugs, is more likely to result in feelings or unreality.

You’re paranoid. You’re certain people are saying bad things about you, or are trying to hurt you, or steal your money, or put you away in a nursing home. You’re convinced your partner is having an affair, is being unfaithful to you.

You’re hallucinating. You see things that are not there. You hear things that are not there. You see your best friend who’s been dead for 20 years. He’s accusing you of something, he’s threatening you—and you’re terrified. Psychosis, caused by drugs, is more likely to result in hallucinations.

Depression, anxiety, and panic occurs in more than 30% of patients with AD, LBD, or FTD. Distinguishing anxiety and depression from dementia, or deciding how much of a patient’s symptoms are anxiety, how much depression, and how dementia is art more than science and requires experience, expertise and patience on the part of the physician. It’s not simple and it’s not straight-forward.

Once the dementia of AD, or LBD, or FTD have progressed, it’s relatively easy to recognize they’re something wrong with the patient. However, distinguishing one dementia from another: AD from LBD, AD from FTD, LBD from FTD is difficult—even at post-mortem examination. There are treatments for dementia, but none of them are specific for AD, LBD, or FTD. Lacking such specific treatments, distinguishing AD from LBD, or AD from FTD, or LBD from FTD is not, at this time, crucial.

Recognizing or diagnosing dementia when it begins, distinguishing it from anxiety or depression, and being certain the dementia is not related to a treatable condition: thyroid disease, vitamin B12 or thiamine deficiency requires experience and expertise. How far an evaluation should go and how many tests should be done is decided on a case by case basis.

A reasonable evaluation consists of taking a good history.

This includes a history of high blood pressure, unexplained fevers, heart disease, stroke, lung disease, liver disease, kidney disease, thyroid disease, diabetes, and cancer.

This includes a history of mental disorders: anxiety, bi-polar disorder, depression, psychosis, schizophrenia.

This includes a history of alcohol abuse, illicit drug use, prescription and non prescription drugs.

This includes a family history of AD, PD, and mental disorders.

This includes an occupational history listing exposures to toxins in the workplace including: aluminum, carbon monoxide, copper, fungicides, herbicides, iron, mercury, manganese.

This includes a physical and neurological examination, a Mini-mental status examination, an examination for anxiety, and depression.

This includes blood tests for vitamin B-12 and folate, liver, kidney, and thyroid function tests, sodium, potassium, chloride, and bicarbonate, and if suspected a serological test for syphilis, a test for AIDS or Lyme disease.

This includes an MRI of the brain.

Additional tests including a lumbar puncture ( a spinal tap) and a PET-scan for AD are ordered at the discretion of the physician.

In AD there is atrophy: shrinkage of the brain. The changes are more marked in the hippocampus: a region of the temporal lobe that stores memories and in a region called the nucleus basalis.

At post-mortem examination, under the microscope, in affected regions the brain cells, neurons, are shrunken, dying, and inside of them are twisted fibers, called neuro-fibrillary tangles and deposited on them is a protein called Tau. Some neurons have disappeared and in their place are tombstones, marking where the neuron had been: the marking are composed of neurofibrillary tangles, remnants of the neuron’s dendrites and axons, the processes that protrude from the neuron and connect it with other neurons. Neurofibrillary tangles initially occur in the anterior and medial parts of the temporal lobe.

As AD progresses, neurofibrillary tangles accumulate in other brain regions, especially the association cortices. The association cortices are regions of the brain that process and associate information: they combine visual with auditory information, auditory with sensory information, and they “name” the information, they describe it to you.

Neurofibrillary tangles are not confined to AD. Neurofibrillary tangles, but not amyloid plaques, are found in FTD, PSP, CBD, post-encephalitis Parkinson, and the dementia associated with boxing: dementia puglistica.

In AD, around the small blood vessels in the regions most affected, are deposits of an amorphous gel-like protein called amyloid. In some regions, in addition to the neurofibrillary tangles there are amyloid plaques. Amyloid when it deposits around the walls of blood vessels, weakens the walls. This can result in hemorrhages inside the brain. The hemorrhages vary from microscopic without causing symptoms to major hemorrhages that may be life-threatening. As AD progresses, amyloid accumulates around blood vessels in the association cortices, and amyloid plaques form in the association cortices.

In addition to neurofibrillary tangles and amyloid plaques other changes can include the presence of granules in some neurons called granulo-vacuolar degeneration. This occurs in the hippocampus. Their significance is not known. .

The early and marked changes in the nucleus basalis and hippocampus are responsible for the early and characteristic symptoms of AD: difficulty remembering recent events. Think of your memory as a video recorder: first you must see the event: you must be alert enough to see it. This involves the nucleus basalis. Next, you must record the event. This involves the hippocampus. Next, you must store the event in a temporary file. This involves the hippocampus. Next, important events, are transferred to permanent files stored throughout the cortex. When AD affects the nucleus basalis and hippocampus, you have difficulty recording and storing recent events.

As AD progresses, neurofibrillary tangles and amyloid plaques deposit in the association cortices. You begin to have difficulty retrieving information, you begin to have difficulty associating visual, auditory, and sensory information, you begin to have difficulty describing what you see and hear, and you begin to see and hear things no one else sees or hears: you hallucinate.

There are 100 billion neurons in the brain: 100 X 109 neurons. Each neuron makes 10,000 connections or synapses with other neurons. This means there are 100 X 1013 synapses or 1,000,000 gigabytes of storage in your brain. Like a super-computer your brain has a vast storage capacity. As AD and LBD progress, your search engine, your “Google” becomes defective.

In 10.0 % of patients there’s a family history of AD, in 90% there’s not. At least 5 genes have a role in AD.

The gene for the amyloid precursor protein, APP, on Chromosome 21.

The gene for the pre-senilin I protein on Chromosome 14.

The gene for the pre-senilin 2 protein on Chromosome 1)

A gene on Chromosome !2.

A gene on Chromosome 19.

APP is a long protein that to be activated must be split into fragments called peptides. A peptide consists of a chain of amino acids. It’s believed that a mutant gene on Chromosome 21 produces a mutant APP that’s split into a 40 to 43 amino acid-long peptide chain. This chain forms into what is called a “beta sheath.” The “beta sheath” is an abnormal configuration and through a complex and not well understood process leads to the formation of amyloid plaques. In Down’s syndrome, a disorder of mental retardation associated with three instead of two Chromosome-21s, the extra Chromsome-21 results in an increased production of APP. The increased levels of APP result in an acceleration of AD: A high percent of patients with Down’s Syndrome, several times higher than the general population, develop AD at a relatively young age: in the 40s instead of their 60s and 70s.

Other chromosome 21 genes, such as the gene coding for superoxide dismutase-1,(SOD-1) may be involved in AD. SOD, catalase and glutathione peroxidase are the major enzymes involved in inactivating the toxic free radicals generated by the mitochondria the “oil refineries and power plants” of the cell.

The presence of certain genes increase or decrease the vulnerability to AD. Thus people who have what is called the ApoE-4 allele, have an increased risk of developing AD while people who have the ApoE-2 allele have a decreased risk of developing AD.

Aluminum, the most common metal, has in some studies been associated with an increased risk of AD. The role of aluminum, especially aluminum from cooking pots, is controversial and at this time, unproven.

Inside every neuron is a system of micro-tubules, these are like an underground tunnels that transport protein from one part of the cell to another. The Tau protein is an important part of the micro-tubules. In AD, the Tau proteins become hyper-phosphorylated: extra phosphate molecules are attached to them. This alters the structure of the Tau protein. And, in some as yet not understood way, the micro-tubules “collapse” as Tau proteins deposit on them. It’s as though you were building a tunnel and the bricks (the Tau proteins) you were using were defective and the tunnel collapsed as you built it.

Neurofibrillary tangles containing Tau proteins are found in AD, in FTD, in CBD, and in PSP. In FTD a mutant gene on chromosome 17 has been found that produces a mutant Tau protein, one that deposits on the neurofibrillary tangles in FTD and CBD. Similar genes have NOT been found for the Tau proteins in AD and PSP. It’s possible that such genes will be found on Chromosome 17 or on another Chromosome. It’s also possible that a virus, or a toxin, and not a gene, is responsible for the abnormal Tau protein in AD and in PSP.

There is debate among researchers as to whether the severity of the dementia in AD, the loss of intellectual function, correlates with the presence of neuro-fibrillary tangles, amyloid plaques or both. Current thinking is that the number and location of the neurofibrillary tangles best correlates with the severity of the dementia.

An unresolved question is why is AD characterized by neurofibrillary tangles and amyloid plaques. In diseases such as FTD, CBD, and PSP, there are neurofibrillary tangles but NO plaques. Neurofibrillary tangles are, by themselves, sufficient to result in dementia. So, why are there neurofibrillary tangles AND plaques in AD? What is the presence of both neurofibrillary tangles and amyloid plaques telling us about AD?

The neurofibrillary tangles in AD resemble the tangles in FTD, but the ones in FTD contain a Tau protein formed from a mutant gene on Chromosome 17, the ones in AD contain a Tau protein NOT formed from a mutant gene. What is the significance of this?

In PD and in LBD the dementia correlates with the presence of Lewy bodies. But many patients with LBD have changes of AD: neurofibrillary tangles and amyloid plaques. Similarly, many patients with AD have changes of LBD. What is the significance of this relationship? Understanding these relationships will, in time, lead to an understanding, a treatment, and a cure for AD, for LBD, for FTD, for CBD, for PSP and PD.

The cause of AD, like the cause of PD is unknown. Treatment of AD, like treatment of PD is symptomatic. In AD early changes occur in the neurons of the nucleus basalis. These neurons contain acetyl choline, a major chemical messenger. Acetyl choline is involved in memory and alertness. Drugs, anti-cholinergics, drugs that block the actions of acetyl choline, decrease the tremor in PD, but decrease memory and alertness. Treatment of AD, and of LBD, centers on using drugs that block an enzyme, choline acetyl-transferase (abbreviated CAT) , that breaks down acetyl choline: blocking CAT increases acetyl choline in the brain.

Exelon and Aricept block CAT, increase acetyl choline in the brain, and improve memory and alertness. Exelon also blocks an enzyme, butyryl cholinesterase, increases butyryl choline in the brain, this may further improve memory and alertness. Aricept and Exelon are most useful early in AD and LBD. These is a suggestion that both Aricept and Exelon may slow the progression of AD and LBD. This is, to date, unproven.

Glutamate is an excitatory amino acid that acts as a chemical messenger in the brain. Excess glutamate is thought, by some researchers, to damage neurons. Glutamate stimulates neurons through three receptors. The more important one are the NMDA and the AMPA receptors. Namenda blocks the actions of glutamate on the NMDA receptors Namenda alone or combined with Aricept or Exelon is helpful in improving alertness and memory in some patients with AD and LBD.

Some AD patients, like some LBD patients become psychotic: they are agitated, delusional, paranoid, and hallucinate. In such patients anti-psychotic drugs such as Abilify, Risperidol, and Seroquel are helpful. Some AD patients develop epileptic seizures or myoclonus. Such patients require anti-convulsant drugs.

These is some evidence that inflammation may play a role in AD and LBD. Based on this some neurologists advocate the use of non steroidal anti-inflammatory drugs. Whether the potential risk of these drugs, gastro-intestinal bleeding, is equal to the potential benefit is decided on a case by case basis.

Some have proposed that oxidative stress causes or worsens AD and on this basis the following recommendations are made at the Lieberman Parkinson Clinic. All recommendations MUST be discussed with your own doctor.

B-1, thiamine, 100 mg /day
B-2, riboflavin, 100 mg /day
B-3, niacin, 100 mg /day
B-5, pantothenic acid, 100 /day
B-6, pyridoxine, 100 mg /day AT LEAST 4 hours BEFORE taking carbidopa/levodopa if you taking carbidopa/levodopa
B-7, biotin, 100 mg /day, double the amount if on anti-biotics for an infection folic acid, 200 micrograms twice/day
B-12, 50 micrograms twice/day C, ascorbic acid, 500 mg twice/day

How is Parkinson's disease diagnosed?

Parkinson’s disease is usually diagnosed by a neurologist who can evaluate symptoms and their severity. There is no test that can clearly identify the disease. Sometimes people with suspected Parkinson’s disease are given anti-Parkinson’s drugs to see if they respond. Other tests, such as brain scans, can help doctors decide if a patient has true Parkinson’s disease or some other disorder that resembles it.

Microscopic brain structures called Lewy bodies, which can be seen only during an autopsy, are regarded as a hallmark of classical Parkinson’s. Autopsies have uncovered Lewy bodies in a surprising number of older persons without diagnosed Parkinson’s –  8% of people over 50, almost 13% of people over 70, and almost 16% of those over 80, according to one study.

How many people are affected by Parkinson's disease?

In the United States, at least 500,000 people are believed to suffer from Parkinson’s disease, and about 50,000 new cases are reported annually. These figures are expected to increase as the average age of the population increases. The disorder appears to be slightly more common in men than women. The average age of onset is about 60. Both prevalence and incidence increase with advancing age; the rates are very low in people under 40 and rise among people in their 70s and 80s. Parkinson’s disease is found all over the world. The rates vary from country to country, but it is not clear whether this reflects true ethnic and/or geographic differences or discrepancies in data collection.

Some experts believe Parkinson’s disease is something of an “iceberg phenomenon,” lurking undetected in as many as 20 people for each known Parkinson’s patient. A few researchers contend that almost everyone would develop Parkinson’s eventually if they lived long enough.

Is there any treatment for Parkinson's disease?

There is no cure for Parkinson’s disease. Many patients are only mildly affected and need no treatment for several years after the initial diagnosis. When symptoms grow severe, doctors usually prescribe levodopa (L-dopa), which helps replace the brain’s dopamine. Sometimes doctors prescribe other drugs that affect dopamine levels in the brain. In patients who are very severely affected, a kind of brain surgery known as pallidotomy has reportedly been effective in reducing symptoms. Another kind of brain surgery, in which healthy dopamine-producing tissue is transplanted into the brain, is also being tested. Finally, researchers are trying to identify substances that will prevent dopamine-producing brain cells from dying.

A variety of medications provide dramatic relief from the symptoms, but no drug can stop the progression of the disease. In some cases, surgery is an appropriate treatment. Some doctors recommend physical therapy or muscle-strengthening exercises.

What are the symptoms of Parkinson's disease?

Often, the first symptom of Parkinson’s disease is tremor (trembling or shaking) of a limb, especially when the body is at rest. The tremor often begins on one side of the body, frequently in one hand. Other common symptoms include slow movement (bradykinesia), an inability to move (akinesia), rigid limbs, a shuffling gait and a stooped posture. People with Parkinson’s disease often show reduced facial expressions and speak in a soft voice. Occasionally, the disease also causes depression, personality changes, dementia, sleep disturbances, speech impairments or sexual difficulties. The severity of Parkinson’s symptoms tends to worsen over time.

What causes Parkinson's disease?

Although there are many theories about the cause of Parkinson’s disease, none has ever been proven. Researchers have reported families with apparently inherited Parkinson’s for more than a century. However, until recently, the prevailing theory held that one or more environmental factors caused the disease. Severe Parkinson’s-like symptoms have been described in people who took an illegal drug contaminated with the chemical MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and in people who contracted a particularly severe form of influenza during an epidemic in the early 1900s. Recent studies of twins and families with Parkinson’s have suggested that some people have an inherited susceptibility to the disease that may be influenced by environmental factors. The strong familial inheritance of the chromosome 4 gene is the first evidence that a gene alteration alone may lead to Parkinson’s disease in some people.

What is the prognosis for Parkinson's disease?

Parkinson’s disease is both chronic, meaning it persists over a long period of time, and progressive, meaning its symptoms grow worse over time.  Although some people become severely disabled, others experience only minor motor disruptions. Tremor is the major symptom for some patients, while for others tremor is only a minor complaint and other symptoms are more troublesome.  No one can predict which symptoms will affect an individual patient, and the intensity of the symptoms also varies from person to person.