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Parkinson's disease is a neurodegenerative disease of the substantia nigra
(an area in the basal ganglia). The disease was first discovered and its
symptoms documented in 1817 (Essay on the Shaking Palsy) by the English
physician Dr. James Parkinson; the associated biochemical changes in the
brain of patients were identified in the 1960s.
The disease is a progressive movement disorder of the extrapyramidal system,
which controls and adjusts communication between neurons in the brain and
muscles in the human body.
The cause of Parkinson's disease is not known. Geneticists have since 1997
found nine different specific genetic defects, each of which causes the
disease in one or a few families with extraordinarily high incidences of the
disease, but such families are rare. While a strong inheritance pattern
occurs in only a very small percentage of cases, an affected individual is
three to four times more likely than an unaffected individual to have a
close relative with Parkinson's. Having a parent with Parkinson's raises
one's lifetime risk of developing the disorder threefold, from the general
population's figure of 2% to about 6%.
A popular theory holds that the disease might result in most cases from the
combination of a subtle genetically determined vulnerability to
environmental toxins along with mild exposure to those toxins. The toxins
most strongly suspected at present are certain pesticides and industrial
metals. Minor past episodes of head trauma are also more commonly reported
by sufferers than by others in the population. While emotional or a
psychological trauma can precipitate the initial symptoms or aggravate
existing symptoms, this is not the actual cause of the disorder.
The symtoms of Parkinson's disease result principally from loss of some of
the brain cells that use dopamine as their neurotransmitter. Most of the
dopamine-using cells reside in the substantia nigra (in the pathway
projecting to the striatum, both of which are major components of the
extrapyramidal system) that regulates the coordination of movement. Brain
cells producing other brain chemicals such as norepinephrine, serotonin and
acetylcholine exhibit minor damage in Parkinson's disease, accounting for
some of the wide array of symptoms.
The mechanism by which the brain cells in Parkinson's are lost appears to
center on an abnormal accumulation of the protein alpha-synuclein in the
damaged cells. This protein forms blobs called Lewy bodies. The precise
mechanism whereby aggregates of alpha-synuclein damage the cells is not
known. The aggregates may be merely a normal reaction by the cells as part
of their effort to correct a different, as-yet unknown, insult. It does
appear that alpha-synuclein aggregation is enhanced by the presence of
dopamine and the byproducts of dopamine production.
Symptoms may vary among patients, and additionally may vary greatly over
time in a single patient, but commonly include:
* tremor (while this is the best known symptom, it is not displayed by an
estimated 30% of patients),
* rigidity (increased tone or stiffness in the muscles),
* bradykinesia (slowness of movement),
* failing balance,
* walking problems.
Additonally, patients might show:
* anxiety or panic attacks
* speech problems (vocal cords can also be affected, causing monotonous,
soft speech qualities),
* dementia, in approximately 20% of all patients, typically starting with
slowing of thought and progressing to difficulty organizing thoughts
* stooped posture,
* sleep disturbances,
* altered sexual function,
* loss of sense of smell,
* oily skin,
* difficulty in swallowing.
Symptoms usually only begin to appear after about 80% of the dopamine in the
brain has been lost. The level of dopamine will continue to fall slowly over
time, with an attendant worsening of symptoms. The disease is not lethal.
It is an incapacitating disease, disturbing some important human functions
and in some cases resulting in a substantial reduction in quality of life.
As in many neurologic diseases, psychological complications are often
extremely serious and require the patient's family members and relatives to
pay keen attention to the emotional fragility that usually follows the
emergence of the disease; indeed, the depression which often results is seen
by many as one of the worst aspects of the disease. In some cases drugs are
employed, especially in the fight against depression (given that
Parkinson's-related depression is mainly induced by a complex of
chemical-physical factors). Also, some common side effects of therapy can
put the patient in a condition of humble self-consideration. External help
is required to control the administration of the prescribed therapy: since
patients are often confused or depressed, there is a risk of their
improperly implementing the therapeutic regimen if left to their own
devices, leading to symptoms not being adequately controlled.
Parkinson's disease is very widespread, with about 150-200 cases per 100,000
population at any given time. About 2% of the population develops the
disease some time during life. Cases are reported at all ages, though it is
quite rare in people younger than 30 and the average age at which symptoms
begin is 58-60; the risk of developing it substantially increases with age.
It occurs in all parts of the world, but appears to be more common in people
of European ancestry than in those of African ancestry. Those of east Asian
ancestry have an intermediate risk. It is more common in rural than urban
areas and men are affected slightly more often than women.
The treatment of Parkinson's disease mainly relies on replacing dopamine
with levodopa or mimicking its action with dopamine agonists such as
pramipexole, ropinirole, pergolide or bromocriptine. Levodopa is a dopamine
precursor that is transfomed into dopamine by the brain). This is almost
always supplemented with carbidopa, a substance which prevents levodopa from
being metabolized in the gut, liver and other tissues, thus allowing more
levodopa to reach the brain and thus allows a reduction in dosage, thus
reducing some of the side effects. The most frequent side effects of these
dopaminergic drugs are nausea, sleepiness, dizziness, involuntary writhing
movements and visual hallucinations.
As in many other diseases, the therapy requires a continuing regimen of
medicines, the dosage of which has to be specifically[ calculated for each
single case and might vary during the evolution of the disease. The
treatment is complex and usually consists of a mixture of substances
(basically focused on levodopa), some of which compensate side effects of
others. Amantadine hydrochloride, anticholinergics and COMT inhibitors
tolcapone, entacapone are sometimes prescribed. Foods rich in proteins can
reduce the uptake of levodopa, because the same uptake system is used both
by proteins and levodopa. However, this can usually be dealt with by
redistributing meal times: in many cases it is advisable to move the
consumption of proteins towards the evening, so to have symptoms appearing
when the patient has less need of mobility. While these therapies are a good
attempt at treating the symptoms, they are not a cure - they do not attack
the underlying cause of the disease; that is to say, they do not restore the
brain's dopamine production.
Regular physical exercise and/or therapy are beneficial to the patient and
essential for maintaining and improving mobility, flexibility, balance and a
range of motion, and for a better resistance against many of the secondary
symptoms and side effects.
Surgical interventions are currently being researched, and deep brain
stimulation is presently the most popular and effective such treatment. In
the future, implantation of cells genetically engineered to produce dopamine
or stem cells that transform into dopamine-producing cells may become available.
Even these, however, will not constitute cures because they do not address
the widespread loss of several different types of cells in the brain and
even for the dopamine-producing cells, do not re-establish all of the
original connections with neighboring brain cells. A true cure will have to
detect the earliest signs of the disorder before they cause important
symptoms and will intervene in the process that damages the brain cells in
the first place.
Parkinson's disease does not necessarily affect intellectual integrity,
apart from the emotional effects of eventual psychological complications,
and in those cases where the patient is still compos mentis, their role in
the treatment is fundamental. The patient's cooperation is required in order
to provide the physicians with all the details that might help in the making
a correct diagnosis and consequent determination the best appropriated
therapy. Conversely, it is crucial for doctors to explain the precise extent
of the disease's progress, and provide as much information as possible about
the prescribed therapy, how the symptoms and side effects can be reduced.
Working together in this manner, the patient and doctor can ensure the
maximum quality of life for the sufferer.
There are other disorders that are called Parkinson-Plus diseases. These
include Shy-Drager Syndrome (SDS), Progressive Supranuclear Palsy (PSP) and
Olivopontocerebellar Atrophy (OPCA which is also called Multiple System
Atrophy). Patients often begin with typical Parkinson's disease symptoms and
these Parkinson-Plus diseases can only be diagnosed when other symptoms
become apparent after some years. These Parkinson-Plus diseases usually
progress more quickly than the typical main illness, and the usual
anti-Parkinson's medications do not work as well at controlling symptoms.
Secondary parkinsonism (or briefly Parkinsonism) is a term used for a
symptom constellation that is similar to that of Parkinson's disease but is
caused by other disorders or medications. Major reasons for secondary
parkinsonism are stroke, encephalitis, narcotics, toxins and carbon monoxide
There are other idiopathic (of unknown cause) conditions as Parkinson's
disease that may cause parkinsonism. In these conditions the problem is not
the deficient production of dopamine but the inefficient binding of dopamine
to its receptors located on globus pallidus.
One famous sufferer of young-onset Parkinson's is Michael J. Fox, who has
written a book about his experience of the disease. The film Awakenings
(starring Robin Williams and Robert de Niro and based on genuine cases)
deals sensitively and largely accurately with a similar disease,
postencephalitic parkinsonism; sadly, the state of the art in treatment
remains roughly the same as it was at the time of the events depicted, the
1960s, although patients with postencephalitic parkinsonism lose benefit
from their medication far faster than do patients with Parkinson's disease.
Other famous people with Parkinson's include Muhammad Ali, Pope John Paul
II, former Attorney General Janet Reno, photographer Margaret Bourke-White
and Farnsworth Wright, editor of Weird Tales magazine in the 1930s, Barry