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Parkinson's disease (also known as PD or Parkinson disease) is a degenerative disorder of the central
nervous system, that affects the control of muscles, and so may affect movement, speech and posture.
Parkinson's disease belongs to a group of conditions called movement disorders. It is often characterized
by muscle rigidity, tremor, a slowing of physical movement (bradykinesia), and in extreme cases, a loss of
physical movement (akinesia). The primary symptoms are due to excessive muscle contraction, normally caused
by the insufficient formation and action of dopamine, which is produced in the dopaminergic neurons of the
brain. PD is both chronic, meaning it persists over a long period of time, and progressive.

PD is the most common cause of parkinsonism, a group of similar symptoms. PD is also called "primary
parkinsonism" or "idiopathic PD" ("idiopathic" meaning of no known cause). While most forms of parkinsonism
are idiopathic, there are some cases where the symptoms may result from toxicity, drugs, genetic mutation,
head trauma, or other medical disorders.

Parkinson disease affects movement (motor symptoms). Typical other symptoms include disorders of mood,
behavior, thinking, and sensation (non-motor symptoms). Individual patients' symptoms may be quite
dissimilar; progression is also distinctly individual.

There are four major dopamine pathways in the brain; the nigrostriatal pathway, referred to above,
mediates movement and is the most conspicuously affected in early Parkinson's disease. The other pathways
are the mesocortical, the mesolimbic, and the tuberoinfundibular. These pathways are associated with,
respectively: volition and emotional responsiveness; desire, initiative, and reward; and sensory processes
and maternal behavior. Reduction in dopamine along the non-striatal pathways is the likely explanation
for much of the neuropsychiatric pathology associated with Parkinson's disease.

Motor symptoms
The cardinal symptoms are:

tremor: normally 4-7Hz tremor, maximal when the limb is at rest, and decreased with voluntary movement.
It is typically unilateral at onset. This is the most apparent and well-known symptom. However, an estimated
30% of patients have little perceptible tremor; these are classified as akinetic-rigid. rigidity: stiffness;
increased muscle tone. In combination with a resting tremor, this produces a ratchety, "cogwheel" rigidity
when the limb is passively moved. bradykinesia/akinesia: respectively, slowness or absence of movement.
Rapid, repetitive movements produce a dysrhythmic and decremental loss of amplitude. postural instability:
failure of postural reflexes, which leads to impaired balance and falls.

Other motor symptoms include:

Gait and posture disturbances:
Shuffling: gait is characterized by short steps, with feet barely leaving the ground, producing an audible
shuffling noise. Small obstacles tend to trip the patient

Decreased arm swing: a form of bradykinesia
Turning "en bloc": rather than the usual twisting of the neck and trunk and pivoting on the toes, PD patients
keep their neck and trunk rigid, requiring multiple small steps to accomplish a turn.

Stooped, forward-flexed posture.
In severe forms, the head and upper shoulders may be bent at a right angle relative to the trunk (camptocormia).
Festination: a combination of stooped posture, imbalance, and short steps. It leads to a gait that gets
progressively faster and faster, often ending in a fall.
Gait freezing:
"freezing" is another word for akinesia, the inability to move. Gait freezing is characterized by inability to
move the feet, especially in tight, cluttered spaces or when initiating gait.

Dystonia:
abnormal, sustained, painful twisting muscle contractions, usually affecting the foot and ankle in PD patients.
This causes toe flexion and foot inversion, interfering with gait.
Speech and swallowing disturbances

Hypophonia: soft speech.
Speech quality tends to be soft, hoarse, and monotonous.

Festinating speech: excessively rapid, soft, poorly-intelligible speech.

Drooling: most likely caused by a weak, infrequent swallow and stooped posture.

(Non-motor causes of speech/language disturbance in both expressive and receptive language: these include
decreased verbal fluency and cognitive disturbance especially related to comprehension of emotional content
of speech and of facial expression[3]

Dysphagia: impaired ability to swallow.
Can lead to aspiration, pneumonia, and ultimately death.

Other motor symptoms:
fatigue (up to 50% of cases);
masked facies (a mask-like face also known as hypomimia), with infrequent blinking; [4]
difficulty rolling in bed or rising from a seated position;
micrographia (small, cramped handwriting);
impaired fine motor dexterity and coordination;
impaired gross motor coordination;
Poverty of movement: overall loss of accessory movements, such as decreased arm swing when walking, as well as
spontaneous movement.

Non-motor symptoms

Mood disturbances
Estimated prevalance rates of depression vary widely according to the population sampled and methodology used.
Reviews of depression estimate its occurrence in anywhere from 20-80% of cases.[5] Estimates from community
samples tend to find lower rates than from specialist centres. Most studies use self-report questionnaires such
as the Beck Depression Inventory which may overinflate scores due to physical symptoms. Studies using diagnostic
interviews by trained psychiatrists also report lower rates of depression.

More generally, there is an increased risk for any individual with depression to go on to develop Parkinson's
disease at a later date.
[6]
Seventy percent of individuals with Parkinson's disease diagnosed with pre-existing depression go on to develop
anxiety. Ninety percent of Parkinson's disease patients with pre-existing anxiety subsequently develop depression);
apathy or abulia.

Cognitive disturbances
Slowed reaction time; both voluntary and involuntary motor responses are significantly slowed.
executive dysfunction, characterized by difficulties in: differential allocation of attention, impulse control,
set shifting, prioritizing, evaluating the salience of ambient data, interpreting social cues, and subjective time
awareness. This complex is present to some degree in most Parkinson's patients; it may progress to:
dementia: a later development in approximately 20-40% of all patients, typically starting with slowing of thought
and progressing to difficulties with abstract thought, memory, and behavioral regulation.
memory loss; procedural memory is more impaired than declarative memory. Prompting elicits improved recall.
medication effects: some of the above cognitive disturbances are improved by dopaminergic medications, while
others are actually worsened.
[7]

Sleep disturbances
Excessive daytime somnolence;
Initial, intermediate, and terminal insomnia;
Disturbances in REM sleep: disturbingly vivid dreams, and REM Sleep Disorder, characterized by acting out of
dream content;

Sensation disturbances
impaired visual contrast sensitivity, spatial reasoning, colour discrimination, convergence insufficiency
(characterized by double vision) and oculomotor control dizziness and fainting; usually attributable orthostatic
hypotension, a failure of the autonomous nervous system to adjust blood pressure in response to changes in body
position impaired proprioception (the awareness of bodily position in three-dimensional space) loss of sense
of smell (anosmia), pain: neuropathic, muscle, joints, and tendons, attributable to tension, dystonia, rigidity,
joint stiffness, and injuries associated with attempts at accommodation

Autonomic disturbances
oily skin and seborrheic dermatitis;
urinary incontinence, typically in later disease progression
constipation and gastricdysmotility, severe enough to endanger comfort and even health altered sexual function:
characterized by profound impairment of sexual arousal, behavior, orgasm, and drive is found in mid and late
Parkinson disease. Current data addresses male sexual function almost exclusively.

Diagnosis

18F PET scan shows decreased dopamine activity in the basal ganglia, a pattern which aids in diagnosing
Parkinson's disease.There are currently no blood or laboratory tests that have been proven to help in
diagnosing sporadic PD. Therefore the diagnosis is based on medical history and a neurological examination.
The disease can be difficult to diagnose accurately. Early signs and symptoms of PD may sometimes be dismissed
as the effects of normal aging. The physician may need to observe the person for some time until it is apparent
that the symptoms are consistently present. Doctors may sometimes request brain scans or laboratory tests in
order to rule out other diseases. However, CT and MRI brain scans of people with PD usually appear normal.

Descriptive epidemiology
The worldwide prevalence of Parkinson's disease is 4 to 6 million people. There are over 1.5 million in China
alone. The disease usually has a long, subtle onset, so diagnosis occurs most often after many years of
subclinical disease [citation needed]. Prevalence estimates range from a low of 7 per 100,000 in Ethiopia to
a high of 329.3 per 100,000 in Nebraska, U.S.A. (although that figure was arrived at using capture-recapture
estimates), and 328.3 cases per 100,000 in the Parsi community in Bombay, India. The greatest prevalence of
any country is the U.S.A., with between 100 and 250 cases per 100,000.[citation needed]

The average age at which symptoms begin is 55-60, and although cases at ages as low as 11 have been reported
it is highly unusual for people under 30 to develop Parkinson's. 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 in developed countries, but
the converse is true in poorer countries, leading Tanner to speculate about environmental causes
[citation needed]. Men are affected at a rate about double that of women, especially in the older age groups.
There is a suggestion of increased prevalence in the California Hispanic population.[8] About 2% of the
population develops the disease some time during life [citation needed].

Incidence has been estimated by several groups, starting with northern California.[8] They observed age and
sex corrected incidence of 13.4 per 100,000/year. They note a rapid increase in incidence with age, male
rates nearly double female rates, and an elevated rate amongst Hispanics. This study was followed by a group
in Spain [9] who used the two-stage survey technique pioneered in the Copiah County study [citation needed]
to survey a cohort age 65 to 85. Within that group, incidence adjusted for age and sex was 186.8/100,000
per year, with men's rates being 2.55 times that of women. For the same age group, Van den Eeden and colleagues
observed an incidence of roughly 120/100,000/year. Soon thereafter the Rotterdam sudy was published [10]
using techniques similar to the Spanish group and Copiah County. They note age-specific incidence rates from
0.3 per 1000 person-years in subjects aged 55 to 65 years, to 4.4 per 1000 person-years for those aged =85
year, and a sex ratio of 1.55 for male incidence

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