Where is parkinson disease

Early symptoms of Parkinson's disease are subtle and occur gradually. For example, affected people may feel mild tremors or have difficulty getting out of a chair.

They may notice that they speak too softly, or that their handwriting is slow and looks cramped or small. Friends or family members may be the first to notice changes in someone with early Parkinson's. They may see that the person's face lacks expression and animation, or that the person does not move an arm or leg normally.

People with Parkinson's often develop a parkinsonian gait that includes a tendency to lean forward, small quick steps as if hurrying forward, and reduced swinging of the arms. They also may have trouble initiating or continuing movement. Symptoms often begin on one side of the body or even in one limb on one side of the body.

As the disease progresses, it eventually affects both sides. However, the symptoms may still be more severe on one side than on the other. A number of disorders can cause symptoms similar to those of Parkinson's disease. People with Parkinson's-like symptoms that result from other causes are sometimes said to have parkinsonism.

While these disorders initially may be misdiagnosed as Parkinson's, certain medical tests, as well as response to drug treatment, may help to distinguish them from Parkinson's. Since many other diseases have similar features but require different treatments, it is important to make an exact diagnosis as soon as possible. There are currently no blood or laboratory tests to diagnose nongenetic cases of Parkinson's disease.

Medically reviewed by Seunggu Han, M. Early signs. Risk factors. Exposure to air pollutants may amplify risk for depression in healthy individuals.

Costs associated with obesity may account for 3. Related Coverage. What is the life expectancy for people with Parkinson's? Medically reviewed by Nancy Hammond, MD. Why do I feel shaky, weak, and tired? What can I do about it? The majority of Parkinson's patients are treated with medications to relieve the symptoms of the disease. These medications work by stimulating the remaining cells in the substantia nigra to produce more dopamine levodopa medications or by inhibiting some of the acetylcholine that is produced anticholinergic medications , therefore restoring the balance between the chemicals in the brain.

It is very important to work closely with the doctor to devise an individualized treatment plan. Side effects vary greatly by class of medication and patient. Developed more than 30 years ago, levodopa is often regarded as the gold standard of Parkinson's therapy.

Levodopa works by crossing the blood-brain barrier, the elaborate meshwork of fine blood vessels and cells that filter blood reaching the brain, where it is converted into dopamine. Since blood enzymes called AADCs break down most of the levodopa before it reaches the brain, levodopa is now combined with an enzyme inhibitor called carbidopa.

The addition of carbidopa prevents levodopa from being metabolized in the gastroinstenal tract, liver and other tissues, allowing more of it to reach the brain. Therefore, a smaller dose of levodopa is needed to treat symptoms. This advance also helps reduce the severe nausea and vomiting often experienced as a side effect of levodopa. For most patients, levodopa reduces the symptoms of slowness, stiffness and tremor.

It is especially effective for patients that have a loss of spontaneous movement and muscle rigidity. This medication, however, does not stop or slow the progression of the disease. Levodopa is available as a standard or immediate release formula or a long-acting or "controlled-release" formula. Controlled release may provide a longer duration of action by increasing the time it takes for the gastrointestinal tract to absorb the medication.

Side effects may include nausea, vomiting, dry mouth and dizziness. Dyskinesias abnormal movements may occur as the dose is increased.

In some patients, levodopa may cause confusion, hallucinations or psychosis. Bromocriptine, pergolide, pramipexole and ropinirole are medications that mimic the role of chemical messengers in the brain, causing the neurons to react as they would to dopamine.

They can be prescribed alone or with levodopa and may be used in the early stages of the disease or administered to lengthen the duration of effectiveness of levodopa. These medications generally have more side effects than levodopa, so that is taken into consideration before doctors prescribe dopamine agonists to patients. Side effects may include drowsiness, nausea, vomiting, dry mouth, dizziness and feeling faint upon standing.

While these symptoms are common when starting a dopamine agonist, they usually resolve over several days. In some patients, dopamine agonists may cause confusion, hallucinations or psychosis. Entacapone and tolcapone are medications that are used to treat fluctuations in response to levodopa. An electrical circuit is made up of numerous wires connected in such a way that when a light switch is turned on, a light bulb will beam.

Similarly, a neuron that is excited will transmit its energy to neurons that are next to it. Neurons have a cell body with branching arms, called dendrites, which act like antennae and pick up messages. Axons carry messages away from the cell body. Impulses travel from neuron to neuron, from the axon of one cell to the dendrites of another, by crossing over a tiny gap between the two nerve cells called a synapse. Chemical messengers called neurotransmitters allow the electrical impulse to cross the gap.

Nerve cells in the substantia nigra produce the neurotransmitter dopamine and are responsible for relaying messages that plan and control body movement. For reasons not yet understood, the dopamine-producing nerve cells of the substantia nigra begin to die off in some individuals. When 80 percent of dopamine is lost, PD symptoms such as tremor, slowness of movement, stiffness, and balance problems occur.

Body movement is controlled by a complex chain of decisions involving inter-connected groups of nerve cells called ganglia. Information comes to a central area of the brain called the striatum, which works with the substantia nigra to send impulses back and forth from the spinal cord to the brain. The basal ganglia and cerebellum are responsible for ensuring that movement is carried out in a smooth, fluid manner Fig. These impulses are passed from neuron to neuron, moving quickly from the brain to the spinal cord and, finally, to the muscles.

When dopamine receptors in the striatum are not adequately stimulated, parts of the basal ganglia are either under- or over-stimulated. In particular, the subthalamic nucleus STN becomes overactive and acts as a brake on the globus pallidus interna GPi , causing shutdown of motion and rigidity.

When the GPi is overstimulated, it has an over-inhibitory effect on the thalamus, which in turn decreases thalamus output and causes tremor Fig. The action of dopamine is opposed by another neurotransmitter called acetylcholine.

In PD the nerve cells that produce dopamine are dying. The PD symptoms of tremor and stiffness occur when the nerve cells fire and there isn't enough dopamine to transmit messages. High levels of glutamate, another neurotransmitter, also appear in PD as the body tries to compensate for the lack of dopamine. Symptoms of PD vary from person to person, as does the rate of progression.