Parkinson Disease

IV

Diagnosis

Diagnosing Parkinson disease may be difficult, particularly in the early stages of the disease when symptoms resemble other medical conditions, and misdiagnosis occurs occasionally. No single laboratory test can diagnose the disease. Blood tests are performed to eliminate conditions such as a low thyroid, which may result in slowness of movement. Brain imaging techniques, such as magnetic resonance image (MRI), positron emission tomography (PET scan), and single photon emission computed tomography (SPECT), may be used to help doctors exclude other medical conditions, such as stroke or brain tumors, that produce symptoms similar to those of Parkinson disease. Doctors quiz patients about their exposure to drugs, viruses, and environmental toxins to determine if a particular factor may be causing a parkinsonism disorder. They document the medical history of the patient’s blood relatives to determine the likelihood of a genetic predisposition for Parkinson disease or other disorders. And they carefully observe a patient’s muscular activity over a period of time—as the disease progresses, motions particular to Parkinson disease become more obvious.

Doctors usually diagnose Parkinson disease if a patient develops two or more of the principal symptoms, at least one of which is tremor or bradykinesia. The diagnosis is usually confirmed if people with suspected Parkinson disease respond well to drug treatment. Those with parkinsonism disorders or other medical conditions with similar symptoms typically do not respond to the drugs used in treating Parkinson disease.

V

Treatment

There is no known cure for Parkinson disease—that is, no treatment that prevents the disease from progressing. But the symptoms of the disease can be controlled by various drugs and, in some cases, by surgery.

A

Drug Therapy

Most symptoms of Parkinson disease arise from a deficiency of dopamine in the brain. But simply giving a patient a dose of dopamine to restore depleted stores is ineffective because dopamine cannot pass from the bloodstream to the brain. Drugs that treat Parkinson disease, known as antiparkinson drugs, use other methods to temporarily restore dopamine in the brain or closely mimic dopamine’s actions. In this section, each drug is designated by its generic name, followed by trade name examples in parentheses.

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A

1

Levodopa

The most effective antiparkinson drug available is levodopa (Laradopa), an oral drug introduced in 1967 that treats bradykinesia, rigidity, tremor, and difficulty walking. Levodopa’s structure enables it to enter the brain, where it transforms into dopamine.

When levodopa is taken alone, however, the body breaks down about 95 percent of the drug into dopamine before it reaches the brain. Instead of being used by the brain, the dopamine travels throughout the body, producing side effects, including nausea and vomiting, before it is broken down, or metabolized, by the liver and other tissues. Combining levodopa with a drug such as carbidopa enables more levodopa to enter the brain before it converts into dopamine. Carbidopa/levodopa (Atamet, Sinemet) lessens rigidity and bradykinesia but is less effective in treating tremor or balance problems. A similar drug combining carbidopa and benserazide (Madopar) is available in Canada and Europe.

Carbidopa/levodopa produces side effects in some people. As many as half of the people who take this drug for two to five years begin to notice fluctuations in the drug’s effectiveness, known as an on-off effect. Others develop dyskinesia—involuntary movements such as jerking or twitching. As Parkinson disease progresses, the effectiveness of carbidopa/levodopa decreases and patients need higher and more frequent doses to control their symptoms. Depending upon the severity of symptoms, most doctors combine carbidopa/levodopa with other drugs to enhance levodopa’s effects.

A

2

Dopamine Agonists

Dopamine agonists mimic the action of dopamine by activating nerve cells in the striatum. Dopamine agonists are increasingly used alone in the early stages of Parkinson disease in order to lower a patient’s risk of developing the dyskinesia associated with levodopa therapy. Later in the course of the disease they are more likely to be combined with carbidopa/levodopa to alleviate that drug’s on-off effects. Side effects range from nausea, headache, and nasal congestion to nightmares and hallucinations. Dopamine agonists include pergolide (Permax), paramipexole (Mirapex), and ropinerole (Requip).

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