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Naf87 Naf87
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6 years ago
John is 63 years old and receives home care by an occupational therapist twice a week. His therapist is currently working with John on maintaining joint flexibility and balance.
 
  John demonstrates resting tremor, so his therapist is also working on adaptive techniques, so John can continue to use his hands to write, use the computer, and cook simple meals. John's wife assists with his mobility and walks slowly beside him, holding his arm. Sometimes she needs to help him open his prescription bottles, so he can take his medicine, a combination of levodopa and carbidopa.
 
  What motor disease does John demonstrate? One of his signs is resting tremor. What is the difference between a resting tremor and an intention tremor?
 
  What is the advantage of combining levodopa with carbidopa? What is the benefit of anticholinergic drugs in the management of Parkinson disease?
 
  Parkinson disease involves the destruction of the substantia nigra and the nigrostriatal pathway. Where are these structures anatomically?
 
  The patient with Parkinson disease typically presents with a masklike facial expression. Why does he or she have a masklike facial expression? How are the eyes, mouth, and laryngopharynx affected by this disease?
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6 years ago
John is expressing the signs and symptoms of Parkinson disease. The resting tremor that exists in Parkinson disease is a rhythmic movement that occurs when the limb is inactive. When an intended movement is initiated in the limb, the tremor disappears. The tremor is also absent when the individual is asleep. Intention tremor, on the other hand, is absent when the limb is at rest. When an intended movement is initiated, the tremor worsens. Intention tremor is a result of cerebellar dysfunction and the inability for the cerebellum to control the movement of the limb to the intended target.

Levodopa, when administered alone, is largely metabolized before it enters the brain. When this happens, it can no longer cross the blood-brain barrier and produce its therapeutic effect. Carbidopa is beneficial because it inhibits decarboxylase, the enzyme responsible for metabolizing levodopa to dopamine in the systemic circulation. As a result, more levodopa is available to enter cerebral circulation and a smaller dose is needed to have therapeutic value.

Unlike levodopa, which acts to increase dopamine levels, anticholinergic drugs inhibit cholinergic activity in the central nervous system. They function to reduce the effects that occur when cholinergic neurons work without the inhibitory action of dopamine.

The substantia nigra is a dopamine-producing center of the midbrain. The axons of these cells form a tract, called the nigrostriatal pathway, to the striatum of the basal ganglia. This tract carries dopamine to the striatum and modulates basal ganglion activity.
As muscle rigidity and bradykinesis progress, voluntary and involuntary movement of the facial muscles is lost. The result is a masklike facial appearance and inability to express emotion through facial movements. Blinking becomes impaired, and in conjunction with altered autonomic function, excess lacrimation and tearing occur. The muscles of the tongue, mouth, and throat are also affected by rigidity. Eating, speaking, and swallowing become increasingly difficult. With autonomic change, there is excessive salivation and drooling.
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