Reference no: EM133517074
Assignment:
Case Study: Parkinson's Disease
A physician examined Tarek, a 66-year-old man, because he displayed symptoms of Parkinson's disease: resting tremor, muscle rigidity, and bradykinesia (slowness in the initiation and continuation of movement). This made it difficult for Tarek to perform daily tasks such as getting dressed, bathing, and many other activities. Further physical examination and a thorough history, together with an MRI to rule out alternative possibilities, confirmed the diagnosis. The physician placed Tarek on a dopamine agonist that can cross the blood-brain barrier and said that this could be supplemented later by levodopa, a monoamine oxidase inhibitor (MAOI), anticholinergics, and other medications.
Parkinson's disease is characterized by the degeneration of dopaminergic neurons in the substantia nigra of the midbrain, with concomitant loss of their projections to the dorsal striatum along the nigrostriatal pathway. This loss in dopaminergic neurotransmission results in involuntary motor control; the primary manifestation of Parkinson's disease. Dopamine is derived from L-dopa (levodopa) and is a monoamine degraded within presynaptic axons by the enzyme monoamine oxidase (MAO). Dopaminergic neurons produce effects that are antagonized by ACh released by other neurons that synapse in the striatum. A drug must be able to cross the blood-brain barrier to be effective in treating neurological disorders such as Parkinson's disease.
Questions
1. What are the monoamines and what are some examples?
2. What is the blood-brain barrier?
3. How would a dopamine agonist, levodopa, and an MAOI benefit Tarek with his Parkinson's disease?
4. What is an anticholinergic drug, and how would such a drug benefit Tarek?
5. Aside from voluntary motor control, name one other function served by dopamine in the brain and the associated brain region.
6. Parkinson's disease is also associated with the accumulation of Lewy bodies in the brain. What are Lewy bodies and how do they contribute to the pathophysiology of Parkinson's disease?