antiparkinson drug
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What is an antiparkinson drug?
Antiparkinson drugs treat the symptoms of Parkinson's disease and other parkinsonism conditions. Parkinson's disease results from the degeneration of cells in the substantia nigra and locus ceruleus, which leads to a dopamine deficiency and inhibits activity within the basal ganglia.
Major antiparkinson drugs include levodopa, dopamine-receptor agonists, amantadine, COMT (catechol-O-methyltransferase) inhibitors, MAO-B (monoamine oxidase B) inhibitors, and muscarinic receptor antagonists. Levodopa increases dopamine in the brain, while dopamine-receptor agonists stimulate dopamine receptors. Amantadine, an antiviral drug, can also reduce tremor and bradykinesia symptoms by triggering dopamine release.
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What disease are antiparkinson drugs used to treat?
Antiparkinson drugs are used to treat Parkinson disease and other conditions of parkinsonism. Parkinsonism is a group of neurological disorders that cause loss of motor function due to the degeneration of neurons in the area of the brain that controls movement. Parkinson disease, the most common form of parkinsonism, is characterized by tremor, muscle rigidity, slowness in movement, and postural instability. Antiparkinson drugs include levodopa, dopamine-receptor agonists, amantadine, COMT (catechol-O-methyltransferase) inhibitors, MAO-B (monoamine oxidase B) inhibitors, and muscarinic receptor antagonists.
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How do antiparkinson drugs help people with Parkinson's disease?
Antiparkinson drugs help manage the symptoms of Parkinson's disease and parkinsonism, which are characterized by motor function loss due to neuron degeneration in the brain. These drugs include levodopa, which converts to dopamine in the brain, addressing dopamine deficiency. Dopamine-receptor agonists stimulate dopamine production, while amantadine promotes dopamine release and reduces neuronal overactivity.
Levodopa is often combined with carbidopa to increase its effectiveness and reduce side effects, allowing many patients to live reasonably normal lives. Although these drugs modify the symptoms, they are not a cure for Parkinson's disease.
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What are some common types of antiparkinson drugs?
Antiparkinson drugs treat symptoms of Parkinson's disease and parkinsonism. Main types include levodopa, which converts to dopamine in the brain, and dopamine-receptor agonists like pergolide and bromocriptine, which stimulate dopamine receptors. Other drugs include COMT inhibitors (e.g., tolcapone) and MAO-B inhibitors (e.g., selegiline), which prevent dopamine breakdown, and amantadine and muscarinic receptor antagonists. Levodopa is often supplemented with carbidopa to increase its delivery to the brain.
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What are possible side effects of taking antiparkinson drugs?
Antiparkinson drugs, used to manage symptoms of Parkinson's disease, can have several side effects. Levodopa, a common treatment, may cause involuntary movements, hallucinations, nausea, vomiting, and changes in mood or behavior, especially after long-term use. Other drugs, like chlorpromazine and haloperidol, can cause drowsiness, altered blood pressure or heart rate, and tremors. Prolonged use of some antipsychotic drugs can also lead to movement disorders resembling Parkinson's disease, such as tardive dyskinesia. In rare cases, neuroleptic malignant syndrome, a potentially fatal neurological side effect, can occur.
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How do doctors decide which antiparkinson drug to prescribe to a patient?
The selection of an antiparkinson drug depends on various factors, and doctors consider these before prescribing.
The most effective treatment is levodopa, which converts to dopamine in the brain, addressing the dopamine deficiency characteristic of parkinsonism. However, its long-term use can lead to side effects; thus, it is often combined with carbidopa to enhance levodopa's effectiveness and reduce side effects. Other drugs include dopamine-receptor agonists, amantadine, COMT inhibitors, MAO-B inhibitors, and muscarinic receptor antagonists. In advanced cases, deep brain stimulation or other surgical interventions might be considered to alleviate symptoms.
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antiparkinson drug, any drug used to treat the symptoms of Parkinson disease or other conditions of parkinsonism. The major antiparkinson drugs are levodopa, dopamine-receptor agonists, amantadine, and the so-called COMT (catechol-O-methyltransferase) inhibitors, MAO-B (monoamine oxidase B) inhibitors, and muscarinic receptor antagonists.
Levodopa
The first drug that was discovered to successfully relieve symptoms of Parkinson disease was the amino acid l-3,4-dihydroxyphenylalanine (levodopa, or l-dopa). Levodopa is the precursor of the neurotransmitter dopamine, a marked decrease in which is the primary neuropathological feature of parkinsonism. When given orally in large daily doses, some levodopa is able to escape metabolism in the bloodstream and enter the brain, where surviving dopamine neurons convert it to dopamine through the process of decarboxylation (the removal of a carboxyl group, COOH). To increase the delivery of levodopa to the brain, levodopa therapy is supplemented with carbidopa (an analog of levodopa), which inhibits the decarboxylation (and hence breakdown) of levodopa to dopamine prior to crossing the blood-brain barrier (dopamine itself cannot penetrate the blood-brain barrier). As a result, greater amounts of levodopa are able to reach the brain, enabling the administration of lower doses of the drug and thereby reducing the risk for severe side effects.
The primary side effect associated with large doses of levodopa is an increased risk for schizophrenia-like episodes, presumably because of excess formation of dopamine. The use of levodopa to treat Parkinson disease, moreover, is not the radical cure that it was once thought to be but only a measure that modifies the symptoms of the disease.
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Dopamine-receptor agonists
Dopamine-receptor agonists work by binding to dopamine receptors on dopaminergic neurons (the neurons that normally synthesize and use dopamine) in the neurotransmitter’s absence. Stimulation of the receptors increases dopaminergic activity in the brain, thereby lessening the severity of parkinsonism symptoms. Examples of dopamine-receptor agonists include pergolide, ropinirole, pramipexole, and bromocriptine. These drugs are modified chemically so as to be able to gain access to the brain. Side effects of dopamine-receptor agonists include hallucination and mental confusion.
COMT and MAO-B inhibitors
COMT inhibitors, such as tolcapone and entacapone, block the enzymatic breakdown of dopamine by the catechol-O-methyltransferase enzyme. These drugs commonly are given in conjunction with the combination of levodopa and carbidopa, since they inhibit COMT degradation of levodopa in peripheral tissues, thereby increasing levodopa’s half-life in the blood and enabling greater amounts of the drug to cross the blood-brain barrier.
Similar to COMT inhibitors, MAO-B inhibitors slow the degradation of dopamine in the brain. Best known of these agents is selegiline, which extends the effects of levodopa and often is prescribed in combination with levodopa and carbidopa.
Muscarinic receptor antagonists
Abnormal activity of the neurotransmitter acetylcholine is responsible for producing certain symptoms of parkinsonism. This activity is mediated by the binding of acetylcholine to muscarinic acetylcholine receptors in the brain (the receptors are named for their sensitivity to the chemical muscarine and their selectivity for acetylcholine). Thus, agents that block the receptors, such as benztropine mesylate and trihexyphenidyl, are administered to reduce symptoms, though their actions are modest. These drugs are also suspected of increasing dopamine levels in the brain. Sedative actions and effects on vision, however, limit their use in elderly patients.
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Amantadine
The antiviral drug amantadine, which is used in the treatment of influenza A infection, also has some ability to reduce symptoms of tremor and bradykinesia (slowness of movement) in patients affected by Parkinson disease. While its mechanism of action in this capacity is unclear, it has been found to trigger the release of dopamine from neurons in the brain. It also blocks excitatory signaling and neuronal overactivity associated with movement. Confusion, dizziness, nausea, and vomiting are listed among its side effects.