Transported into the CNS and converted to dopamine (which does not enter the CNS); also converted to dopamine in periphery

Amerliorates all clinical features of parkinsonism, particularly effective in relieving bradykinesia

GI upset, arrhythmias, dyskinesias, on-off and wearing-off phenomena, behavioral disturbances
l-DOPA → nausea
1/3 of patients respond very well, 1/3 less well, 1/3 unable to tolerate or no response

Parkinson’s disease: Most efficacious therapy but not always used as the first drug due to development of disabling response fluctuations over time

Peripheral dopa decarboxylase inhibitor which reduces peripheral conversion of Levodopa to dopamine; does not enter CNS

Decreases side effects from

peripheral dopamine excess

Increases amount of L-dopa that can enter CNS

Antiviral agent

May potentiate dopaminergic function by influencing synthesis, release or reuptake of dopamine

CNS effects (restlessness, depression, irritability, insomnia, hallucinations, confusion);
Acute toxic psychosis, livedo reticularis, peripheral edema;
heart failure, postural hypotension, urinary retention, GI disturbances

CI: patients with heart failure or seizures

D₂ receptor agonist

GI effects, postural hypotension, dyskinesias, mental disturbances (e.g., delusions, ↓ impulse control)

Pleural & retroperitoneal fibrosis, erhthromelalgia (ergot-derived)

Sudden sleep attacks

Prior use for Parkinson’s

D₁ and D₂ receptor agonist

“Sudden sleep attacks

Not available due to association with valvular heart disease

D₃ receptor agonist; smooths out fluctuations in Levodopa response

Scavenge H₂O₂ and ↑ neurotrophic activity in dopaminergic cultures

“Sudden sleep attacks

Parkinson’s

Relatively pure D₂ agonist

“Sudden sleep attacks

Parkinson’s

Potent dopamine agonist

High incidence of nausea and vomiting
dyskinesias, drowsiness, chest pain, sweating, hypotension

Sudden sleep attacks

Injection used for off-periods of akinesia, rescue treatment in levodopa-induced dyskinesia

Inhibits MAO-B selectively and MAO-A in higher doses – inhibits breakdown of dopamine; increases dopamine in neurons; may have neuroprotective effects

May increase adverse effects of levodopa

CNS stimulation

Hypertensive crisis with tyramine

Parkinson’s; enhances and prolongs effects of levodopa; smooths levodopa response

MAO-B inhibitor, more potent in preventing MPTP-induced parkinson’s

“

CNS stimulation

Hypertensive crisis with tyramine

Parkinson’s; adjunctive to levodopa

Inhibits COMT in periphery (does not enter CNS); ↓ metabolism of levodopa and prolongs its action

↑ levodopa toxicity (nausea, dyskinesias, confusion); GI effects, orthostatic ↓ BP, sleep disturbances, orange urine

Parkinson’s

Like entacapone, but enters CNS

Hepatotoxicity (death from acute hepatic failure), ↑ liver enzymes, red color in body fluids (orange urine)

Parkinson’s

Antagonist at M receptors in basal ganglia; reduce tremor and rigidity, little effect on bradykinesia

Antimuscarinic effects: sedation, mydriasis, urinary ret., dry mouth

Acute suppurative parotitis

(complication of dry mouth)

Poorly tolerated by elderly

Antagonist at M receptors in basal ganglia; reduce tremor and rigidity, little effect on bradykinesia

Antimuscarinic effects: sedation, mydriasis, urinary ret., dry mouth

Acute suppurative parotitis

(complication of dry mouth)

Poorly tolerated by elderly