TREATMENT OF PARKINSONS DISEASE

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Parkinson's disease is an age-related degenerative brain disorder that results in the breakdown of certain brain tissue. It is most famous for causing slow movements, tremors, balance issues, and other issues. The majority of cases occur for unknown reasons, but some are hereditary. Although the condition cannot be cured, there are numerous available treatments. Treatment Carbidopa-Levodopa Patients with Parkinson's disease (PD) must take levodopa treatment within two years after the start of symptoms. Levodopa, the most effective treatment for Parkinson's disease (PD), is usually used with carbidopa, an aromatic acid decarboxylase inhibitor, to significantly reduce the likelihood of nausea. Increasing the dosage of carbidopa and levodopa beyond the currently advised 1:4 ratio has been shown to increase on time without dyskinesia while decreasing off time. Adrenergic agonists Dopamine receptor agonists stimulate dopamine receptors and delay levodopa-related adverse effects such motor fluctuations and dyskinesias when given early in the course of therapy. There isn't enough evidence, though, to prove that early dopamine agonist therapy slows the progression of the condition or even improves long-term quality of life. Common non-ergot dopamine agonists used in clinical settings include pramipexole, etc

Antagonists of the adenosine receptor An adenosine A2 receptor antagonist is used in addition to levodopa in PD patients experiencing off episodes. Patients who experience motor abnormalities brought on by levodopa may receive a minor benefit from the medicine, which is available in tablets. Although it has been seen to worsen or cause vertigo, hallucinations, dyskinesia, and other symptoms, it is typically well-managed. MAO inhibitors Selegiline and rasagiline, although commonly used in early, mild PD, are helpful in individuals with moderately advanced PD who have motor issues with levodopa. It has been demonstrated that safinamide, another MAOI, reduces daily and early-morning off times while increasing mean on time without distracting dyskinesia. A reversible MAOI, safinamide also lowers neuronal glutamate release, inhibits voltage-dependent activated sodium channel, limits dopamine absorption in brain neurons, and absorbs calcium ion entry.

Catechol O-Methyltransferase (COMT) inhibitors By preventing the central and peripheral breakdown of levodopa and tolcapone, respectively, they raise the levels of levodopa and dopamine in the central nervous system. The usage of tolcapone has been constrained due to hepatotoxicity. The triple-combination therapy of levodopa ,carbidopa, and entacapone is available but frequently denied by third-party payers. Anticholinergics Anticholinergic medications like trihexyphenidyl and benztropine work to counteract the effects of acetylcholine at muscarinic receptors postsynaptic to striatal interneurons. They are primarily used to lessen tremor and have no effect on bradykinesia. The side effects of acetylcholine antagonists include memory loss, hallucinations, dry mouth, diarrhea, and urinary retention.

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