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In the previous lecture we started discussing parkinson’s disease we talked about its symptoms causes and treatment options so today we’ll start talking about parkinson’s disease treatment and we’ll begin with levodopa first remember that the main problem is the degeneration of dopaminergic neurons in basal ganglia so can we use dopamine as a drug to compensate
This degeneration the answer is no because dopamine does not cross the blood-brain barrier but we can use levodopa which is the metabolic precursor of dopamine it is actively transported into the cns and converted to dopamine by dopamine decarboxylase enzyme but there will be another problem as dopamine decarboxylase enzyme is also found in the gastrointestinal
Tract and peripheral tissues so more than 95 of levodopa is decarboxylated to dopamine in the periphery resulting in nausea vomiting cardiac arrhythmias and hypotension and less than five percent enters the cns so to solve this issue and enhance the effects of levodopa on the cns levodopa should be co-administered with a dopamine decarboxylase inhibitor that
Does not cross the blood-brain barrier such as bensrizide or carbidopa these agents diminish the metabolism of levodopa in the periphery thereby increasing the availability of levodopa to the cns the addition of carbidopa lowers the dose of levodopa needed by four to five fold and consequently decreases the severity of the side effects arising from peripherally
Formed dopamine adverse effects include anorexia nausea and vomiting and this occur because of stimulation of the chemoreceptor trigger zone tachycardia and ventricular extracestols that result from dopaminergic action on the heart and hypotension may also develop adrenergic action on the iris causes midriosis brownish saliva and urine because of the melanin
Pigment produced from catecholamine oxidation visual and auditory hallucinations and abnormal involuntary movements may develop these effects reflect over activity of dopamine in the basal ganglia levodopa can also cause mood changes depression psychosis and anxiety fluctuations in motor response may be produced also called on all as levodopa has an extremely
Short half-life one to two hours which causes fluctuations in plasma concentration and ingestion of meals particularly if high in protein interferes with the transport of levodopa into the cns so levodopa should be taken on an empty stomach 30 minutes before a meal drug interactions include vitamin b6 increases the peripheral metabolism of levodopa and diminishes
Its effectiveness co-administration of levodopa and mao inhibitors can produce a hypertensive crisis caused by enhanced catecholamine production that’s all for this video in the next lecture we’ll continue talking about parkinson’s disease treatment so subscribe click on the bell icon and keep following us
Transcribed from video
Pharmacology [CNS] 3- Parkinson's Disease Treatment [Part 1: Levodopa Carbidopa and Benserazide ] By Medical Videos [ ANIMATED ]
