Parkinson’s disease was first described by sir James Parkinson. It is characterised by tremor, rigidity, bradykinesia, and loss of postural reflexes.

In idiopathic parkinsonism there is degeneration of the dopamine-containing neurons in the substantia nigra, resulting in dopamine deficiency. Hence, the balance between inhibitory dopaminergic neurons and excitatory cholinergic neurons is disturbed resulting in relative cholinergic overreactivity.

Classification :

  1. Drugs influencing brain dopaminergic system

a. Dopamine precursor: levodopa

b. Dopamine agonists: bromocriptine, pergolide, pramipexole, ropinirole

c. Dopamine releasing drug: amantadine

d. MAO-B inhibitors: rasagiline

e. COMT inhibitors: tolcapone, entacapone

f. Peripheral decarboxylase inhibitors: carbidopa, benserazide

  1. Drugs influencing brain cholinergic system

a. Centrally acting anticholinergic drugs: benzhexol, procyclidine, benztropine

b. Antihistaminics with anticholinergic activity: promethazine, diphenyhydramine

The main aim of drug therapy in parkinsonism is to either enhance dopamine activity or reduce cholinergic activity in the striatum.


Levodopa is the main drug for the treatment of idiopathic parkinsonism. Dopamine does not cross BBB hence its immediate precursor levodopa is used. It is converted to dopamine by decarboxylase enzyme. A large amount of the drug is converted to dopamine in the peripheral tissues by peripheral decarboxylase enzyme. Only a small amount of levodopa enters the brain. Therefore levodopa is always used in combination with carbidopa /benserazide(peripheral decarboxylase inhibitors) which does not cross the BBB. ; peripheral metabolism of levodopa is reduced, thus increasing its bioavailability in the basal ganglia. Levodopa improves all the clinical symptom of parkinsonism, but does not stop the progression of the disease.


An oral administration levodopa is rapidly absorbed from the small intestine by an active transport system. Amino acids present in food may interfere with absorption of levodopa hence it should be given 30-60 minutes before meal. Active transport of levodopa into the brain may be inhibited by competition from dietary amino acids. The main metabolic products of levodopa are homovanilic acid(HVA) and 3,4- dihydroxyphenylacetic acid (DOPAC). The metabolites are excreted in urine.


  1. GIT: nausea, vomiting, anorexia are common in early treatment with levodopa.
  2. CVS: the commonest cardiovascular side effect is postural hyprtension which is usually asymptomatic. It can also cause tachycardia, palpitation, rarely cardiac arrhythmias.
  3. Abnormal movements: dyskinesia, tics, choreoathetoid movements.
  4. Alteration in smell and taste sensation
  5. Mental changes like insomnia, confusion, delusions, euphoria, depression and nightmares.
  6. Fluctuations in response: after 3-5 years of therapy with progressing disease control becomes poor and fluctuations in symptom occur frequently. Wearing off is due to decrease in plasma concentration of levodopa towards the end of a dose interval. End of dose deterioration can also be improved by administering levodopa in smaller and more frequent doses. THATS ALL ABOUT LEARN ABOUT ANTIPARKINSONIAN DRUGS

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