Dopaminergic Enhancers

This group of drugs act to boost dopaminergic (+ cholinergic transmission) within the brain. They are most classically used to treat Parkinson’s characterised by DA loss in the substantia nigra.


This is a precursor of dopamine which is uptaken by the CNS and converted to dopamine

– It is given with Carbidopa, a peripheral DDC inhibitor which stops the peripheral conversion of L- DOPA to dopamine which would stop the drug from crossing the BBB.

– It gives clinical improvement in many patients and lasts 2-5 years.


Side effects
  • Dyskinesia (repetitive involuntary movements) in 80% of patients
  •  Early onset psychosis and schizophrenia like symptoms (hallucinations)
  • Cardiovascular –> Palpitations + Hypotension (consider midodrine, a-agonist to ­arterial resistance)
  • Daytime sleepiness
  • Nausea and vomiting –> due to D2 activation of chemoreceptive trigger zone
  • It is important to not acutely stop Levodopa due to the risk of neuroleptic malignant syndrome.
  • N.B. Not used in patients with psychosis, glaucoma and peptic ulcers

DA receptor agonists

e.g. Pramipexole + Ropinirole + Bromocriptine

These are selective dopaminergic agonists, given as alternative first line drugs or in combination 

Side effects
  • Similar to levodopa + can induce profound hypotension.
  • Impulse control disorders + Daytime somnolence
  • Bromocriptine and cabergoline can cause excessive fibrosis
  • Therefore, before treatment all patient should have Echocardiogram, ESR, creatinine + CXR

MAO-B inhibitors

e.g. Selegiline

This is a selective MAO-B inhibitor that decreases DA metabolism to prolong its action
– Has few side effects, but can precipitate “serotonin syndrome” if taken with SSRIs/TCAs

N.B. As first-line treatments. It can be difficult to know which one of these to give, as each of these 3 therapies has their own benefits and disadvantages:

i) L-DOPA ➔ Gives the best improvements in symptoms, but highest rate of motor complications
– In addition, gives reduced effectiveness with time

ii) DA-agonists ➔ Less improvement in symptoms but offset by fewer motor complications
– However direct agonist activity gives highest rate of hallucinations and impulsivity

iii) MAO-Bi’s ➔ Like DA-agonists, less improvement in symptoms but fewer motor complications
– Less likely to give impulsivity etc but should not be used if patients taking SSRIs

COMT inhibitors

e.g. Entacapone + Tolcapone
This reduces peripheral metabolism of levodopa, increasing bioavailability to reach the CNS
– Used to augment effect of Carbidopa + L-dopa in a combined treatment for Parkinson’s disease


This is an anti-influenza drug that blocks the M2 ion channel but has CNS activity

The mechanism of action in the CNS is not known but the net result is to increase DA release and therefore has become useful in the management of early Parkinson. 

Side effects
  • Ataxia
  • Confusion


This is a blocker of the dopamine reuptake protein

– It increases the DA transmission at the synapse, used to enhance functioning in ADHD 

Side effects
  • Abdominal pain
  • Nausea
  • Appetite suppression
  • Insomnia

CNS Muscarinic antagonists

e.g.Benztropine + Procyclidine

These drugs block muscarinic receptors in CNS and suppress overactivity in the striatum

– Indicated more for the management of drug-induced parkinsonism as opposed to idiopathic.
– Potent in the treatment of tremor and rigidity in Parkinson’s and EPSE’s from antipsychotics

Side effects
  • Anticholinergic effects (dry mouth, tachycardia, dilation)
  • Not used in glaucoma


The intended purpose of this website is to be used as a resource for revision for exams. It should not be used as a guideline or reference for clinical practice/decision making or by patients looking for medical information or advice. In2Med takes no responsibility for any loss or damaged resulting from the use of information from this website.

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