Bromocriptine effects

Those for the D2 receptor (e.g. bromocriptine) have a particular value in the treatment of Parkinson s disease by reproducing the effects of the dopamine lost through degeneration of the nigrostriatal tract (Chapter 15). They are also used to reduce the undesirable effects of prolactinaemia (high plasma prolactin), such as amenorrhoea and galactorrhoea. 

Bromocriptine directly binds to the D2 receptors on the lac-totroph cells to exert its effect. Bromocriptine normalizes prolactin level, restores menstrual cycles, and reduces tumor size in approximately 90% of patients.49 Adverse effects such as nausea, dizziness, and orthostatic hypotension often limit 5% to 10% of patients from continuing treatment. Thus, start bromocriptine at a low dose (e.g., 0.625-1.25 mg) at bedtime... 

Bromocriptine, used in theory to reverse DA blockade, reduces rigidity, fever, or CK levels in up to 94% of patients. Amantadine has been used successfully in up to 63% of patients. Dantrolene has been used as a skeletal muscle relaxant, with favorable effects on temperature, respiratory rate, and CK in up to 81% of patients. 

The well-known emetic effect of ergot alcaloids in dogs was particularly pronounced with bromocriptine, even with oral doses of as low as 0.1 mg/kg. 

Six patients with Parkinson s disease were withdrawn from their antiparkinsonian medications (L-DOPA/carbidopa, bromocriptine, or lisuride) (Rabey et al. 1992, 1993). After 12 hours off medication, the subjects ate 250 g of cooked fava beans. Significant improvements in motor symptoms were noted, comparable to those seen with 125 mg of L-DOPA and 12.5 mg of carbidopa. In fact, three subjects developed severe dyskinesias after fava ingestion, akin to those seen after larger doses of pharmaceutical L-DOPA. Plasma levels of L-DOPA increased after fava ingestion in a manner comparable to that seen with administration of oral L-DOPA. These results suggest that the L-DOPA contained in fava beans was transported into the CNS and converted to dopamine. In five nonparkinsonian, healthy volunteers, a similar increase in plasma L-DOPA was observed after fava ingestion, although much lower. The difference in plasma L-DOPA between normal volunteers and parkinsonian patients is apparently due to a residual effect of carbidopa in the subjects with Parkinson s disease. Without carbidopa, the L-DOPA from fava is rapidly converted to dopamine in the blood stream and never crosses the blood-brain barrier. 

L-DOPA can be initiated at 50 mg taken at bedtime and increased stepwise over a few weeks until the symptoms are relieved. Bromocriptine can be initiated at 7.5 mg at bedtime, pramipexole is often dosed at 0.125-0.375 mg at night, and ropinirole, which has an indication for RLS, is typically administered at 0.25-3 mg at bedtime. These medications are not without side effects. They may cause nausea and, over time, insomnia. Less commonly, these medications can cause hallucinations or involuntary movements called dyskinesias. These side effects usually resolve rapidly upon discontinuing the medication. 

Bromocriptine is a dopamine agonist acting by direct stimulation of the dopamine receptors. In Parkinson s disease, it is reserved for use in patients who are intolerant to levodopa or in whom levodopa alone is not sufficient. Orphenadrine is an antimuscarinic indicated in Parkinson s disease. Antimuscarinics tend to be more effective than levodopa in targeting tremor rather than rigidity and bradykinesia. Moclobemide is an antidepressant referred to as a reversible monoamine oxidase inhibitor (RIAAA) type A. 

The dopamine agonist bromocriptine produces the male-odor induced effects, while they are prevented by pimozide, which blocks dopaminergic transmission (Kaba etal, 1992). 

Dopamine receptor agonists. Deficient dopaminergic transmission in the striatum can be compensated by ergot derivatives (bromocriptine p. 114], lisu-ride, cabergoline, and pergolide) and nonergot compounds (ropinirole, prami-pexole). These agonists stimulate dopamine receptors (D2, D3, and D sub-types), have lower clinical efficacy than levodopa, and share its main adverse effects. 

Bromocriptine, a dopaminomimetic that is a dopamine D2 receptor agonist, possesses expressed antiparkinsonian activity. It is used for treating all phases of idiopathic and post-encephalic Parkinsonism. However, it has a number of undesirable side effects, even causing mental disturbances in long-term use. The most common synonyms are parlodel, bromergon, and others. 

Pharmacology Bromocriptine, a dopamine agonist, may relieve akinesia, rigidity, and tremor in patients with Parkinson s disease. It produces its therapeutic effect by directly stimulating the dopamine receptors in the corpus striatum. 

Bromocriptine (Parl el) [Antiparkinsonian Agent/Dopamine Receptor Agonist] Uses Parkin on Dz, hyperprolactinemia, acromegaly, pituitary tumors Action Direct-acting on the striatal dopamine receptors X prolactin secretion Dose Initial, 1.25 mg PO bid titrate to effect, w/ food Caution [B, ] Contra Severe ischemic heart Dz or PVD Disp Tabs, caps SE X BP, Raynaud phenomenon (vasospastic disorder resulting in discoloration of the fmgers/toes), dizziness, N, hallucinations Interactions T Effects W/ erythromycin, fluvoxamine, nefazodone, sympathomimetics, antihypertensives X effects W/ phenothiazines, antipsychotics EMS Monitor BP may cause intolerance to EtOH OD May cause NA, severe hypotension give IV fluids symptomatic and supportive... 

Type B effects are rare but should be recognized. They include oedema of the lower limbs (bromocriptine, amantadine), livedo reticularis (amantadine), diarrhoea (tolcapone, entacapone), paroxysmal hypertension and dysregulation of blood pressure control (selegiline), narcoleptic phenomena (pramipex-ole), and insomnia (all dopaminergic agonists). 

---