Since cabergoline is not approved in the U.S. for Parkinsons Disease, but for hyperprolactinemia, the drug remains on the market. The lower doses required for treatment of hyperprolactinemia have been found to be not associated with clinically significant valvular heart disease or cardiac valve regurgitation. Interactions
No interactions were noted with levodopa or selegiline. The drug should not be combined with other ergot derivatives. Dopamine antagonists such as antipsychotics and metoclopramide counteract some effects of cabergoline. The use of antihypertensive drugs should be intensively monitored because excessive hypotension may result from the combination. Pharmacology
Pharmacodynamics
Cabergoline is a long-acting dopamine D2 receptor agonist. In-vitro rat studies show a direct inhibitory effect of cabergoline on the prolactin secretion in the lactotroph cells of the pituitary gland and cabergoline decreases serum prolactin levels in reserpinized rats. Although cabergoline is commonly described principally as a D2 receptor agonist, it also possesses significant affinity for the dopamine D3, and D4, serotonin 5-HT1A, 5-HT2A, 5-HT2B, and 5-HT2C, and α2-adrenergic receptors, as well as moderate/low affinity for the dopamine D1, serotonin 5-HT7, and α1-adrenergic receptors. Cabergoline functions as an partial or full agonist at all of these receptors except for the 5-HT7, α1-adrenergic, and α2-adrenergic receptors, where it acts as an antagonist. Cabergoline has been associated with cardiac valvulopathy due to activation of 5-HT2B receptors. Pharmacokinetics
Following a single oral dose, resorption of cabergoline from the gastrointestinal (GI) tract is highly variable, typically occurring within 0.5 to 4 hours. Ingestion with food does not alter its absorption rate.
High rates of impetigo are a marker for widespread streptococcal transmission. Diagnosis
Chorea is distinctive, if the health care provider is familiar with it. The diagnosis is then made by the typical acute onset in the weeks following a sore throat or other minor infection, plus evidence of inflammation (raised CRP and/or ESR) and evidence of recent streptococcal infection. To confirm recent streptococcal infection:

Throat culture
Anti-DNAse B titre (peaks at 8–12 weeks after infection)
Anti-streptolysin O titre (peaks at 3–5 weeks)None of these tests are 100% reliable, particularly when the infection was some months previously. Further testing is directed more towards alternative diagnoses and other manifestations of rheumatic fever:

Echocardiography
EEG
Lumbar puncture
Magnetic resonance imaging or computed tomography scan of the brain (alterations in caudate nucleus and putaminal enlargement have been described in some patients)

Management
Management of Sydenhams chorea is based on the following principles:

Eliminate the streptococcus – it may not be of any use for the index patient but further spread of that specific clone will be prevented. Treat the movement disorder
Immunosuppression
Prevention of relapses and further cardiac damage
Manage the disabilityThere is a UFMG rating scale for Sydenhams chorea, from Brazilian Universidade Federal de Minas Gerais (UFMG), for research purposes, but it only looks at motor function not psychiatric/behavioural symptoms. Occupational therapy and physiotherapy is useful for maintaining function and muscle tone. Treatment with sodium valproate is effective for controlling symptoms, but it doesn’t speed up recovery. Haloperidol was used previously, but caused serious side effects e.g. tardive dyskinesia.