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==== Levodopa ==== | ==== Levodopa ==== | ||
<callout type="success">{{fa>arrow-circle-right?color=green}} See main article: **[[meds:dopamine-agonists:carbidopa-levodopa|]]**</callout> | <callout type="success">{{fa>arrow-circle-right?color=green}} See main article: **[[meds:dopamine-agonists:carbidopa-levodopa|]]**</callout> | ||
- | Administration of dopamine alone is ineffective because dopamine cannot cross the blood–brain barrier. Thus, the main treatment for all patients with Parkinson's is levodopa, a dopamine precursor. When ingested alone, levodopa is rapidly converted to dopamine outside the CNS. Thus carbidopa, a DOPA decarboxylase inhibitor (DDCI), is added to inhibit the conversion of levodopa to dopamine outside the CNS. | + | The main treatment for PD is levodopa, a dopamine precursor (since dopamine itself cannot cross the blood–brain barrier). When taken orally, levodopa is rapidly converted to dopamine outside the CNS. Thus carbidopa, a DOPA decarboxylase inhibitor (DDCI), is added to inhibit the conversion of levodopa to dopamine outside the CNS. |
+ | |||
+ | ==== On-Off Phenomenon ==== | ||
+ | The on-off phenomenon is a consequence of sustained levodopa treatment in patients with Parkinson's disease. It is characterized by a switch between mobility and immobility, which occurs as an end-of-dose or “wearing off” worsening of motor function or, much less commonly, as sudden and unpredictable motor fluctuations.[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1033307/|Lees, A. J. (1989). The on-off phenomenon. Journal of Neurology, Neurosurgery & Psychiatry, 52(Suppl), 29-37.]])] | ||
==== Dopamine Agonists ==== | ==== Dopamine Agonists ==== | ||
- | Dopamine agonists such as [[meds:dopamine-agonists:ropinirole|ropinirole]] and [[meds:dopamine-agonists:pramipexole|pramipexole]] are also used. | + | Dopamine agonists include the ergot derivatives: [[meds:dopamine-agonists:bromocriptine|bromocriptine]], cabergoline, dihydroergocryptine, lisuride, and pergolide. There are also the non-ergot derivatives: apomorphine, piribedil, [[meds:dopamine-agonists:pramipexole|pramipexole]], [[meds:dopamine-agonists:ropinirole|ropinirole]], rotigotine. |
==== Dopamine Agonist Withdrawal Syndrome (DAWS) ==== | ==== Dopamine Agonist Withdrawal Syndrome (DAWS) ==== | ||
Dopamine agonist withdrawal syndrome (DAWS) is a complication that affects up to 19% of PD patients who undergo a dopamine agonist taper. It was initially described in 2010 as a severe stereotypical cluster of psychiatric and physical symptoms occurring with dopamine agonist withdrawal.[([[https://www.ncbi.nlm.nih.gov/pubmed/28104232|Yu, X. X., & Fernandez, H. H. (2017). Dopamine agonist withdrawal syndrome: A comprehensive review. Journal of the neurological sciences, 374, 53-55.]])][([[https://www.ncbi.nlm.nih.gov/pubmed/23686524|Nirenberg, M. J. (2013). Dopamine agonist withdrawal syndrome: implications for patient care. Drugs & aging, 30(8), 587-592.]])] The symptoms of DAWS include anxiety, panic attacks, dysphoria, depression, agitation, irritability, suicidal ideation, fatigue, orthostatic hypotension, nausea, vomiting, diaphoresis, generalized pain, and drug cravings. | Dopamine agonist withdrawal syndrome (DAWS) is a complication that affects up to 19% of PD patients who undergo a dopamine agonist taper. It was initially described in 2010 as a severe stereotypical cluster of psychiatric and physical symptoms occurring with dopamine agonist withdrawal.[([[https://www.ncbi.nlm.nih.gov/pubmed/28104232|Yu, X. X., & Fernandez, H. H. (2017). Dopamine agonist withdrawal syndrome: A comprehensive review. Journal of the neurological sciences, 374, 53-55.]])][([[https://www.ncbi.nlm.nih.gov/pubmed/23686524|Nirenberg, M. J. (2013). Dopamine agonist withdrawal syndrome: implications for patient care. Drugs & aging, 30(8), 587-592.]])] The symptoms of DAWS include anxiety, panic attacks, dysphoria, depression, agitation, irritability, suicidal ideation, fatigue, orthostatic hypotension, nausea, vomiting, diaphoresis, generalized pain, and drug cravings. | ||
- | |||
- | ==== On-Off Phenomenon ==== | ||
- | The on-off phenomenon is a consequence of sustained levodopa treatment in patients with Parkinson's disease. It is characterized by a switch between mobility and immobility, which occurs as an end-of-dose or “wearing off” worsening of motor function or, much less commonly, as sudden and unpredictable motor fluctuations.[([[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1033307/|Lees, A. J. (1989). The on-off phenomenon. Journal of Neurology, Neurosurgery & Psychiatry, 52(Suppl), 29-37.]])] | ||
===== Resources ===== | ===== Resources ===== | ||
== For Providers == | == For Providers == | ||
* [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2658001/|Poewe, W., et al. "Diagnosis and management of Parkinson’s disease dementia." International journal of clinical practice 62.10 (2008): 1581-1587.]] | * [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2658001/|Poewe, W., et al. "Diagnosis and management of Parkinson’s disease dementia." International journal of clinical practice 62.10 (2008): 1581-1587.]] |