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==Medical Therapy==
==Medical Therapy==
The mainstay of therapy for motor symptoms of Parkinson disease are:  
The mainstay of therapy for motor symptoms of Parkinson disease are:  
* Levodopa: This drug is the most effective in controlling motor symptoms in [[Parkinson's disease|PD]] patients (2_8). If we use [[levodopa]] alone, it will convert to [[dopamine]] in the peripheral circulation, so we combine it with a decarboxylase inhibitor like [[carbidopa]] to prevent this. The ratio of carbidopa_levodopa in tablets are 10/100, 25/100 or 25/250.(9_10) The [[adverse effects]] of this drug includes elevated serum [[homocysteine]], low levels of [[vitamin B12]], elevated [[methylmalonic acid]] and sensorimotor peripheral neuropathy.(17 ta 20) It can also cause motor fluctuations, [[dyskinesia]], [[cramps]] and [[dystonia]].(21_22) One of the concerns regarding long term use of [[levodopa]] is that it may be increase the rate of [[dopamine]] [[Neuron|neurons]] degeneration(37) but other studies demonstrated  that it does not damage [[Neuron|neurons]].(39_40)
* Levodopa: This drug is the most effective in controlling motor symptoms in [[Parkinson's disease|PD]] patients.<ref name="pmid24756517">{{cite journal |vauthors=Connolly BS, Lang AE |title=Pharmacological treatment of Parkinson disease: a review |journal=JAMA |volume=311 |issue=16 |pages=1670–83 |date=2014 |pmid=24756517 |doi=10.1001/jama.2014.3654 |url=}}</ref><ref name="pmid23279439">{{cite journal |vauthors=Ferreira JJ, Katzenschlager R, Bloem BR, Bonuccelli U, Burn D, Deuschl G, Dietrichs E, Fabbrini G, Friedman A, Kanovsky P, Kostic V, Nieuwboer A, Odin P, Poewe W, Rascol O, Sampaio C, Schüpbach M, Tolosa E, Trenkwalder C, Schapira A, Berardelli A, Oertel WH |title=Summary of the recommendations of the EFNS/MDS-ES review on therapeutic management of Parkinson's disease |journal=Eur. J. Neurol. |volume=20 |issue=1 |pages=5–15 |date=January 2013 |pmid=23279439 |doi=10.1111/j.1468-1331.2012.03866.x |url=}}</ref> If we use [[levodopa]] alone, it will convert to [[dopamine]] in the peripheral circulation, so we combine it with a decarboxylase inhibitor like [[carbidopa]] to prevent this. The ratio of carbidopa_levodopa in tablets are 10/100, 25/100 or 25/250.<ref name="pmid15706700">{{cite journal |vauthors= |title=Parcopa: a rapidly dissolving formulation of carbidopa/levodopa |journal=Med Lett Drugs Ther |volume=47 |issue=1201 |pages=12 |date=January 2005 |pmid=15706700 |doi= |url=}}</ref><ref name="pmid20925074">{{cite journal |vauthors=Ondo WG, Shinawi L, Moore S |title=Comparison of orally dissolving carbidopa/levodopa (Parcopa) to conventional oral carbidopa/levodopa: A single-dose, double-blind, double-dummy, placebo-controlled, crossover trial |journal=Mov. Disord. |volume=25 |issue=16 |pages=2724–7 |date=December 2010 |pmid=20925074 |doi=10.1002/mds.23158 |url=}}</ref> The [[adverse effects]] of this drug includes elevated serum [[homocysteine]], low levels of [[vitamin B12]], elevated [[methylmalonic acid]] and sensorimotor peripheral neuropathy.<ref name="pmid18785232">{{cite journal |vauthors=Toth C, Brown MS, Furtado S, Suchowersky O, Zochodne D |title=Neuropathy as a potential complication of levodopa use in Parkinson's disease |journal=Mov. Disord. |volume=23 |issue=13 |pages=1850–9 |date=October 2008 |pmid=18785232 |doi=10.1002/mds.22137 |url=}}</ref><ref name="pmid20582991">{{cite journal |vauthors=Toth C, Breithaupt K, Ge S, Duan Y, Terris JM, Thiessen A, Wiebe S, Zochodne DW, Suchowersky O |title=Levodopa, methylmalonic acid, and neuropathy in idiopathic Parkinson disease |journal=Ann. Neurol. |volume=68 |issue=1 |pages=28–36 |date=July 2010 |pmid=20582991 |doi=10.1002/ana.22021 |url=}}</ref><ref name="pmid23836370">{{cite journal |vauthors=Ceravolo R, Cossu G, Bandettini di Poggio M, Santoro L, Barone P, Zibetti M, Frosini D, Nicoletti V, Manganelli F, Iodice R, Picillo M, Merola A, Lopiano L, Paribello A, Manca D, Melis M, Marchese R, Borelli P, Mereu A, Contu P, Abbruzzese G, Bonuccelli U |title=Neuropathy and levodopa in Parkinson's disease: evidence from a multicenter study |journal=Mov. Disord. |volume=28 |issue=10 |pages=1391–7 |date=September 2013 |pmid=23836370 |doi=10.1002/mds.25585 |url=}}</ref><ref name="pmid25168395">{{cite journal |vauthors=Uncini A, Eleopra R, Onofrj M |title=Polyneuropathy associated with duodenal infusion of levodopa in Parkinson's disease: features, pathogenesis and management |journal=J. Neurol. Neurosurg. Psychiatry |volume=86 |issue=5 |pages=490–5 |date=May 2015 |pmid=25168395 |doi=10.1136/jnnp-2014-308586 |url=}}</ref> It can also cause motor fluctuations, [[dyskinesia]], [[cramps]] and [[dystonia]].<ref name="pmid20880751">{{cite journal |vauthors=Calabresi P, Di Filippo M, Ghiglieri V, Tambasco N, Picconi B |title=Levodopa-induced dyskinesias in patients with Parkinson's disease: filling the bench-to-bedside gap |journal=Lancet Neurol |volume=9 |issue=11 |pages=1106–17 |date=November 2010 |pmid=20880751 |doi=10.1016/S1474-4422(10)70218-0 |url=}}</ref><ref name="pmid25488260">{{cite journal |vauthors=Aquino CC, Fox SH |title=Clinical spectrum of levodopa-induced complications |journal=Mov. Disord. |volume=30 |issue=1 |pages=80–9 |date=January 2015 |pmid=25488260 |doi=10.1002/mds.26125 |url=}}</ref> One of the concerns regarding long term use of [[levodopa]] is that it may be increase the rate of [[dopamine]] [[Neuron|neurons]] degeneration<ref name="pmid15372588">{{cite journal |vauthors=Olanow CW, Agid Y, Mizuno Y, Albanese A, Bonuccelli U, Bonucelli U, Damier P, De Yebenes J, Gershanik O, Guttman M, Grandas F, Hallett M, Hornykiewicz O, Jenner P, Katzenschlager R, Langston WJ, LeWitt P, Melamed E, Mena MA, Michel PP, Mytilineou C, Obeso JA, Poewe W, Quinn N, Raisman-Vozari R, Rajput AH, Rascol O, Sampaio C, Stocchi F |title=Levodopa in the treatment of Parkinson's disease: current controversies |journal=Mov. Disord. |volume=19 |issue=9 |pages=997–1005 |date=September 2004 |pmid=15372588 |doi=10.1002/mds.20243 |url=}}</ref> but other studies demonstrated  that it does not damage [[Neuron|neurons]].<ref name="pmid11553992">{{cite journal |vauthors=Rajput AH |title=The protective role of levodopa in the human substantia nigra |journal=Adv Neurol |volume=86 |issue= |pages=327–36 |date=2001 |pmid=11553992 |doi= |url=}}</ref><ref name="pmid21917769">{{cite journal |vauthors=Parkkinen L, O'Sullivan SS, Kuoppamäki M, Collins C, Kallis C, Holton JL, Williams DR, Revesz T, Lees AJ |title=Does levodopa accelerate the pathologic process in Parkinson disease brain? |journal=Neurology |volume=77 |issue=15 |pages=1420–6 |date=October 2011 |pmid=21917769 |doi=10.1212/WNL.0b013e318232ab4c |url=}}</ref>
 
* Dopamine agonists:
* Dopamine agonists:
* Monoamine oxidase (MAO) B inhibitors:
* Monoamine oxidase (MAO) B inhibitors:

Revision as of 07:51, 20 April 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Medical Therapy

The mainstay of therapy for motor symptoms of Parkinson disease are:

  • Levodopa: This drug is the most effective in controlling motor symptoms in PD patients.[1][2] If we use levodopa alone, it will convert to dopamine in the peripheral circulation, so we combine it with a decarboxylase inhibitor like carbidopa to prevent this. The ratio of carbidopa_levodopa in tablets are 10/100, 25/100 or 25/250.[3][4] The adverse effects of this drug includes elevated serum homocysteine, low levels of vitamin B12, elevated methylmalonic acid and sensorimotor peripheral neuropathy.[5][6][7][8] It can also cause motor fluctuations, dyskinesia, cramps and dystonia.[9][10] One of the concerns regarding long term use of levodopa is that it may be increase the rate of dopamine neurons degeneration[11] but other studies demonstrated  that it does not damage neurons.[12][13]
  • Dopamine agonists:
  • Monoamine oxidase (MAO) B inhibitors:
  • Anticholinergic agents:
  • Amantadine:
  • Catechol-O-methyl transferase (COMT) inhibitors:
  • Estrogen:
  • Other agents:

Treatment choices for some of the nonmotor symptoms of PD are:

  • Psychosis:
  • Dementia:
  • Daytime sleepiness:
  • Fatigue:
  • Depression:
  • Constipation:
  • Sialorrhea:
  • Rhinorrhea:
  • Sexual dysfunction:
  • Ortostatic hypotention:

References

  1. Connolly BS, Lang AE (2014). "Pharmacological treatment of Parkinson disease: a review". JAMA. 311 (16): 1670–83. doi:10.1001/jama.2014.3654. PMID 24756517.
  2. Ferreira JJ, Katzenschlager R, Bloem BR, Bonuccelli U, Burn D, Deuschl G, Dietrichs E, Fabbrini G, Friedman A, Kanovsky P, Kostic V, Nieuwboer A, Odin P, Poewe W, Rascol O, Sampaio C, Schüpbach M, Tolosa E, Trenkwalder C, Schapira A, Berardelli A, Oertel WH (January 2013). "Summary of the recommendations of the EFNS/MDS-ES review on therapeutic management of Parkinson's disease". Eur. J. Neurol. 20 (1): 5–15. doi:10.1111/j.1468-1331.2012.03866.x. PMID 23279439.
  3. "Parcopa: a rapidly dissolving formulation of carbidopa/levodopa". Med Lett Drugs Ther. 47 (1201): 12. January 2005. PMID 15706700.
  4. Ondo WG, Shinawi L, Moore S (December 2010). "Comparison of orally dissolving carbidopa/levodopa (Parcopa) to conventional oral carbidopa/levodopa: A single-dose, double-blind, double-dummy, placebo-controlled, crossover trial". Mov. Disord. 25 (16): 2724–7. doi:10.1002/mds.23158. PMID 20925074.
  5. Toth C, Brown MS, Furtado S, Suchowersky O, Zochodne D (October 2008). "Neuropathy as a potential complication of levodopa use in Parkinson's disease". Mov. Disord. 23 (13): 1850–9. doi:10.1002/mds.22137. PMID 18785232.
  6. Toth C, Breithaupt K, Ge S, Duan Y, Terris JM, Thiessen A, Wiebe S, Zochodne DW, Suchowersky O (July 2010). "Levodopa, methylmalonic acid, and neuropathy in idiopathic Parkinson disease". Ann. Neurol. 68 (1): 28–36. doi:10.1002/ana.22021. PMID 20582991.
  7. Ceravolo R, Cossu G, Bandettini di Poggio M, Santoro L, Barone P, Zibetti M, Frosini D, Nicoletti V, Manganelli F, Iodice R, Picillo M, Merola A, Lopiano L, Paribello A, Manca D, Melis M, Marchese R, Borelli P, Mereu A, Contu P, Abbruzzese G, Bonuccelli U (September 2013). "Neuropathy and levodopa in Parkinson's disease: evidence from a multicenter study". Mov. Disord. 28 (10): 1391–7. doi:10.1002/mds.25585. PMID 23836370.
  8. Uncini A, Eleopra R, Onofrj M (May 2015). "Polyneuropathy associated with duodenal infusion of levodopa in Parkinson's disease: features, pathogenesis and management". J. Neurol. Neurosurg. Psychiatry. 86 (5): 490–5. doi:10.1136/jnnp-2014-308586. PMID 25168395.
  9. Calabresi P, Di Filippo M, Ghiglieri V, Tambasco N, Picconi B (November 2010). "Levodopa-induced dyskinesias in patients with Parkinson's disease: filling the bench-to-bedside gap". Lancet Neurol. 9 (11): 1106–17. doi:10.1016/S1474-4422(10)70218-0. PMID 20880751.
  10. Aquino CC, Fox SH (January 2015). "Clinical spectrum of levodopa-induced complications". Mov. Disord. 30 (1): 80–9. doi:10.1002/mds.26125. PMID 25488260.
  11. Olanow CW, Agid Y, Mizuno Y, Albanese A, Bonuccelli U, Bonucelli U, Damier P, De Yebenes J, Gershanik O, Guttman M, Grandas F, Hallett M, Hornykiewicz O, Jenner P, Katzenschlager R, Langston WJ, LeWitt P, Melamed E, Mena MA, Michel PP, Mytilineou C, Obeso JA, Poewe W, Quinn N, Raisman-Vozari R, Rajput AH, Rascol O, Sampaio C, Stocchi F (September 2004). "Levodopa in the treatment of Parkinson's disease: current controversies". Mov. Disord. 19 (9): 997–1005. doi:10.1002/mds.20243. PMID 15372588.
  12. Rajput AH (2001). "The protective role of levodopa in the human substantia nigra". Adv Neurol. 86: 327–36. PMID 11553992.
  13. Parkkinen L, O'Sullivan SS, Kuoppamäki M, Collins C, Kallis C, Holton JL, Williams DR, Revesz T, Lees AJ (October 2011). "Does levodopa accelerate the pathologic process in Parkinson disease brain?". Neurology. 77 (15): 1420–6. doi:10.1212/WNL.0b013e318232ab4c. PMID 21917769.

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