Entacapone improves complex movement performance in patients with Parkinson’s disease

Müller, Thomas; Erdmann, Christoph; Muhlack, Siegfried; Bremen, Dirk; Przuntek, H.; Woitalla, Dirk

doi:10.1016/j.jocn.2006.02.008

Cited by 11 publications

(4 citation statements)

References 19 publications

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“…Hierzu zählen insbesondere Dyskinesien und Levodopa-induzierte psychische Störungen, z. B. Halluzinationen [54]. Nach Beginn einer Therapie mit einem COMT-Hemmer kann es sinnvoll sein, die Levodopa-Tagesdosis zu reduzieren, vor allem in der zweiten Tageshälfte, in der sich kumulative Effekte bemerkbar machen können.…”

Section: Praktische Hinweise Zur Therapie Mit Mao-bund Comt-hemmernunclassified

Grundlagen und Stellenwert der COMT- und MAO-B-Inhibitoren in der Therapie des idiopathischen Parkinson-Syndroms

Woitalla¹,

Krüger²,

Lorenzl³

et al. 2020

Fortschr Neurol Psychiatr

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ZusammenfassungCOMT- und MAO-B-Hemmer gehören neben den Dopamin-Agonisten und Levodopa zu den etablierten Pharmaka zur Behandlung des idiopathischen Parkinson-Syndroms (IPS). Die MAO-B-Hemmer Selegilin und Rasagilin entfalten auch in der Monotherapie einen symptomatischen Therapieeffekt, während Safinamid und COMT-Hemmer nur zur Kombinationstherapie mit Levodopa zugelassen sind. Beide Substanzklassen verlängern die Wirkdauer von Levodopa und optimieren die Wirkung der Therapie. Klinisch messbar resultiert eine Verlängerung der ON-Zeit. Der Einsatz von MAO-B-Inhibitoren erfolgte in der Vergangenheit auch unter der Vorstellung einer neuroprotektiven Wirkung. Trotz der aufgrund experimenteller Daten postulierten Wirkung ließ sich dieser Effekt in klinischen Studien bislang nicht zweifelsfrei belegen.

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Section: Praktische Hinweise Zur Therapie Mit Mao-bund Comt-hemmernunclassified

Grundlagen und Stellenwert der COMT- und MAO-B-Inhibitoren in der Therapie des idiopathischen Parkinson-Syndroms

Woitalla¹,

Krüger²,

Lorenzl³

et al. 2020

Fortschr Neurol Psychiatr

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“…Inhibition of COMT by entacapone prolongs the half-life of levodopa (Nutt et al 1994;Ruottinen and Rinne 1996) and this is associated with improved clinical efficacy in PD patients (Kaakkola and Wurtman 1993;Nutt et al 1994;Ruottinen and Rinne 1996;Parkinson Study Group 1997;Rinne 1998;Poewe 2002Grandas et al 2007;Deuschl et al 2007;Müller et al 2007) and in experimental models of parkinsonism (Smith et al 2003;Marin et al 2005Marin et al , 2006. By extending the half-life of levodopa with entacapone, it is possible to deliver the drug in a way that is less pulsatile, thereby allowing the benefit of levodopa with a reduced risk for motor complications.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…COMT inhibitors such as entacapone (Fenelon et al 2003;Deuschl et al 2007;Müller et al 2007). Administration of a single dose of levodopa with a COMT inhibitor increases the levodopa plasma area under the curve and its elimination half-life without augmenting peak plasma levels (Nutt et al 1994;Heikkinen et al 2002).…”

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confidence: 99%

Entacapone potentiates the long-duration response but does not normalize levodopa-induced molecular changes

Marı́n¹,

Aguilar²,

Mengod³

et al. 2008

Neurobiology of Disease

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Coadministration of entacapone with levodopa attenuates motor complications in experimental models of Parkinson's disease. The mechanisms underlying entacapone effects are unknown. We investigated the effect of entacapone, on: long duration response (LDR) to levodopa, levodopa-induced postsynaptic pharmacodynamic mechanisms and molecular changes in hemiparkinsonian rats. 6-hydroxydopamine-unilaterally lesion rats were treated with levodopa (25 mg /kg)+vehicle; levodopa+entacapone (30 mg/kg) or saline, twice daily for 22 days. The LDR and the apomorphine-induced rotations were measured. In situ hybridization was performed measuring the expression of striatal preproenkephalin, preprodynorphin and dopamine D-3 receptors mRNAs, subthalamic cytochrome oxidase mRNA and nigral glutamic acid decarboxylase mRNA. Entacapone potentiated the LDR but did no modify neither the apomorphine-induced rotational behavior nor the molecular changes. Our results suggest that the effects of entacapone on levodopa-induced motor response are no mediated by postsynaptic mechanisms and that administration of entacapone is not able to normalize the molecular alterations induced by levodopa in the basal ganglia.

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“…In clinical trials, combined treatment with levodopa and entacapone has a notable effect on the control of dyskinesia. Entacapone can enhance the duration of the effect of each dose of levodopa, and can preferentially improve motor symptoms of PD patients 13,14 . Compared with levodopa/carbidopa, treatment with entacapone/levodopa/carbidopa results in an improved quality of life in PD patients with mild, or minimal, non‐disabling motor fluctuations 15–19 …”

Section: Introductionmentioning

confidence: 99%

Entacapone promotes cAMP-dependent colonic Cl− secretion in rats

Li¹,

Zheng²,

et al. 2011

Neurogastroenterology &Amp; Motility

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Entacapone improves complex movement performance in patients with Parkinson’s disease

Cited by 11 publications

References 19 publications

Grundlagen und Stellenwert der COMT- und MAO-B-Inhibitoren in der Therapie des idiopathischen Parkinson-Syndroms

Grundlagen und Stellenwert der COMT- und MAO-B-Inhibitoren in der Therapie des idiopathischen Parkinson-Syndroms

Entacapone potentiates the long-duration response but does not normalize levodopa-induced molecular changes

Entacapone promotes cAMP-dependent colonic Cl− secretion in rats

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