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Neurological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
There are no treatments which halt the degeneration of dopaminergic neurones, but the consequences can be mitigated by: Increasing dopamine production (L-DOPA, with a peripheral DOPA decarboxylase inhibitor)Direct dopamine agonistsDrugs which inhibit dopamine breakdown (COMT inhibitors)
Psychiatry
Published in Seema Khan, Get Through, 2020
Levodopa is used in combination with a dopa-decarboxylase inhibitor. This inhibitor prevents the metabolism of levodopa to dopamine within the periphery and therefore allows more dopamine to penetrate the blood – brain barrier to act on the corpus striatum.
Neurology, ophthalmology and psychiatry
Published in Shibley Rahman, Avinash Sharma, MRCP Part 2 Best of Five Practice Questions, 2018
Shibley Rahman, Avinash Sharma
A 60-year-old man has the clinical diagnosis of idiopathic Parkinson’s disease. He is commenced on treatment with L-dopa and dopa decarboxylase inhibitor therapy. However, he continues to have a troublesome tremor.
A novel treatment option for intrajejunal levodopa administration
Published in Expert Review of Neurotherapeutics, 2023
In Parkinson’s disease (PD), there is a dopamine deficiency that has been well substituted since the 1960s, which allows the disease to be successfully treated [1]. Since dopamine does not cross the blood-brain barrier, levodopa (L-3,4-dihydroxyphenylalanine) is administered. As under physiological conditions a high proportion of levodopa is being metabolized into dopamine in the periphery before passing the blood-brain-barrier, the DOPA-decarboxylase inhibitors (DDI) were introduced, increasing the bioavailability of levodopa by about ten times. That is why levodopa is only given with the decarboxylase inhibitors benserazide or carbidopa in a ratio of 4 to 1 [1]. Levodopa is also degraded peripherally by the enzyme catechol-O-methyl transferase (COMT), which is why the additional administration of a COMT inhibitor has proven itself in levodopa therapy [1].
What are the main considerations when prescribing pharmacotherapy for Parkinson’s disease?
Published in Expert Opinion on Pharmacotherapy, 2022
MAO-B-I are generally well tolerated. They are less potent than dopamine agonists. They are applied with varying dosages even in a transdermal fashion [16]. Introduction of dopamine agonists and amantadine is generally performed cautiously and slowly. This kind of drug titration avoids or reduces onset of leg edema, nausea, and vertigo particularly in the case of dopamine agonists. Supplementation with the peripheral dopamine receptor blocker domperidone, if available, for amelioration of nausea, or i.e. midodrine for compensation of dopamine replacement induced orthostatic blood pressure, if reimbursed, counteracts these common frequent side effects of dopamine replacement. Application of peripheral acting COMT-I’s only makes sense in combination with L-dopa/dopa decarboxylase inhibitor formulations.
State-of-the-art pharmacotherapy for autonomic dysfunction in Parkinson’s disease
Published in Expert Opinion on Pharmacotherapy, 2020
Cecilia Quarracino, Matilde Otero-Losada, Francisco Capani, Santiago Pérez-Lloret
An initial double-blind, randomized, cross-over study did not observe any hemodynamic difference after orthostatic stress in the 15 patients treated with levodopa-dopa decarboxylase inhibitor plus entacapone 200 mg or placebo [79]. Another study that included 5 PD and 7 Multiple system atrophy (MSA) patients failed to detect any blood pressure modification in PD patients when comparing entacapone 400 mg vs. placebo and invasive pharmacological testing but did observe a moderate blood-pressor effect in MSA patients in a dose-dependent fashion [80]. Along this line, one cross-sectional study designed to evaluate factors related to OH in 103 PD patients reported a reduced risk (p < 0.01) or OH in those treated with entacapone when compared with patients treated with levodopa or other antiparkinsonian drugs [33]. Further studies are needed to study the role of entacapone and the cardiovascular system.