Fluoxetine in Parkinson's disease

Simons, Jorik

doi:10.1002/mds.870110517

Cited by 32 publications

(14 citation statements)

References 3 publications

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“…There are conflicting results whether SSRI can be used safely in PD [3][4][5] or not [6][7][8]. All of these studies included patients that experienced a worsening of parkinsonian signs.…”

Section: Discussionmentioning

confidence: 99%

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Start of a selective serotonin reuptake inhibitor (SSRI) and increase of antiparkinsonian drug treatment in patients on levodopa

Vijver

Roos

Jansen

et al. 2002

Brit J Clinical Pharma

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Aims We determined whether the start of selective serotonin reuptake inhibitors (SSRI) in levodopa users was followed by a faster increase of antiparkinsonian drug treatment. Methods Selected were all levodopa users of 55 years and older from the PHARMO prescription database. The rate of increase of antiparkinsonian drug treatment was compared using Cox's proportional hazard model for starters of SSRI (n=15) with starters of tricyclic antidepressants (TCA) (n=31) and with patients not using antidepressants (n=304), and was adjusted for age, gender, and duration of levodopa use. Results The hazard ratio for the SSRI group compared with the TCA group was 4.2 (95% confidence interval 1.4, 12.6) and compared with the second control group was 2.7 (1.2, 5.2). Conclusions The start of SSRI therapy in levodopa users is followed by a faster increase of antiparkinsonian drug treatment.

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“…There are conflicting results whether SSRI can be used safely in PD [3][4][5] or not [6][7][8]. All of these studies included patients that experienced a worsening of parkinsonian signs.…”

Section: Discussionmentioning

confidence: 99%

“…There are no controlled studies with selective serotonin reuptake inhibitors (SSRI) [2]. There are conflicting reports whether SSRI worsen symptoms of PD [3][4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Start of a selective serotonin reuptake inhibitor (SSRI) and increase of antiparkinsonian drug treatment in patients on levodopa

Vijver

Roos

Jansen

et al. 2002

Brit J Clinical Pharma

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“…In a case-series of 5 PD patients treated with L-DOPA and either cabergoline or placebo, fluoxetine (10–20 mg p.o. id) worsened UPDRS part III subscore in two patients [211]. In a 1-month add-on study of 14 PD patients with depression, fluoxetine (20 mg p.o.…”

Section: Sert Inhibitorsmentioning

confidence: 99%

Monoamine Reuptake Inhibitors in Parkinson’s Disease

Huot

Fox

Brotchie

2015

Parkinson's Disease

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The motor manifestations of Parkinson's disease (PD) are secondary to a dopamine deficiency in the striatum. However, the degenerative process in PD is not limited to the dopaminergic system and also affects serotonergic and noradrenergic neurons. Because they can increase monoamine levels throughout the brain, monoamine reuptake inhibitors (MAUIs) represent potential therapeutic agents in PD. However, they are seldom used in clinical practice other than as antidepressants and wake-promoting agents. This review article summarises all of the available literature on use of 50 MAUIs in PD. The compounds are divided according to their relative potency for each of the monoamine transporters. Despite wide discrepancy in the methodology of the studies reviewed, the following conclusions can be drawn: (1) selective serotonin transporter (SERT), selective noradrenaline transporter (NET), and dual SERT/NET inhibitors are effective against PD depression; (2) selective dopamine transporter (DAT) and dual DAT/NET inhibitors exert an anti-Parkinsonian effect when administered as monotherapy but do not enhance the anti-Parkinsonian actions of L-3,4-dihydroxyphenylalanine (L-DOPA); (3) dual DAT/SERT inhibitors might enhance the anti-Parkinsonian actions of L-DOPA without worsening dyskinesia; (4) triple DAT/NET/SERT inhibitors might exert an anti-Parkinsonian action as monotherapy and might enhance the anti-Parkinsonian effects of L-DOPA, though at the expense of worsening dyskinesia.

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“…Depression was not improved with the use of fluoxetine. In a placebo-controlled study of a new dopamine agonist reported by Simons [18,Class IIa], five patients in the placebo group were started on fluoxetine. Motor disability was found to increase by 20% to 25% in two of these patients.…”

Section: Diet and Lifestylementioning

confidence: 99%

Depression in Parkinson’s disease

Richard

2000

Curr Treat Options Neurol

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Depression is very common in Parkinson's disease (PD), but its severity and particular symptoms vary. It can often be difficult to diagnose because many of the symptoms typically associated with depression (eg, sleep difficulties, fatigue) can be seen in nondepressed patients with PD, and signs thought to represent depression (eg, lack of facial expression, slowness) can be produced by PD itself. Apathy, although a possible feature of depression, can exist apart from depression and is often associated with cognitive impairment. Therefore, when evaluating patients with PD for possible depression, one should concentrate on the psychological or ideational aspects of the illness. One must determine whether the patient feels sad or hopeless or has a marked inability to enjoy life. Once it has been determined that the patient has clinically significant depressive symptoms, it is important to let him or her know that depression is an aspect of PD requiring treatment, just like the motor manifestations of the disease. The idea of adding antidepressant medications and the possibility of psychotherapy should be introduced. A very reasonable first-choice antidepressant is either sertraline or paroxetine. Because of isolated case reports of worsening motor function associated with institution of a selective serotonin reuptake inhibitor (SSRI), one should keep track of when the medication was started so that the patient can be seen again within a month. It is important from a psychological perspective to have regular follow-up visits when treating depression. If the SSRIs are ineffective or not tolerated, nortriptyline is a good next choice. It has fewer anticholinergic effects and is less likely to cause or worsen orthostatic hypotension than other tricyclic antidepressants. Amitriptyline, although an old favorite of neurologists, is very sedating and has too much anticholinergic activity to be well tolerated in the higher doses needed to treat depression. If a patient could benefit from a dopamine agonist from a motor standpoint and his or her depressive symptoms are mild, consider using pramipexole, which may improve mood and motivation (although this has not yet been proven in a well-controlled trial). It is a good idea to keep patients on antidepressant therapy at least 6 months; many patients require long-term treatment. If a patient is severely depressed, he or she should be referred to a psychiatrist, who may consider admission to the hospital and possible electroconvulsive therapy.

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Fluoxetine in Parkinson's disease

Cited by 32 publications

References 3 publications

Start of a selective serotonin reuptake inhibitor (SSRI) and increase of antiparkinsonian drug treatment in patients on levodopa

Start of a selective serotonin reuptake inhibitor (SSRI) and increase of antiparkinsonian drug treatment in patients on levodopa

Monoamine Reuptake Inhibitors in Parkinson’s Disease

Depression in Parkinson’s disease

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