Date: Wed, 19 Mar 1997 07:51:53 -0500
From: Whit Garberson <firstname.lastname@example.org>
From my limited experience, SSRIs can exacerbate the neuromotor symptoms of Parkinson's Disease.
Date: Wed, 19 Mar 1997 23:52:34 +0700
From: Albert Maramis <email@example.com>
SSRIs can cause depletion of dopamine. In Parkinson's Disease it is better to use dopaminergic antidepressants: MAOIs, bupropion, and amineptine.
Date: Wed, 19 Mar 1997 10:42:16 -0800 (PST)
From: firstname.lastname@example.org (James Ferrell)
Clinically it is clear that SSRIs can cause akathisia, jaw clenching, and worsening of Parkinson's Disease (extrapyramidal symptoms like those that dopamine antagonists cause), as well as neuroendocrine symptoms like those of hyperprolactinemia (which dopamine antagonists also cause). One plausible mechanism for this is that SSRIs cause reversible depletion of dopamine stores. There may be other contributing mechanisms as well.
Date: Sat, 22 Mar 1997 20:12:19 +0000
From: "M. J. Eales" <email@example.com>
A recent article by Kapur & Remington (Serotonin-dopamine interaction and its relevance to schizophrenia, Am J Psychiat 153 (1996), 466-476) clarified this (for me). The authors provide evidence that stimulation of 5HT2 receptors in the basal ganglia inhibits dopamine release. This is suggested to be one of the reasons why atypical antipsychotics, most of which have 5HT2 antagonist activity, have fewer extrapyramidal effects. It also explains EPS caused occasionally by SSRIs.
I had a lady with early Parkinson's whose pill-rolling tremor was made much worse by venlafaxine.
Date: Sat, 22 Mar 1997 17:13:57 -0500
From: "Andy Cheshire" <firstname.lastname@example.org>
Sertraline is a fairly potent inhibitor of dopamine release. Even stronger than buproprion if I recall correctly.
It is hypothesized that in the basal ganglia there is an interaction between serotonergic and dopaminergic neurons via axoaxonal synapses. Serotonin released from the serotonin axon binds with serotonin receptor on the dopamine axon and inhibits its release of dopamine. The subtype involved here is 5-HT2. This explains the increase in EPS on some patients receiving SSRI.
Date: Thu, 27 Mar 1997 08:38:50 -0700
From: "Dr. Alan Gelenberg" <email@example.com>
All SSRIs have been associated with motor function deterioration in depressed patients with Parkinson's Disease. The most cases reported are with fluoxetine; the least, with sertraline. Although bupropion theoretically should be a good antidepressant to use in this population, due to its dopamine agonist properties, a neurologist and expert in Parkinson's Disease whom we consulted has been unimpressed with its efficacy. TCAs are usually poorly tolerated by patients with Parkinson's Disease and can worsen orthostatic hypotension. MAOIs also can cause hypotension and possibly, when combined with levodopa, a hypertensive crisis.
Date: Thu, 27 Mar 1997 13:51:37 -0500
From: "Laura Fochtmann" <lfochtmann@MAIL.PSYCHIATRY.SUNYSB.Edu>
In terms of treating depression in patients with Parkinson's Disease, ECT is quite effective and deserves mention. Independent of its effects on mood, it also has beneficial effects in alleviating Parkinsonism and "on-off" phenomena. Since the Parkinson's patients tend to be sensitive to the cognitive effects of ECT, we generally decrease the l-dopa dosage prior to ECT to minimize associated delirium. In this regard, unilateral treatment or decreased treatment frequency (twice a week) may also be considered.
Date: Tue, 01 Apr 1997 23:37:05 -0800
From: Eduardo Dunayevich <firstname.lastname@example.org>
To my knowledge the only antidepressants shown in controlled trials to be effective in treating depression associated with Parkinson's Disease are tricyclics.
Date: Wed, 2 Apr 1997 17:49:18 +1200
From: email@example.com (David Menkes)
This is also my understanding. By virtue of their antimuscarinic activity, they are also of some use themselves in treating co-morbid Parkinsonian symptoms. Imipramine and other tricyclics were commonly used in Parkinson's Disease prior to the advent of l-dopa and tended to improve tremor rather more than bradykinesia.
I was puzzled by Dr. Gelenberg's comment earlier that TCAs are especially poorly tolerated in Parkinson's Disease; my practice is to use them judiciously (for example, nortriptyline causes relatively little orthostasis, and may be preferred for this reason) and manage emergent side-effects as one normally would in the elderly.
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Prepared by David Gotlib, M.D. (firstname.lastname@example.org).
Revised: April 6, 1997
Original tips copyright 1997 original authors.
Web page copyright 1997 David Gotlib.