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1 ompleted both assessments (18 placebo and 16 pramipexole).
2 4 and D2 receptor subtypes in the effects of pramipexole.
3 with pregabalin as compared with placebo and pramipexole.
4 ly lower with pregabalin than with 0.5 mg of pramipexole.
5 cessary, placebo recipients were assigned to pramipexole.
6 of inefficacy or an adverse event related to pramipexole.
7 ne patient who became hypomanic while taking pramipexole.
8 educed by treatment with the antioxidant S(-)pramipexole.
9 ntribute to the anti-parkinsonian effects of pramipexole.
10 ompound to compare the results obtained with pramipexole.
11 le, and two in the group receiving 0.5 mg of pramipexole.
12 ificant difference between early and delayed pramipexole (-0.4 points, 95% CI -2.2 to 1.4, p=0.65).
13 Patients were randomly assigned to receive pramipexole, 0.5 mg 3 times per day with levodopa placeb
14 e, to receive double-blind either placebo or pramipexole (1.5 mg a day) and followed them up for 15 m
16 th 300 mg of pregabalin, 178 with 0.25 mg of pramipexole, 180 with 0.5 mg of pramipexole, and 179 wit
17 scale scores was greater for patients taking pramipexole (48%) than for those taking placebo (21%).
22 Overall, 180 (81%) of patients given early pramipexole and 179 (84%) patients given delayed pramipe
25 nsistent with the neurochemical effect, both pramipexole and bromocriptine prevented 3-AP-induced los
29 fective in RLS, including dopamine agonists (pramipexole and ropinirole) and alpha2 delta ligands (ga
32 pamine agonists, particularly ropinirole and pramipexole, and management of motor and behavioral comp
33 lin, three in the group receiving 0.25 mg of pramipexole, and two in the group receiving 0.5 mg of pr
35 eks, the VAS pain score decreased 36% in the pramipexole arm and 9% in the placebo arm (treatment dif
36 th pregabalin at a dose of 300 mg per day or pramipexole at a dose of 0.25 mg or 0.5 mg per day or 12
37 ignificantly lower with pregabalin than with pramipexole at a dose of 0.5 mg (2.1% vs. 7.7%, P=0.001)
39 valence model revealed that after 8 weeks on pramipexole, BPD patients attended more readily to feedb
40 d in healthy subjects after a single dose of pramipexole, but its potential to induce abnormalities i
42 p=0.64); however, at week 8, BPD patients on pramipexole demonstrated a significantly greater tendenc
43 2.1) for early and -14.6% (2.0) for delayed pramipexole (difference -0.5 percentage points, 95% CI -
46 d with the placebo group, patients receiving pramipexole experienced gradual and more significant imp
48 nausea), and 22 (10%) patients in the early pramipexole group and 17 (8%) in the delayed pramipexole
50 om baseline was significantly reduced in the pramipexole group compared with the levodopa group: 7.1%
51 pramipexole group and 17 (8%) in the delayed pramipexole group had serious events, two of which (hall
52 ipexole group and 61 patients in the delayed pramipexole group were included in the neuroimaging subs
55 minergic neuronal loss, the dopamine agonist pramipexole has exhibited neuroprotective properties.
56 algesia and/or were disabled, treatment with pramipexole improved scores on assessments of pain, fati
58 l neuroprotectant selegiline and patients on pramipexole in the SPECT study appear to have been clini
59 ne the safety and antidepressant efficacy of pramipexole in treatment-resistant bipolar depression.
60 lective dopamine (DA) D2/D3 receptor agonist pramipexole in two models of nigrostriatal (NS) degenera
61 ned to identify whether early versus delayed pramipexole initiation has clinical and neuroimaging ben
62 synaptic alterations, chronic treatment with pramipexole is associated not only with a reduced risk o
63 We recently reported that the D2/D3 agonist pramipexole may have pro-cognitive effects in euthymic p
66 In vitro and animal studies suggest that pramipexole may protect and that levodopa may either pro
67 ssigned to receive placebo or flexibly dosed pramipexole (mean maximum dose=1.7 mg/day, SD=1.3) added
69 ents pre- and post 8 weeks of treatment with pramipexole or placebo by using the Iowa Gambling Task (
71 Treatment with dopamine agonists such as pramipexole or ropinirole allows levodopa to be delayed,
72 of rates of augmentation with pregabalin and pramipexole over a period of 40 or 52 weeks of treatment
75 ients with fibromyalgia were randomized 2:1 (pramipexole:placebo) to receive 4.5 mg of pramipexole or
76 sencephalic (VM) cultures in the presence of pramipexole (PPX) and other drugs with dopamine (DA) D3
77 vative LIGA20, the dopamine receptor agonist pramipexole (PPX) and the caspase inhibitor Z-VAD-FMK bu
81 ipexole and 179 (84%) patients given delayed pramipexole reported adverse events (most frequently nau
82 ere significant targets for locally perfused pramipexole, ropinirole, and gabapentin, which significa
90 ater, and the D3-preferring dopamine agonist pramipexole to identify D3-mediated regional cerebral bl
92 ine, some outcomes showed a better trend for pramipexole treatment than for placebo, but failed to re
95 series of compounds structurally related to pramipexole were designed, synthesized, and evaluated as
97 group received a single oral dose of 0.25mg pramipexole, whereas a second group received a single or
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