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1 ompleted both assessments (18 placebo and 16 pramipexole).
2 le, and two in the group receiving 0.5 mg 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 4 and D2 receptor subtypes in the effects of pramipexole.
7 of inefficacy or an adverse event related to pramipexole.
8 ne patient who became hypomanic while taking pramipexole.
9 educed by treatment with the antioxidant S(-)pramipexole.
10 ntribute to the anti-parkinsonian effects of pramipexole.
11 ompound to compare the results obtained with 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%).
23 Overall, 180 (81%) of patients given early pramipexole and 179 (84%) patients given delayed pramipe
26 nsistent with the neurochemical effect, both pramipexole and bromocriptine prevented 3-AP-induced los
30 fective in RLS, including dopamine agonists (pramipexole and ropinirole) and alpha2 delta ligands (ga
33 pamine agonists, particularly ropinirole and pramipexole, and management of motor and behavioral comp
34 lin, three in the group receiving 0.25 mg of pramipexole, and two in the group receiving 0.5 mg of pr
36 eks, the VAS pain score decreased 36% in the pramipexole arm and 9% in the placebo arm (treatment dif
37 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
38 ignificantly lower with pregabalin than with pramipexole at a dose of 0.5 mg (2.1% vs. 7.7%, P=0.001)
40 valence model revealed that after 8 weeks on pramipexole, BPD patients attended more readily to feedb
41 d in healthy subjects after a single dose of pramipexole, but its potential to induce abnormalities i
44 p=0.64); however, at week 8, BPD patients on pramipexole demonstrated a significantly greater tendenc
45 2.1) for early and -14.6% (2.0) for delayed pramipexole (difference -0.5 percentage points, 95% CI -
50 d with the placebo group, patients receiving pramipexole experienced gradual and more significant imp
52 nausea), and 22 (10%) patients in the early pramipexole group and 17 (8%) in the delayed pramipexole
54 om baseline was significantly reduced in the pramipexole group compared with the levodopa group: 7.1%
55 pramipexole group and 17 (8%) in the delayed pramipexole group had serious events, two of which (hall
56 ipexole group and 61 patients in the delayed pramipexole group were included in the neuroimaging subs
60 minergic neuronal loss, the dopamine agonist pramipexole has exhibited neuroprotective properties.
61 algesia and/or were disabled, treatment with pramipexole improved scores on assessments of pain, fati
63 l neuroprotectant selegiline and patients on pramipexole in the SPECT study appear to have been clini
64 ne the safety and antidepressant efficacy of pramipexole in treatment-resistant bipolar depression.
65 lective dopamine (DA) D2/D3 receptor agonist pramipexole in two models of nigrostriatal (NS) degenera
67 ned to identify whether early versus delayed pramipexole initiation has clinical and neuroimaging ben
68 synaptic alterations, chronic treatment with pramipexole is associated not only with a reduced risk o
69 We recently reported that the D2/D3 agonist pramipexole may have pro-cognitive effects in euthymic p
72 In vitro and animal studies suggest that pramipexole may protect and that levodopa may either pro
73 ssigned to receive placebo or flexibly dosed pramipexole (mean maximum dose=1.7 mg/day, SD=1.3) added
75 effects of 2 weeks of the D(2)-like agonist pramipexole on reward learning and used functional magne
77 ents pre- and post 8 weeks of treatment with pramipexole or placebo by using the Iowa Gambling Task (
79 Treatment with dopamine agonists such as pramipexole or ropinirole allows levodopa to be delayed,
80 of rates of augmentation with pregabalin and pramipexole over a period of 40 or 52 weeks of treatment
83 ients with fibromyalgia were randomized 2:1 (pramipexole:placebo) to receive 4.5 mg of pramipexole or
84 sencephalic (VM) cultures in the presence of pramipexole (PPX) and other drugs with dopamine (DA) D3
85 vative LIGA20, the dopamine receptor agonist pramipexole (PPX) and the caspase inhibitor Z-VAD-FMK bu
89 ipexole and 179 (84%) patients given delayed pramipexole reported adverse events (most frequently nau
90 ere significant targets for locally perfused pramipexole, ropinirole, and gabapentin, which significa
100 d to the D3R-selective agonists PD128907 and pramipexole, the latter of which is used to treat patien
101 s (50% female) were randomized to 2 weeks of pramipexole (titrated to 1 mg/day) or placebo in a doubl
102 ater, and the D3-preferring dopamine agonist pramipexole to identify D3-mediated regional cerebral bl
104 The depressed group then received open-label pramipexole treatment for 6 weeks (0.5 mg/day titrated t
105 ine, some outcomes showed a better trend for pramipexole treatment than for placebo, but failed to re
108 series of compounds structurally related to pramipexole were designed, synthesized, and evaluated as
109 e most common adverse events associated with pramipexole were transient anxiety and weight loss.
110 group received a single oral dose of 0.25mg pramipexole, whereas a second group received a single or
111 efficiently at 4 weeks post-inoculation than pramipexole, which partially rescued it at both time poi