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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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