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1 etic-neuralgia patient abruptly discontinued pregabalin.
2 randomly assigned: 117 to placebo and 116 to pregabalin.
3 ain processing may respond to agents such as pregabalin.
4 te to precursors for GABA analogues, such as pregabalin.
5 cium-independent) dye release are reduced by pregabalin.
7 0 mg/day of pregabalin (-9.2), 600 mg/day of pregabalin (-10.3), and lorazepam (-12.0) were significa
8 y disorder were randomly assigned to receive pregabalin (150 mg/day or 600 mg/day), lorazepam (6 mg/d
9 received daily treatment, 182 with 300 mg of pregabalin, 178 with 0.25 mg of pramipexole, 180 with 0.
10 point compared with placebo (-8.4 +/- 0.8): pregabalin, 300 mg (-12.2 +/- 0.8, P<.001), 450 mg (-11.
11 were randomized to 4 weeks of treatment with pregabalin, 300 mg/d (n = 91), 450 mg/d (n = 90), or 600
12 tine (nine of 14 studies); 7.7 (6.5-9.4) for pregabalin; 7.2 (5.9-9.21) for gabapentin, including gab
13 ven placebo (73%, N=50 of 69), 600 mg/day of pregabalin (71%, N=50 of 70), or 150 mg/day or pregabali
14 le score in the patients given 150 mg/day of pregabalin (-9.2), 600 mg/day of pregabalin (-10.3), and
16 y adds to our understanding of the action of pregabalin, a drug used for treatment of partial seizure
17 igned to evaluate the efficacy and safety of pregabalin, a novel alpha(2)-delta ligand, for treatment
18 -5-phosphonopentanoic acid], suggesting that pregabalin action depends on NMDA receptor activation.
20 reating fibromyalgia, compared with placebo, pregabalin alone is associated with a small increase in
21 potent neuropathic analgesics gabapentin and pregabalin (alpha2delta-1 and alpha2delta-2), were also
24 nderwent randomization, of whom 108 received pregabalin and 101 received placebo; after randomization
27 cing pain, and newly developed ones, such as pregabalin and duloxetine, while specifically marketed f
28 he most frequent adverse events reported for pregabalin and lorazepam were somnolence and dizziness.
29 he primary analyses involved a comparison of pregabalin and placebo over a period of 12 weeks with us
31 d a comparison of rates of augmentation with pregabalin and pramipexole over a period of 40 or 52 wee
32 of the alpha-2-delta ligands (gabapentin and pregabalin) and the norepinephrine/serotonin reuptake in
33 serotonin-noradrenaline reuptake inhibitors, pregabalin, and gabapentin; a weak recommendation for us
34 us adverse events reported by patients given pregabalin, and no withdrawal syndrome was associated wi
35 vior, and could be rescued by the analgesic, pregabalin, and the libido-enhancing drugs, apomorphine
37 ralgia compared with placebo, gabapentin and pregabalin are associated with a modest increase in the
43 cities were significantly more common in the pregabalin arms, being more evident with the higher dose
44 get 75 mg twice daily and 150 mg twice daily pregabalin arms, respectively (P = .009 and P = .007, co
45 ovides support and a mechanism of action for pregabalin as a possible effective therapy in the treatm
46 n in patients with RLS who were treated with pregabalin as compared with placebo and pramipexole.
51 nts were randomly assigned to receive either pregabalin at a dose of 150 mg per day that was adjusted
52 signed to receive 52 weeks of treatment with pregabalin at a dose of 300 mg per day or pramipexole at
53 -delta Type 1 substantially reduces specific pregabalin binding in CNS regions that are known to pref
56 three-step synthesis of the medicinal agent pregabalin (commercialized by Pfizer under the trade nam
65 sted leg-pain intensity score was 3.4 in the pregabalin group and 3.0 in the placebo group (adjusted
66 sted leg-pain intensity score was 3.7 in the pregabalin group and 3.1 in the placebo group (adjusted
70 cebo; after randomization, 2 patients in the pregabalin group were determined to be ineligible and we
71 observation-carried-forward end point, the 3 pregabalin groups and the alprazolam group had significa
72 ntly (P<.02) improved by the 300- and 600-mg pregabalin groups, but not by the 450-mg pregabalin (wee
81 ral nervous system (CNS) binding protein for pregabalin in vivo, a mutant mouse with an arginine-to-a
82 ) mice, the acute systemic administration of pregabalin increased the threshold for SD initiation in
91 antiepileptic drugs (topiramate, lacosamide, pregabalin, levetiracetam), hypothermia, magnesium, pyri
98 lds up to 74%, including the important drugs pregabalin, memantine, and the antimalarial artemisinin.
101 acebo with those of 150, 300, and 450 mg/day pregabalin on pain, sleep, fatigue, and health-related q
103 [1-(aminomethyl)cyclohexaneacetic acid] and pregabalin (PGB) [(S)-(+)-3-isobutyl-GABA or (S)-3-(amin
112 e CaV2.1 (P/Q-type) calcium channel subunit, pregabalin slowed the speed of SD propagation in vivo.
113 by 4.5 points, among participants receiving pregabalin than among those receiving placebo (P<0.001),
115 roved or much improved was also greater with pregabalin than with placebo (71.4% vs. 46.8%, P<0.001).
116 40 or 52 weeks was significantly lower with pregabalin than with pramipexole at a dose of 0.5 mg (2.
117 the development of a new synthetic route for pregabalin that proceeds with an overall yield of 74%.
118 of suicidal ideation in the group receiving pregabalin, three in the group receiving 0.25 mg of pram
127 ms, being more evident with the higher dose, pregabalin was generally well tolerated by most patients
131 -mg pregabalin groups, but not by the 450-mg pregabalin (week 1, P = .06; week 4, P = .32) and the al
132 oembolic stroke patients, whereas gabapentin/pregabalin were favored in subarachnoid hemorrhage, intr
133 ocular pressure and a promising therapeutic, pregabalin, which binds to CACNA2D1 protein and lowers i
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