ライフサイエンスコーパス: gabapentin

1 le and ropinirole) and alpha2 delta ligands (gabapentin).

2 stsynaptic blockade of calcium channels (for gabapentin).

3 effects more potently and efficaciously than gabapentin.

4 of newer antidepressants and three trials of gabapentin.

5 ome reporting for trials of off-label use of gabapentin.

6 or for the anti-epileptic and analgesic drug gabapentin.

7 h amitriptyline, carbamazepine, diazepam and gabapentin.

8 e taking the placebo and in some patients on gabapentin.

9 d research, were extensively used to promote gabapentin.

10 ad complete resolution of nausea when taking gabapentin.

11 , after she was placed on the anticonvulsant gabapentin.

12 rmine the specificity of hBCATc for the drug gabapentin.

13 4 patients enrolled in an open-lbel trial of gabapentin.

14 that was also reversed by pre-incubation in gabapentin.

15 from slices that had been pre-incubation in gabapentin.

16 e half were pre-incubated in aCSF containing gabapentin.

17 e pain during neuropathy that is reversed by gabapentin.

18 domain of thrombospondin-2 was prevented by gabapentin.

19 dorsal horn neurons that could be blocked by gabapentin.

20 with highest correlations for acesulfame and gabapentin.

21 CaV2.2 and alpha2delta-1 is not disrupted by gabapentin.

22 pine and have been successfully treated with gabapentin.

23 ts noted improvement in symptoms when taking gabapentin.

24 (hazard ratio [HR] 0.78 [95% CI 0.63-0.97]), gabapentin (0.65 [0.52-0.80]), and topiramate (0.64 [0.5

25 carbamazepine was significantly better than gabapentin (0.75 [0.63-0.90]), and estimates suggest a n

26 , double-blind study was designed to compare gabapentin (1,200-2,400 mg/day) (n=75 patients) with pla

27 Gabapentin (1,200-2,400 mg/day) is safe and efficacious

28 ed a masked, crossover, therapeutic trial of gabapentin (1,200mg/day) versus memantine (40 mg/day) fo

29 the first time that the alpha2delta ligands gabapentin [1-(aminomethyl)cyclohexaneacetic acid] and p

30 pine (26%), topiramate (25%), pregabalin and gabapentin (10%).

31 Subjects received either gabapentin (1200 mg/day) or matched placebo.

32 95; 95% CI, -1.44 to -0.47), and 2 trials of gabapentin (-2.05; 95% CI, -2.80 to -1.30).

33 y whereas intrathecal morphine (1microg) and gabapentin (200microg) partially reversed thermal and me

34 ed to be higher in patients taking high-dose gabapentin (3,300-3,600 mg/day) than in those taking sta

35 is, we did an open-label study in which oral gabapentin 300 mg thrice daily was given for every other

36 900 mg) and 347 at 8 weeks (113 placebo, 114 gabapentin 300 mg, and 120 gabapentin 900 mg).

37 71 participants at 4 weeks (119 placebo, 123 gabapentin 300 mg, and 129 gabapentin 900 mg) and 347 at

38 shes per day were randomly assigned placebo, gabapentin 300 mg/day, or gabapentin 900 mg/day by mouth

39 43) and 31% (16 to 46) in the group assigned gabapentin 300 mg; and 49% (42 to 56) and 46% (34 to 58)

40 Gabapentin (50mg/kg, i.p.) significantly reduced vlPAG n

41 (119 placebo, 123 gabapentin 300 mg, and 129 gabapentin 900 mg) and 347 at 8 weeks (113 placebo, 114

42 (113 placebo, 114 gabapentin 300 mg, and 120 gabapentin 900 mg).

43 56) and 46% (34 to 58) in the group assigned gabapentin 900 mg.

44 assigned placebo, gabapentin 300 mg/day, or gabapentin 900 mg/day by mouth in three divided doses fo

45 We conducted a gabapentin (900 mg) challenge in healthy human subjects

46 m of this study was to assess the effects of gabapentin, a drug effective in neuropathic pain patient

47 e oligonucleotides to knock down Cavbeta and gabapentin, a drug that binds to and inhibits alpha2delt

48 ng pain; thus, there is a rationale to study gabapentin, a drug that increases the threshold to exper

49 Gabapentin, a drug useful in several neurological and ps

50 micked the effect of conditioned medium, and gabapentin, a high-affinity antagonist of TSP binding to

51 Blocking Cavalpha2delta1 with gabapentin, a ligand for the Cavalpha2delta1 proteins, o

52 s in nucleus accumbens, we demonstrated that gabapentin, a specific alpha2delta-1 antagonist, prefere

53 enaline reuptake inhibitors, pregabalin, and gabapentin; a weak recommendation for use and proposal a

54 a provide complementary new information that gabapentin administered systemically and spinally can ef

55 lpha2delta2 pharmacological blockade through gabapentin administration promoted corticospinal structu

56 verage 5.6%) and between day (average 4.8%), gabapentin administration was associated with an average

57 risk of preeclampsia among women exposed to gabapentin after adjustment.

58 may account for the differential effects of gabapentin after chronic ethanol.

59 ined treatment v 49%; 95% CI, 26% to 58% for gabapentin alone) and scores (56%; 95% CI, 26% to 71% fo

60 ined treatment v 60%; 95% CI, 33% to 73% for gabapentin alone).

61 ctively alleviate hot flashes, compared with gabapentin alone, in patients with inadequate hot flash

62 weaned off the antidepressant and receiving gabapentin alone.

63 ntrathecal administration of 10-30 microg of gabapentin also produced a significant effect on the mec

64 The effect of gabapentin, an anticonvulsant drug that is also effectiv

65 Pretreatment with gabapentin, an inhibitor of the alpha2delta1 subunit, bl

66 2019, and 306 were randomly assigned (153 to gabapentin and 153 to placebo).

67 Eighty-four patients received gabapentin and 70 (83%) completed the study; 81 received

68 d for treatment of neuropathic pain, such as gabapentin and amitriptyline.

69 enytoin proved ineffective, while valproate, gabapentin and carbamazepine varied in their potencies,

70 Gabapentin and duloxetine reversed mechanical hyperalges

71 Side effects included unsteadiness with gabapentin and lethargy with memantine.

72 ast potential interaction is associated with gabapentin and levetiracetam.

73 l antiepileptic agents, including valproate, gabapentin and phenytoin, reduced the ability of astrocy

74 target of the potent neuropathic analgesics gabapentin and pregabalin (alpha2delta-1 and alpha2delta

75 The therapeutic drugs gabapentin and pregabalin (PGB), which are both alpha(2)

76 ostherpetic neuralgia compared with placebo, gabapentin and pregabalin are associated with a modest i

77 Gabapentin and pregabalin are structurally related compo

78 The interaction of gabapentin and pregabalin with conventional antiepilepti

79 effectiveness of the alpha-2-delta ligands (gabapentin and pregabalin) and the norepinephrine/seroto

80 opioids for non-cancer pain, gabapentinoids (gabapentin and pregabalin), benzodiazepines, and Z-drugs

81 Gabapentinoids, gabapentin and pregabalin, are recommended in multimodal

82 t of voltage-gated calcium channels binds to gabapentin and pregabalin, mediating the analgesic actio

83 ponsive to a variety of therapies, including gabapentin and topiramate.

84 ly comparable to what has been reported with gabapentin and with some newer antidepressants.

85 tremor patients (primidone, propranolol, and gabapentin) and several candidates hypothesized to reduc

86 One hundred thirteen patients received gabapentin, and 89 (78.8%) completed the study; 116 rece

87 lic antidepressants (such as nortriptyline), gabapentin, and a compounded topical gel containing bacl

88 LRP1 regulates alpha2delta binding to gabapentin, and influences calcium channel trafficking a

89 athic rats as compared to the approved drug, gabapentin, and previously published sEH inhibitors.

90 clonidine, soy phyto-oestrogens, vitamin E, gabapentin, and several of the newer antidepressants, wi

91 Gabapentin antagonizes the interaction of thrombospondin

92 Gabapentin antagonizes thrombospondin binding to alpha2d

93 Gabapentin appears to increase human brain GABA levels.

94 sion in the literature regarding efficacy of gabapentin as a candidate addiction therapy.

95 The use of gabapentin as an effective analgesic agent for neuropath

96 cluding ergothioneine, carnitine, carnosine, gabapentin, as well as four cations, including MPP(+) ,

97 pha2delta amino acid, R217A, eliminates both gabapentin binding and analgesic efficacy.

98 ison suggests that alpha(2)delta-4 lacks the gabapentin binding motifs characterized for alpha(2)delt

99 2+) -dependent reduction in affinity of (3)H-gabapentin binding to alpha2delta-1.

100 However, the effect on (3)H-gabapentin binding was not reproduced by the synaptogeni

101 ha2delta-1 might reciprocally influence (3)H-gabapentin binding.

102 pha(2)delta-2; this was confirmed by a [(3)H]gabapentin-binding assay.

103 In vitro studies indicate that gabapentin binds to the alpha(2)delta-1 (hereafter refer

104 ), and NICU admission among women exposed to gabapentin both early and late in pregnancy (RR, 1.35 [1

105 tained tactile allodynia which is reduced by gabapentin but not the potent cyclooxygenase inhibitor k

106 ), visual acuity improved significantly with gabapentin, but not with baclofen.

107 drugs reduced median eye speed (p < 0.001), gabapentin by 32.8% and memantine by 27.8%, and improved

108 so determined electrophysiologically whether gabapentin causes displacement of beta subunits from Ca(

109 s compounded for neuropathic pain (ketamine, gabapentin, clonidine, and lidocaine), nociceptive pain

110 Gabapentin compared with placebo also significantly impr

111 of opioids increased with benzodiazepine and gabapentin coprescription.

112 ne, and lidocaine), or mixed pain (ketamine, gabapentin, diclofenac, baclofen, cyclobenzaprine, and l

113 In conclusion, gabapentin did not provide a significant therapeutic adv

114 y was adequately powered, but treatment with gabapentin did not result in significantly lower pain sc

115 Requiring >=2 gabapentin dispensings moved the RR to 1.40 (1.03-1.90,

116 Gabapentin displayed a complex behavior where the featur

117 ubunit but not in the presence of beta4b; 3) gabapentin does not affect Ca(v)2.1 voltage-dependent ga

118 to neuronal alpha(2)delta-1 and suggest that gabapentin does not directly target TSP/alpha(2)delta-1

119 Gabapentin does not seem to have direct Ca2+ channel blo

120 se information is available on the safety of gabapentin during pregnancy.

121 nued on their current antidepressant without gabapentin) during which time they completed validated d

122 .36], p < 0.001), SGA among women exposed to gabapentin early (1.17 [1.02-1.33], p = 0.02), late (1.3

123 Gabapentin effects on glutamate are not known.

124 In this report, we examined gabapentin effects on trafficking and voltage-dependent

125 Gabapentin effects were blocked in the presence of a spe

126 risk of preterm birth among women exposed to gabapentin either late (RR, 1.28 [1.08-1.52], p < 0.01)

127 not find evidence for an association between gabapentin exposure during early pregnancy and major mal

128 e sought to evaluate the association between gabapentin exposure during pregnancy and risk of adverse

129 rmations and cardiac defects associated with gabapentin exposure during the first trimester (T1), and

130 care unit admission (NICUa) associated with gabapentin exposure early, late, or both early and late

131 in; 7.2 (5.9-9.21) for gabapentin, including gabapentin extended release and enacarbil; and 10.6 (7.4

132 r alternative treatment options to off-label gabapentin for the management of chronic pelvic pain and

133 panies to develop and publish articles about gabapentin for the medical literature, and planning to s

134 Efficacy of gabapentin for the treatment of alcohol use disorder in

135 dies has evaluated newer antidepressants and gabapentin for treating hot flashes.

136 inary support for the safety and efficacy of gabapentin for treatment of cannabis dependence that mer

137 that opioids, tramadol, benzodiazepines, and gabapentin (for radiculopathy) are effective for pain re

138 y of a calcium channel/GABA modulating drug, gabapentin, for the treatment of cannabis dependence.

139 e examined reporting practices for trials of gabapentin funded by Pfizer and Warner-Lambert's subsidi

140 Gabapentin (GBP) and S(+)-3-isobutyl-gamma-aminobutyric

141 The antiepileptic and antiallodynic drug gabapentin (GBP) binds to the alpha2delta-1 and alpha2de

142 Accumulating evidence indicates that gabapentin (GBP), a prescription drug, is prone to misus

143 he effects of electroacupuncture (EA) versus gabapentin (GP) for hot flashes among survivors of breas

144 Confusion was also more frequent in the gabapentin group (7 [8%] vs 1 [1.2%]; P = .06).

145 hange from baseline was -1.1 (SD 2.0) in the gabapentin group and -0.9 (SD 1.8) in the placebo group

146 hange from baseline was -1.4 (SD 2.3) in the gabapentin group and -1.2 (SD 2.1) in the placebo group

147 erage NRS pain score was 4.3 (SD 2.3) in the gabapentin group and 4.5 (SD 2.2) in the placebo group.

148 was 7.1 (standard deviation [SD] 2.6) in the gabapentin group and 7.4 (SD 2.2) in the placebo group.

149 in the placebo group (10 [7%] of 153 in the gabapentin group compared with 3 [2%] of 153 in the plac

150 During the first 6 weeks, the naltrexone-gabapentin group had a longer interval to heavy drinking

151 ore women had a serious adverse event in the gabapentin group than in the placebo group (10 [7%] of 1

152 res of pain were significantly better in the gabapentin group than in the placebo group.

153 omparable in the 2 groups (15 [13.3%] in the gabapentin group vs 11 [9.5%] in the placebo group).

154 pentin group were dizziness (20 [24%] in the gabapentin group vs 4 [4.9%] in the control group; P<.00

155 oup; P<.001) and somnolence (19 [23%] in the gabapentin group vs 5 [6%] in the control group; P = .00

156 rienced significantly more frequently in the gabapentin group were dizziness (20 [24%] in the gabapen

157 and infection were all more frequent in the gabapentin group, but withdrawals were comparable in the

158 rexone-alone group but not in the naltrexone-gabapentin group, while a history of alcohol withdrawal

159 visual disturbances were more common in the gabapentin group.

160 iated with better response in the naltrexone-gabapentin group.

161 intent-to-treat analysis, subjects receiving gabapentin had a statistically significant reduction in

162 Moreover, gabapentin had no effect on reinstatement of sucrose see

163 These findings indicate that gabapentin has a measurable antinociceptive effect and a

164 Gabapentin has come into clinical use as adjunctive ther

165 he alpha-2-delta receptor modulators such as gabapentin have shown early promising results in multimo

166 The risk of suicidal acts was increased for gabapentin (hazard ratio [HR], 1.42; 95% confidence inte

167 Gabapentin impairs the T-cell receptor-driven calcium re

168 racetamol and opiates in 97% of patients and gabapentin in 45% of patients.

169 e beneficial effect of Cavbeta antisense and gabapentin in allergic airway inflammation.

170 nstitutional trial to assess the efficacy of gabapentin in controlling hot flashes in women with brea

171 To assess the efficacy and safety of gabapentin in patients with fibromyalgia.

172 Intraperitoneal injection of 30-60 mg/kg of gabapentin in resiniferotoxin-treated rats significantly

173 CaV2.2 cell-surface expression is reduced by gabapentin in the presence of wild-type alpha2delta-1 (b

174 ould be employed when considering the use of gabapentin in transplant recipients, especially when com

175 aimed to measure the efficacy and safety of gabapentin in women with chronic pelvic pain and no obvi

176 oes not alter cP450 enzymes (lamotrigine and gabapentin) in monotherapy for 6 months or more were fol

177 (6.5-9.4) for pregabalin; 7.2 (5.9-9.21) for gabapentin, including gabapentin extended release and en

178 Gabapentin increased the amplitudes of evoked GABA recep

179 (fMRI) in normal volunteers, we studied the gabapentin-induced modulation of brain activity in respo

180 Gabapentin infused directly into the CeA also blocked de

181 use selective inhibition of alpha2delta-1 by gabapentin infusion into wild-type VMH significantly inc

182 v)2.1 Ca2+ channels in X. laevis oocytes; 2) gabapentin inhibition occurs in the presence of the Ca2+

183 endent on beta-subunit concentration; and 5) gabapentin inhibition of Ca(v)2.1 trafficking can be rev

184 Our principal findings are as follows: 1) gabapentin inhibits trafficking of recombinant Ca(v)2.1

185 e.g., capsaicin), antiepileptic drugs (e.g., gabapentin), injection of other agents (e.g., botulinum

186 esence of wild-type alpha2delta-1 (but not a gabapentin-insensitive alpha2delta-1 mutant), the intera

187 The alpha2delta ligand gabapentin interacts with alpha2delta-1, and inhibits ca

188 minophen are preferred analgesic agents, and gabapentin is a contextual third choice, in neurocritica

189 y target pathological channels; for example, gabapentin is a ligand of alpha2delta voltage-activated

190 Gabapentin is a nonhormonal agent that also can reduce h

191 Gabapentin is a structural analog of GABA that has antic

192 concentrations predict clinical efficacy of gabapentin is an area worthy of exploration.

193 This mechanism may help to explain why gabapentin is both effective and selective in the treatm

194 The anticonvulsant gabapentin is effective in reducing the subjective pain

195 Gabapentin is effective in the control of hot flashes at

196 Gabapentin is effective in the treatment of pain and sle

197 Gabapentin is effective in treating some chronic pain co

198 activation, thus supporting the concept that gabapentin is more effective in modulating nociceptive t

199 Gabapentin is well established as an effective treatment

200 Despite the therapeutic efficacy of gabapentin, its molecular and cellular mechanisms of act

201 nd marketed in the United States: felbamate, gabapentin, lamotrigine, and topiramate.

202 In contrast, the new AEDs gabapentin, lamotrigine, levetiracetam, tiagabine, topir

203 xploratory analysis suggests that the use of gabapentin, lamotrigine, oxcarbazepine, and tiagabine, c

204 randomly assigned to receive carbamazepine, gabapentin, lamotrigine, oxcarbazepine, or topiramate.

205 randomly assigned to receive carbamazepine, gabapentin, lamotrigine, oxcarbazepine, or topiramate.

206 Gabapentin, marketed for the treatment of seizures and n

207 Our findings suggest that gabapentin may be an effective treatment for many patien

208 We suggest that gabapentin may cause acute renal dysfunction by a mechan

209 xcitatory synapse formation and suggest that gabapentin may function therapeutically by blocking new

210 Gabapentin may reduce these symptoms and help prevent ea

211 neration antipsychotics, iliac fascia block, gabapentin, melatonin, lower levels of intraoperative pr

212 In vivo, gabapentin microinjected in the nucleus accumbens core a

213 This preliminary evidence shows that gabapentin might have a role in treatment of chemotherap

214 Gabapentin monotherapy appears to be efficacious for the

215 uli was sensitive to systemic treatment with gabapentin, morphine and the cannabinoid WIN 55,212-2, b

216 addition, IB-MECA was equally efficacious as gabapentin (Neurontin) or amitriptyline, but respectivel

217 rough litigation concerning the promotion of gabapentin (Neurontin, Pfizer, Inc., New York, New York)

218 tructurally and pharmacologically related to gabapentin (Neurontin; Pfizer Inc., New York, NY).

219 tingly, this interaction is not inhibited by gabapentin on a molecular level and is not detectable on

220 in turn, dependence reverses the effects of gabapentin on CeA neurons, and suggest that gabapentin r

221 Here, we investigated the effect of gabapentin on GABAergic transmission in CeA slices, on e

222 potential effect of systemic and intrathecal gabapentin on tactile allodynia induced by resiniferotox

223 -controlled trial was to study the effect of gabapentin on the perception of pruritus and its behavio

224 ents with downbeat nystagmus will respond to gabapentin or baclofen.

225 Inhibiting alpha2delta-1 with gabapentin or disrupting the alpha2delta-1-NMDAR interac

226 endent processes with Cavalpha2delta1 ligand gabapentin or genetic Cavalpha2delta1 knockdown blocks T

227 Furthermore, systemic administration of gabapentin or intrathecal injection of alpha2delta-1Tat

228 n period to a maximum dosage of 3600 mg/d of gabapentin or matching placebo.

229 Patients were randomized to the study drug (gabapentin or placebo) at a starting dose of 300 mg oral

230 Hot flashes can be managed with venlaxafine, gabapentin, or-potentially-stress management.

231 aternal age, race/ethnicity, indications for gabapentin, other pain conditions, hypertension, diabete

232 he SF-36 and POMS also significantly favored gabapentin (P< or =.01).

233 d sleep interference showed improvement with gabapentin (P<.001).

234 tion have shown improvements with oestrogen, gabapentin, paroxetine, and clonidine, but little or no

235 Maternal use of gabapentin, particularly late in pregnancy, was associat

236 Topiramate, onabotulinum toxin type A, gabapentin, petasites and tizanidine are among the agent

237 hibition of host pyramidal cells and blocked gabapentin preference (i.e. relieved ongoing pain) in a

238 and thromboembolic stroke patients, whereas gabapentin/pregabalin were favored in subarachnoid hemor

239 rs of the glutamatergic system, riluzole and gabapentin, prolong survival.

240 Safety information was defined for gabapentin, propofol, sevoflurane, the combination of ri

241 Mice administered gabapentin recovered upper extremity function after cerv

242 Systemic gabapentin reduced ethanol intake in dependent, but not

243 the presence of central sensitization; (ii) gabapentin reduced the activation in the brainstem, only

244 We found that (i) gabapentin reduced the activations in the bilateral oper

245 Primidone, propranolol, and gabapentin reduced the amplitude (power) of the patholog

246 Overall, our results suggest that gabapentin reduces the number of beta4a-bound Ca(v)2.1 c

247 A gabapentin regimen (topical or oral) had been recommende

248 gabapentin on CeA neurons, and suggest that gabapentin represents a potential medication for treatme

249 Collectively, these findings show that gabapentin reverses behavioral measures of ethanol depen

250 d GEPR-9s, and this effect may contribute to gabapentin's effectiveness in anxiety and pain in which

251 Importantly, gabapentin's effects on drug seeking were not due to a g

252 Gabapentin seems to decrease hot flashes by approximatel

253 Using a rat neuropathic pain model in which gabapentin-sensitive tactile allodynia develops after ti

254 Gabapentin significantly reduced APN median eye speed in

255 Relative to placebo, gabapentin significantly reduced cannabis use as measure

256 Trials were for off-label uses of gabapentin sponsored by Pfizer and Parke-Davis, and docu

257 sitisation which in turn can be inhibited by gabapentin, suggesting a potential role in the pathogene

258 By contrast, gabapentin suppressed allodynia in both CFA and PSNL mod

259 em, only during central sensitization; (iii) gabapentin suppressed stimulus-induced deactivations, on

260 Spinal administration of the anticonvulsant gabapentin suppresses allodynia by an unknown mechanism.

261 ible acute renal dysfunction after beginning gabapentin therapy for chronic pain due to diabetic neur

262 Mood and quality of life also improve with gabapentin therapy.

263 Gabapentin (titrated from 900 to 3600 mg/d or maximum to

264 randomly assigned in a 1:1 ratio to receive gabapentin (titrated to a maximum dose of 2700 mg daily)

265 The addition of gabapentin to naltrexone improved drinking outcomes over

266 by their ability to inhibit binding of [(3)H]gabapentin to pig brain membranes and for their potency

267 The ability of gabapentin to suppress this pathway may be important for

268 used to communicate favorable messages about gabapentin to their physician colleagues.

269 Lamotrigine, gabapentin, topiramate, and oxcarbazepine are available

270 Systemic baclofen, gabapentin, tramadol, and morphine dose-dependently atte

271 A significantly greater proportion of gabapentin-treated patients compared with placebo-treate

272 Gabapentin-treated patients displayed a significantly gr

273 By intent-to-treat analysis, gabapentin-treated patients' mean daily pain score at th

274 atistically significant differences favoring gabapentin treatment were observed in measures of qualit

275 The three gabapentin trials decreased hot flashes by 35% to 38% co

276 The SSRIs or SNRIs, clonidine, and gabapentin trials provide evidence for efficacy; however

277 normalities with neurological symptoms, with gabapentin-type anticonvulsants, and is among the first

278 Gabapentin-unexposed pregnancies served as the reference

279 mg/day [N=50]), naltrexone (50 mg/day) with gabapentin (up to 1,200 mg/day [N=50]) added for the fir

280 ted a double-blind crossover trial comparing gabapentin (up to 900 mg/day) to baclofen (up to 30 mg/d

281 evidence of potential harms associated with gabapentin use, it is important that clinicians consider

282 Gabapentin users had increased risk in subgroups of youn

283 signed to receive both an antidepressant and gabapentin versus being weaned off the antidepressant an

284 o or fewer, 0.87, 0.85-0.90), and treatment (gabapentin vs carbamazepine, 0.71, 0.59-0.86; topiramate

285 The dose of gabapentin was 1,800 mg per os, in a single administrati

286 The promotion of gabapentin was a comprehensive and multifaceted process.

287 Gabapentin was also associated with significantly greate

288 Gabapentin was associated with an increase in mean HSA,

289 or baseline values); only the higher dose of gabapentin was associated with significant decreases in

290 ed whether the combination of naltrexone and gabapentin was better than naltrexone alone and/or place

291 This effect did not endure after gabapentin was discontinued.

292 Gabapentin was generally well tolerated.

293 or not the antidepressant was continued when gabapentin was started, there was an approximately 50% m

294 ts with APN, the reduction of nystagmus with gabapentin was substantial and 8 of these elected to con

295 In the 2.3% with demyelinating disease, gabapentin was the most likely second analgesic (50.0%).

296 atistically significant differences favoring gabapentin were reported.

297 the effectiveness of the anticonvulsant drug gabapentin, which is a specific inhibitor of BCATc.

298 ocally perfused pramipexole, ropinirole, and gabapentin, which significantly counteracted optogenetic

299 Some newer antidepressants and gabapentin, within 4 weeks of therapy initiation, decrea

300 lozapine, duloxetine, clonazepam, ramelteon, gabapentin, zonisamide, and yokukansan.