ライフサイエンスコーパス: neuroleptic

1 ved prescriptions for more than one atypical neuroleptic).

2 ng memory than treatment with a conventional neuroleptic.

3 se patients when they are taking an atypical neuroleptic.

4 he therapeutic and in the adverse effects of neuroleptics.

5 n elderly patients treated with conventional neuroleptics.

6 ort treatment with low doses of conventional neuroleptics.

7 erved for patients receiving mostly atypical neuroleptics.

8 and decreased following exposure to atypical neuroleptics.

9 ume and the reverse for exposure to atypical neuroleptics.

10 n the early stages of treatment with typical neuroleptics.

11 b-group of subjects chronically treated with neuroleptics.

12 ly, and 27 had received typical and atypical neuroleptics.

13 renia is confounded by the widespread use of neuroleptics.

14 esolimbic dopamine with a profile similar to neuroleptics.

15 ho were refractory to treatment with typical neuroleptics.

16 results for D-cycloserine plus conventional neuroleptics.

17 mediating the delayed therapeutic action of neuroleptics.

18 dication was switched to any of the atypical neuroleptics.

19 iving prescriptions for atypical and typical neuroleptics.

20 een implicated in the therapeutic effects of neuroleptics.

21 antidepressants (3.2); clonidine (2.3); and neuroleptics (0.9).

22 ics and 22,648 (58.6%) received any atypical neuroleptic (1,207 [5.3%] received clozapine; 10,970 [48

23 olanzapine=38.5%, risperidone=28.0%, typical neuroleptics=14.5%, quetiapine=0.0%).

24 aloperidol group required less median rescue neuroleptics (2.0 mg) than the placebo + haloperidol gro

25 or each of the four then available atypical neuroleptics after the medication switch.

26 e overall clinical profile of this classical neuroleptic agent.

27 criteria for partial response to traditional neuroleptic agents.

28 r disease who were and were not treated with neuroleptic agents.

29 r disease who were and were not treated with neuroleptic agents.

30 n that treatment with clozapine, an atypical neuroleptic, ameliorates this deficit in clinically resp

31 He responded quickly to neuroleptic and was noted to be an easily engageable per

32 n the study: 15,984 (41.4%) received typical neuroleptics and 22,648 (58.6%) received any atypical ne

33 enic patients who had received minimal or no neuroleptics and 34 patients with chronic illness whose

34 AD patients who had taken neuroleptics and AD brains that also contained Lewy bodi

35 (mainly amphetamines) in 40% of cases, while neuroleptics and antidepressants were of poor benefit.

36 lume increased following exposure to typical neuroleptics and decreased following exposure to atypica

37 increase could not be clearly attributed to neuroleptics and may be related to antidepressant treatm

38 nce that supports the safety and efficacy of neuroleptics and neuromodulatory approaches in treatment

39 Thirty-four patients were taking typical neuroleptics, and 10 were unmedicated.

40 of drugs will be reviewed: benzodiazepines, neuroleptics, and atypical antipsychotics, including sid

41 apine, moderate with risperidone and typical neuroleptics, and low with quetiapine.

42 ticulum proteins that bind certain steroids, neuroleptics, and psychotropic drugs, form a trimeric co

43 me measures to treatment status, exposure to neuroleptics, and symptoms was examined.

44 ave diabetes than those who received typical neuroleptics, and the prevalence of diabetes was signifi

45 anesthesia, pharmacologic non-REM sleep, and neuroleptic anesthesia.

46 Repeated treatments with neuroleptics are associated with biochemical and morphol

47 and the associated structural changes after neuroleptics are discontinued.

48 Traditional neuroleptics are the standard treatment for TS, but ther

49 d to establish the role of agents other than neuroleptics as clinical therapies for the treatment of

50 Such events may underlie the aetiology of neuroleptic associated cerebral oedema and neuroleptic m

51 ognitive function when added to conventional neuroleptics at a dose of 50 mg/d.

52 In the patients who had never received neuroleptics at baseline (N = 87), the mean cumulative i

53 (22.3%) and the 89 patients who had received neuroleptics before baseline for 1-30 days (24.6%); howe

54 ; however, the 131 patients who had received neuroleptics before baseline for more than 30 days tende

55 The CNS metabolic response to a neuroleptic challenge in treatment-responsive and nonres

56 We have found that the commonly used neuroleptics chlorpromazine, trifluoperazine and clozapi

57 (33-35 degrees C for 1 h) with phenothiazine neuroleptics (chlorpromazine & promethazine) as additive

58 nd metoclopramide, but not with the atypical neuroleptic clozapine, led to markedly enhanced FosB-lik

59 Like the atypical neuroleptic clozapine, NT77L blocked the climbing behavi

60 io similar to that observed for the atypical neuroleptic clozapine.

61 s, but is completely blocked by the atypical neuroleptic clozapine.

62 ecause of its high affinity for the atypical neuroleptic clozapine.

63 cidate the muscarinic action of the atypical neuroleptics clozapine and olanzapine.

64 ht patients were being treated with atypical neuroleptics (clozapine [N=26], olanzapine [N=31], rispe

65 ffect of chronic treatment with two atypical neuroleptics, commonly used to treat schizophrenia.

66 re recent data support the adjunctive use of neuroleptics, deep-brain stimulation, and neurosurgical

67 ously observed in patients receiving typical neuroleptics did not occur in patients treated with cloz

68 lamic deficits, whereas those taking typical neuroleptics did not.

69 was to examine the clinical course following neuroleptic discontinuation of patients with recent-onse

70 Treatment with typical neuroleptics does not reverse this deficit.

71 nt of negative symptoms was predicted by low neuroleptic dose and low baseline SANS total score.

72 Only eight (15%) received a daily neuroleptic dose higher than 200 mg of chlorpromazine eq

73 Exploratory analysis suggested that neuroleptic dose is correlated with changes in all 3 dom

74 ents without tardive dyskinesia when age and neuroleptic dose were controlled for.

75 gative symptoms, extrapyramidal symptoms, or neuroleptic dose.

76 The butyrophenone neuroleptic droperidol is very effective in aborting acu

77 e stimuli and an alteration, correlated with neuroleptic drug dosage, in the functional coupling betw

78 The neuroleptic drug eticlopride, a highly selective D(2) re

79 y hepatic effects of chlorpromazine (CPZ), a neuroleptic drug known for years to induce intrahepatic

80 suggests a focal compensatory response that neuroleptic drug regimens may augment.

81 rug, risperidone, and an older, conventional neuroleptic drug, haloperidol, in terms of the rate of r

82 exacerbation of extrapyramidal effects with neuroleptic drugs and betel nut (Areca catechu); increas

83 chizophrenia who were and were not receiving neuroleptic drugs and normal control subjects were obtai

84 umans or experimental animals with classical neuroleptic drugs can lead to abnormal, tardive movement

85 val and exposure to either benzodiazepine or neuroleptic drugs do not account for the lack of marked

86 Typical neuroleptic drugs elicit their antipsychotic effects mai

87 se changes are consistent with the idea that neuroleptic drugs lead to "compensation" and "adaptation

88 of rats treated acutely and chronically with neuroleptic drugs of different classes.

89 he comparison of the effects of 2 classes of neuroleptic drugs on regional brain functional activitie

90 awal are inadequate to escape the effects of neuroleptic drugs on regional cerebral glucose metabolis

91 Typical and atypical neuroleptic drugs produced contrasting regulatory effect

92 mon is related to manic depression, in which neuroleptic drugs should be used with caution.

93 chiatry, such as L-DOPA, methylphenidate and neuroleptic drugs, act on dopaminergic mechanisms.

94 TS, but there is increasing interest in non-neuroleptic drugs, behavioural therapies, and surgical a

95 f L-dopa and severe sensitivity reactions to neuroleptic drugs.

96 20%-40% of patients treated chronically with neuroleptic drugs.

97 r = 3 weeks) or stopped treatment with depot neuroleptic drugs.

98 and both gender and longterm responsivity to neuroleptic drugs.

99 and D4) is a target for typical and atypical neuroleptic drugs.

100 ain regions that are functionally altered by neuroleptic drugs.

101 ute to their clinical advantage over typical neuroleptic drugs.

102 ed without evidence of axon terminal loss or neuroleptic effects on dysbindin-1 or VGluT-1.

103 The authors hypothesized that neuroleptics enhance striatal glutamatergic neurotransmi

104 pal personality disorder who had no previous neuroleptic exposure and in 14 normal comparison subject

105 mus in schizophrenic patients are related to neuroleptic exposure and symptom severity.

106 Globus pallidus enlargement correlated with neuroleptic exposure and with age of onset of psychosis.

107 Subjects with prior neuroleptic exposure had larger basal ganglia volumes an

108 These results were not influenced by neuroleptic exposure history, postmortem interval, or ag

109 Patients' neuroleptic exposure was calculated over the 2 years by

110 ive syndrome related to undisclosed previous neuroleptic exposure, or 'soft age-related' parkinsonian

111 ere unrelated to age, postmortem interval or neuroleptic exposure.

112 r placebo (n=24) added to their conventional neuroleptic for an 8-week, double-blind trial.

113 l or substance abuse or dependence, and were neuroleptic free for a minimum of 21 days.

114 s in basal ganglia in five subjects who were neuroleptic free, five subjects who were being treated w

115 schizophrenia in the current study had been neuroleptic-free for at least 3 weeks.

116 Neuroleptic-free schizophrenia subjects exhibited the hi

117 Patients with < or = 10 years on neuroleptics had a five times greater chance of remissio

118 Patients receiving atypical neuroleptics had a mean P50 ratio that fell between thes

119 = 15) for whom lithium, anticonvulsants, and neuroleptics had been ineffective, had produced intolera

120 s and 34 patients with chronic illness whose neuroleptics had been withdrawn.

121 ily treatments with two chemically divergent neuroleptics, haloperidol (1 mg/kg i.p./day) and eticlop

122 Chronic treatments with two typical neuroleptics, haloperidol and metoclopramide, but not wi

123 I diabetes after initiation of some atypical neuroleptics has been reported, primarily in studies inv

124 results suggest that chronic treatments with neuroleptics having different effects on cognitive and m

125 y sought to determine whether other atypical neuroleptics improve P50 ratios.

126 ine has been found to be superior to typical neuroleptics in ameliorating the symptoms of refractory

127 maging of patients under regimens of chronic neuroleptics in particular in the context of forthcoming

128 psychotic approved in 1989, and conventional neuroleptics in the Department of Veterans Affairs (VA)

129 trations than the patients receiving typical neuroleptics in the previous trial.

130 Discontinuation of neuroleptics increased the chances of remission fourfold

131 of patients receiving predominantly typical neuroleptics increased, while the opposite was observed

132 levels may protect against the expression of neuroleptic-induced dyskinesia.

133 A role in these neuroleptic-induced dyskinesias may be played by a struc

134 anifest significant psychiatric symptoms and neuroleptic-induced extrapy-ramidal side effects and hav

135 Persistent, neuroleptic-induced oral dyskinesias could therefore be

136 The present results support the view that neuroleptic-induced reductions in DA transmission do not

137 There was no evidence that treatment with neuroleptics influenced the fertility rate in women with

138 These two neuroleptics inhibit tau dephosphorylation by PP-2B thro

139 ght, Language, and Communication scale or to neuroleptic level.

140 hich lower doses (0.25-1.0 microg) exhibit a neuroleptic-like action.

141 The neuroleptic-like effects of neurotensin (NT) are thought

142 r antinociception, while exhibiting atypical neuroleptic-like effects.

143 syndrome and 13 cases of risperidone-induced neuroleptic malignant syndrome against three criteria se

144 They assessed 19 cases of clozapine-induced neuroleptic malignant syndrome and 13 cases of risperido

145 Nine of the 19 cases of clozapine-related neuroleptic malignant syndrome and eight of the 13 cases

146 Neuroleptic malignant syndrome can occur in patients giv

147 de effect profiles overlap considerably with neuroleptic malignant syndrome criteria, and atypical an

148 thors' goal was to analyze reported cases of neuroleptic malignant syndrome in patients given clozapi

149 ypotension, acute urinary retention, and the neuroleptic malignant syndrome or rhabdomyolysis.

150 Neuroleptic malignant syndrome should be treated by disc

151 eight of the 13 cases of risperidone-related neuroleptic malignant syndrome were designated as having

152 Published clinical findings on neuroleptic malignant syndrome were integrated with data

153 as to develop a pathophysiological model for neuroleptic malignant syndrome with greater explanatory

154 Insufficient evidence exists for "atypical" neuroleptic malignant syndrome with novel antipsychotics

155 s will be discussed: malignant hyperthermia, neuroleptic malignant syndrome, anticholinergic poisonin

156 gnosis, and treatment of serotonin syndrome, neuroleptic malignant syndrome, malignant hyperthermia,

157 ess may constitute a trait vulnerability for neuroleptic malignant syndrome, which, when coupled with

158 esponsible for most, if not all, features of neuroleptic malignant syndrome.

159 ntagonism, produces the clinical syndrome of neuroleptic malignant syndrome.

160 other end-organs that function abnormally in neuroleptic malignant syndrome.

161 cal antipsychotics and resembles "classical" neuroleptic malignant syndrome.

162 ted them as high or low probability of being neuroleptic malignant syndrome.

163 signated as having high probability of being neuroleptic malignant syndrome.

164 xicities unrelated to (but misattributed as) neuroleptic malignant syndrome.

165 f neuroleptic associated cerebral oedema and neuroleptic malignant syndrome.

166 the schizophrenia patients receiving typical neuroleptics (mean=19.8% [SD=21.0%] versus 110.1% [SD=87

167 only patients who had never been exposed to neuroleptic medication (n = 15) were considered.

168 nship between the 2-year exposure to typical neuroleptic medication and change in basal ganglia volum

169 Neuroleptic medication can provoke severe sensitivity re

170 Recent reports suggest that neuroleptic medication changes basal ganglia volume.

171 and end of a 2-year period and who received neuroleptic medication during this time.

172 nic patients may be mitigated by the type of neuroleptic medication they receive.

173 database, patients with schizophrenia whose neuroleptic medication was switched showed significantly

174 patients with DSM-IV schizophrenia receiving neuroleptic medication were given oral glucose tolerance

175 abnormalities are due to chronic morbidity, neuroleptic medication, and/or hospitalization, or wheth

176 ere not confounded by dementia, Braak score, neuroleptic medication, cerebral infarcts, or Lewy bodie

177 Neuroleptic medication, however, affects the size of the

178 either the absence or the inadequate use of neuroleptic medication.

179 ne percent of the patients were treated with neuroleptic medication; most of these patients received

180 ed to evaluate the effectiveness of atypical neuroleptic medications in actual clinical practice.

181 s with tardive dyskinesia who were receiving neuroleptic medications were enrolled.

182 ion, successful treatment typically requires neuroleptic medications, necessitating intervention by m

183 s may have serious effects: poor response to neuroleptic medications, poor clinical outcomes, and dir

184 with schizophrenia (40 men and 30 women; 29 neuroleptic naive and 41 previously treated) and 81 heal

185 Seventy-three patients were neuroleptic naive, 14 had received treatment for less th

186 nts with schizophrenia (58 men, 42 women; 39 neuroleptic naive, 61 previously treated) and 110 health

187 nctioning were obtained for 130 patients (51 neuroleptic naive, 79 previously treated) and 130 health

188 At 6-month follow-up, both the neuroleptic-naive and previously treated patients showed

189 rdive dyskinesia among patients who had been neuroleptic-naive at baseline (22.3%) and the 89 patient

190 sode schizophrenic patients, who were mostly neuroleptic-naive at intake, the authors examined the re

191 In the neuroleptic-naive group, volumes did not correlate with

192 Sixteen right-handed and neuroleptic-naive men with schizotypal personality disor

193 CIPANTS: This naturalistic study involved 54 neuroleptic-naive men with SPD and 54 male HC subjects a

194 A group of 261 neuroleptic-naive patients aged 55 or above were identif

195 s by dopamine occurred both in first-episode neuroleptic-naive patients and in previously treated chr

196 We studied 17 neuroleptic-naive patients at the early stages of illnes

197 The neuroleptic-naive patients did not differ from the healt

198 previously compared healthy volunteers with neuroleptic-naive patients experiencing their first epis

199 audate nucleus volume reported in studies of neuroleptic-naive patients experiencing their first epis

200 Seventy-four neuroleptic-naive patients with DSM-IV schizophrenia wer

201 tudy represents the largest sample of mostly neuroleptic-naive patients with first-episode schizophre

202 Neuroleptic-naive patients with schizophrenia (N=90) and

203 -electrode array system for 25 first-episode neuroleptic-naive patients with schizophrenia at baselin

204 n the early stages of schizophrenia, even in neuroleptic-naive patients, and may be the result of int

205 atment, since the differences are evident in neuroleptic-naive patients.

206 already evident at the first presentation of neuroleptic-naive patients.

207 than the healthy comparison subjects and the neuroleptic-naive patients.

208 r entorhinal cortex volume in first-episode, neuroleptic-naive psychotic disorders may not be a confo

209 rs sought to examine basal ganglia volume in neuroleptic-naive psychotic patients.

210 ic studies were conducted in newly diagnosed neuroleptic-naive schizophrenic and non-schizophrenic ps

211 MRI scans were acquired from 21 male, neuroleptic-naive subjects recruited from the community

212 n two distinct working memory tasks in these neuroleptic-naive subjects with schizotypal personality

213 l power was also reduced in the subset of 19 neuroleptic-naive, first-episode schizophrenic patients

214 Twenty-one of the patients were neuroleptic-naive; of the 75 previously treated patients

215 Like atypical neuroleptics, NT69L blocked the climbing behavior in rat

216 Nevertheless, we found that neuroleptics of both classes regulated transcription fac

217 cal and behavioral effects that characterize neuroleptics of different classes.

218 ly treated patients, 48 had received typical neuroleptics only, and 27 had received typical and atypi

219 by whether patients received a conventional neuroleptic or each of the four then available atypical

220 izophrenia treated with typical and atypical neuroleptics over 4 months in 1999 in the Veterans Healt

221 rs and who had been nonresponsive to typical neuroleptics participated in the study.

222 otonin reuptake inhibitor citalopram and the neuroleptic perphenazine with placebo for the treatment

223 These data suggest that NT69L may have neuroleptic properties in humans and may be useful in th

224 oceptive neurons, regulating the response to neuroleptics, psychotomimetics, and drugs of abuse, and

225 ion of abnormally hyperphosphorylated tau by neuroleptics raises an intriguing possibility that the c

226 ears) and 2.6 years after discontinuation of neuroleptics (range 1 month to 9 years).

227 ses are related to concurrent treatment with neuroleptics rather than a direct effect of antidepressa

228 ese results confirm previous data indicating neuroleptic resistance is associated with early onset.

229 The authors compared age at onset in neuroleptic-resistant and -responsive schizophrenic pati

230 e men (mean = 21.2 years, SD = 6.1, N = 75), neuroleptic-resistant men (mean = 19.4 years, SD = 4.7,

231 effects model indicated that male and female neuroleptic-resistant patients did not differ significan

232 euroleptic-responsive patients suggests that neuroleptic-resistant patients differ premorbidly as wel

233 nset between males and females is smaller in neuroleptic-resistant patients than in neuroleptic-respo

234 (mean = 19.4 years, SD = 4.7, N = 119), and neuroleptic-resistant women (mean = 20.1 years, SD = 6.3

235 s disease or after treatment with L-dopa and neuroleptics, respectively.

236 Thirty-eight acutely psychotic and neuroleptic responsive (by history) newly admitted inpat

237 ive as an antipsychotic for the treatment of neuroleptic responsive inpatients with acute schizophren

238 The mean ages at onset in the neuroleptic-responsive men (mean = 21.2 years, SD = 6.1,

239 n mean age at onset, whereas male and female neuroleptic-responsive patients did.

240 er in neuroleptic-resistant patients than in neuroleptic-responsive patients suggests that neurolepti

241 77) were fairly similar, whereas that of the neuroleptic-responsive women (mean = 24.2 years, SD = 8.

242 The effect of gender and neuroleptic responsivity on age at onset was related to

243 Severe neuroleptic sensitivity reactions are associated with si

244 nd its limited response to L-dopa and severe neuroleptic sensitivity.

245 In contrast, a third antagonist, the neuroleptic spiperone, produced an almost complete suppr

246 The results were unaffected by neuroleptic status or smoking history.

247 with the antipsychotic efficacy of atypical neuroleptics such as clozapine.

248 xtrapyramidal side effects caused by typical neuroleptics such as haloperidol.

249 the synapse), as is apparently the action of neuroleptics targeting dopamine receptors.

250 more frequent extrapyramidal side effects of neuroleptics than did the patients with Alzheimer's dise

251 rains of schizophrenic patients treated with neuroleptics than in those without this treatment.

252 By contrast, haloperidol, a typical neuroleptic that acts preferentially at D2-class recepto

253 6, 9, and 12 months after the institution of neuroleptic therapy among 307 psychiatric outpatients ov

254 was lower after gradually discontinuing oral neuroleptic therapy or stopping depot injections, early

255 nts with schizophrenia after withdrawal from neuroleptic therapy were located by a computerized liter

256 tpatients) were withdrawn abruptly from oral neuroleptic therapy, and 204 discontinued treatment grad

257 s high within 6 months of discontinuing oral neuroleptic therapy, particularly in hospitalized patien

258 up, three of these patients remained free of neuroleptic therapy.

259 ts in the two groups who were not exposed to neuroleptics, there was little difference in frequency o

260 ortex of brains from schizophrenics and from neuroleptic-treated and nonmedicated controls.

261 No comparable changes were found in neuroleptic-treated or untreated controls.

262 Previous studies, mostly involving neuroleptic-treated patients, have suggested enlarged ba

263 with psychotic depression received either no neuroleptic treatment (N = 11) or treatment for less tha

264 s also been associated with poor response to neuroleptic treatment and worse long-term outcome.

265 iduals with schizophrenia but do not require neuroleptic treatment because of their less severe sympt

266 that in a cohort of young patients receiving neuroleptic treatment early in their illness, cognitive

267 renia and the roles of chronic morbidity and neuroleptic treatment in these abnormalities remain uncl

268 ivation of striatal dopamine (DA) neurons by neuroleptic treatment or by electrical stimulation of th

269 Possible confounding influences of neuroleptic treatment were analyzed by comparing subject

270 common in schizophrenia in association with neuroleptic treatment were not supported.

271 e disorder who had residual symptoms despite neuroleptic treatment were randomly assigned to receive

272 diagnosis was predicted by hospitalization, neuroleptic treatment, duration of illness, enduring imp

273 e confounding roles of chronic morbidity and neuroleptic treatment, remain unclear.

274 Stage 3 sleep increased during neuroleptic treatment, while stage 4 sleep did not chang

275 medicated patients and size increases after neuroleptic treatment.

276 reased caudate volume may reflect effects of neuroleptic treatment.

277 tor blockade and may moderate the effects of neuroleptic treatment.

278 schizophrenic patients through the course of neuroleptic treatment.

279 nia following discontinuation of maintenance neuroleptic treatment.

280 esia is a serious and common complication of neuroleptic treatment.

281 ce in age at onset is related to response to neuroleptic treatment.

282 striatal structures associated with typical neuroleptic treatment.

283 or the induction of antipsychotic actions by neuroleptic treatments, was downregulated by chronic tre

284 at the completion of a 6- to 8-week atypical neuroleptic trial, and at a 2- to 4-year follow-up.

285 dine, stimulants, and antidepressants, while neuroleptic use increased only slightly.

286 Secondary end points were rescue neuroleptic use, delirium recall, comfort (perceived by

287 illness and may not be secondary to previous neuroleptic use.

288 ved with haloperidol may also apply to other neuroleptics used in Alzheimer's disease patients with p

289 All classes of neuroleptics used were implicated in producing tardive d

290 olumes, whereas a higher dose of an atypical neuroleptic was associated only with higher thalamic vol

291 he treated group, a higher dose of a typical neuroleptic was associated with higher caudate, putamen,

292 ceiving prescriptions for different atypical neuroleptics was examined with multiple logistic regress

293 enia, receipt of a prescription for atypical neuroleptics was significantly associated with diabetes

294 e controlled, patients who received atypical neuroleptics were 9% more likely to have diabetes than t

295 less than 40 years old, all of the atypical neuroleptics were associated with a significantly increa

296 hen patients treated with different atypical neuroleptics were compared, only the clozapine group had

297 Patients treated with atypical neuroleptics were those who received prescriptions for c

298 Atypical and typical neuroleptics, when administered chronically, can bring a

299 This study determined if augmentation of neuroleptics with 3 g/day of ethyl eicosapentaenoic acid

300 It appears that 5 days of neuroleptic withdrawal are inadequate to escape the effe