ライフサイエンスコーパス: extrapyramidal

1 scending fibers, corticospinal/pyramidal and extrapyramidal.

2 th PSEN1 mutations had pyramidal (21 [25%]), extrapyramidal (12 [14%]), or cerebellar (three [4%]) si

3 ssociated with more local injection-site and extrapyramidal adverse effects.

4 effect on oculomotor systems or significant extrapyramidal adverse effects.

5 including assessments reliant on pyramidal, extrapyramidal and cerebellar systems.

6 alopathy, psychiatric, cognitive, epileptic, extrapyramidal and inflammatory cerebrospinal fluid (CSF

7 important in the dopaminergic regulation of extrapyramidal and limbic NT release in conscious animal

8 orders (for example, migraine and seizures), extrapyramidal and movement disorders, mental health dis

9 rodegenerative disease of the cerebellum and extrapyramidal and pyramidal systems, nevertheless suffe

10 m was not associated with the development of extrapyramidal clinical disorders, including parkinsonis

11 ting that some may later develop symptomatic extrapyramidal disease.

12 Interestingly, no weight gain, no extrapyramidal disorder except rare akathisia were obser

13 nce at least twice the rate for placebo were extrapyramidal disorder, somnolence, and tremor.

14 athies were more commonly associated with an extrapyramidal disorder.

15 t disorders with ophthalmic symptoms include extrapyramidal disorders such as Parkinson disease-assoc

16 Features overlap with common extrapyramidal disorders: idiopathic torsion dystonia, i

17 ), decreased weight, dilated cardiomyopathy, extrapyramidal dysfunction and gross neuro-muscular defe

18 rmalities of motor control characteristic of extrapyramidal dysfunction suggest impairment of broader

19 al optic atrophy and later-onset spasticity, extrapyramidal dysfunction, and cognitive deficit.

20 Clinical features include extrapyramidal dysfunction, onset in childhood, and a re

21 and movement disorders, including ataxia and extrapyramidal dysfunction.

22 pressants and Panax ginseng; exacerbation of extrapyramidal effects with neuroleptic drugs and betel

23 done was well tolerated, with no evidence of extrapyramidal effects, cardiac events, or seizures.

24 was associated with more discontinuation for extrapyramidal effects.

25 , communication, feeding, and education) and extrapyramidal features contributed significantly to the

26 , communication, feeding, and education) and extrapyramidal features contributed significantly to the

27 d in patients with progressive dementia with extrapyramidal features in endemic regions or with relev

28 ease may explain some characteristics of the extrapyramidal features of DLB and its limited response

29 al ganglia disease, variably presenting with extrapyramidal features similar to those of Huntington's

30 s a neuropsychiatric disease associated with extrapyramidal features which differ from those of Parki

31 ignificant percentage of AD patients exhibit extrapyramidal features, and many PD patients develop de

32 No patient had tremor or other extrapyramidal features.

33 on, hearing loss, pigmentary retinopathy and extrapyramidal features.

34 admixture of cognitive, neuropsychiatric and extrapyramidal features.

35 No extrapyramidal impairments associated with basal ganglia

36 (5) marked early hypertonia and symptoms of extrapyramidal involvement.

37 cant differences between treatment groups on extrapyramidal measures nor significant adverse drug int

38 s were lower in individuals with more severe extrapyramidal motor abnormalities as measured by the Un

39 higher cognitive processes and modulation of extrapyramidal motor activity.

40 es that can be accompanied by a pyramidal or extrapyramidal motor disorder.

41 (encephalopathy, epilepsy, and pyramidal and extrapyramidal motor disorders) that are primarily attri

42 ntial association of anti-Tat antibodies and extrapyramidal motor dysfunction in PWH.

43 sed striatal dopamine levels, and consequent extrapyramidal motor dysfunction.

44 sed striatal dopamine levels, and consequent extrapyramidal motor dysfunction.

45 that early-life stress is protective against extrapyramidal motor effects of antipsychotic drugs in t

46 l results predict the clinical expression of extrapyramidal motor side effects at high doses.

47 adverse event reports of akathisia or other extrapyramidal motor side effects; mean scores on motor

48 ers of the study population had at least one extrapyramidal motor sign (EPMS), with bradykinesia bein

49 Treatment-emergent adverse event rates of extrapyramidal motor symptoms (KarXT, zero [0%] vs place

50 chotic drugs is limited by the occurrence of extrapyramidal motor symptoms, which are caused by dopam

51 control facial movement [4-7]: a subcortical extrapyramidal motor system drives spontaneous facial ex

52 This would indicate that extrapyramidal movement abnormalities constitute the cor

53 Neurological symptomatology consisted of extrapyramidal movement abnormalities, spasticity, ataxi

54 Patients almost invariably have prominent extrapyramidal movement abnormalities, which are rarely

55 compacta and ventral tegmental area regulate extrapyramidal movement and important cognitive function

56 ted with Leigh syndrome, was the most common extrapyramidal movement disorder among pediatric patient

57 Parkinsonism was the most prevalent extrapyramidal movement disorder in adults and was commo

58 notype was novel, with 50% having a dystonic extrapyramidal movement disorder, and 70% a behavioral s

59 ntraneuronal inclusions (Lewy bodies) and an extrapyramidal movement disorder.

60 levels, optic nerve deficits, ataxia and an extrapyramidal movement disorder.

61 ndrial disease and with 1 or more predefined extrapyramidal movement disorders (parkinsonism, dystoni

62 Extrapyramidal movement disorders associated with mitoch

63 We found a high prevalence of extrapyramidal movement disorders including cerebellar a

64 rs], 30 adult [age range, 20-81 years]) with extrapyramidal movement disorders were identified.

65 , stagnant psychomotor development, abnormal extrapyramidal movements and nephrosis.

66 Patients suffer from extrapyramidal movements, spasticity, ataxia, and cognit

67 pyramidal (n = 20), cerebellar (n = 14), or extrapyramidal (n = 12) signs, myoclonus (n = 12), visua

68 Extensive extrapyramidal neurodegenerative and reorganizational ch

69 Low expression was observed also in many extrapyramidal nuclei, such as the globus and ventral pa

70 ing features including cognitive impairment, extrapyramidal or peripheral motor involvement, and atax

71 Although some patients also displayed other extrapyramidal or pyramidal signs, these were always les

72 ironmental manganese (Mn) toxicity causes an extrapyramidal, parkinsonian-type movement disorder with

73 encephalon), constituting a major descending extrapyramidal pathway for control over midbrain and bra

74 n in intrinsic cortical, thalamocortical and extrapyramidal pathways.

75 [40.07%]), followed by PPA (76 [28.46%]) and extrapyramidal phenotypes (69 [25.84%]).

76 hese results demonstrate a potential role of extrapyramidal plasticity during functional recovery aft

77 d had predominant ataxia, and 18% had a pure extrapyramidal presentation.

78 Individuals with extrapyramidal presentations had milder neurological dis

79 ehavioural, cognitive, metabolic, motor, and extrapyramidal presentations will be critically appraise

80 ypic axes - motor neuron, frontotemporal and extrapyramidal - rather than the unitary approach of com

81 imbic brain region nucleus accumbens vs. the extrapyramidal region striatum; this effect is fully blo

82 ctivity and screened in models predictive of extrapyramidal side effect (EPS) liability.

83 rial SPECT brain images, serum prolactin and extrapyramidal side effect ratings were obtained for an

84 APDs) have been hypothesized to show reduced extrapyramidal side effects (EPS) due to their rapid dis

85 on is based solely on their ability to cause extrapyramidal side effects (EPS), including tardive dys

86 mechanistically related to the production of extrapyramidal side effects (EPS).

87 g (APD) associated with an increased risk of extrapyramidal side effects (EPSs) and hyperprolactinemi

88 Extrapyramidal side effects (n = 7) emerged at a thresho

89 mains of the Neuropsychiatric Inventory) and extrapyramidal side effects (Simpson Angus Scale scores

90 rden); and group 4, dopaminergic antagonism (extrapyramidal side effects and hyperprolactinemia).

91 Based on lower rates of acute extrapyramidal side effects associated with second-gener

92 motor functions and to the induction of the extrapyramidal side effects associated with the use of t

93 Positive psychotic symptoms and extrapyramidal side effects at baseline appear to be pow

94 It has a low incidence of extrapyramidal side effects but may cause agranulocytosi

95 humans and may be useful in the treatment of extrapyramidal side effects caused by typical neurolepti

96 profile.Atypical antipsychotics show reduced extrapyramidal side effects compared to first generation

97 neurons, whereas their potential to produce extrapyramidal side effects correlates with their propen

98 psychotic agent with less tendency to induce extrapyramidal side effects in man.

99 drugs to exhibit antipsychotic efficacy and extrapyramidal side effects in schizophrenia patients.

100 setting of neurological symptoms, including extrapyramidal side effects of antipsychotic treatment.

101 s disease tended to experience more frequent extrapyramidal side effects of neuroleptics than did the

102 negative symptoms, level of functioning, and extrapyramidal side effects over baseline.

103 ss active in behavioral models predictive of extrapyramidal side effects than in the mouse climbing a

104 mean severity of both psychotic symptoms and extrapyramidal side effects than those in the haloperido

105 hopathology) and safety (in terms of reduced extrapyramidal side effects).

106 levation and related sexual side effects; 6) extrapyramidal side effects, akathisia, and tardive dysk

107 with secondary sources of variance including extrapyramidal side effects, anxiety/depression, and psy

108 fectiveness measures that favored clozapine (extrapyramidal side effects, disruptiveness), bootstrap

109 Positive and negative symptoms, extrapyramidal side effects, quality of life, and level

110 conditioned avoidance response assay, while extrapyramidal side effects, such as catalepsy, emerged

111 tors contribute to the low risk of producing extrapyramidal side effects, which is the defining chara

112 ted by less anxiety and depression and fewer extrapyramidal side effects.

113 improved significantly over baseline only in extrapyramidal side effects.

114 e flattening were associated with changes in extrapyramidal side effects.

115 psychotic effect in humans without producing extrapyramidal side effects.

116 zapine had less tardive dyskinesia and fewer extrapyramidal side effects.

117 o antipsychotic agents and the production of extrapyramidal side effects.

118 there was little difference in frequency of extrapyramidal side effects.

119 sociated with an extremely low prevalence of extrapyramidal side effects.

120 h has low antipsychotic efficacy but induces extrapyramidal side effects.

121 ant schizophrenic patients without eliciting extrapyramidal side effects.

122 patients in the intervention group had mild extrapyramidal side effects.

123 t available, the number of participants with extrapyramidal side-effects (EPS) and the mean scores of

124 ic drugs differ in their propensity to cause extrapyramidal side-effects (EPS), but their dose-effect

125 of many current medications are the observed extrapyramidal side-effects (EPS), postulated to arise f

126 ogeneous group of disorders with progressive extrapyramidal signs and neurological deterioration, cha

127 as well as the development of myoclonus and extrapyramidal signs are consistent manifestations of di

128 eimer's disease (AD) is often accompanied by extrapyramidal signs attributed to nigrostriatal dysfunc

129 ulative antipsychotic doses, and presence of extrapyramidal signs early in treatment.

130 Extrapyramidal signs frequently accompany Alzheimer's di

131 Age and severity of extrapyramidal signs have been consistently associated w

132 Thus, extrapyramidal signs in AD correlate best with tangle pa

133 the basal ganglia or subthalamic nucleus and extrapyramidal signs in AD.

134 neuropil threads were positively related to extrapyramidal signs in AD.

135 disease associated with age and severity of extrapyramidal signs is related primarily to their combi

136 and combined effects of age and severity of extrapyramidal signs on the risk of incident dementia in

137 (mMMS) score, and the presence or absence of extrapyramidal signs or psychotic features.

138 In phase A, extrapyramidal signs tended to be greater with the stand

139 amination scores was slower, the presence of extrapyramidal signs was decreased, and the development

140 The presence of extrapyramidal signs was determined using the Unified Pa

141 Patients with AD (with or without extrapyramidal signs) did not show neuronal loss in the

142 threads was increased in AD (with or without extrapyramidal signs) nigra compared to control tissue,

143 nce of myoclonus, seizures, pyramidal signs, extrapyramidal signs, and cerebellar signs) from all ind

144 ter psychiatric symptoms, cerebellar ataxia, extrapyramidal signs, and extensive calcifications on br

145 ertension, diabetes mellitus, heart disease, extrapyramidal signs, depression, psychosis, aggression,

146 e of frontal lobe release signs, presence of extrapyramidal signs, gait disturbance, history of falls

147 typical cases, svPPA-tau showed significant extrapyramidal signs, greater executive impairment, and

148 llitus, heart disease, incident strokes, and extrapyramidal signs, only conventional antipsychotic us

149 nts included abnormal involuntary movements, extrapyramidal signs, psychiatric symptoms, and medical

150 ding frontotemporal dementia, pyramidal, and extrapyramidal signs.

151 function, and three of them developed subtle extrapyramidal signs.

152 ough a subgroup developed moderate to severe extrapyramidal signs.

153 All subjects developed extrapyramidal signs.

154 duced, although there was a mild increase in extrapyramidal signs; 112 patients met the criteria for

155 Safety was assessed using adverse events, Extrapyramidal Symptom (EPS) rating scales, laboratory v

156 nternational Neuropsychiatric Interview, and extrapyramidal symptom assessments indicating normal to

157 For all extrapyramidal symptom measures, sertindole was clinical

158 These findings support an atypical extrapyramidal symptom profile and the potential of a si

159 to explain the therapeutic efficacy and low extrapyramidal symptom profile of atypical antipsychotic

160 The extrapyramidal symptom profile of risperidone was compar

161 elated to 1) change in negative symptoms, 2) extrapyramidal symptom profile, 3) effect on prolactin l

162 There were no significant changes in Extrapyramidal Symptom Rating Scale scores and no cases

163 While Extrapyramidal Symptom Rating Scale scores were signific

164 Extrapyramidal Symptom Rating Scale total scores at endp

165 am and laboratory results, and scores on the Extrapyramidal Symptom Rating Scale.

166 to scores on the dyskinesia subscale of the Extrapyramidal Symptom Rating Scale.

167 Rating Scale, the Mini-Mental State, and the Extrapyramidal Symptom Rating Scale.

168 placebo in mean change from baseline in the extrapyramidal symptom rating scales.

169 rom baseline in lipid and glucose levels and extrapyramidal symptom ratings.

170 ssessed by recording adverse events and with extrapyramidal symptom scales and electrocardiograms at

171 luded spontaneously reported adverse events, extrapyramidal symptom scores, serum prolactin concentra

172 Extrapyramidal symptom severity scores were 1.4 (95% CI=

173 The incidence of extrapyramidal symptom-related treatment-emergent advers

174 e risperidone and olanzapine groups reported extrapyramidal symptoms (24% and 20%, respectively).

175 One subject experienced moderate extrapyramidal symptoms (akasthisia) during RWJ-37796 in

176 or antipsychotic drugs which will not induce extrapyramidal symptoms (EPS) and tardive dyskinesias (T

177 ng there is a potential risk of exacerbating extrapyramidal symptoms (EPS) if H3R antagonists were us

178 regard to both the antipsychotic action and extrapyramidal symptoms (EPS) of antipsychotic drugs (AP

179 H] = 87), stroke (NNH = 53 for risperidone), extrapyramidal symptoms (NNH = 10 for olanzapine; NNH =

180 rrected QT-interval prolongation (p = 0.16), extrapyramidal symptoms (p = 0.31), excessive sedation (

181 ter TTR (SMD=-0.27) and a lower incidence of extrapyramidal symptoms (RR=0.31, NNH=7) compared with h

182 Extrapyramidal symptoms (Simpson-Angus Scale, Barnes Aka

183 Extrapyramidal symptoms and akathisia were similar in th

184 The incidence of extrapyramidal symptoms and changes in the levels of lip

185 nd because treatment is often accompanied by extrapyramidal symptoms and dyskinesias.

186 Safety and tolerability evaluations included extrapyramidal symptoms and effects on weight, prolactin

187 otic agents in producing significantly fewer extrapyramidal symptoms and having a lower risk of tardi

188 that has associated chronic cocaine use with extrapyramidal symptoms and striatal dopaminergic deplet

189 ated patients had a significant reduction in extrapyramidal symptoms and subjective measures of stiff

190 psychotic medications should be examined for extrapyramidal symptoms and tardive dyskinesia.

191 Three rating scales were used to assess extrapyramidal symptoms as well as the occurrence of adv

192 % of treated patients develop characteristic extrapyramidal symptoms caused by haloperidol-induced to

193 th anti-NMDA receptor antibodies both showed extrapyramidal symptoms following initiation of treatmen

194 and is necessary to reduce the expression of extrapyramidal symptoms induced by chronic haloperidol t

195 safe and effective antipsychotics devoid of extrapyramidal symptoms liability, sedation, and catalep

196 patients treated with OFC and fluoxetine in extrapyramidal symptoms or serious adverse events.

197 es carrying a single parkin mutation without extrapyramidal symptoms or signs also had psychiatric sy

198 atients with respect to prolactin elevation, extrapyramidal symptoms or weight gain.

199 rious side effects and significantly greater extrapyramidal symptoms relative to pimozide.

200 experienced statistically significantly more extrapyramidal symptoms than haloperidol-treated multipl

201 s of haloperidol produced significantly more extrapyramidal symptoms than placebo or sertindole.

202 at improvement in positive, negative, and/or extrapyramidal symptoms was associated with mood improve

203 Severity of extrapyramidal symptoms was low in both groups, with no

204 Severity of extrapyramidal symptoms was mild at baseline and through

205 hereas the incidence of QTc prolongation and extrapyramidal symptoms was similar between groups, more

206 ebo group (p = .60), and a global measure of extrapyramidal symptoms was similar between treatment gr

207 Extrapyramidal symptoms were assessed using the Simpson-

208 indistinguishable from placebo, and rates of extrapyramidal symptoms were not dose related.

209 f somnolence, weight gain, restlessness, and extrapyramidal symptoms were similar in the two groups.

210 The frequency and severity of extrapyramidal symptoms were similar in the two treatmen

211 Adverse events related to extrapyramidal symptoms were spontaneously reported by 1

212 in the domains of symptoms, quality of life, extrapyramidal symptoms, and a synthetic measure of mult

213 ant even after lifetime medication exposure, extrapyramidal symptoms, and abnormal involuntary moveme

214 Anticholinergic use, extrapyramidal symptoms, and estimated IQ had little eff

215 and negative symptoms, comorbid depression, extrapyramidal symptoms, and overall drug safety.

216 athy, clubfoot, absent deep tendon reflexes, extrapyramidal symptoms, and persistently deficient myel

217 events, laboratory parameters, vital signs, extrapyramidal symptoms, and suicidality.

218 ncluding weight gain, metabolic dysfunction, extrapyramidal symptoms, and tardive dyskinesia), especi

219 s on overall psychopathology, response rate, extrapyramidal symptoms, and tardive dyskinesia.

220 ol-treated patients experienced worsening of extrapyramidal symptoms, as indicated by several measure

221 scular events, as well as metabolic effects, extrapyramidal symptoms, falls, cognitive worsening, car

222 Safety measures included adverse events, extrapyramidal symptoms, laboratory assessments, and sui

223 se of atypical features, including exclusive extrapyramidal symptoms, normal eye movements, and norma

224 ignificant cognitive impairment, increase in extrapyramidal symptoms, or central anticholinergic effe

225 y differential effects on positive symptoms, extrapyramidal symptoms, or mood).

226 but not with age, gender, negative symptoms, extrapyramidal symptoms, or neuroleptic dose.

227 lactic benztropine) in compliance, symptoms, extrapyramidal symptoms, or overall quality of life, and

228 Although olanzapine is associated with fewer extrapyramidal symptoms, other side effects may offset t

229 iapine was well tolerated and did not induce extrapyramidal symptoms, sustained elevations of prolact

230 Measures of extrapyramidal symptoms, weight gain, and somnolence wer

231 owever, haloperidol carries a higher rate of extrapyramidal symptoms, whereas olanzapine is associate

232 oncentration correlated with the severity of extrapyramidal symptoms.

233 rates of dysphoria, depressive symptoms, and extrapyramidal symptoms.

234 t is clinically effective with a low risk of extrapyramidal symptoms.

235 mptoms of schizophrenia; quality of life; or extrapyramidal symptoms.

236 impson-Angus Rating Scale was used to assess extrapyramidal symptoms.

237 onventional antipsychotic agents in terms of extrapyramidal symptoms.

238 e apparently unrelated subjects with similar extrapyramidal symptoms.

239 renia (PNS), and minimal positive/depressive/extrapyramidal symptoms.

240 events and the use of medications related to extrapyramidal symptoms.

241 There was minimal risk of extrapyramidal symptoms.

242 isorders comprising cerebellar ataxia and/or extrapyramidal symptoms.

243 sedation, akathisia (for aripiprazole), and extrapyramidal symptoms.

244 dverse events at the injection site and more extrapyramidal symptoms.

245 performance and shows reduced liability for extrapyramidal symptoms.

246 toms without marked positive, depressive, or extrapyramidal symptoms.

247 tolerated and associated with a low rate of extrapyramidal symptoms; neither weight gain nor clinica

248 hisia Scale, and Modified Simpson-Angus [for Extrapyramidal Symptoms] Scale) and electromechanical as

249 ncluding cases with motor neuron disease and extrapyramidal syndromes.

250 us pain modulation system, the thalamus, the extrapyramidal system, non-noxious somatosensory systems

251 rological dichotomies (e.g. pyramidal versus extrapyramidal systems) from the perspective of modern a

252 d central nervous system (CNS) vasculitis to extrapyramidal to cognitive phenotypes.

253 Visual hallucinations, illusions and extrapyramidal tract signs were more frequent as clinica