ライフサイエンスコーパス: tardive

1 Patients aged 18-80 years with tardive dyskinesia (>/=3 months before screening) were r

2 e a greater cumulative 12-month incidence of tardive dyskinesia (36.9%).

3 Twenty patients with tardive dyskinesia (mean duration = 43.7 months) were vi

4 Tardive dyskinesia (TD) has no well-accepted treatments

5 VCMs) in rats is similar in many respects to tardive dyskinesia (TD) in humans.

6 induced by chronic haloperidol as a model of tardive dyskinesia (TD) in rats, we confirmed the antidy

7 There is controversy over whether tardive dyskinesia (TD) is solely a consequence of antip

8 extrapyramidal side effects (EPS), including tardive dyskinesia (TD).

9 They examined the cumulative incidence of tardive dyskinesia 1, 3, 6, 9, and 12 months after the i

10 uthors' goal was to compare the incidence of tardive dyskinesia among patients receiving olanzapine a

11 ence in the 12-month cumulative incidence of tardive dyskinesia among patients who had been neurolept

12 cumulative incidence of persistent emergent tardive dyskinesia among the 255 patients without dyskin

13 Patients assigned to clozapine had less tardive dyskinesia and fewer extrapyramidal side effects

14 which participates in antipsychotic-induced tardive dyskinesia and in levodopa-induced dyskinesia.

15 ditional targets are considered for treating tardive dyskinesia and negative and cognitive symptoms.

16 tardive dyskinesia or for the persistence of tardive dyskinesia and the associated structural changes

17 role of HP metabolites in the development of tardive dyskinesia are discussed.

18 arkinson's disease, Huntington's chorea, and tardive dyskinesia arise from an imbalance between these

19 The incidence of newly emergent tardive dyskinesia at any visit after baseline, at the f

20 ys of exposure) who did not have evidence of tardive dyskinesia at baseline.

21 short mean durations and use of nonstandard tardive dyskinesia definitions.

22 of protein-oxidized products associated with tardive dyskinesia did not pass Bonferroni correction, h

23 rences, 2% and 22%), and higher incidence of tardive dyskinesia for chlorpromazine versus clozapine (

24 The authors studied the risk of tardive dyskinesia for older patients in the early stage

25 The weighted mean annual incidence of tardive dyskinesia for second-generation antipsychotics

26 analysis (P<.001) and with lower symptoms of tardive dyskinesia in a secondary analysis including onl

27 The authors studied the incidence of tardive dyskinesia in elderly institutionalized patients

28 were to investigate the rate (incidence) of tardive dyskinesia in elderly patients beginning treatme

29 anched-chain amino acids in the treatment of tardive dyskinesia in men with psychiatric disorders was

30 The risk of tardive dyskinesia in older outpatients is high, even wi

31 nce-daily valbenazine significantly improved tardive dyskinesia in participants with underlying schiz

32 fficacy and tolerability in the treatment of tardive dyskinesia in phase 2 studies.

33 to identify risk factors for development of tardive dyskinesia in this age group.

34 yramidal symptoms and having a lower risk of tardive dyskinesia in vulnerable clinical populations at

35 Stratified by age, annual tardive dyskinesia incidence rates were 0.35% with secon

36 ed for 463 925 person-years), the annualized tardive dyskinesia incidence was 3.9% for second-generat

37 Tardive dyskinesia incidence was higher with second-gene

38 Lack of awareness of tardive dyskinesia is a common feature in schizophrenia

39 Tardive dyskinesia is a movement disorder affecting 20%-

40 Tardive dyskinesia is a persistent movement disorder ind

41 Tardive dyskinesia is a serious and common complication

42 measure was a frequency count of videotaped tardive dyskinesia movements.

43 g > or =1 year and reporting on new cases of tardive dyskinesia or dyskinesia were systematically rev

44 thesis cannot account for the time course of tardive dyskinesia or for the persistence of tardive dys

45 Forty-three patients with schizophrenia and tardive dyskinesia participated in the study.

46 Tardive dyskinesia patients had significantly higher con

47 8, age 41.2 years, 71.2% male, 62.0% white), tardive dyskinesia prevalence rates were 13.1% for secon

48 Differences in tardive dyskinesia rates between diagnostic groups found

49 Tardive dyskinesia rates for patients beginning treatmen

50 To provide an update on tardive dyskinesia rates in patients treated with first-

51 Tardive dyskinesia results from exposure to dopamine rec

52 Current evidence supports a lower tardive dyskinesia risk for second-generation antipsycho

53 e correlations observed between decreases in tardive dyskinesia symptoms and decreases in aromatic am

54 Tardive dyskinesia symptoms correlated positively with m

55 ived placebo (N=18) in the percent change in tardive dyskinesia symptoms from baseline to the end of

56 The reduction in tardive dyskinesia symptoms in the amino acids group was

57 Patients were also rated for tardive dyskinesia symptoms with the Abnormal Involuntar

58 the >/=30% and >/=60% levels of decrease in tardive dyskinesia symptoms.

59 on antipsychotics are expected to cause less tardive dyskinesia than first-generation antipsychotics.

60 showed significantly less awareness of their tardive dyskinesia than patients without the deficit syn

61 e (N = 87), the mean cumulative incidence of tardive dyskinesia was 3.4% and 5.9% at 1 and 3 months,

62 A greater risk of tardive dyskinesia was associated with history of ECT tr

63 Persistent emergent tardive dyskinesia was defined according to scores on th

64 Awareness of tardive dyskinesia was only modestly related to two of t

65 Lack of awareness of tardive dyskinesia was stable over time.

66 The cumulative rates of tardive dyskinesia were 25%, 34%, and 53% after 1, 2, an

67 Patients with tardive dyskinesia were prohibited from assignment to pe

68 hotic treatment and presumably long-standing tardive dyskinesia were randomly assigned to receive bra

69 t Scale and research diagnostic criteria for tardive dyskinesia were used to define the comparative i

70 aspartate in their CSF than patients without tardive dyskinesia when age and neuroleptic dose were co

71 One hundred fifty-eight subjects with tardive dyskinesia who were receiving neuroleptic medica

72 e potential of a significantly lower risk of tardive dyskinesia with olanzapine than with haloperidol

73 group, the observed incidence of persistent tardive dyskinesia with risperidone seemed to be much lo

74 e found to be beneficial in the treatment of tardive dyskinesia, although this finding was not confir

75 including weight gain and the possibility of tardive dyskinesia, are reviewed.

76 tress and glutamatergic neurotransmission in tardive dyskinesia, both of which may be relevant to the

77 ation antipsychotics have a reduced risk for tardive dyskinesia, compared to first-generation antipsy

78 acids constitute a novel, safe treatment for tardive dyskinesia, with a strong potential for providin

79 6 mg/day provided a significant reduction in tardive dyskinesia, with favourable safety and tolerabil

80 r a mood disorder who had moderate or severe tardive dyskinesia.

81 lerability of valbenazine as a treatment for tardive dyskinesia.

82 ch may be relevant to the pathophysiology of tardive dyskinesia.

83 idence rates of long-term treatment-emergent tardive dyskinesia.

84 term effects of valbenazine in patients with tardive dyskinesia.

85 Symptom Rating Scale scores and no cases of tardive dyskinesia.

86 be examined for extrapyramidal symptoms and tardive dyskinesia.

87 ) receptor polymorphism on susceptibility to tardive dyskinesia.

88 mented the efficacy of vitamin E in treating tardive dyskinesia.

89 or efficacy of vitamin E in the treatment of tardive dyskinesia.

90 its inferences about adverse effects such as tardive dyskinesia.

91 response rate, extrapyramidal symptoms, and tardive dyskinesia.

92 linical symptoms, and occurrence of incident tardive dyskinesia.

93 tus has been implicated as a risk factor for tardive dyskinesia.

94 as Parkinson disease, Alzheimer disease, and tardive dyskinesia.

95 in AIMS scores for patients with refractory tardive dyskinesia.

96 al examination is required to identify early tardive dyskinesia.

97 s had at least moderate unawareness of their tardive dyskinesia.

98 4% versus 53%) and significantly less severe tardive dyskinesia.

99 otentially contribute to the pathogenesis of tardive dyskinesia.

100 , conceptual disorganization, akathisia, and tardive dyskinesia.

101 authors studied the use of tetrabenazine for tardive dyskinesia.

102 patients with schizophrenia, 11 of whom had tardive dyskinesia.

103 ine transporter-2 inhibitor-in patients with tardive dyskinesia.

104 extrapyramidal side effects, akathisia, and tardive dyskinesia; 7) cataracts; and 8) myocarditis.

105 not induce extrapyramidal symptoms (EPS) and tardive dyskinesias (TDs).

106 on, the question as to whether patients with tardive dystonia have an underlying vulnerability remain

107 suggesting that the pathogenetic changes in tardive dystonia may become irreversible after long-term

108 picture, risk factors and natural history of tardive dystonia resulting from dopamine-receptor antago

109 Overall, the phenomenology of tardive dystonia was indistinguishable from that of prim

110 uroleptics used were implicated in producing tardive dystonia, which was found to develop at any time

111 have also been reported for DBS treatment of tardive dystonia, writer's cramp, cranial dystonia, myoc

112 the right, were significantly more common in tardive dystonia.

113 ical neuroleptic drugs can lead to abnormal, tardive movements that persist long after the drugs are

114 orbidities misinterpreted as bradykinesia, a tardive syndrome related to undisclosed previous neurole

115 ic tremor, peripheral trauma-induced tremor, tardive tremor and rabbit syndrome, paroxysmal tremors (