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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) can occur in people exposed to d
5                                              Tardive dyskinesia (TD) has no well-accepted treatments
6 VCMs) in rats is similar in many respects to tardive dyskinesia (TD) in humans.
7 induced by chronic haloperidol as a model of tardive dyskinesia (TD) in rats, we confirmed the antidy
8            There is controversy over whether tardive dyskinesia (TD) is solely a consequence of antip
9 zine therapeutic effects in the treatment of tardive dyskinesia (TD).
10 extrapyramidal side effects (EPS), including tardive dyskinesia (TD).
11    They examined the cumulative incidence of tardive dyskinesia 1, 3, 6, 9, and 12 months after the i
12 uthors' goal was to compare the incidence of tardive dyskinesia among patients receiving olanzapine a
13 ence in the 12-month cumulative incidence of tardive dyskinesia among patients who had been neurolept
14  cumulative incidence of persistent emergent tardive dyskinesia among the 255 patients without dyskin
15      Patients assigned to clozapine had less tardive dyskinesia and fewer extrapyramidal side effects
16  which participates in antipsychotic-induced tardive dyskinesia and in levodopa-induced dyskinesia.
17 ditional targets are considered for treating tardive dyskinesia and negative and cognitive symptoms.
18 tardive dyskinesia or for the persistence of tardive dyskinesia and the associated structural changes
19 role of HP metabolites in the development of tardive dyskinesia are discussed.
20 arkinson's disease, Huntington's chorea, and tardive dyskinesia arise from an imbalance between these
21              The incidence of newly emergent tardive dyskinesia at any visit after baseline, at the f
22 ys of exposure) who did not have evidence of tardive dyskinesia at baseline.
23  short mean durations and use of nonstandard tardive dyskinesia definitions.
24 of protein-oxidized products associated with tardive dyskinesia did not pass Bonferroni correction, h
25 rences, 2% and 22%), and higher incidence of tardive dyskinesia for chlorpromazine versus clozapine (
26              The authors studied the risk of tardive dyskinesia for older patients in the early stage
27        The weighted mean annual incidence of tardive dyskinesia for second-generation antipsychotics
28 analysis (P<.001) and with lower symptoms of tardive dyskinesia in a secondary analysis including onl
29 horea associated with Huntington disease and tardive dyskinesia in adults.
30         The authors studied the incidence of tardive dyskinesia in elderly institutionalized patients
31  were to investigate the rate (incidence) of tardive dyskinesia in elderly patients beginning treatme
32 anched-chain amino acids in the treatment of tardive dyskinesia in men with psychiatric disorders was
33                                  The risk of tardive dyskinesia in older outpatients is high, even wi
34 nce-daily valbenazine significantly improved tardive dyskinesia in participants with underlying schiz
35 fficacy and tolerability in the treatment of tardive dyskinesia in phase 2 studies.
36  to identify risk factors for development of tardive dyskinesia in this age group.
37 yramidal symptoms and having a lower risk of tardive dyskinesia in vulnerable clinical populations at
38                    Stratified by age, annual tardive dyskinesia incidence rates were 0.35% with secon
39 ed for 463 925 person-years), the annualized tardive dyskinesia incidence was 3.9% for second-generat
40                                              Tardive dyskinesia incidence was higher with second-gene
41                         Lack of awareness of tardive dyskinesia is a common feature in schizophrenia
42                                              Tardive dyskinesia is a movement disorder affecting 20%-
43                                              Tardive dyskinesia is a persistent movement disorder ind
44                                              Tardive dyskinesia is a serious and common complication
45  measure was a frequency count of videotaped tardive dyskinesia movements.
46 g > or =1 year and reporting on new cases of tardive dyskinesia or dyskinesia were systematically rev
47 thesis cannot account for the time course of tardive dyskinesia or for the persistence of tardive dys
48  Forty-three patients with schizophrenia and tardive dyskinesia participated in the study.
49                                              Tardive dyskinesia patients had significantly higher con
50 8, age 41.2 years, 71.2% male, 62.0% white), tardive dyskinesia prevalence rates were 13.1% for secon
51                               Differences in tardive dyskinesia rates between diagnostic groups found
52                                              Tardive dyskinesia rates for patients beginning treatmen
53                      To provide an update on tardive dyskinesia rates in patients treated with first-
54                                              Tardive dyskinesia results from exposure to dopamine rec
55            Current evidence supports a lower tardive dyskinesia risk for second-generation antipsycho
56 e correlations observed between decreases in tardive dyskinesia symptoms and decreases in aromatic am
57                                              Tardive dyskinesia symptoms correlated positively with m
58 ived placebo (N=18) in the percent change in tardive dyskinesia symptoms from baseline to the end of
59                             The reduction in tardive dyskinesia symptoms in the amino acids group was
60                 Patients were also rated for tardive dyskinesia symptoms with the Abnormal Involuntar
61  the >/=30% and >/=60% levels of decrease in tardive dyskinesia symptoms.
62 on antipsychotics are expected to cause less tardive dyskinesia than first-generation antipsychotics.
63 showed significantly less awareness of their tardive dyskinesia than patients without the deficit syn
64 e (N = 87), the mean cumulative incidence of tardive dyskinesia was 3.4% and 5.9% at 1 and 3 months,
65                            A greater risk of tardive dyskinesia was associated with history of ECT tr
66                          Persistent emergent tardive dyskinesia was defined according to scores on th
67                                 Awareness of tardive dyskinesia was only modestly related to two of t
68                         Lack of awareness of tardive dyskinesia was stable over time.
69                      The cumulative rates of tardive dyskinesia were 25%, 34%, and 53% after 1, 2, an
70                                Patients with tardive dyskinesia were prohibited from assignment to pe
71 hotic treatment and presumably long-standing tardive dyskinesia were randomly assigned to receive bra
72 t Scale and research diagnostic criteria for tardive dyskinesia were used to define the comparative i
73 aspartate in their CSF than patients without tardive dyskinesia when age and neuroleptic dose were co
74        One hundred fifty-eight subjects with tardive dyskinesia who were receiving neuroleptic medica
75 tential for significant side effects such as tardive dyskinesia with long-term therapy, levodopa/carb
76 e potential of a significantly lower risk of tardive dyskinesia with olanzapine than with haloperidol
77  group, the observed incidence of persistent tardive dyskinesia with risperidone seemed to be much lo
78 ic dysfunction, extrapyramidal symptoms, and tardive dyskinesia), especially with long-term use.
79 e found to be beneficial in the treatment of tardive dyskinesia, although this finding was not confir
80 ls ineligible owing to treatment resistance, tardive dyskinesia, and history of suicide attempts.
81 t disorders, including Huntington's disease, tardive dyskinesia, and Tourette's syndrome.
82 including weight gain and the possibility of tardive dyskinesia, are reviewed.
83 tress and glutamatergic neurotransmission in tardive dyskinesia, both of which may be relevant to the
84 ation antipsychotics have a reduced risk for tardive dyskinesia, compared to first-generation antipsy
85 acids constitute a novel, safe treatment for tardive dyskinesia, with a strong potential for providin
86 6 mg/day provided a significant reduction in tardive dyskinesia, with favourable safety and tolerabil
87 ch may be relevant to the pathophysiology of tardive dyskinesia.
88 idence rates of long-term treatment-emergent tardive dyskinesia.
89 horea associated with Huntington disease and tardive dyskinesia.
90 ine transporter-2 inhibitor-in patients with tardive dyskinesia.
91 cern about long-term adverse effects such as tardive dyskinesia.
92  (VMAT2) inhibitor approved for treatment of tardive dyskinesia.
93 lerability of valbenazine as a treatment for tardive dyskinesia.
94 r a mood disorder who had moderate or severe tardive dyskinesia.
95  Symptom Rating Scale scores and no cases of tardive dyskinesia.
96  be examined for extrapyramidal symptoms and tardive dyskinesia.
97 ) receptor polymorphism on susceptibility to tardive dyskinesia.
98 mented the efficacy of vitamin E in treating tardive dyskinesia.
99 or efficacy of vitamin E in the treatment of tardive dyskinesia.
100 its inferences about adverse effects such as tardive dyskinesia.
101  response rate, extrapyramidal symptoms, and tardive dyskinesia.
102 linical symptoms, and occurrence of incident tardive dyskinesia.
103 term effects of valbenazine in patients with tardive dyskinesia.
104 tus has been implicated as a risk factor for tardive dyskinesia.
105 as Parkinson disease, Alzheimer disease, and tardive dyskinesia.
106  in AIMS scores for patients with refractory tardive dyskinesia.
107 al examination is required to identify early tardive dyskinesia.
108 s had at least moderate unawareness of their tardive dyskinesia.
109 4% versus 53%) and significantly less severe tardive dyskinesia.
110 otentially contribute to the pathogenesis of tardive dyskinesia.
111 , conceptual disorganization, akathisia, and tardive dyskinesia.
112 authors studied the use of tetrabenazine for tardive dyskinesia.
113  patients with schizophrenia, 11 of whom had tardive dyskinesia.
114  extrapyramidal side effects, akathisia, and tardive dyskinesia; 7) cataracts; and 8) myocarditis.
115 not induce extrapyramidal symptoms (EPS) and tardive dyskinesias (TDs).
116 f abuse, depression, Alzheimer's disease and tardive dyskinesias, and mediates subsequent long-term n
117 on, the question as to whether patients with tardive dystonia have an underlying vulnerability remain
118  suggesting that the pathogenetic changes in tardive dystonia may become irreversible after long-term
119 picture, risk factors and natural history of tardive dystonia resulting from dopamine-receptor antago
120                Overall, the phenomenology of tardive dystonia was indistinguishable from that of prim
121 uroleptics used were implicated in producing tardive dystonia, which was found to develop at any time
122 have also been reported for DBS treatment of tardive dystonia, writer's cramp, cranial dystonia, myoc
123 the right, were significantly more common in tardive dystonia.
124 ical neuroleptic drugs can lead to abnormal, tardive movements that persist long after the drugs are
125 orbidities misinterpreted as bradykinesia, a tardive syndrome related to undisclosed previous neurole
126 ally debilitating side-effects, most notably tardive syndromes and parkinsonism, as well as potential
127 ics and specific therapies for the different tardive syndromes and the treatment of drug-induced park
128 tetrabenazine, the first drugs indicated for tardive syndromes, have improved outcomes for many patie
129 ic tremor, peripheral trauma-induced tremor, tardive tremor and rabbit syndrome, paroxysmal tremors (

 
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