ライフサイエンスコーパス: tic

1 Information on 29 tic symptoms was elicited.

2 Attrition was low (12/126, or 9.5%); tic worsening was reported by 4% of children (5/126).

3 io, 7.6; 95% confidence interval, 2.0-26.5), tic disorders (8.4; 2.4-29.6), and obsessive-compulsive

4 1.1%]; adjusted RR, 11.8; 95% CI, 9.4-14.7), tic disorders (28 cases [0.8%] vs 24 controls [0.2%]; ad

5 10.4 years) with ADHD, combined type, and a tic disorder participated.

6 iagnostic criteria: presence of OCD and/or a tic disorder, prepubertal symptom onset, episodic course

7 ese findings suggest that comorbidity with a tic disorder has a limited effect on ADHD outcome.

8 In addition, tic disorders were not associated with stimulant use.

9 This study thus shows that, although tics originate in the striatum, their timing depends on

10 IRR, 1.51; 95% CI, 1.28-1.77; P < .001) and tic disorders (n = 993; IRR, 1.35; 95% CI, 1.21-1.50; P

11 isorder (OR, 3.4; CI, 1.3-8.7; P = .02), and tic disorders (OR, 8.7; CI, 1.3-57.7; P = .02).

12 ming based on incoming cortical activity and tic history.

13 ming based on incoming cortical activity and tic history.

14 To evaluate the impact of comorbid ADHD and tic disorders from a lifespan perspective, the authors s

15 We rated ADHD and tic symptoms weekly and monitored adverse effects, labor

16 on-deficit/hyperactivity disorder (ADHD) and tic disorders.

17 Attention-deficit/hyperactivity disorder and tic disorders appeared to be independent in course: in c

18 disorders (obsessive-compulsive disorder and tic disorders) associated with streptococcal infections

19 ing the propensity for both tic learning and tic expression, respectively.

20 and to determine which children with OCD and tic disorders will benefit from immunomodulatory therapi

21 sk of mental disorders, specifically OCD and tic disorders, after a streptococcal throat infection.

22 ks of mental disorders, particularly OCD and tic disorders.

23 or children with infection-triggered OCD and tic disorders.

24 t of obsessive-compulsive disorder (OCD) and tic disorders, a concept termed pediatric autoimmune neu

25 with obsessive-compulsive disorder (OCD) and tic disorders, designated as pediatric autoimmune neurop

26 um is involved in the pathogenesis of TS and tic-related OCD.

27 may contribute to the habitual behaviour and tics of this syndrome.

28 sm and modulation of Tourette's syndrome and tics.

29 re involved in the pathophysiology of TS and tics.

30 effects were countered by the benchmark anti-tic therapy haloperidol (0.3 mg/kg, IP).

31 Absence of ideal anti-tic drugs, combined with knowledge that uncomplicated ca

32 emi-involuntary behaviors, whether these are tics or eye blinks.

33 ymptoms of motor disinhibition presenting as tics and psychiatric manifestations, such as attention d

34 can disinhibit automatic behaviors, such as tics in Tourette syndrome.

35 I activities were analysed 2 s before and at tic onset irrespective of the clinical phenomenology.

36 perculum (PO) predominantly activated before tic onset (P < 0.05, corrected for multiple comparisons)

37 hereby also reducing the propensity for both tic learning and tic expression, respectively.

38 ost effective target for DBS to control both tics and associated comorbidities, and further clarify f

39 ourette's syndrome severity as determined by tic severity and rates of commonly comorbid disorders su

40 Tourette syndrome (TS) is characterized by tics, sensorimotor gating deficiencies, and abnormalitie

41 a Tourette syndrome (TS) is characterized by tics, which are transiently worsened by stress, acute ad

42 reotyped movements and vocalizations called 'tics'.

43 ing the role of the basal ganglia in causing tics and Tourette syndrome.

44 to examine whether PPI deficits characterize tic-related OCD.

45 motor and vocal behaviors that characterize tics in TS, as well as for the urges that often accompan

46 We characterized tic disorders along with a wide range of neuropsychiatri

47 disorders include tremors, dystonia, chorea, tics, myoclonus, stereotypies, restless legs syndrome, a

48 Other than chorea, tics and obsessive-compulsive disorder, which constitute

49 ity among children with Tourette and chronic tic disorder.

50 including Tourette syndrome (TS) and chronic tic disorders (CTDs), are assumed to be strongly familia

51 increase the risk of Tourette's and chronic tic disorders (TD/CTD), but previous studies have been u

52 ittle data concerning Tourette's and chronic tic disorders (TD/CTD).

53 D patients with and without comorbid chronic tic disorders or schizotypal personality disorder may re

54 monotherapy; patients with comorbid chronic tic disorders showed a preferential response.

55 This may be a consequence of chronic tic control in these patients, or a known fronto-striata

56 th and without comorbid diagnoses of chronic tic disorder or schizotypal personalty disorder.

57 sorder and/or Tourette's syndrome or chronic tic disorder and 21 healthy comparison subjects were eva

58 17 years, with impairing Tourette or chronic tic disorder as a primary diagnosis, randomly assigned t

59 ulsive disorder (OCD) and Tourette's/chronic tic disorders (TD/CTD) with autoimmune diseases (ADs) is

60 Tourette syndrome/chronic tic disorder (TS/CT) and obsessive-compulsive disorder (

61 ree with 7 showing Tourette syndrome/chronic tic phenotype (TS-CTD) were evaluated with whole exome s

62 on the best therapeutic approach to chronic tic disorders and comorbid attention-deficit/hyperactivi

63 oms in children and adolescents with chronic tic disorders and ADHD diagnoses.

64 ent of children and adolescents with chronic tic disorders and comorbid ADHD.

65 ty-one children and adolescents with chronic tic disorders, including Tourette disorder and comorbid

66 and OFCC1 genes that segregated with chronic tic phenotype.

67 lated phenotypic spectrum, including chronic tics (CT) and Obsessive Compulsive Disorder (OCD), are g

68 ith co-occurring Tourette's syndrome/chronic tics may have different underlying genetic susceptibilit

69 and co-occurring Tourette's syndrome/chronic tics were included in the analysis (p=0.01).

70 79 with OCD plus Tourette's syndrome/chronic tics), 5,667 ancestry-matched controls, and 290 OCD pare

71 ics (i.e. age of onset, presence of comorbid tics, positive family history) and symptom theme, with p

72 cuits may result in their failure to control tic behaviors or the premonitory urges that generate the

73 efrontal excitation, thus helping to control tics and possibly contributing to the cortical hyperexci

74 out the need for follow-up invasive, diagnos tic, or therapeutic interventional procedures.

75 mance or personality traits in singers drive tic development, could also be true.

76 , frequency of, and radiotracer input during tics in each of 72 scans from 6 patients with TS.

77 ne of the many stressors that can exacerbate tic/Tourette's or OCD in a subset of such patients.

78 Therefore, we examined tic disorders in an ongoing prospective follow-up study

79 a fertile ground of motor hyperactivity for tic learning.

80 DA, which produce increased propensities for tic learning and expression, respectively.

81 ay counter both the increased propensity for tic expression, by increasing excitability in the indire

82 ct pathway, and the increased propensity for tic learning, by shifting plasticity in the indirect pat

83 The risk for tic disorders among relatives of probands with tic disor

84 ndividuals with ADHD are at greater risk for tic disorders, the presence of tic disorders has a limit

85 blings, and offspring) had similar risks for tic disorders despite different degrees of shared enviro

86 y early age (mean = 6.3 years, SD = 2.7, for tics; mean = 7.4 years, SD = 2.7, for OCD).

87 There is no cure for tics, and symptomatic therapy includes behavioral and ph

88 of comprehensive behavioral intervention for tics or 8 sessions of supportive treatment for 10 weeks.

89 Medications for tics are often effective but can cause adverse effects.

90 atients required ongoing pharmacotherapy for tics after surgery, and patients improved significantly

91 circuit-based neural mechanisms that govern tic generation in Tourette's syndrome.

92 ADHD (12%) than those without ADHD (4%) had tic disorders.

93 Heightened tic severity was also associated with greater engagement

94 Behaviourally, higher tic severity was correlated with slower task performance

95 Neurally, higher tic severity was associated with enhanced activation of

96 s elements, including chorea, hyperactivity, tics, emotional lability, and obsessive-compulsive sympt

97 me adult patients continue to have impairing tics.

98 support the involvement of the cerebellum in tic production; (iii) furnishes predictions on the amoun

99 sociation areas are critically implicated in tic generation, similar to movements triggered internall

100 Ten patients (91%) reported improvement in tic severity soon after DBS.

101 mulation led to a significant improvement in tic severity, with an overall acceptable safety profile.

102 ert with basal ganglia, are also involved in tic production.

103 eal musculature that is commonly involved in tic symptoms.

104 robust clinically significant reductions in tic and ADHD symptoms in children and adolescents with c

105 tacts, and programming settings resulting in tic suppression were commonly associated with a subjecti

106 anglia-cerebellar-thalamo-cortical system in tic generation; (ii) suggests an explanation of the syst

107 nglia networks, which are likely involved in tics and behavioural expressions of Gilles de la Tourett

108 syndrome and other tic disorders results in tics due to cortical activation of the abnormal striatal

109 evalence of comorbid difficulties, including tics, obsessive-compulsive behaviors, and attention defi

110 oking was strongly correlated with increased tic severity and with the presence of comorbid OCD in th

111 a moderate environmental stressor, increases tic-like responses and elicits TS-like sensorimotor gati

112 ased regional volumes accompanied increasing tic symptom severity and motoric disinhibition as demons

113 tivation determined the timing of individual tics via an accumulation process of inputs that was depe

114 vity in determining the timing of individual tics.

115 factors underlying the timing of individual tics.

116 to rule out the possibility of drug-induced tic exacerbation in individual patients.

117 hat patients have in suppressing involuntary tics.

118 e pathophysiology underlying the involuntary tics of Gilles de la Tourette syndrome (GTS) remains unk

119 DA amplifies the tendency to execute learned tics and also provides a fertile ground of motor hyperac

120 Lifetime tic symptom data were obtained from direct structured in

121 essarily all) children with mild to moderate tic disorder.

122 ith controls, subjects with ADHD showed more tic disorders at baseline and more new onsets were repor

123 mary motor cortex and are predicted by motor tic severity and white-matter microstructure (FA) within

124 the system-level mechanisms underlying motor tic production: in this respect, the model predicts that

125 Motor tics are a cardinal feature of Tourette syndrome and are

126 al disorder characterized by vocal and motor tics and associated with cortical-striatal-thalamic-cort

127 ic disorder characterized by vocal and motor tics.

128 der characterized by chronic vocal and motor tics.

129 ined by the presence of both vocal and motor tics.

130 r-thalamo-cortical system to study how motor tics are generated in Tourette syndrome.

131 Overall, there was a 48% reduction in motor tics and a 56.5% reduction in phonic tics at final follo

132 rome (TS) is characterized by multiple motor tics plus one or more vocal (phonic) tics, which charact

133 trongly associated with the genesis of motor tics in TS--are paradoxically elevated in individuals wi

134 isinhibition leads to the formation of motor tics resembling those expressed during Tourette syndrome

135 here was no evidence (group data) that motor tics or vocal tics changed in frequency or severity duri

136 in sensorimotor cortex was noted with motor tics.

137 or system to produce a surplus of movements (tics) and high performance (exquisite singing).

138 rtal children with ADHD and chronic multiple tic disorder (who had participated in an 8-week, double-

139 ychiatric disorder characterized by multiple tics and sensorimotor abnormalities, the severity of whi

140 y use of standard assessment scales for OCD, tics, anxiety, depression, and global function.

141 re than 85% of clinical exacerbations in OCD/tic behavior in patients who met criteria for PANDAS had

142 lable way to ensure hepaative application of tic protection.

143 ion adjustments and objective assessments of tic severity until database lock 1 month after the final

144 In contrast, at the beginning of tic action, significant fMRI activities were found in se

145 MAYA, which encodes a version of the game of tic-tac-toe and interactively competes against a human o

146 The heritability of tic disorders was estimated to be 0.77 (95% CI, 0.70-0.8

147 ing was used to estimate the heritability of tic disorders.

148 The impact of tic disorders on the outcome of attention deficit hypera

149 mpulsive disorder and for the persistence of tic symptoms into adulthood.

150 tic generation and enabled the prediction of tic timing based on incoming cortical activity and tic h

151 tic generation and enabled the prediction of tic timing based on incoming cortical activity and tic h

152 ater risk for tic disorders, the presence of tic disorders has a limited impact on ADHD outcome.

153 factors affecting the temporal properties of tic expression are still unknown.

154 losely replicated the temporal properties of tic generation and enabled the prediction of tic timing

155 losely replicated the temporal properties of tic generation and enabled the prediction of tic timing

156 drome, which leads to impaired regulation of tic behaviors.

157 prefrontal hypertrophy in the regulation of tic symptoms, the current findings suggest that neural p

158 ng correlated inversely with the severity of tic symptoms across both samples (r = -0.34; P = .01).

159 ignificantly associated with the severity of tic symptoms in orbitofrontal, midtemporal, and parieto-

160 The severity of tic symptoms in the Tourette group correlated inversely

161 s correlated positively with the severity of tic symptoms.

162 cal relevance in determining the severity of tic symptoms.

163 help to modulate the course and severity of tic symptoms.

164 correlated with measures of the severity of tic symptoms.

165 us correlated inversely with the severity of tic symptoms.

166 ns correlated inversely with the severity of tic, obsessive-compulsive disorder, and attention-defici

167 correlate significantly with the severity of tic, obsessive-compulsive disorder, or attention-deficit

168 resents the most severe end of a spectrum of tic disorders that, in aggregate, affect approximately 5

169 dence supporting the theory that symptoms of tic disorders or obsessive-compulsive disorder (OCD) may

170 d rate of ADHD remission was 20% and that of tic remission, 65%.

171 cological interventions for the treatment of tic disorders.

172 (iii) furnishes predictions on the amount of tics generated when striatal dopamine increases and when

173 udy, we aimed to explore the neural basis of tics in patients with Tourette syndrome by using event-r

174 n hypothesized to bring about the control of tics during adolescence.

175 ttle is known about the neural correlates of tics and associated urges.

176 The neural correlates of tics are not well understood and have not been imaged se

177 In children, exacerbations of tics and obsessive symptoms may occur after infection wi

178 have an important role in the expression of tics, and a poststreptococcal autoimmune cause has been

179 The generation of tics was limited by absolute and relative tic refractory

180 cating these structures in the generation of tics.

181 ndicated that OCD patients with a history of tics had lower levels of PPI.

182 suggest that OCD patients with a history of tics may have greater impairment in sensorimotor gating

183 ons, absence childhood and family history of tics, inability to suppress the movements and coexistenc

184 se findings suggest that the pathogenesis of tics involves an impaired modulation of neuronal activit

185 choir's enchantment, the sole perception of tics as a disorder falls short of the properties of the

186 Persistence of tics beyond young adulthood and a previous suicide attem

187 ains specifiers to delineate the presence of tics and degree of insight.

188 actors underlying the temporal properties of tics expressed in Tourette syndrome and other tic disord

189 ity suggests that the number and severity of tics are a function of the degree to which the system fo

190 motor circuits to attenuate the severity of tics.

191 o be engaged in the voluntary suppression of tics.

192 ex during the acute voluntary suppression of tics.

193 the SMA, that may lead to the suppression of tics.

194 nglia are thought to produce the symptoms of tics, obsessive-compulsive disorder, and attention-defic

195 ve effects of which commonly exceed those of tics.

196 cortical activation determined the timing of tics but did not determine their form.

197 a compensatory and neuromodulatory effect on tic-related symptoms.

198 the anteromedial globus pallidus interna on tic severity and common comorbidities.

199 Tourette syndrome (TS) is a childhood-onset tic disorder associated with abnormal development of bra

200 ildren with obsessive-compulsive disorder or tic disorders occurring in association with streptococca

201 ns of obsessive-compulsive disorder (OCD) or tic disorders, including Tourette syndrome, were randoml

202 a diagnosis of any mental disorder, OCD, or tic disorders.

203 presumed streptococcus-associated OCD and/or tics and 82 healthy comparison children who were matched

204 h obsessive-compulsive disorder (OCD) and/or tics believed to be associated with streptococcal infect

205 ren with streptococcus-associated OCD and/or tics than in the healthy children.

206 istinct subgroup of subjects with OCD and/or tics who have enlarged basal ganglia.

207 tween obsessive-compulsive disorder (OCD) or tics/Tourette's syndrome in childhood to antecedent grou

208 can help to differentiate them from organic tics.

209 ics expressed in Tourette syndrome and other tic disorders have eluded clinicians and scientists for

210 ition typical of Tourette syndrome and other tic disorders results in tics due to cortical activation

211 expressed during Tourette syndrome and other tic disorders.

212 ibility of an overrepresentation of perioral tics in this group of highly achieving young vocal artis

213 ients, particularly in those with persistent tics, history of suicide attempts, and psychiatric comor

214 01), with equal response in motor and phonic tic symptoms (P<.01 for both).

215 gumentativeness), 2) purely motor and phonic tic symptoms, 3) compulsive phenomena (e.g., touching of

216 al score (-5.8 [2.9]; P=.01); and the phonic tic severity score (-2.2 [2.6]; P=.04).

217 s characterized by multiple motor and phonic tics and high comorbidity rates with other neurobehavior

218 the presence of fluctuating motor and phonic tics.

219 haracterized by involuntary motor and phonic tics.

220 the presence of involuntary motor and phonic tics.

221 n motor tics and a 56.5% reduction in phonic tics at final follow-up.

222 multiple motor and one or more vocal/phonic tics.

223 e motor tics plus one or more vocal (phonic) tics, which characteristically wax and wane.

224 odevelopmental approach to the pre- and post-tic sensorimotor urges, and (2) the TS treatment with de

225 Hdc knockout mice exhibited potentiated tic-like stereotypies, recapitulating core phenomenology

226 eps minor (FM) WM that significantly predict tic severity in TS.

227 the striatum and the timing of the previous tic.

228 The probands' tic symptoms were grouped by using agglomerative hierarc

229 d 9 patients (five females) with psychogenic tics representing 4.9% of all 184 patients first evaluat

230 A single dose of nicotine reduced tic severity as assessed by blind video scoring in the m

231 Likewise, desipramine significantly reduced tic symptoms (Yale Global Tic Severity Scale; 30% decrea

232 of tics was limited by absolute and relative tic refractory periods that were derived from an interna

233 in contrast to low rates of ADHD remission, tic disorders mostly remitted.

234 ither very small or based on parent-reported tics in population-based (nonclinical) twin samples.

235 Movements resembling tics are observed in a small proportion of patients with

236 nce and clinical features of PMDs resembling tics during the last 3.5 years in our centre.

237 ourette syndrome, those with PMDs resembling tics were older: 36.3 versus 18.7 years (p=0.014) at pre

238 The resulting tics and their neuronal representation within the striat

239 ity in these regions accompanied more severe tic symptoms, suggesting that faulty activity in these c

240 e sensorimotor putamen predicted more severe tics.

241 bitual responses correlated with more severe tics.

242 first-line treatments for moderate to severe tics, are often associated with adverse effects.

243 illes de la Tourette syndrome (TS), who show tic-like movements, are impaired in grip-load force cont

244 son subjects during spontaneous or simulated tics.

245 Subjects from a specialty tic disorders clinic were randomly assigned to receive 8

246 premonitory urges that generate spontaneous tic behaviors.

247 ndrome group was stronger during spontaneous tics than during voluntary tics in the somatosensory and

248 uppression of voluntary movement rather than tics was required during a Go-NoGo task.

249 responses; we also review the evidence that tics engage the habit-learning circuitry.

250 Our findings, taken together, suggest that tics are caused by the combined effects of excessive act

251 the basis of these findings, we suggest that tics are exaggerated, maladaptive, and persistent motor

252 s, our observations strengthen the view that tics may be related to motor learning.

253 The tic response rate was substantial (58% vs 5%; desipramin

254 both the deficits in habit learning and the tic symptoms of TS are likely to be consequences of the

255 Thus, the precise time of the tic expression depends on the interaction between the su

256 This informal observational study on the tic prevalence in 40 young singers was carried out durin

257 ircadian-gated process, and as a result, the tic mutant is defective in rhythmic JA responses to path

258 We showed that the tic mutant is hypersensitive to growth-repressive effect

259 tical activity contributes to triggering the tic event and that the recently discovered basal ganglia

260 ute, respectively, to the development of the tics of Tourette's syndrome, the obsessions of OCD, the

261 terns of neural activity associated with the tics.

262 allowed the spontaneous expression of their tics.

263 The spatial properties of these tics are dependent on the location of the focal disinhib

264 The functional abnormalities correlated to tic severity in all cortico-basal ganglia networks, name

265 ponding roughly to the human putamen, led to tic-like stereotypies after either acute stress or d-amp

266 have been used to study behaviors similar to tics as well as to pursue potential pathophysiological d

267 MAIN OUTCOME MEASURES: Total tic score on the Yale Global Tic Severity Scale and the

268 The constellation of motor and vocal tics and certain of the other neuropsychiatric symptoms

269 ctivity (ADHD) behaviors and motor and vocal tics during long-term treatment with methylphenidate.

270 ette's syndrome by releasing motor and vocal tics from regulatory control.

271 d DBS approach could improve motor and vocal tics in Tourette syndrome.

272 al disorder characterized by motor and vocal tics.

273 der characterized by chronic motor and vocal tics.

274 usly exhibiting a variety of motor and vocal tics.

275 ic disorder characterised by motor and vocal tics.

276 is characterized by multiple motor and vocal tics.

277 ized by the presence of both motor and vocal tics.

278 order characterized by impairing motor-vocal tics.

279 vealed a trend between the severity of vocal tics and Bmax values.

280 idence (group data) that motor tics or vocal tics changed in frequency or severity during maintenance

281 atient with prominent coprolalia, such vocal tics were associated with activity in prerolandic and po

282 rtant model of impulse control is volitional tic suppression in Tourette syndrome.

283 Images acquired during periods of voluntary tic suppression were compared with images acquired when

284 uring spontaneous tics than during voluntary tics in the somatosensory and posterior parietal cortice

285 follows a developmental time course in which tics become increasingly more controlled during adolesce

286 fe and effective treatment for children with tic disorders and ADHD.

287 fety of guanfacine in treating children with tic disorders and attention deficit hyperactivity disord

288 h activity was significantly correlated with tic occurrence in the group included medial and lateral

289 Many genes (3627) correlated with tic severity in TS (p < 0.05) among which GABA- (p = 2.1

290 ntify genes whose expression correlated with tic severity in TS, and to identify genes differentially

291 pus callosum size correlated positively with tic severity.

292 c disorders among relatives of probands with tic disorders increased proportionally to the degree of

293 tical thickness in sensorimotor regions with tic symptoms suggest that these brain regions are import

294 the relatively small sample of subjects with tic disorders, our conclusions should be considered prel

295 genes observed in blood that correlate with tics or are alternatively spliced are involved in the pa

296 ty clinic diagnoses, patients diagnosed with tics or Tourette's by physicians in the community were s

297 Probands with tics or obsessive-compulsive personality disorder were n

298 edicated children with ADHD with and without tic disorders.

299 a well-matched group of 103 children without tics.

300 ng-rewriting compulsions, repetitive writing tics) and disinhibition (uttering syllables/words, echol