ライフサイエンスコーパス: tic

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

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

3 1.1%]; adjusted RR, 11.8; 95% CI, 9.4-14.7), tic disorders (28 cases [0.8%] vs 24 controls [0.2%]; ad

4 level of sensorimotor noise that accompanies tics may be particularly high in Tourette syndrome, and

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

6 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

7 ming based on incoming cortical activity and tic history.

8 ming based on incoming cortical activity and tic history.

9 Ss), other tic disorders, ascertainment, and tic severity were examined.

10 ds to a large reduction in tic frequency and tic intensity in individuals with TS.

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

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

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

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

15 antly predicted both Tourette's syndrome and tic spectrum disorders status in the population-based sa

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

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

18 nostic biomarkers of functional dystonia and tics, where clinical diagnosis is often also more challe

19 nal underpinnings of waiting impulsivity and tics using multi-modal neuroimaging protocol.

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

21 re involved in the pathophysiology of TS and tics.

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

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

24 nt tics to chronic tic disorders, as well as tic persistence and lifetime tic severity.

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

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

27 ted HRT (p < 0.01), controlling for baseline tic severity, tic medication, and attention deficit hype

28 ict one-year outcome; these include baseline tic severity, subsyndromal autism spectrum symptoms, and

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

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

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

32 valuate change in the severity of bothersome tics.

33 Two bothersome tics on the Hopkins Motor/Vocal Tic Scale (HM/VTS) were

34 Tourette's Disorder (TD) is characterized by tics that cause distress and impairment.

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

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

37 reotyped movements and vocalizations called 'tics'.

38 dren at follow-up, although in several cases tics were apparent only when the child was observed remo

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

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

41 pleted a baseline assessment to characterize tic severity, premonitory urges, medical history, and ps

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

43 ity among children with Tourette and chronic tic disorder.

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

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

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

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

48 duals with Tourette syndrome (TS) or chronic tic disorder (CTD) have an elevated risk of subsequent s

49 17 years, with impairing Tourette or chronic tic disorder as a primary diagnosis, randomly assigned t

50 mes, and Tourette syndrome and other chronic tic disorders.

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

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

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

54 ting conversion of transient tics to chronic tic disorders, as well as tic persistence and lifetime t

55 and OFCC1 genes that segregated with chronic tic phenotype.

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

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

58 79 with OCD plus Tourette's syndrome/chronic tics), 5,667 ancestry-matched controls, and 290 OCD pare

59 a familial disorder, regardless of comorbid tic disorder status.

60 dividuals with OCD with and without comorbid tics, compared with relatives of unaffected individuals.

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

62 primary motor (M1) cortex that differentiate tics from voluntary movements.

63 ted from the CM thalamus that differentiated tic from voluntary movement, and this physiological feat

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

65 ne with the neuronal changes observed during tic expression following disinhibition of the striatal m

66 power decrease in M1 that was present during tics and voluntary movements.

67 ygenic risk scores correlate with worst-ever tic severity and may represent a potential predictor of

68 lso significantly correlated with worst-ever tic severity and was higher in case subjects with a fami

69 hereas elevation of androgens can exacerbate tic disorders.

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

71 m on the 12-month anniversary of their first tic.

72 a fertile ground of motor hyperactivity for tic learning.

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

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

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

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

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

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

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

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

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

82 lation (DBS) can be an effective therapy for tics and comorbidities in select cases of severe, treatm

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

84 animals shows repetitive rotations and head tics with juvenile onset.

85 Heightened tic severity was also associated with greater engagement

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

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

88 Remarkably, however, tics were present in all children at follow-up, although

89 me adult patients continue to have impairing tics.

90 s collectively indicate that DBS may improve tics and OCB, the effects may develop over several month

91 urrounding GPi and CM thalamus that improved tics for some patients but were ineffective for others.

92 ck intervention may be helpful for improving tic symptoms.

93 theses about potential targets for improving tics and comorbidities.

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

95 proactive and reactive) were not impaired in tic disorders.

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

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

98 om improvement, and the networks involved in tic improvement may differ across surgical targets.

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

100 eal musculature that is commonly involved in tic symptoms.

101 tion and volitional inhibition are normal in tic disorders, whereas automatic inhibition is impaired-

102 it nonetheless leads to a large reduction in tic frequency and tic intensity in individuals with TS.

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

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

105 rks that were correlated with improvement in tics or comorbid obsessive-compulsive behaviour and to p

106 was 13 months to reach a 40% improvement in tics, and there were no significant differences across t

107 as positively correlated with improvement in tics; the model predicted clinical improvement scores (P

108 ral networks associated with improvements in tics and comorbid obsessive-compulsive behaviour, compar

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

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

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

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

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

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

115 vity in determining the timing of individual tics.

116 factors underlying the timing of individual tics.

117 was time-locked to the onset of involuntary tics but was not present during voluntary movements.

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

119 At a genetic level, tic disorders represent a continuous spectrum of disease

120 vestigated whether, at the population level, tic-related OCD has a stronger familial load than non-ti

121 ers, as well as tic persistence and lifetime tic severity.

122 The Ash1l(+/-) mice manifested tic-like behaviors and compulsive behaviors that could b

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 terized by the occurrence of vocal and motor tics.

128 ic disorder characterized by vocal and motor tics.

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

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

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

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

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

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

135 ve-compulsive disorder (OCD) included a new "tic-related" specifier.

136 ed OCD has a stronger familial load than non-tic-related OCD.

137 of OCD in relatives of individuals with non-tic-related OCD (e.g., risk for full siblings: aHR = 10.

138 257 with tic-related OCD and 20,975 with non-tic-related OCD), we identified all twins, full siblings

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

140 lable way to ensure hepaative application of tic protection.

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

142 s demonstrate the preliminary enhancement of tic severity reductions by augmenting HRT with DCS compa

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

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

145 The primary outcome measure of tic severity was the Yale Global Tic Severity Scale admi

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

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

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

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

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

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

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

153 s correlated positively with the severity of tic symptoms.

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

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

156 cological interventions for the treatment of tic disorders.

157 (R(2) = .16%, p empirical = .07, Q = .14) of tics in the Avon Longitudinal Study of Parents and Child

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

159 The defining character of tics is that they can be transiently suppressed by volit

160 PRS predicted the presence and chronicity of tics, and symptom severity of obsessive-compulsive disor

161 s found a significant polygenic component of tics occurring in a general population cohort based on P

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

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

164 cating these structures in the generation of tics.

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

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

167 er in case subjects with a family history of tics than in simplex case subjects.

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

169 of movement and influence the initiation of tics in TS.

170 In humans, clinical manifestation of tics cannot be captured via functional imaging due to mo

171 The involuntary (or voluntary) nature of tics has been the subject of considerable debate, and it

172 ation study in relation to the occurrence of tics and associated traits in a general population cohor

173 s that might contribute to the occurrence of tics.

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

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

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

177 it was recently argued that the presence of tics in Tourette syndrome could result in a blurring of

178 mechanism responsible for the production of tics with that used in suppressing them.

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

180 neurofeedback from the SMA-for reduction of tics in adolescents with TS.

181 pants had significantly greater reduction of tics on the Yale Global Tic Severity Scale after real ne

182 motor circuits to attenuate the severity of tics.

183 ditions, but correlated with the severity of tics.

184 ed to TD and specifically to the severity of tics.

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

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

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

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

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

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

191 We identified 43 children with recent onset tics (mean 3.3 months since tic onset) and re-examined 3

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

193 ly associated with involuntary movements, or tics.

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

195 can help to differentiate them from organic tics.

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

197 unification of Tourette's syndrome and other tic disorders in future diagnostic schemata.

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

199 expressed during Tourette syndrome and other tic disorders.

200 eterminants of Tourette's syndrome and other tic disorders.

201 urette's polygenic risk scores (PRSs), other tic disorders, ascertainment, and tic severity were exam

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

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

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

205 the presence of fluctuating motor and phonic tics.

206 haracterized by involuntary motor and phonic tics.

207 erized by the occurrence of motor and phonic tics.

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

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

210 sic deoxyribozyme-based automaton that plays tic-tac-toe(42), to direct structural reconfiguration (S

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

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

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

214 the striatum and the timing of the previous tic.

215 ition in a group of 19 patients with primary tic disorders and 15 healthy volunteers.

216 that its cardinal manifestation - prominent tics - may be ameliorated by a peripheral, sensory inter

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

218 r therapy with D-cycloserine (DCS) to reduce tic severity in a placebo-controlled quick-win/fast-fail

219 lity, entrain brain oscillations, and reduce tics in TS.

220 risk to test whether Tourette's and related tic disorders have an underlying shared genetic etiology

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

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

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

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

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

226 The resulting tics and their neuronal representation within the striat

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

228 e sensorimotor putamen predicted more severe tics.

229 bitual responses correlated with more severe tics.

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

231 .01), controlling for baseline tic severity, tic medication, and attention deficit hyperactivity diso

232 son subjects during spontaneous or simulated tics.

233 ith recent onset tics (mean 3.3 months since tic onset) and re-examined 39 of them on the 12-month an

234 premonitory urges that generate spontaneous tic behaviors.

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

236 event the initial excitation of the striatal tic focus-a hypothesis we have previously introduced.

237 However, strong evidence supporting tic-related OCD as a distinct subtype of OCD is lacking.

238 le for use outside of the clinic to suppress tics and PU in TS.

239 group exhibited lower severity for targeted tics (d = 1.30, p < 0.001) relative to the placebo group

240 iting slightly greater severity for targeted tics.

241 oural level this has led to the concept that tics result from a failure of inhibition.

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

243 This finding supports the notion that tics along a spectrum from nonclinical to clinical sympt

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

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

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

247 iting the nascent excitation released by the tic generator.

248 lsive behaviors that could be rescued by the tic-relieving drug haloperidol.

249 metimes ignore repetitive stimuli (e.g., the tic of a clock) or detect meaningful repetition (e.g., c

250 ion, and that they prevent expression of the tic by inhibiting the nascent excitation released by the

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

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

253 tor output could be increased to prevent the tic from reaching the threshold for expression, although

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

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

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

257 ong clinicians is that for most children the tics are temporary, disappearing within a few months.

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

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

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

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

262 hat waiting impulsivity in TD was related to tic severity, to functional connectivity of orbito-front

263 dren had more than minimal impairment due to tics.

264 rved familial patterns of OCD in relation to tics were not seen in relation to other neuropsychiatric

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

266 , and are often preceded by a strong urge-to-tic-referred to as a premonitory urge (PU).

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

268 uture for predicting conversion of transient tics to chronic tic disorders, as well as tic persistenc

269 Motor and vocal tics are common in childhood.

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 ), which is characterized by motor and vocal tics, is not in general considered as a product of impul

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

274 al disorder characterized by motor and vocal tics.

275 der characterized by chronic motor and vocal tics.

276 ized by repetitive motor movements and vocal tics.

277 e mechanisms are recruited during volitional tic suppression, and that they prevent expression of the

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

279 ay constitute a potential mechanism by which tics are generated.

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

281 ween 1967 and 2007 (n = 4,085,367; 1257 with tic-related OCD and 20,975 with non-tic-related OCD), we

282 isorders, SIBs are typically associated with tic disorders, most commonly Tourette syndrome, and neur

283 h this map was significantly correlated with tic improvement (P < 0.017).

284 nd cerebellum was positively correlated with tic improvement; the model predicted clinical improvemen

285 n is impaired-a deficit that correlated with tic severity and thus may constitute a potential mechani

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

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

288 c inhibition were positively correlated with tic severity.

289 risk of OCD in relatives of individuals with tic-related OCD was considerably greater than the risk o

290 ition was abnormal/impaired in patients with tic disorders.

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

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

293 iency has been independently associated with tics in humans and with repetitive behavioral pathology

294 ry motor area (SMA) has been associated with tics in Tourette syndrome (TS).

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 fic action, shares some common features with tics.

298 for healthy controls, whereas patients with tics exhibited strong positive compatibility effects, bu

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

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