ライフサイエンスコーパス: apraxia

1 rogressive nonfluent aphasia and progressive apraxia.

2 in motion perception and its relationship to apraxia.

3 al and temporal features of movement in limb apraxia.

4 ming and response implementation deficits in apraxia.

5 rom neuropsychological studies of upper limb apraxia.

6 -use difficulties experienced by people with apraxia.

7 profound ataxia, camptocormia and oculomotor apraxia.

8 erentiated from bvFTD, svPPA and SCI by limb apraxia.

9 t may also be impaired in some patients with apraxia.

10 l as asymmetrical limb-kinetic and ideomotor apraxia.

11 both asymmetrical limb-kinetic and ideomotor apraxia.

12 specific deficits in patients suffering from apraxia.

13 hat they shed light on the human syndrome of apraxia.

14 enable us to advance traditional accounts of apraxia.

15 Daily Living Scale as well as recovery from apraxia.

16 s underlying right-hemisphere constructional apraxia.

17 sorders, particularly ataxia with oculomotor apraxia 1 (AOA1) and spinocerebellar ataxia with axonal

18 Ataxia with oculomotor apraxia 1 is caused by mutation in the APTX gene, which

19 ical disease known as ataxia with oculomotor apraxia 1 is caused by mutations in the APTX gene that e

20 europathological diseases: ataxia oculomotor apraxia 1, spinocerebellar ataxia with neuronal neuropat

21 ble APTX mutations in ataxia with oculomotor apraxia 1.

22 Ataxia oculomotor apraxia-1 (AOA1) is a neurological disorder caused by mu

23 Ataxia oculomotor apraxia-1 is a neurological disorder that arises from mu

24 ological disorder known as ataxia oculomotor apraxia-1.

25 degenerative disorder ataxia with oculomotor apraxia 2 (AOA-2) is caused by defects in senataxin, a p

26 degenerative diseases ataxia with oculomotor apraxia 2 (AOA2) and amyotrophic lateral sclerosis 4 (AL

27 -deficient mutants in ataxia with oculomotor apraxia 2 neurodegenerative disease.

28 rological disorders: AOA2 (ataxia oculomotor apraxia 2) and ALS4 (amyotrophic lateral sclerosis 4).

29 f mutated, results in ataxia with oculomotor apraxia 4 (AOA4) and microcephaly with early-onset seizu

30 Z) to neurodegeneration in ataxia oculomotor apraxia-4 (AOA4) and Charcot-Marie-Tooth disease (CMT2B2

31 ered symptoms; whereas, syndromes 4 ("phobia-apraxia"), 5 ("fever-adenopathy"), and 6 ("weakness-inco

32 cessing deficits constitute a key symptom of apraxia, a disorder of motor cognition frequently observ

33 utants are reminiscent of human ocular motor apraxia, a neurodevelopmental disorder characterized by

34 Several recent studies of apraxia after stroke have made advances in understanding

35 ences of this imbalance can be symptoms like apraxia, agnosia or sundowning.

36 phere-damaged patients with and without limb apraxia and a normal control group to examine preprogram

37 Disease-specific profiles of limb apraxia and associated deficits can be observed.

38 ure suggests that the presence or absence of apraxia and associated parietal deficits may be clinical

39 edictions with 75% accuracy, the recovery of apraxia and independence level at 9 months.

40 eral presentation, clumsy useless limb, limb apraxia and myoclonus, four had cortical sensory impairm

41 BCoS offers a quick and valid way to detect apraxia and predict functional recovery.

42 disorder characterized by ataxia, oculomotor apraxia, and choreoathetosis.

43 tal cerebellar ataxia, hypotonia, oculomotor apraxia, and mental retardation.

44 vermis and by ataxia, hypotonia, oculomotor apraxia, and neonatal breathing dysregulation.

45 ling, extended lifespan, and rescued ataxia, apraxia, and social abnormalities but did not rescue tre

46 henotype of recessive ataxia with oculomotor apraxia (AOA).

47 y-onset progressive ataxia with ocular motor apraxia (AOA1).

48 sclerosis (ALS4) and ataxia with oculomotor apraxia (AOA2).

49 The clinical features of interest were: limb apraxia, apraxia of speech (AOS), and left parietal symp

50 The volitional impairments of alien limb and apraxia are a defining feature of the corticobasal syndr

51 Ataxia with oculomotor apraxia (ataxia-telangiectasia-like syndrome [AOA]; MIM

52 XRCC1 gene are associated with ocular motor apraxia, axonal neuropathy, and progressive cerebellar a

53 motor articulatory planning deficit (speech apraxia) combined with a variable degree of agrammatism.

54 on, characterized by asymmetric rigidity and apraxia, cortical sensory deficits, dystonia and myoclon

55 Clinical diagnoses of progressive apraxia, corticobasal degeneration and progressive supra

56 We found that aphasia and speech apraxia could be retrieved easily through ICD-10 diagnos

57 Regression analysis showed that limb apraxia could successfully differentiate between AD and

58 hypotonia, cerebral atrophy and speech delay/apraxia/dysarthria.

59 cerebellar dysfunction, oromotor/oculomotor apraxia, emotional lability and mutism in patients after

60 ations associated with ataxia and oculomotor apraxia encode proteins with huge losses in protein stab

61 Q, associated with ataxia but not oculomotor apraxia, encodes a protein with a mild defect in stabili

62 ith congruent tools in individuals with limb apraxia following left hemisphere stroke (LCVA), a disor

63 Mutism/speech apraxia has been well documented as a toxic effect of cy

64 to movement deficits, and that patients with apraxia have difficulty in selecting movements.

65 Ideomotor apraxia (IMA) is often associated with damage of the dom

66 ent actions with familiar objects (ideomotor apraxia; IMA), along with five control subjects.

67 rebellar degeneration, ataxia and oculomotor apraxia in man.

68 rlapping cognitive symptoms, and measures of apraxia, in particular, appear to be a promising discrim

69 rain and cerebellar malformation, oculomotor apraxia, irregular breathing, developmental delay, and a

70 Ideomotor limb apraxia is a classic neurological disorder manifesting a

71 This finding suggests that ideomotor limb apraxia is associated with disruption of the neural repr

72 bellar vermis, ataxia, hypotonia, oculomotor apraxia, neonatal breathing abnormalities, and mental re

73 ing benign essential blepharospasm (BEB) and apraxia of eyelid opening (ALO).

74 Vertical gaze palsy and apraxia of eyelid opening were more commonly observed in

75 tonias: blepharospasm, hemifacial spasm, and apraxia of eyelid opening.

76 yndrome primarily defined by the presence of apraxia of speech (AoS) and/or expressive agrammatism.

77 cal features of interest were: limb apraxia, apraxia of speech (AOS), and left parietal symptoms of d

78 speech features indicative of dysarthria and apraxia of speech (AOS).

79 Childhood apraxia of speech (CAS) is conceived as an impairment of

80 Progressive apraxia of speech (PAOS) is a neurodegenerative motor-sp

81 It is debated whether primary progressive apraxia of speech (PPAOS) and progressive agrammatic aph

82 hildren presented with features of childhood apraxia of speech (the same speech disorder associated w

83 When compared to the patients with mixed apraxia of speech and agrammatism, the patients with pro

84 mporal lobes compared to patients with mixed apraxia of speech and agrammatism.

85 age and gender to 22 patients who had mixed apraxia of speech and agrammatism.

86 PURPOSE OF REVIEW: Autism, childhood apraxia of speech and central auditory processing disord

87 patterns emerged: (1) NFPA, characterized by apraxia of speech and deficits in processing complex syn

88 rtant papers pertaining to acquired aphasia, apraxia of speech and dysarthria with special attention

89 is approach, we found no association between apraxia of speech and lesions of the left insula, anteri

90 rebral artery (which can independently cause apraxia of speech and many other deficits).

91 help define the pathobiology of progressive apraxia of speech and may have consequences for developm

92 ove our understanding of primary progressive apraxia of speech and provide some important prognostic

93 r in which patients present with an isolated apraxia of speech and show focal degeneration of superio

94 bility, we examined the relationship between apraxia of speech and the insula in three unique ways: (

95 e aim of this study was to determine whether apraxia of speech can present as an isolated sign of neu

96 A syndrome characterized by progressive pure apraxia of speech clearly exists, with a neuroanatomic c

97 Others have confirmed that patients with apraxia of speech commonly have damage to the anterior i

98 These subjects with primary progressive apraxia of speech included eight females and four males,

99 Apraxia of speech is a disorder of speech motor planning

100 Progressive apraxia of speech is a neurodegenerative syndrome affect

101 Primary progressive apraxia of speech is a recently described neurodegenerat

102 nt studies have established that progressive apraxia of speech is not a homogenous disease but rather

103 gopaenic progressive aphasia and progressive apraxia of speech may be seen as points in a space of co

104 executive dysfunction and dysarthria without apraxia of speech or frank agrammatism.

105 Presenting features of progressive apraxia of speech or nonfluent aphasia are strongly asso

106 upathy and 4R-tauopathy in agPPA may rely on apraxia of speech presence.

107 In eight subjects the apraxia of speech remained the predominant feature.

108 Thirteen subjects with primary progressive apraxia of speech underwent two serial comprehensive cli

109 Apraxia of speech was associated with 4R-tauopathy in ag

110 n patients with and without insular lesions, apraxia of speech was associated with structural damage

111 autopsy-confirmed patients with progressive apraxia of speech who were followed over 10 years.

112 that some subjects with primary progressive apraxia of speech will rapidly evolve and develop a deva

113 Twelve subjects were identified as having apraxia of speech without any signs of aphasia based on

114 rate clinical entities: 'primary progressive apraxia of speech' when AoS occurs in the absence of exp

115 a of damage in chronic stroke patients with 'apraxia of speech', a disorder of motor planning and pro

116 related individuals diagnosed with childhood apraxia of speech, a rare disorder enriched for causativ

117 ent in the subjects with primary progressive apraxia of speech, but there was individual variability.

118 rain injury can lead to a condition known as apraxia of speech, in which patients are impaired in the

119 SP) can sometimes present with a progressive apraxia of speech, nonfluent aphasia, or a combination o

120 with CBD and PSP present with a progressive apraxia of speech, nonfluent aphasia, or a combination o

121 asis of the most persistent and severe form, apraxia of speech, remains elusive.

122 temporal dementia, corticobasal syndrome and apraxia of speech, there is greater cortical pathology t

123 hough it typically presents with concomitant apraxia of speech, this is not always the case.

124 t present with agrammatism in the absence of apraxia of speech, which we will refer to as progressive

125 Only two patients eventually developed apraxia of speech, while parkinsonism was absent-to-mild

126 speech disfluencies resembling those seen in apraxia of speech.

127 use deficits in verbal fluency, such as pure apraxia of speech.

128 ore common syndrome of mixed agrammatism and apraxia of speech.

129 actually related to the primary progressive apraxia of speech.

130 avioural change, executive dysfunction, limb apraxia or Parkinsonism.

131 d more severe speech abnormalities (oromotor apraxia, P=0.007).

132 fixations, presumably due to constructional apraxia patients' damage to the right-hemisphere regions

133 cades to the right can impair constructional apraxia patients' perception of location shifts.

134 elopmental delay, typical facies, oculomotor apraxia, polydactyly, and subtle posterior fossa abnorma

135 d ubiquitinated inclusions, parkinsonism and apraxia predicted corticobasal pathology, and nonfluent

136 ,000 population), and ataxia with oculomotor apraxia (prevalence, 0.4 per 100,000 population) were th

137 ith speech may reflect motor coordination or apraxia, problems with processing language may reflect a

138 Constructional apraxia refers to the inability of patients to copy accu

139 In the largest prospective study of apraxia-related lesions to date, we performed voxel-base

140 completed background assessments to quantify apraxia severity.

141 mpared with congruent tools as a function of apraxia severity.

142 The clinical relevance of apraxia stands in stark contrast to the paucity of thera

143 a coherent interpretation of the results of apraxia studies remains hampered by the lack of a standa

144 Ataxia-oculomotor apraxia syndrome 1 is an early onset cerebellar ataxia t

145 e gyrus may play a role in the mutism/speech apraxia syndrome seen with cyclosporine/tacrolimus neuro

146 h hydrolase, is mutated in ataxia-oculomotor apraxia syndrome.

147 iabilities and correlations between the BCoS apraxia tasks and counterpart tests from the literature.

148 dity and functional predictive values of the apraxia tests in the Birmingham Cognitive Screen (BCoS)

149 elopment with mild epilepsy and speech delay/apraxia to severe developmental and epileptic encephalop

150 contains DNL3 and the ataxia with oculomotor apraxia type 1 (AOA) gene product aprataxin.

151 ent cell lines, human Ataxia with Oculomotor Apraxia Type 1 (AOA1) and DT40 chicken B cell, we found

152 Telangiectasia (A-T) and Ataxia with Ocular Apraxia Type 1 (AOA1) are devastating neurological disor

153 Ataxia oculomotor apraxia type 1 (AOA1) is an autosomal recessive disease

154 Ataxia with oculomotor apraxia type 1 (AOA1) is an early onset progressive spin

155 he recessive disorder ataxia with oculomotor apraxia type 2 (AOA2) and a dominant juvenile form of am

156 generative disorders: ataxia with oculomotor apraxia type 2 (AOA2) and amyotrophic lateral sclerosis

157 h's ataxia (FRDA) and ataxia with oculomotor apraxia type 2 (AOA2) are the two most frequent forms of

158 Ataxia oculomotor apraxia type 2 (AOA2) is a rare autosomal recessive cere

159 d cells from patients with ataxia oculomotor apraxia type 2 (ref. (9)) and in BRCA1-mutated cancer ce

160 in the neurological disorders ataxia-ocular apraxia type 2 and juvenile amyotrophic lateral sclerosi

161 axia: 0.55 points/yr, ataxia with oculomotor apraxia type 2: 1.14 points/yr, POLG-ataxia: 1.56 points

162 P leads to late-onset ataxia with oculomotor apraxia type 4 (AOA4) in humans and embryonic lethality

163 Limb apraxia was associated with intact preprogramming but im

164 f these remapping deficits in constructional apraxia was confirmed through a highly significant corre

165 The prevalence of limb apraxia was highest in PCA, amnestic AD, lvPPA and nfvPP

166 in agPPA, while pure agrammatic PPA without apraxia was linked to 3R-tauopathy.

167 PNFA, combined with limb apraxia was significantly more common in PGRN mutation c

168 misphere stroke patients with constructional apraxia were compared to patients without constructional

169 Patients with constructional apraxia were found to be significantly impaired in posit

170 pansion carriers, nonfluent aphasia and limb apraxia were significantly more common in GRN mutation c

171 rrelated with the severity of alien limb and apraxia, which we suggest share a core deficit in motor

172 by progressive asymmetric limb rigidity and apraxia with dystonia, myoclonus, cortical sensory loss