ライフサイエンスコーパス: apraxia

1 in motion perception and its relationship to apraxia.

2 al and temporal features of movement in limb apraxia.

3 ming and response implementation deficits in apraxia.

4 l as asymmetrical limb-kinetic and ideomotor apraxia.

5 both asymmetrical limb-kinetic and ideomotor apraxia.

6 specific deficits in patients suffering from apraxia.

7 profound ataxia, camptocormia and oculomotor apraxia.

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

9 enable us to advance traditional accounts of apraxia.

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

11 Daily Living Scale as well as recovery from apraxia.

12 s underlying right-hemisphere constructional apraxia.

13 rogressive nonfluent aphasia and progressive apraxia.

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

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

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

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

18 ble APTX mutations in ataxia with oculomotor apraxia 1.

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

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

21 ological disorder known as ataxia oculomotor apraxia-1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 rebellar degeneration, ataxia and oculomotor apraxia in man.

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

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

60 Ideomotor limb apraxia is a classic neurological disorder manifesting a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 Apraxia of speech is a disorder of speech motor planning

79 Primary progressive apraxia of speech is a recently described neurodegenerat

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

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

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

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

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

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

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

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

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

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

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

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

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

93 actually related to the primary progressive apraxia of speech.

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

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

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

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

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

99 ,000 population), and ataxia with oculomotor apraxia (prevalence, 0.4 per 100,000 population) were th

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 Limb apraxia was associated with intact preprogramming but im

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

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

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

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

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

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

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