ライフサイエンスコーパス: agnosia

1 r reflex nystagmus, suggesting a 'vestibular agnosia'.

2 the routing of information in the forebrain (agnosia).

3 visual stream and suffered from visual form agnosia.

4 patients with clinically apparent vestibular agnosia.

5 d can produce the typical symptoms of finger agnosia.

6 Visual agnosia (15/183; 8.2%), substantial brain atrophy (27/18

7 ent in the published data cohort (eg, visual agnosia [5.6%, 3.9-7.2], aphasia [23.0%, 20.0-26.0], and

8 derate Alzheimer's disease, including visual agnosia (55.1%, 95% CI 45.7-64.6), aphasia (57.9%, 48.6-

9 lanced; however, the link between vestibular agnosia and imbalance was confounded by the presence of

10 the need for patients to exhibit associative agnosia and/or prosopagnosia: many authors have used the

11 vides a framework for understanding auditory agnosias and makes specific predictions to direct future

12 mechanisms and brain substrates of auditory agnosias and related disorders of auditory object proces

13 entrotemporal-fusiform network (resulting in agnosia) and the left hemisphere language network (resul

14 erage], were designated as having vestibular agnosia, and displayed worse posturography than non-vest

15 lance in acute TBI, its link with vestibular agnosia, and potential clinical impact, by prospective l

16 Thus, impaired balance and vestibular agnosia are co-localized to the inferior longitudinal fa

17 nce of amusia as a distinct form of auditory agnosia, but does not support the hypothesis that bilate

18 We tested a patient (HJA) with visual agnosia due to bilateral lesions of the ventral occipito

19 vioral switching or a possible interoceptive agnosia following hippocampal damage.

20 However, in humans category specific visual agnosia follows inferior temporal cortex but not LPFC da

21 owledge for objects in a patient with visual agnosia (H.J.A.).

22 D.F., a patient with severe visual form agnosia, has been the subject of extensive research duri

23 osopagnosia could predict subclinical facial agnosia in an independent lesion cohort (n = 31).

24 osopagnosia and predicted subclinical facial agnosia in an independent lesion cohort.

25 to confirm directly that D.F.'s visual form agnosia is associated with extensive damage to the ventr

26 ance on tasks commonly used to assess finger agnosia is modulated by changes in hand posture.

27 In conclusion, vestibular agnosia mediates imbalance in traumatic brain injury bot

28 Loss of shape recognition in visual-form agnosia occurs without equivalent losses in the use of v

29 this imbalance can be symptoms like apraxia, agnosia or sundowning.

30 That vestibular agnosia patients show worse balance, but without increas

31 ayed worse posturography than non-vestibular-agnosia patients, despite no difference in vestibular sy

32 ons in bimodal learning in modality-specific agnosia (prosopagnosia, phonagnosia).

33 Aphasia, agnosia, seizures and visual field defects were observed

34 es include behavioural dementia, associative agnosia, semantic forms of primary progressive aphasia a

35 range from sensory or motor deficits (visual agnosia, sensory hypersensitivity, atonic episodes, rest

36 emporal lobe that correlated with vestibular agnosia severity.

37 , which resulted in a persisting visual-form agnosia that has been extensively characterized at the b

38 yday life; others interpret the criterion of agnosia to require pervasive recognition impairments aff

39 Patients with vestibular agnosia were also more unbalanced; however, the link bet

40 ing behavioral abnormalities and associative agnosia when predominantly right-sided, semantic Primary

41 mporal ablations in monkeys produce a visual agnosia which causes severe 'psychic blindness' in the f

42 suoperceptual skills and apperceptive visual agnosia with predominant posterior atrophy corresponding

43 deficits in object perception in visual-form agnosia without the exploitation of both structural and

44 g their fingers, a condition known as finger agnosia, yet are relatively unimpaired in sensation and