ライフサイエンスコーパス: visual hallucination

1 ere the primary outcome is an improvement in visual hallucinations.

2 suggest three mechanisms underlying complex visual hallucinations.

3 alterations in visual perception, including visual hallucinations.

4 frequently had a good levodopa response and visual hallucinations.

5 One-third of patients experienced visual hallucinations.

6 ry hallucinations, but not the subgroup with visual hallucinations.

7 y in visual recognition to social vision and visual hallucinations.

8 considering current models for mechanisms of visual hallucinations.

9 ple system atrophy, including a patient with visual hallucinations.

10 al hallucinations, relative to those without visual hallucinations.

11 sential components of a model of oscillating visual hallucinations.

12 echanism underlying 5-HT2A receptor-mediated visual hallucinations.

13 of visual perceptual alterations, including visual hallucinations.

14 al feedback mechanisms can enhance patterned visual hallucinations.

15 utes to the observed regularity of geometric visual hallucinations.

16 These are experienced as geometric visual hallucinations.

17 nitive function in patients with and without visual hallucinations.

18 was made for reporting of persistent formed visual hallucinations.

19 and executive function, were associated with visual hallucinations.

20 n the clinical study of whom 32% experienced visual hallucinations.

21 eelings of presence and passage) and complex visual hallucinations.

22 particularly for patients with a history of visual hallucinations.

23 the left ILF (P = .02) than patients without visual hallucinations.

24 istinct mechanisms and when and how to treat visual hallucinations.

25 erse events for ADS-5102 vs placebo included visual hallucinations (15 [23.8%] vs 1 [1.7%]), peripher

26 early-onset DLB over early-onset AD included visual hallucinations (15 [46.9%] vs 42 [11.6%]), slowne

27 sm symptoms-71 years (66-92 years), six with visual hallucinations-72 years (64-90 years), seven with

28 differences in ocular pathology between the visual hallucination and non-visual hallucination groups

29 hy patient group included hyper-religiosity, visual hallucinations and cross-modal sensory experience

30 econdary outcomes included impact ratings of visual hallucinations and electrophysiological measures.

31 Visual hallucinations and illusions are thought to be ca

32 Fifty patients with visual hallucinations and illusions secondary to degener

33 ctively contribute to the pathophysiology of visual hallucinations and may explain their predominantl

34 d synPC4 pattern scores were associated with visual hallucinations and motor impairment, respectively

35 Visual hallucinations and motor severity were associated

36 s associated with the presence of persistent visual hallucinations and persistent delusions.

37 d cognitive decline with new-onset recurrent visual hallucinations and progressive lethargy.

38 disease (81 without hallucinations, 19 with visual hallucinations) and 34 healthy age-matched contro

39 variables persecutory ideation, auditory and visual hallucinations, and diagnosis of probable psychos

40 he possible neuronal events at the origin of visual hallucinations, and further suggests that brain o

41 ypes include myoclonic seizures, auditory or visual hallucinations, and renal failure.

42 down processes in shifting the complexity of visual hallucinations, and to assess whether these techn

43 Procaine-induced visual hallucinations appeared associated with greater g

44 Visual hallucinations are a core feature of dementia wit

45 Visual hallucinations are common in older people and are

46 Visual hallucinations are common in Parkinson's disease

47 Visual hallucinations are common in Parkinson's disease

48 However, irrespective of mechanism, visual hallucinations are difficult to treat.

49 Visual hallucinations are frequent, disabling complicati

50 The neural mechanisms of visual hallucinations are largely unknown.

51 in Parkinson's disease and, with respect to visual hallucinations, are an important predictor of cog

52 predominant effects induced by LSD included visual hallucinations, audiovisual synesthesia, and posi

53 sing activities of daily living, depression, visual hallucinations, best-corrected visual acuity (BCV

54 n in Alzheimer's disease, as were persistent visual hallucinations, but patients who had dementia wit

55 tional connectivity changes with Parkinson's visual hallucinations, but the biological factors underl

56 -HT2A receptors may lead to the formation of visual hallucinations by increasing cortical excitabilit

57 Visual hallucinations can be a major hallmark of late st

58 Here we show that visual hallucinations can be induced in the normal popul

59 Visual hallucinations can be phenomenologically divided

60 ly-impaired individuals who experience vivid visual hallucinations (Charles Bonnet syndrome).

61 between the presence of the Ser23 allele and visual hallucinations (chi2 = 7.5, df = 1, P = 0.006) (P

62 estones of advanced disease (frequent falls, visual hallucinations, cognitive disability and need for

63 older and had an extremely low frequency of visual hallucinations compared with Parkinson's disease.

64 grey matter atrophy patterns associated with visual hallucinations, comparing Parkinson's disease hal

65 he link between abnormal visual function and visual hallucinations, considering current models for me

66 In the matched sample, visual hallucinations continued to be less common in wom

67 ionships of persistent psychiatric symptoms (visual hallucinations, delusions, depression) to plaques

68 estones of advanced disease (frequent falls, visual hallucinations, dementia and need for residential

69 ribed by several different authors as formed visual hallucinations due to disturbances of the visual

70 , the hallucinators, all of whom experienced visual hallucinations, exhibited grey matter atrophy wit

71 (e.g., emotions, thoughts, and olfactory and visual hallucinations) exhibits no clear relation to the

72 ons to the hippocampus and cortex, while the visual hallucinations experienced by subjects with Demen

73 ve decline and core clinical features (e.g., visual hallucinations, fluctuating cognition, parkinsoni

74 h Lewy bodies is characterised clinically by visual hallucinations, fluctuating cognitive function, p

75 ch in peduncular hallucinosis, a syndrome of visual hallucinations following subcortical lesions long

76 Patients in the visual hallucinations group had similar disease duration

77 ogy between the visual hallucination and non-visual hallucination groups.

78 ses revealed that patients with a history of visual hallucinations had lower fractional anisotropy in

79 cted for multiple comparisons, patients with visual hallucinations had significantly greater disease

80 70]) than the ADP group and a lower risk for visual hallucinations (HR, 0.56 [95% CI, 0.45-0.71]) and

81 98]), apathy (HR, 0.79 [95% CI, 0.71-0.87]), visual hallucinations (HR, 0.76 [95% CI, 0.64-0.90]), ir

82 Visual hallucinations, illusions and extrapyramidal trac

83 profile correlated strongly with ratings of visual hallucinations, implying that intrinsic brain act

84 Impact measures of visual hallucinations improved in both placebo and activ

85 nary incontinence in 50% and dementia in 39%.Visual hallucinations in 0%.

86 Visual hallucinations in Lewy body disease (LBD) can be

87 devices and gain a greater understanding of visual hallucinations in mental disorders.

88 The literature related to visual hallucinations in ophthalmological settings from

89 ructural connectivity changes that accompany visual hallucinations in Parkinson's disease and the org

90 The exact pathogenesis of visual hallucinations in Parkinson's disease is not know

91 mographic and ophthalmological correlates of visual hallucinations in Parkinson's disease, the combin

92 endently contributing to the pathogenesis of visual hallucinations in Parkinson's disease.

93 connectome, and lead to the hypothesis that visual hallucinations in patients with COS may be becaus

94 of visual cortex may reduce the frequency of visual hallucinations in people with CBS, particularly i

95 onnet Syndrome (CBS), a phenomenon involving visual hallucinations in people with visual impairments.

96 ) funded a research programme to investigate visual hallucinations in the key and high burden areas o

97 topological and hodological neural basis of visual hallucinations integrating grey and white matter

98 reases appeared to correlate positively with visual hallucination intensity.

99 al hallucinations measured by the North East Visual Hallucinations Interview, with a moderate-to-larg

100 VH were assessed using a North-East-Visual-Hallucinations-Interview that captures phenomenol

101 ons, disinhibition, auditory hallucinations, visual hallucinations, irritability, personality change,

102 Current research into visual hallucination is predominantly ophthalmology-led,

103 Complex visual hallucinations may affect some normal individuals

104 Transient monocular visual loss or complex visual hallucinations may lead to neuroanatomic ambiguit

105 a significant reduction in the frequency of visual hallucinations measured by the North East Visual

106 tion and the wider clinical context in which visual hallucinations occur.

107 ness and transient delusions and auditory or visual hallucinations occurred in the majority.

108 than those with no Lewy body disease to have visual hallucinations of misperception, peripheral hallu

109 where loss of vision leads to complex, vivid visual hallucinations of objects, people, and whole scen

110 ent, migraine coma, Charles Bonnet syndrome (visual hallucinations of the blind), schizophrenia, hall

111 rs for early progression to dementia include visual hallucinations, older age and biomarker changes s

112 ented due to homonymous visual disturbances, visual hallucinations or incidental homonymous visual fi

113 r there is a single underlying mechanism for visual hallucinations or they have different disease-dep

114 any drug (OR, 9.41; 95% CI, 5.26-16.85), and visual hallucinations (OR, 2.13; 95% CI, 1.10-4.13).

115 The milestones of dementia (P < 0.0005) and visual hallucinations (P = 0.02) as well as the accumula

116 ently presented with catatonia, auditory and visual hallucinations, paranoia, aggression, mood dysreg

117 ng cognitive impairment, attention deficits, visual hallucinations, parkinsonism, and other neuropsyc

118 ficits included a small visual field defect, visual hallucinations, prosopagnosia, topographical diso

119 ns in subjects with Parkinson's disease with visual hallucinations, relative to those without visual

120 2.1 [5.1] years; P = .03), had more frequent visual hallucinations that did not achieve significance

121 ommon and sometimes curious, if not bizarre, visual hallucinations, the forms of which suggest that e

122 these spontaneous fluctuations can subserve visual hallucinations, the functional MRI brain activity

123 to both fMRI and iEEG, induced a topographic visual hallucination: the patient described seeing indoo

124 cking of this oscillation is correlated with visual hallucinations, thought disorder, and disorganiza

125 significant and consistent risk factors for visual hallucinations, together with new evidence to sug

126 The Charles Bonnet syndrome is a disorder of visual hallucinations typically occurring in older perso

127 Visual hallucinations (VH) are common in Parkinson's dis

128 For many years, visual hallucinations (VH) in idiopathic Parkinson's dis

129 recuneus, and anterior cingulate metabolism; visual hallucinations (VH) with bilateral dorsolateral-f

130 arise in Parkinson's disease (PD) including visual hallucinations (VH).

131 ht into the pathophysiological mechanisms of visual hallucinations (VHs) in patients with Parkinson d

132 Visual hallucinations (VHs) occur in macular degeneratio

133 The frequency of delusions and visual hallucinations was increased in Parkinson's disea

134 in neuropathological correlate of persistent visual hallucinations was the presence of less severe ta

135 bodies, which is hypothesized to account for visual hallucinations, we found connectivity with this r

136 dality of the hallucination: lesions causing visual hallucinations were connected to the lateral geni

137 at death 75.5 +/- 8.0 years) and persistent visual hallucinations were documented in 63%.

138 ies and Alzheimer's disease for auditory and visual hallucinations were especially pronounced for pat

139 ligible patients admitting to having complex visual hallucinations were interviewed to explore the ch

140 Visual hallucinations were more common in the group with

141 n model the four independent determinants of visual hallucinations were rapid eye movement sleep beha

142 erential diagnosis, depicting other forms of visual hallucination which result from a variety of non-