ライフサイエンスコーパス: dural

1 ) had a potentially causal cranial or spinal dural abnormality, 5 (11%) had an alternative cause, and

2 ways reveals a potential cause, most often a dural abnormality.

3 rtance of inflammatory mediator (IM)-induced dural afferent sensitization to this pain syndrome, the

4 trigeminal ganglion from 40 mechanosensitive dural afferents (conduction velocitity: 0.3-6.6 m s(-1))

5 6 m s(-1)) and nine mechanically insensitive dural afferents (MIAs) (conduction velocitity: 0.3-2.8 m

6 sistent pronociceptive neural adaptations in dural afferents and enhanced responses to an established

7 lays a dominant role in the sensitization of dural afferents because of the combination of the densit

8 asting increase in identified rat trigeminal dural afferents labelled for neuronal nitric oxide synth

9 d labeling for CGRP in identified trigeminal dural afferents that persisted long after discontinuatio

10 IMs modulated a number of currents in dural afferents, including those both expected and/or pr

11 appear to contribute to the sensitization of dural afferents, the Cl(-) current is the primary mechan

12 ression of neuronal nitric oxide synthase in dural afferents, which is critical for enhanced sensitiv

13 of the dura and subsequent sensitization of dural afferents.

14 ic neurotransmitter expression in identified dural afferents.

15 belling of neuronal nitric oxide synthase in dural afferents.

16 resented with severe tumoral calcinosis with dural and carotid artery calcifications.

17 sioning of the A11 significantly facilitated dural and noxious pinch and innocuous brush evoked firin

18 antly inhibited peri-middle meningeal artery dural and noxious pinch evoked firing of neurons in the

19 M) to measure the diameter changes of single dural and pial vessels in the awake mouse during volunta

20 are involved in the descending modulation of dural and/or cutaneous facial trigeminovascular nocicept

21 A similar sensitization was elicited by dural application of NTG and SNAP.

22 After dural application with MO, mechanical thresholds of the

23 he transverse sinus partially overlapped the dural area that shows the greatest density of mast cells

24 of abnormal connections between branches of dural arteries and venous sinuses or veins.

25 morrhage, cerebrovascular malformations, and dural arteriovenous fistula affecting the basal ganglia,

26 Dural arteriovenous fistula is a very rare cause of myel

27 sistant pulsatile tinnitus caused by a small dural arteriovenous fistula revealed in computed tomogra

28 r center demonstrating right T7 to T8 spinal dural arteriovenous fistula.

29 ssa dural sinus anatomy in two patients with dural arteriovenous fistula.

30 Rare causes of tinnitus include cranial dural arteriovenous fistulas (DAVFs), which are usually

31 reflux (CVR) in patients with lateral sinus dural arteriovenous fistulas (DAVFs).

32 the follow-up clinically and radiologically, dural arteriovenous fistulas should be kept in mind in t

33 In arteriovenous malformations and dural arteriovenous fistulas, ASL is very sensitive to d

34 In cases of severe dural AV fistula in the cavernous sinus, the pituitary g

35 in 21 patients with angiographically proved dural AV fistula of the cavernous sinus were retrospecti

36 that typically presents as a meningioma-like dural-based mass.

37 -to-male ratio, 4:1), with 93% presenting as dural-based masses mimicking meningioma.

38 with laser-Doppler flowmetry measurements of dural blood flow (DBF), we examined whether CGRP and men

39 as headaches, but little is known about the dural blood flow regulation during behavior.

40 ion of CGRP caused a significant increase in dural blood flow; however, neither method of CGRP admini

41 Leakage of plasma proteins from dural blood vessels was first detected 4 h after GTN inf

42 CGRP dilated dural, but not pial, vessels and significantly reduced s

43 inical application of OCTA in a patient with dural carotid-cavernous sinus fistula (CCF), which was c

44 normal episcleral venous plexus secondary to dural CCF.

45 Dural cerebral veins (CV) are required for cerebrospinal

46 n our overall sample, the odds of successful dural culture was almost two-fold compared with scalp (O

47 lecular and cellular processes that regulate dural CV development in mammals and describe venous malf

48 SF) leak occurs when there is an osseous and dural defect at the skull base, with direct communicatio

49 ncidence of Chiari I malformation (6.4%) and dural ectasia (42.6%); and physical examination findings

50 ogic lesions, such as optic pathway gliomas, dural ectasia and aqueduct stenosis.

51 ome include scoliosis, chest wall deformity, dural ectasia, joint hypermobility, and acetabular protr

52 Dural enhancement was seen on 96 of 97 (99%) postoperati

53 the surgical margin and for the presence of dural enhancement, fluid, and air.

54 receptor activation in the vlPAG attenuated dural-evoked Adelta-fiber neurons (maximally by 19%) and

55 Some dural fibers issued collateral branches to the pia at th

56 Dural IMs produced long-lasting generalized cutaneous al

57 ine release selectively in rats treated with dural IMs.

58 pamine release selectively in rats receiving dural IMs; CPP was blocked by intra-NAc alpha-flupenthix

59 d not expand; neuronal response threshold to dural indentation and skin stimulation did not decrease;

60 er treatment; neuronal response threshold to dural indentation, which initially decreased after IS, i

61 th compounds potently blocked the neurogenic dural inflammation following trigeminal ganglion stimula

62 -HT(1F) receptor agonist (SSOFRA), inhibited dural inflammation in the neurogenic plasma protein extr

63 -HT(1F) receptor agonists inhibit neurogenic dural inflammation, a model of migraine headache, indica

64 well as the axonal size distribution of the dural innervation.

65 of the GON (20 s to 5 min) enhanced afferent dural input in 8/20 neurones.

66 dache, where it is believed that an enhanced dural input to the Vc may generate central sensitisation

67 is unlikely when there is an extensive local dural invasion and given that the molecular mechanisms r

68 ve therapeutic targets for the control of PA dural invasion.

69 w into the dcLNs is directly via an adjacent dural lymphatic network, which may be important for the

70 We show that dural lymphatic vessels absorb CSF from the adjacent sub

71 Dural lymphatic vessels transport fluid into deep cervic

72 trap and displaying complete aplasia of the dural lymphatic vessels, macromolecule clearance from th

73 at 2 and 6 h and increased interleukin 6 in dural macrophages and in rat cerebrospinal fluid at 6 h

74 Because iNOS was expressed in dural macrophages following topical GTN, and in the sple

75 ion and oedema formation after GTN infusion, dural mast cells exhibited granular changes consistent w

76 ate the cAMP-PKA cascade in sensitization of dural mechanonociceptors and suggest that this cascade m

77 eminovascular neuronal tone and Adelta-fiber dural-nociceptive responses, which differs from the way

78 ve in two models of migraine: the neurogenic dural plasma protein extravasation model and the nucleus

79 We studied the dural plasma protein extravasation response after unilat

80 ey points in the management of unintentional dural puncture and of PDPH.

81 approach to the management of unintentional dural puncture and PDPH.

82 an intrathecal catheter as it avoids further dural puncture and seals the hole during the time it is

83 ated spinal anesthesia as well as unintended dural puncture during epidural anesthesia.

84 is associated with a lower incidence of post-dural puncture headaches.

85 The incidence following accidental dural puncture is not as high as previously thought--app

86 tch should not be performed until 24 h after dural puncture to increase its success; however, it shou

87 aumatic and conventional needles in which no dural puncture was done (epidural injections) or without

88 esia; it has not been studied for accidental dural puncture with a large bore needle.

89 subsequent epidural replacement, inadvertent dural puncture, and cesarean section with difficult intu

90 cted to be induced 2 h after IS application: dural receptive fields did not expand; neuronal response

91 Chemical stimulation of their dural receptive fields with inflammatory mediators both

92 racted two aspects of central sensitization: dural receptive fields, which initially expanded by IS,

93 the GON induced an increased excitability of dural responses in 8/12 and 9/10 neurones, respectively.

94 ity of patients, pointing to weakness of the dural sac as one of the etiological factors.

95 patient and poorly depicted posterior fossa dural sinus anatomy in two patients with dural arteriove

96 patients with skull fractures extending to a dural sinus or jugular bulb.

97 patients with skull fractures extending to a dural sinus or jugular bulb.

98 g of the optic disc [p=0.881], and bilateral dural sinus stenosis [p=0.837], Mann-Whitney U test).

99 Some theories - such as the dural sinus stenosis theory - seem to ignore the relatio

100 acute intracranial hemorrhage due to delayed dural sinus thrombosis after endovascular treatment of h

101 t is a rapid, useful method for diagnosis of dural sinus thrombosis and for preoperative mapping of v

102 Dural sinus thrombosis was diagnosed in seven patients,

103 Dural sinus thrombosis was found in four patients.

104 Eighteen patients had suspected dural sinus thrombosis.

105 e are few reported cases of SAH secondary to dural sinus thrombosis; however most of these are convex

106 = 0.83, 1.0), presence of retrograde flow in dural sinuses (kappa = 1), presence of retrograde cortic

107 ctor CT venography depicted thrombosis of 98 dural sinuses or jugular bulbs in 57 (40.7%) of the 140

108 meninges, though are concentrated around the dural sinuses, and have a unique transcriptional profile

109 rospinal fluid barrier situated close to the dural sinuses, the site of recently discovered CNS lymph

110 ered functional lymphatic vessels lining the dural sinuses.

111 We investigated if noxious dural stimulation evokes sensitization of second-order n

112 al activation in the rat showed that noxious dural stimulation induced a 3- to 4-fold increase in the

113 acial and hind-paw allodynia associated with dural stimulation is a useful surrogate of pain associat

114 he facilitatory effect of GON stimulation on dural stimulation suggests a central mechanism at the se

115 The responses to dural stimulation were analysed before and after stimula

116 al nerve (GON) were studied before and after dural stimulation.

117 ould also not be observed at any time during dural stimulation.

118 Topical application on the dural surface of the auditory midbrain in mouse suppress

119 Additionally, the extent of dural thrombosis was overestimated at 2D MR venography i

120 siologically analgesic, are known to inhibit dural trigeminovascular nociceptive responses.

121 Dural vascular malformations are often elusive on all cr

122 Our knowledge of the dural vasculature has been limited to pathological condi

123 T owing to the presence of a fracture near a dural venous sinus or jugular bulb or a high index of cl

124 d only if there is a fracture extending to a dural venous sinus or jugular bulb.

125 eutic approach for a subset of IIH patients: dural venous sinus stenting.

126 iffuse subarachnoid hemorrhage and extensive dural venous sinus thrombosis involving the superior sag

127 'Partial forms' lack significant shared dural venous sinuses (SDVS) and 'Total forms' with SDVS

128 pography of these vessels, running alongside dural venous sinuses, recapitulates the meningeal lympha

129 e rat trigeminal ganglion that innervate the dural venous sinuses.

130 d, as a consequence of thrombosis within the dural venous sinuses.

131 ure (ICP) during locomotion, indicating that dural vessel constriction was not caused passively by co

132 Dural vessel constrictions did not mirror the large incr

133 that, in the awake animal, the diameters of dural vessels are regulated dynamically during behavior

134 To better understand the dynamics of dural vessels during behavior, we used two-photon laser

135 To study how behaviorally driven dynamics of dural vessels might be altered in pathological states, w

136 luntary locomotion drove the constriction of dural vessels, and the dynamics of these constrictions c

137 ot block locomotion-induced constrictions in dural vessels.

138 Immunostaining for CGRP in dural wholemounts revealed a network of fibers extending