戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (left1)

通し番号をクリックするとPubMedの該当ページを表示します
1                                              CRPS IgG significantly increased and prolonged swelling
2                                              CRPS symptoms likely reflect combined effects of axonal
3                    The study included 64,115 CRPS.
4  Fifteen pathologists each interpreted > 150 CRPS/year in all years and together diagnosed 38,813.
5 et where pathologists/endoscopists saw > 600 CRPS each(total 52,760 CRPS), that pathologist, endoscop
6 ndoscopists saw > 600 CRPS each(total 52,760 CRPS), that pathologist, endoscopist, anatomical locatio
7 e superensemble were slightly more accurate (CRPS = 110, 95% CI 102-575) than those made with the bas
8 ent (phenylephrine) in 4 patients with acute CRPS I and 3 patients with resolved CRPS I with that in
9  in the affected limb of patients with acute CRPS I compared to their unaffected limb (p = 0.03), to
10 the abnormal response in patients with acute CRPS I is most likely mediated by an axon reflex and tha
11 ctivation similar to those reported in adult CRPS; (ii) in the CRPS(+) state, stimuli that evoked mec
12  respiratory sinus arrhythmia, do not affect CRPS.
13              Compared with controls, CBP and CRPS, but not OA, had significantly less bilateral hippo
14  were perceived as equivalent in CRPS(+) and CRPS(-) states, the same stimulus produced different pat
15 rs, achieving average RMSE, pinball loss and CRPS of 0.3041, 0.0567 and 0.1683 respectively, with the
16  within-group analysis for CRPS(+) state and CRPS(-) state for brush and cold for the affected and un
17 all-fiber-predominant polyneuropathies cause CRPS-like abnormalities, and pathological studies of ner
18  pathological studies of nerves from chronic CRPS-I patients confirm small-fiber-predominant patholog
19 roke and raises the possibility that chronic CRPS involves a type of spatial neglect.
20                        Compared to controls, CRPS patients particularly showed a significant prolonga
21 n the clinical findings required to diagnose CRPS.
22 logarithmic transformation leads to expected CRPS values which are independent of the order of magnit
23 ng finger tapping of the affected extremity, CRPS patients showed a significant reorganization of cen
24                                          For CRPS patients, pain (measured on a 100-mm visual analog
25 ere performed: (i) within-group analysis for CRPS(+) state and CRPS(-) state for brush and cold for t
26 h fields suggest novel treatment options for CRPS: from targeting autoimmunity to correcting abnormal
27  the NOS substrate l-arginine in plasma from CRPS patients, suggesting reduced miR-939 levels may con
28 -edematous agents in patients suffering from CRPS, and interestingly these therapeutic effects appear
29 ing paw inflammatory response in all groups, CRPS IgG-injected mice displayed sustained, profound mic
30 esults do not apply to patients who have had CRPS for less than 1 year or more than 5 years and do no
31 ng a 6-week period in adult patients who had CRPS from 1 to 5 years.
32                             We recognise how CRPS research may inform mechanistic understanding of FN
33                                     However, CRPS is associated with symptoms that appear similar to
34  with complex regional pain syndrome type I (CRPS I).
35 ; now complex regional pain syndrome type I [CRPS-I]).
36  the complex regional pain syndrome type II (CRPS II or causalgia) in man.
37  genes and that downregulation of miR-939 in CRPS patients may increase expression of these genes, re
38 r morphometry and white matter anisotropy in CRPS patients and matched controls.
39      Our results show that the difference in CRPS between sleep stages exceeds the difference between
40  sought to characterize motor dysfunction in CRPS patients using kinematic analysis and functional im
41 ffected limb were perceived as equivalent in CRPS(+) and CRPS(-) states, the same stimulus produced d
42 ivations in affected and unaffected limbs in CRPS or post-CRPS states.
43 ts that aim to restore S1 representations in CRPS patients, such as sensory discrimination training a
44 obe may explain some CNS-related symptoms in CRPS, including movement disorders and hemineglect/inatt
45 s system may contribute to motor symptoms in CRPS.
46        Abnormalities in the immune system in CRPS have also been demonstrated.
47 p-stage stratification pattern we uncover in CRPS does not break down with advanced age, and surprisi
48 t sympatho-vagal balance strongly influences CRPS.
49 he past decade has offered new insights into CRPS epidemiology, pathophysiology, diagnosis, and treat
50 ulin G (IgG) from patients with longstanding CRPS or healthy volunteers followed by assessment of paw
51 tal nerve injuries in rodents reproduce many CRPS features, further supporting this hypothesis.
52 75) than those made with the baseline model (CRPS = 125, 95% CI 120-168) but had larger uncertainty.
53 recasts the same incidence rate every month (CRPS = 79.4, 95% CI 78.5-80.5) at lead times of 1 to 3 m
54                                         Most CRPS features-spreading pain and skin hypersensitivity,
55                                      For non-CRPS patients, pain increased by 1.4 +/- 4.1 mm and swel
56 ome (CRPS) were compared with those with non-CRPS pain.
57 the 'psychological versus physical' basis of CRPS.
58                   We find that the degree of CRPS in healthy subjects dramatically changes with sleep
59 subjects, we find that the overall degree of CRPS is reduced by approximately 40%, which has importan
60 ings on diagnostic imaging, the diagnosis of CRPS was made.
61 of favorable outcomes following diagnosis of CRPS.
62 the affected limb is an important feature of CRPS I, we investigated whether this supersensitivity al
63 avasation observed in the edematous hands of CRPS patients.
64 or improving understanding and management of CRPS.
65 ding of the pathophysiological mechanisms of CRPS has led to its classification as a chronic primary
66                       Multiple mechanisms of CRPS have been suggested, and recent research has begun
67 tization in a murine tibia fracture model of CRPS.
68 ional passive transfer trauma mouse model of CRPS.
69 of the choroid plexus in the pathogenesis of CRPS.
70 tical role in the global clinical picture of CRPS.
71 dentification of individuals at high risk of CRPS is improving, with several risk factors established
72 ain after limb fracture or in the setting of CRPS.
73 ronic primary pain disorder, and subtypes of CRPS have been updated.
74 anisms underlying pain and other symptoms of CRPS.
75              Although effective treatment of CRPS remains a challenge, evidence-based integrated mana
76 rther advances in diagnosis and treatment of CRPS will require coordinated, international multicentre
77 Many of the advances in our understanding of CRPS have arisen from the development of collaborative r
78 sions: once during an active period of pain (CRPS(+)), and once after symptomatic recovery (CRPS(-)).
79             Eleven trials (754 participants; CRPS type I, 97%), evaluating alendronate (n = 2), clodr
80       These results indicate that persistent CRPS is often contributed to by autoantibodies and highl
81 ffected and unaffected limbs in CRPS or post-CRPS states.
82 r dermatologists to understand and recognize CRPS as a neurological disorder with major dermatologic
83 PS(+)), and once after symptomatic recovery (CRPS(-)).
84                   Bisphosphonates may reduce CRPS pain intensity in the short term, but treatment is
85 r unaffected limbs of patients with resolved CRPS I (p = 0.02), whose sweat response was not signific
86 th acute CRPS I and 3 patients with resolved CRPS I with that in 9 control subjects using the methodo
87 estoring the interest of neurologists in RSD/CRPS should improve patient care and broaden our knowled
88               We propose that persistent RSD/CRPS-I is a post-traumatic neuralgia associated with dis
89 are the Continuous Ranked Probability Score (CRPS) and the Weighted Interval Score (WIS), which can b
90 ing the continuous ranked probability score (CRPS).
91 dictions (continuous rank probability score [CRPS] = 66.8, 95% CI 60.6-148.0) than a baseline model w
92         111 patients with moderate or severe CRPS of 1 to 5 years' duration.
93 ing pain in patients with moderate to severe CRPS of 1 to 5 years' duration.
94               All colorectal polyp specimens(CRPS) for 2011-2017 in a region were categorized using a
95 how cardiorespiratory phase synchronization (CRPS) responds to changes in physiological states and co
96 ties between complex regional pain syndrome (CRPS) and functional neurological disorders (FND) but un
97 ffering from complex regional pain syndrome (CRPS) compared with age- and gender-matched healthy subj
98 phonates for complex regional pain syndrome (CRPS) despite limited evidence of efficacy.
99 se course of complex regional pain syndrome (CRPS) has been unclear until recently.
100              Complex regional pain syndrome (CRPS) in paediatric patients is clinically distinct from
101              Complex regional pain syndrome (CRPS) is a chronic pain condition usually affecting the
102      Chronic complex regional pain syndrome (CRPS) is a debilitating pain condition accompanied by au
103          The complex regional pain syndrome (CRPS) is a disabling neuropathic pain condition that may
104              Complex regional pain syndrome (CRPS) is a rare pain disorder that usually occurs in a l
105              Complex regional pain syndrome (CRPS) occurs after stroke, but most cases develop after
106 atients with complex regional pain syndrome (CRPS) were compared with those with non-CRPS pain.
107 mic signs in complex regional pain syndrome (CRPS), a posttraumatic pain disorder.
108  symptoms of complex regional pain syndrome (CRPS), a rare posttraumatic pain condition.
109  pain (CBP), complex regional pain syndrome (CRPS), and osteoarthritis patients (OA).
110 ons, such as complex regional pain syndrome (CRPS), are not only associated with, but even maintained
111 cteristic of complex regional pain syndrome (CRPS).
112 d in chronic complex regional pain syndrome (CRPS).
113 atients with complex regional pain syndrome (CRPS).
114 criteria for Complex Regional Pain Syndrome (CRPS).
115  Since a critical rate of protein synthesis (CRPS) is known to mediate passage through Start and dete
116                          We demonstrate that CRPS and the traditionally studied respiratory sinus arr
117 ed((fl/fl)) mouse line, we demonstrated that CRPS IgG-induced changes are in part mediated by microgl
118                      These results show that CRPS is associated with a deficit in tactile processing
119  limb edema in both the animal model and the CRPS patient, and that the anti-edematous effects of MP
120 ng counts before applying scores such as the CRPS or WIS can effectively mitigate these difficulties
121 i-IL-6 antibodies were also evaluated in the CRPS fracture model.
122                         We found: (i) in the CRPS(+) state, stimuli that evoked mechanical or cold al
123 to those reported in adult CRPS; (ii) in the CRPS(+) state, stimuli that evoked mechanical or cold al
124 ers and hemineglect/inattention; (iv) in the CRPS(-) state, significant activation differences persis
125 and geometry of the S1 representation of the CRPS hand were largely comparable with those of both the
126  activations during tapping movements of the CRPS-affected hand in 12 patients compared to healthy co
127                               Similar to the CRPS clinical response to glucocorticoids, we now demons
128 ad sensory abnormalities, not limited to the CRPS limb, have been found suggesting that systemic chan
129                                    Using the CRPS on log-transformed values as an example, we list th
130 tion in the two states, suggesting that the 'CRPS brain' responds differently to normal stimuli appli
131 spontaneous neurogenic extravasation in this CRPS model contributed to the development and maintenanc
132                   Evidence mostly applies to CRPS type I and includes non-U.S.-approved formulations
133 nic hindpaw edema in the sciatic transection CRPS model is reversed by a continuous infusion of MP (3
134 nists, such as anakinra, to prevent or treat CRPS via blocking IL-1 actions.
135 econsider the cortical mechanisms underlying CRPS and the rationale for interventions that aim to "re
136 nd in humans (of either sex) with unilateral CRPS.
137       This supersensitivity is reversed when CRPS I resolves.
138           Ten participants (four males) with CRPS of one arm performed temporal order judgements of p
139  after a peripheral injury and overlaps with CRPS.
140 solve uncertainty around which patients with CRPS are most likely to benefit from bisphosphonates.
141         National registries of patients with CRPS have provided us with an invaluable insight into th
142 nt changes in CNS circuitry in patients with CRPS.
143 ion in paediatric patients (9-18 years) with CRPS affecting the lower extremity.

 
Page Top