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1 ing hypersensitivity of dorsal horn neurons (central sensitization).
2 l sensitization) and spinal cord mechanisms (central sensitization).
3 ces proinflammatory microglia activation and central sensitization.
4 ute to heightened clinical pain, perhaps via central sensitization.
5 ll as in normal subjects during experimental central sensitization.
6 d the development of cutaneous allodynia and central sensitization.
7  in the absence, but not in the presence, of central sensitization.
8 a and dorsal horn neurons, thus resulting in central sensitization.
9 the calcium channel alpha2delta-1 subunit in central sensitization.
10 ficient to counteract an already established central sensitization.
11 ed with peripheral sensitization, as well as central sensitization.
12 primary afferent neurons and has been termed central sensitization.
13  in chronic pain by mediating peripheral and central sensitization.
14 rties of other nociceptive neurons and drive central sensitization.
15 phology parameters without and with signs of central sensitization.
16 to prevent hyperalgesia and formalin-induced central sensitization.
17 heral nociceptors, before the development of central sensitization.
18 tability of central (spinal) neurons, termed central sensitization.
19 dministration, a measure of C fiber-mediated central sensitization.
20                     The allodynia reflects a central sensitization.
21 s important in the generation of wind-up and central sensitization.
22 on producing an increase in excitability and central sensitization.
23 bility changes of dorsal horn neurons during central sensitization.
24 d enhanced spinal expression of NCX3 reduced central sensitization.
25 ciceptive pain, peripheral sensitization and central sensitization.
26 mediators, thereby regulating peripheral and central sensitization.
27  spinal cord, an area critically involved in central sensitization.
28 nisms that may be involved in peripheral and central sensitization.
29 se state of chronic pain, which is caused by central sensitization.
30 iour, suggesting a potential role of SOCs in central sensitization.
31             Several mechanisms contribute to central sensitization.
32 d and pain-related brain regions, indicating central sensitization.
33 ansmitter release within the spinal cord and central sensitization.
34 lity, spinal cord synaptic transmission, and central sensitization.
35 ions that we consider indicative of possible central sensitization.
36 n the development of neuronal plasticity and central sensitization.
37 ttle is known about the mediators that drive central sensitization.
38 ith noncardiac chest pain (NCCP), suggesting central sensitization.
39 S play an important role in pain mediated by central sensitization.
40 ral mechanism of cephalic migraine symptoms, central sensitization, also predicting the clinical outc
41 nist suppresses behavioral manifestations of central sensitization, an activity-dependent increase in
42                                              Central sensitization, an activity-dependent increase in
43 of integration in the brainstem, may lead to central sensitization analogous to that described in som
44 periments provide a population-level view of central sensitization and a framework with which to mode
45 naling could be an effective way to suppress central sensitization and alleviate chronic pain.
46                                     To date, central sensitization and astrocyte changes have not bee
47  include altered descending pain modulation, central sensitization and biobehavioural factors.
48 ld provide a neurophysiological mechanism of central sensitization and chronic pain associated with s
49      Microglia play an important role in the central sensitization and chronic pain.
50 ation of Nav1.8(+) afferents in vivo induced central sensitization and conditioned place aversion, th
51 lve the processes of amplification including central sensitization and descending facilitation.
52 ms that may be the prepotent contributors to central sensitization and development of secondary hyper
53  spinal nociceptive processing indicative of central sensitization and for adaptive changes in the sp
54 on of the mutual neuron-glia interactions to central sensitization and hyperalgesia prompts new treat
55  our data have demonstrated that PICs induce central sensitization and hyperalgesia via distinct and
56 have an opposite role and even contribute to central sensitization and hyperalgesia.
57 f the spinal circuits involved in triggering central sensitization and hyperalgesia.
58 ce that activation of CB2 receptors inhibits central sensitization and its contribution to the manife
59 underlying the generation and maintenance of central sensitization and LTP indicates that, although t
60                                              Central sensitization and network hyperexcitability of t
61 trocytes after JNK activation contributes to central sensitization and neuropathic pain facilitation
62 lity in DRG neurons and leads to spinal cord central sensitization and neuropathic pain symptoms.
63 ty in the DRG neurons and led to spinal cord central sensitization and neuropathic pain-like symptoms
64 or (BDNF) signaling appears to contribute to central sensitization and nocifensive behaviors in certa
65 , contributing thereby to activity-dependent central sensitization and pain hypersensitivity.
66 atory synaptogenesis, which together lead to central sensitization and pain state development.
67  are complex and include both peripheral and central sensitization and the involvement of the autonom
68 , leading to hyperexcitable neuronal states, central sensitization and widespread neural plasticity c
69 erapies may target the peripheral drivers of central sensitization and/or the central consequences.
70 le in spinal cord synaptic plasticity (i.e., central sensitization) and pain hypersensitivity after t
71 ed neuronal excitability in the spinal cord (central sensitization), and a syndrome comprising diffus
72  cornea morphology without and with signs of central sensitization, and a group with abnormal cornea
73 secondary mechanical hyperalgesia, a sign of central sensitization, and increased the N13 SEP amplitu
74  excitability of spinal dorsal horn neurons, central sensitization, and the behavioral correlate, hyp
75 es of these circuits, such as peripheral and central sensitization, and the segmental and descending
76                 Nociceptor sensitization and central sensitization are considered to underlie, respec
77      However, synaptic mechanisms underlying central sensitization are incompletely known.
78 rrently available drugs that aim to suppress central sensitization are ineffective, this study stress
79        New findings regarding peripheral and central sensitization are presented in this review.
80                       Manifestations of this central sensitization are windup and long-term potentiat
81 on animal studies, it has been proposed that central sensitization associated to nociception (maladap
82 may contribute to nociceptive plasticity and central sensitization associated with chronic inflammato
83 nce of secondary hyperalgesia and underlying central sensitization associated with persistent pain de
84 f several interplaying mechanisms, including central sensitization, blunting of inhibitory pain pathw
85 n can prevent and/or suppress peripheral and central sensitization by using single-unit recording in
86                           A similar state of central sensitization can be experimentally produced wit
87                                   Diagnosing central sensitization can be particularly difficult.
88                                              Central sensitization caused by spinal disinhibition is
89  of the CCM parameters and sensory tests for central sensitization, (cold pain threshold, mechanical
90 n to peripheral nociceptors, peripheral- and central sensitization contribute to the pathophysiology
91 cent clinical evidence has demonstrated that central sensitization contributes to OA pain.
92 g and inflammation, with both peripheral and central sensitization contributing to joint pain.
93                Nitroglycerin (NTG)-triggered central sensitization (CS) provides a rodent model of mi
94                                              Central sensitization (CS) refers to an increase in the
95 ence suggests that opioid withdrawal induces central sensitization (CS) that is maintained by suprasp
96 tory nature of HS was hypothesized to induce central sensitization (CS; alteration and amplification
97                                           If central sensitization develops, the therapeutic rational
98                                Consequently, central sensitization-driven pain hypersensitivity, but
99 tan intervention counteracted two aspects of central sensitization: dural receptive fields, which ini
100  in the dorsal horn and in the generation of central sensitization during chronic pain states.
101 gnal-regulated kinases (ERKs), which mediate central sensitization during inflammatory pain.
102 ly blocked the development of all aspects of central sensitization expected to be induced 2 h after I
103 spinal dorsal horn that functions to prevent central sensitization following brief, mild, noxious sti
104                                         This central sensitization has been attributed to the enhance
105  dorsal horn neurons and its contribution to central sensitization have been investigated.
106 inal cord dorsal horn neurons, indicative of central sensitization (hyperactivity of dorsal horn neur
107 lar cortex, independently of the presence of central sensitization; (ii) gabapentin reduced the activ
108 the activation in the brainstem, only during central sensitization; (iii) gabapentin suppressed stimu
109 is study reveals that CaMK II contributes to central sensitization in a manner similar to its role in
110 ng the NK1 receptor, shown to be involved in central sensitization in adults, in the negative effects
111 time, the optical control of nociception and central sensitization in behaving mammals and enables se
112 rrent that is believed to be associated with central sensitization in chronic neuropathic pain states
113 t activity-dependent synaptic plasticity and central sensitization in chronic pain.
114 ns may contribute to synaptic plasticity and central sensitization in diabetic neuropathic pain.
115 ion of PKC contributes to the development of central sensitization in dorsal horn neurons produced by
116 tability and represent a useful biomarker of central sensitization in human studies.
117  (OA) pain is associated with peripheral and central sensitization in humans and results in widesprea
118                                              Central sensitization in inflammatory pain conditions re
119                     The results suggest that central sensitization in knee OA is especially apparent
120 e with recent findings regarding the role of central sensitization in pain chronification, especially
121                                 Evidence for central sensitization in pain processing included increa
122 al medulla (RVM) attenuates hyperalgesia and central sensitization in several models of persistent pa
123 tudy tested the hypothesis that induction of central sensitization in the dorsal horn by an intraderm
124 t the combined effects of afferent input and central sensitization in the dorsal horn.
125 gic system is involved in the development of central sensitization in the pain neuraxis, associated w
126 nce phase of secondary hyperalgesia involved central sensitization in Vc neurons conducted by a delay
127 PGE(2)) is a mediator in both peripheral and central sensitization, in part via the prostaglandin E2
128 er assessed in models presumably mediated by central sensitization, including CFA- and capsaicin-indu
129                                              Central sensitization, increased sensitivity in spinal c
130 22 healthy participants, we investigated how central sensitization induced by application of topical
131 fects of sumatriptan (300 microg/kg i.v.) on central sensitization induced by topical application of
132                     The main outcome was the Central Sensitization Inventory (CSI) score (ranging fro
133                                          The Central Sensitization Inventory could be used to counsel
134   The main variable of interest was baseline Central Sensitization Inventory score (measured from 0 t
135                       The mean (SD) baseline Central Sensitization Inventory score was 43.8 (18.2), a
136 y of 239 patients with endometriosis, higher Central Sensitization Inventory scores at baseline were
137 05); however, individuals with high baseline Central Sensitization Inventory scores still had high sc
138                                          The Central Sensitization Inventory scores themselves decrea
139                              Higher baseline Central Sensitization Inventory scores were significantl
140                                          The Central Sensitization Inventory, a validated self-report
141                                              Central sensitization is a form of activity-dependent pl
142                                      Because central sensitization is considered to reflect plasticit
143                                              Central sensitization is maintained by continuing input
144 ribution of specific classes of afferents to central sensitization is possible.
145  in modulating nociceptive transmission when central sensitization is present.
146                                              Central sensitization is thought to play a role in chron
147                      Primary afferent-evoked central sensitization is, in addition, reduced in B2 rec
148 ensory inputs in the central nervous system (central sensitization) is the mechanism accounting for t
149 hnic afferents results in the development of central sensitization manifested as hyperalgesia and inc
150 ults provide evidence for SREP as a possible central sensitization marker with potential clinical uti
151 s and explored its potential usefulness as a central sensitization marker.
152 ible for the genesis of pain in TTH, whereas central sensitization may be involved in transformation
153 r factors besides the endometriosis, such as central sensitization, may play a role in this pain.
154 ion phase of secondary hyperalgesia involved central sensitization mechanisms in Vc neurons that were
155 ed a useful preclinical tool for deciphering central sensitization mechanisms involved in migraine at
156 ed a useful preclinical tool for deciphering central sensitization mechanisms involved in migraine at
157 europathic pain reflects both peripheral and central sensitization mechanisms.
158 icacy in a rat surrogate model indicative of central sensitization, namely phase 2 response of formal
159 ield size, mechanical and thermal coding and central sensitization of deeper dorsal horn neurons that
160 ms have been implicated in neuropathic pain, central sensitization of dorsal horn spinothalamic tract
161 inflammatory mediators induce peripheral and central sensitization of gut-innervating sensory neurons
162  activation was not required for maintaining central sensitization of itch.
163 a within the trigeminal nucleus complex, and central sensitization of medullary dorsal horn neurons i
164 similar mechanisms that result in wind-up or central sensitization of spinal cord neurons.
165                                              Central sensitization of spinothalamic tract (STT) neuro
166 study was designed to examine the effects of central sensitization of spinothalamic tract (STT) neuro
167  enhanced anterior cingulate and PAG reflect central sensitization of the pain matrix, while decrease
168 uch cutaneous allodynia suggests a state of 'central sensitization' of pain transmission pathways and
169 in temporal summation (surrogate measures of central sensitization) on the forearm.
170             For pain, the covered topics are central sensitization, pain-touch and pain-pain interact
171 ensory stimulation, reflecting signatures of central sensitization potentially mediating throbbing he
172  understanding, at a subject-specific level, central sensitization processes that contribute to chron
173 ation of AMPA receptor GluR1 subunits during central sensitization produced by capsaicin injection.
174 ration of JWH133 attenuated these markers of central sensitization, providing a neurobiological basis
175                Issues related to plasticity, central sensitization, psychological confounds, genetics
176                                              Central sensitization refers to the increased synaptic e
177 erents could be the signal that produces the central sensitization responsible for the development of
178 le for the initiation and maintenance of the central sensitization seen in neuropathic pain states.
179                                 Hallmarks of central sensitization, significant spinal astrogliosis a
180 ntervention did not reverse other aspects of central sensitization: spontaneous firing rate and neuro
181 ing of nociceptive information in normal and central sensitization states.
182 ohen d range, 0.906-1.112) and self-reported central sensitization symptoms (Cohen d range, 1.158-1.8
183 igher disability due to pain and more severe central sensitization symptoms (CSS).
184 efits in pain-related anxiety, self-reported central sensitization symptoms, and cost-effectiveness.
185 , a validated self-reported questionnaire of central sensitization symptoms, may identify individuals
186 aires (P < .001), and a higher prevalence of central sensitization syndromes (P < .001).
187 ord to promote excitatory synaptogenesis and central sensitization that contribute to neuropathic pai
188 injury may reduce the initial peripheral and central sensitization that occurs after tissue injury.
189 lgesia) and spinal cord hyperexcitability or central sensitization that results in secondary hyperalg
190 nts of dorsal horn neuronal excitability and central sensitization that underlies hypersensitivity af
191 to injury-induced spinal neuroplasticity and central sensitization that underlies neuropathic pain de
192 the important role of these receptors in the central sensitization that underlies the maintenance of
193 rsal horn of the spinal cord is required for central sensitization, the central facilitation of pain
194  stimulus-induced deactivations, only during central sensitization; this effect was more robust than
195 y in vivo evidence that OA pain is caused by central sensitization through communication between peri
196 th PKA and PKC, and that this contributes to central sensitization through post-translational and CRE
197 mined molecular mechanisms of peripheral and central sensitization to infer chronic pain from HIV inf
198 that PKC is important for the development of central sensitization to peripheral mechanical stimuli.
199 ss of these inhibitory mechanisms that allow central sensitization to proceed.
200 s have demonstrated that both peripheral and central sensitization to pruritogenic stimuli occur duri
201 werful means of preventing the initiation of central sensitization triggered by chemical stimulation
202                                              Central sensitization was indexed through quantitative s
203                    This functions to prevent central sensitization when the noxious stimulus does not
204 modulation associated with capsaicin-induced central sensitization, whereas capsaicin application sti
205           The neuropeptide may help maintain central sensitization, which could serve to enhance guar
206                          CAPS is a result of central sensitization with disinhibition of pain signals
207 atory response, resulting in "peripheral and central sensitization," with the latter resulting from r

 
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