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1  there is more frequent lymph node (20%) and neuropathic (28%) involvement compared with non-IgM AL.
2 and proton spin density can detect and grade neuropathic abnormalities in patients with type 1 diabet
3 6-mediated light-dependent analgesia both in neuropathic and in acute/tonic inflammatory pain models.
4        Cold allodynia is a common symptom of neuropathic and inflammatory pain following peripheral n
5                                              Neuropathic and inflammatory pain promote a large number
6 CB1 PAMs offer a promising strategy to treat neuropathic and inflammatory pain with minimal or no can
7 ipherally induced nociception and alleviated neuropathic and inflammatory pain.
8 iceptive efficacy and tolerance in models of neuropathic and/or inflammatory pain.
9 ced in the posterior insular cortex (pIC) of neuropathic animal, which was significantly correlated w
10  lead to altered nerve morphology, including neuropathic changes which can be associated with chronic
11  quarters of patients presented with pain of neuropathic characteristics, which had a length-dependen
12 es are a global epidemic, and the associated neuropathic complications create a substantial burden on
13                                     However, neuropathic corneal pain (NCP) is currently an ill-defin
14 al studies, which may suggest a direct viral neuropathic effect.
15                                Management of neuropathic foot ulcers in patients with diabetes (DFUs)
16 e beta-glucocerebrosidase gene (GBA) causing neuropathic Gaucher's disease (GD) in homozygotes lead t
17     Mutations in the GBA gene pathogenic for neuropathic GD and complex alleles shift longitudinal co
18                                  Carriers of neuropathic GD mutations (1.4% of patients) had hazard r
19 rkinson's disease (PD) patients, whereas non-neuropathic GD mutations confer intermediate progression
20  sensitization, attenuating inflammatory and neuropathic hyperalgesia.
21 deletion of miR-21 in sensory neurons reduce neuropathic hypersensitivity as well as the extent of in
22                         4a also relieves the neuropathic hypersensitivity induced by oxaliplatin.
23 cipally localized to the hands and the feet, neuropathic in nature and in all study participants asso
24                 Samples from age-matched non-neuropathic individuals were used as controls.
25 on of nociceptive hypersensitivity following neuropathic injury.
26 ac involvement, advanced Mayo disease stage, neuropathic involvement, and liver involvement were inde
27 ing a new contributor to the pathogenesis of neuropathic itch and identifying a new candidate therape
28 and Relevance: Our findings demonstrate that neuropathic-like DE pain symptom severity correlates wit
29                When specifically considering neuropathic-like qualities of DE pain, however, anxiety
30        Mice lacking SerpinA3N developed more neuropathic mechanical allodynia than wild-type (WT) mic
31 ircuit rewiring and that this contributes to neuropathic mechanical allodynia.
32 inhibitor (Sivelastat) in WT mice attenuated neuropathic mechanical allodynia.
33  phenotype that resembles Schwann cells from neuropathic mice.
34                 By contrast, the common, non-neuropathic N370S mutation (1.5% of patients; HR, 1.96;
35 mice in either development or maintenance of neuropathic nociception in either neuropathic pain model
36 hirmer's score), and clinical descriptors of neuropathic ocular pain (NOP) (sensitivity to light or s
37 d that male and female patients with chronic neuropathic orofacial pain show increased functional con
38              Chemotherapy-induced peripheral neuropathic pain (CIPN) is a common and severe debilitat
39              Chemotherapy-induced peripheral neuropathic pain (CIPNP) is a severe dose- and therapy-l
40 E), we revised the Special Interest Group on Neuropathic Pain (NeuPSIG) recommendations for the pharm
41  between structural changes and magnitude of neuropathic pain (NP) remains incompletely understood.
42 al over-expression of Arrb2 reverses chronic neuropathic pain after nerve injury.
43 eripheral monocytes are sufficient in gating neuropathic pain after SNT.
44 peutic target for SCI.SIGNIFICANCE STATEMENT Neuropathic pain after spinal cord injury (SCI) may in p
45 rom segments where patients had a history of neuropathic pain also showed electrophysiological and im
46                                              Neuropathic pain and bladder dysfunction represent signi
47 lts in prolongation of inflammatory pain and neuropathic pain and enhancement of GluN2B-mediated NMDA
48  this study we investigated the incidence of neuropathic pain and examined the presence of nerve dysf
49 changes that arise during the development of neuropathic pain and identify the activation of specific
50 rtant role in multiple preclinical models of neuropathic pain and in inherited human pain phenotypes,
51 w male-dominant microglial signaling in some neuropathic pain and inflammatory pain states, although
52 of extract from Corydalis yanhusuo alleviate neuropathic pain and levo-tetrahydropalmatine (l-THP) is
53  Beyond impaired motor and sensory function, neuropathic pain and loss of bladder control caused by s
54 first-line treatment in chemotherapy-induced neuropathic pain and may be highly efficacious in neurop
55 pain, including trigeminal hypersensitivity, neuropathic pain and migraine.
56 which are associated with the persistence of neuropathic pain and motor dysfunction.
57 t in biology and therapeutically in treating neuropathic pain and neurological disorders.
58 te that trkB.T1 in astrocytes contributes to neuropathic pain and neurological dysfunction following
59 berrant afferent input in the maintenance of neuropathic pain and the potential for targeted chemogen
60 , and led to robust motosensory improvement, neuropathic pain and tissue damage mitigation, and myeli
61 ripheral sensory and motorneuronal function, neuropathic pain and tissue necrosis.
62 play a critical role in mPFC deactivation in neuropathic pain and underlie the mPFC-specific cognitiv
63 Here, we show that both basal mechanical and neuropathic pain are controlled by the microRNA-183 (miR
64                                   Peripheral neuropathic pain arises as a consequence of injury to se
65 ng an important novel therapeutic avenue for neuropathic pain as a class.
66 eclinical profile in two different models of neuropathic pain as well as in a reserpine model of cent
67 ) recommendations for the pharmacotherapy of neuropathic pain based on the results of a systematic re
68 ensory scores were unchanged and below-level neuropathic pain became prominent.
69 P2, and DPP10 are potential drug targets for neuropathic pain because they form a channel complex wit
70  plays a critical role in CeA plasticity and neuropathic pain behaviors in the rat spinal nerve ligat
71 nal blockade of intracellular mGluR5 reduces neuropathic pain behaviours and signalling molecules, wh
72 w-strength evidence that cannabis alleviates neuropathic pain but insufficient evidence in other pain
73 ciception in models of post-surgical and HIV neuropathic pain but only slightly blocked anti-nocicept
74                               Alleviation of neuropathic pain by cannabinoids is limited by their cen
75 a proinflammatory cytokine, IFN-gamma drives neuropathic pain by inducing microglial activation in th
76 ndings suggest that DNMT3a may contribute to neuropathic pain by repressing Kcna2 expression in the D
77  recovery ("remission") from inflammatory or neuropathic pain can be reversed by opioid antagonists.
78 e role of pregabalin in CIBP with a clinical neuropathic pain component is unknown.
79 nsmission in the posterior insular cortex in neuropathic pain condition and the involvement of M2 rec
80  therapeutic strategies for inflammatory and neuropathic pain conditions.
81 ng is male dominant in some inflammatory and neuropathic pain conditions.
82 suggesting that adaptive immune responses in neuropathic pain could be sexually dimorphic.
83  molecule-1alpha (RIM1alpha) participates in neuropathic pain development by binding to and upregulat
84 se findings indicate that G9a contributes to neuropathic pain development through epigenetic silencin
85   Spinal plasticity, a key process mediating neuropathic pain development, requires ubiquitination-de
86 onic non-freezing cold injury is a disabling neuropathic pain disorder due to a sensory neuropathy.
87 eund's adjuvant injection and the late phase neuropathic pain following chronic constriction injury (
88                                              Neuropathic pain following peripheral nerve injury is as
89                                              Neuropathic pain frequently leads to decisions about usi
90 l new mechanisms and therapeutic targets for neuropathic pain from different origins.
91                                              Neuropathic pain from injury to the peripheral and CNS r
92 s critical for DRG neuronal excitability and neuropathic pain genesis.
93                 Whether LY2828360 suppresses neuropathic pain has not been reported, and its signalin
94 ng, we found that individuals with orofacial neuropathic pain have increased infra-slow oscillatory a
95  knowledge of the mechanisms contributing to neuropathic pain in diabetes.
96 or (ST2) signaling in experimental models of neuropathic pain in mice.
97 nic pain, and notably in oxaliplatin-induced neuropathic pain in mice.
98 receptor G2A (GPR132) in oxaliplatin-induced neuropathic pain in mice.
99 ling, and functional profiling can attenuate neuropathic pain in patients carrying the S241T mutation
100 dose of RgIA4 prevented chemotherapy-induced neuropathic pain in rats.
101 vidence suggests that cannabis may alleviate neuropathic pain in some patients, but insufficient evid
102 In this study, we report in individuals with neuropathic pain increased oscillatory neural activity w
103 sults suggest that A3AR-mediated reversal of neuropathic pain increases modulation of GABA inhibitory
104                         We show that chronic neuropathic pain increases PACAP expression at multiple
105                                    Sustained neuropathic pain induced by spinal nerve ligation is acc
106 phrine, TNFalpha, and interleukin-6, and the neuropathic pain induced by the cancer chemotherapy pacl
107 tions, drug discovery, prosthetic design and neuropathic pain investigations.
108              We conclude that development of neuropathic pain involves abnormal homeostatic activity
109                                              Neuropathic pain involves long-lasting modifications of
110                         Chronic, intractable neuropathic pain is a common and debilitating consequenc
111                                              Neuropathic pain is a complex, chronic pain state that o
112                                      Chronic neuropathic pain is a major clinical problem with poorly
113                                              Neuropathic pain is a major, intractable clinical proble
114 experimental animal investigations show that neuropathic pain is associated with altered infra-slow (
115 ence from human investigations suggests that neuropathic pain is associated with altered thalamic bur
116              Significance statement: Chronic neuropathic pain is associated with altered thalamic fir
117                                              Neuropathic pain is caused by a primary lesion or dysfun
118 ng the underlying mechanisms responsible for neuropathic pain is critical if we are to develop more e
119 echanisms responsible for the maintenance of neuropathic pain is imperative for the development of mo
120  a primary dermatological disorder can cause neuropathic pain is still unclear.
121 ent of cortical hyperexcitability underlying neuropathic pain may involve homeostatic plasticity in r
122 new insights in the understanding of the HIV neuropathic pain mechanisms and treatment.SIGNIFICANCE S
123                              Here, we used a neuropathic pain model of perineural HIV envelope glycop
124                                         In a neuropathic pain model of perineural HIV gp120 applicati
125 lar behavioral and pathological changes in a neuropathic pain model of peripheral nerve injury.
126                                         In a neuropathic pain model, LC(:SC) activation reduced hind-
127 tenance of neuropathic nociception in either neuropathic pain model.
128 nical hypersensitivity produced in different neuropathic pain models in adult mice.
129 ne tolerance, in both acute pain and chronic neuropathic pain models.
130 fects in myriad preclinical inflammatory and neuropathic pain models.
131 ids alleviated allodynia and hyperalgesia in neuropathic pain models.
132 se, like alpha2delta-1, it is upregulated in neuropathic pain models.
133 in the spinal cord in a nerve injury-induced neuropathic pain mouse model.
134             Skin biopsies from patients with neuropathic pain often show changes in epidermal innerva
135 nged in a sciatic nerve transection model of neuropathic pain or in the Complete Freund's adjuvant mo
136 . x 12 days) suppressed chemotherapy-induced neuropathic pain produced by paclitaxel without producin
137 yer 5 mPFC pyramidal neurons is abolished in neuropathic pain rats due to a severe reduction of a mus
138                                Therefore, in neuropathic pain rats, the acetylcholine (ACh)-dependent
139 DRGs to elicit neuroprotection and sustained neuropathic pain relief via TGF-beta1 secretion.
140 g the development and maintenance of chronic neuropathic pain remain unclear.
141  progression of spinal plasticity-associated neuropathic pain remains unclear.
142  neurodegenerative diseases, but its role in neuropathic pain remains unclear.
143 ical sensitivity, which resemble features of neuropathic pain reported in humans and other species an
144                RGMa antibody also attenuated neuropathic pain responses, which was associated with fe
145       These findings also support the use of neuropathic pain screening tools in these patients and t
146 dynia) is prevalent in many inflammatory and neuropathic pain settings, with little known of the mech
147  questionnaire, and treatment algorithms for neuropathic pain should now be used in the management of
148 y, we report that individuals with orofacial neuropathic pain show altered functional connectivity be
149                                    Using the Neuropathic Pain Special Interest Group of the Internati
150 ed thalamocortical activity and a persistent neuropathic pain state.
151 triggers pC/EBPbeta in the HIV gp120-induced neuropathic pain state.
152 pathic pain and may be highly efficacious in neuropathic pain states that are refractive to opioid an
153  and dorsal root ganglia that contributes to neuropathic pain states through unknown mechanisms.
154  Cold allodynia occurs as a major symptom of neuropathic pain states.
155 ains present in sensory neurons may modulate neuropathic pain states.
156 nges when the injured animals have developed neuropathic pain states.
157 and central sensitization that contribute to neuropathic pain states.
158  subscale (d = 0.26; P = .026), the SF-MPQ-2 neuropathic pain subscale (d = 0.24; P = .036), and SF-M
159 5], Ocular Surface Disease Index [OSDI], and Neuropathic Pain Symptom Inventory modified for the eye
160                                              Neuropathic pain symptoms respond poorly to available th
161 ads to spinal cord central sensitization and neuropathic pain symptoms.
162 mes where patients are experiencing acquired neuropathic pain symptoms.
163 ong-term treatments to ameliorate peripheral neuropathic pain that includes mechanical allodynia are
164 sic effects in rodent models of experimental neuropathic pain through the A3 adenosine receptor (A3AR
165       In this study we used a mouse model of neuropathic pain to dissociate these factors.
166 tivity in nociceptive neurons and suppresses neuropathic pain transduction in a specific, light-touch
167 gh several efficacious medications exist for neuropathic pain treatment, pain is still underrecognize
168 l for targeted silencing of Abeta-fibers and neuropathic pain treatment.
169  post-traumatic intraneural inflammation and neuropathic pain using the chronic constriction injury (
170  A3AR agonists (IB-MECA and MRS5698) reverse neuropathic pain via a spinal mechanism of action that m
171 d CXCR5 expression in spinal astrocytes, and neuropathic pain was abrogated in Cxcr5-/- mice.
172 igation was to determine whether, in humans, neuropathic pain was also associated with altered infra-
173                                    Orofacial neuropathic pain was associated with significant regiona
174                                              Neuropathic pain was induced by cuffing the right sciati
175                                              Neuropathic pain was induced by partial sciatic nerve li
176 enerated by the spared nerve injury model of neuropathic pain was reversed by ivermectin treatment.
177 m male and female humans with cancer-related neuropathic pain was tested here.
178 B1 signaling would suppress inflammatory and neuropathic pain without producing cannabimimetic effect
179 agonist that attenuates chemotherapy-induced neuropathic pain without producing tolerance and may pro
180 sm (eg, painful cramps, nociceptive pain, or neuropathic pain).
181 ssociation for the Study of Pain grading for neuropathic pain, 100% had probable and 95.2% definite n
182                   In addition, the effect on neuropathic pain, a pain type reported by women treated
183  for neuropathic pain.SIGNIFICANCE STATEMENT Neuropathic pain, a type of moderate to severe chronic p
184 of the complement system in inflammatory and neuropathic pain, although the underlying mechanisms are
185 seases, inflammation, neurodegeneration, and neuropathic pain, among others.
186 cal symptoms, such as diarrhea, fatigue, and neuropathic pain, among others.
187 ials that included 396 patients investigated neuropathic pain, and 12 trials that included 1600 patie
188 ne contribute to the generation of epilepsy, neuropathic pain, and autism spectrum disorders; thus, i
189 atherosclerosis, multiple sclerosis, asthma, neuropathic pain, and diabetic nephropathy, as well as c
190 gies, among which glaucoma, edema, epilepsy, neuropathic pain, and hypoxic tumors.
191  implicated in neurodevelopmental disorders, neuropathic pain, and schizophrenia.
192 I-mtO2(.-)-pCREB-pC/EBPbeta signaling in HIV neuropathic pain, and should help in the development of
193           Use of marijuana for chronic pain, neuropathic pain, and spasticity due to multiple scleros
194 ia, nausea/vomiting related to chemotherapy, neuropathic pain, and spasticity in multiple sclerosis.
195 ility-related disorders, including epilepsy, neuropathic pain, and tinnitus.
196  aggravating stroke, temporal lobe epilepsy, neuropathic pain, and various neurodegenerative diseases
197 ors effectively reduce inflammatory pain and neuropathic pain, arguing against the importance of morp
198                 In rats with postsurgical or neuropathic pain, blockade of opioid signaling in the ro
199                          In a mouse model of neuropathic pain, in vivo two-photon imaging and patch c
200  a potential new target for the treatment of neuropathic pain, including chemotherapy (paclitaxel)-in
201 steroidal anti-inflammatory drugs, drugs for neuropathic pain, opioids, and cannabinoids, to physical
202 adigms in a rat model of oxaliplatin-induced neuropathic pain, showed the better antihypersensitive p
203 have been implicated in nerve injury-induced neuropathic pain, the manner by which injured sensory ne
204 aviors in C57BL/6J male mice were induced by neuropathic pain, unpredictable chronic mild stress, and
205 ing the spinal nerve ligation (SNL) model of neuropathic pain, we found that CXCL13 was persistently
206 T2 represents a valuable strategy to relieve neuropathic pain, we synthesized novel activators (4a-f)
207 re severe dry eye symptoms, ocular pain, and neuropathic pain-like ocular symptoms.
208 led to spinal cord central sensitization and neuropathic pain-like symptoms.
209 his single cluster controls more than 80% of neuropathic pain-regulated genes and scales basal mechan
210 e in silencing sensory neurons and reversing neuropathic pain-related hypersensitivity.
211 c pain, 100% had probable and 95.2% definite neuropathic pain.
212 apeutic target to alleviate inflammatory and neuropathic pain.
213 ent amnesia, dysautonomia, neuromyotonia and neuropathic pain.
214  a cellular target for treating this form of neuropathic pain.
215 expression in the injured DRG and attenuates neuropathic pain.
216  a new role for the RGMa/Neogenin pathway on neuropathic pain.
217 cer pharmacotherapy, leading to debilitating neuropathic pain.
218  contribute to the pathogenesis of orofacial neuropathic pain.
219 y and retraction scars limiting movement) or neuropathic pain.
220 ependent distribution resulting in disabling neuropathic pain.
221 els, expressed by nociceptors, contribute to neuropathic pain.
222  development of more specific treatments for neuropathic pain.
223 ng in rat spared nerve injury (SNI) model of neuropathic pain.
224 that a D1/D5 antagonist transiently inhibits neuropathic pain.
225 e nociceptive system is a basic mechanism of neuropathic pain.
226 ing in small fibre neuropathy and associated neuropathic pain.
227 the somatosensory cortex of a mouse model of neuropathic pain.
228  been suggested to be novel drug targets for neuropathic pain.
229 potentially contributing to the mechanism of neuropathic pain.
230 se and rat peripheral nerve injury models of neuropathic pain.
231  useful in the treatment of inflammatory and neuropathic pain.
232 nal cord persistently attenuated SNL-induced neuropathic pain.
233 ted sodium channel NaV1.7 is dysregulated in neuropathic pain.
234 in microglial activation and pathogenesis of neuropathic pain.
235 mer's disease; and schizophrenia and chronic neuropathic pain.
236 the rat chronic constrictive injury model of neuropathic pain.
237 ity in preclinical models of inflammatory or neuropathic pain.
238 rs including depression, drug addiction, and neuropathic pain.
239 paired heat hyperalgesia in inflammatory and neuropathic pain.
240 bute to hypersensitivity in rodent models of neuropathic pain.
241 potential targets for the pharmacotherapy of neuropathic pain.
242 also inhibited allodynia in a mouse model of neuropathic pain.
243 uent RIM1alpha/CaV2.2 cascade in SNL-induced neuropathic pain.
244 analgesic effect in the treatment of chronic neuropathic pain.
245 hanical hypersensitivity, a major symptom of neuropathic pain.
246 y be a useful analgesic in the management of neuropathic pain.
247 -5p decreased CXCL13 expression, alleviating neuropathic pain.
248 opioid analgesic effects in animal models of neuropathic pain.
249 ipheral nerve injury- and paclitaxel-induced neuropathic pain.
250 ists holds promise as a viable treatment for neuropathic pain.
251 ant role of oligodendrocyte-derived IL-33 in neuropathic pain.
252 ession of MORs in primary sensory neurons in neuropathic pain.
253 activates astrocytes via CXCR5 to facilitate neuropathic pain.
254 as a treatment option for paclitaxel-induced neuropathic pain.
255 ling may be suitable therapeutic targets for neuropathic pain.
256 ain perception and relieves inflammatory and neuropathic pain.
257 he potential of cell-based therapies against neuropathic pain.
258 a crucial contribution to the development of neuropathic pain.
259 on (DRG) and diminishes the opioid effect on neuropathic pain.
260 algesics for the dual treatment of acute and neuropathic pain.
261 ministration of TGF-beta1 potently inhibited neuropathic pain.
262 dations for the pharmacological treatment of neuropathic pain.
263 l nucleus in subjects with chronic orofacial neuropathic pain.
264 timulation, represents a cardinal feature of neuropathic pain.
265 death, axonal retraction, and development of neuropathic pain.
266  calcium channel ligands in the treatment of neuropathic pain.
267 es a substantial unmet need in patients with neuropathic pain.
268 tic silencing as a new treatment modality in neuropathic pain.
269 h the cognitive and the sensory component of neuropathic pain.
270 ntion of chronic cancer chemotherapy-induced neuropathic pain.
271 the rat chronic constrictive injury model of neuropathic pain.
272 itivity in peripheral nerve injury models of neuropathic pain.
273 odone in pain-free states, and in a model of neuropathic pain.
274 nhibition of Panx1 may be useful in treating neuropathic pain.
275 which may contribute to nerve injury-induced neuropathic pain.
276 n the rat spared nerve injury (SNI) model of neuropathic pain.
277 eurological disorders including epilepsy and neuropathic pain.
278 thus promotes post-traumatic axonal loss and neuropathic pain.
279  and treatment algorithms designed to target neuropathic pain.
280 stically distinct models of inflammatory and neuropathic pain.
281 CXCL12/CXCR4 signaling pathway may alleviate neuropathic pain.
282 ined therapeutic target for inflammatory and neuropathic pain.
283 ovel strategy for preventing and controlling neuropathic pain.
284 hanical hypersensitivity, a major symptom of neuropathic pain.
285 nced amygdala activity in an animal model of neuropathic pain.
286  effective in the treatment of some types of neuropathic pain.
287 nctional role in SNI- and paclitaxel-induced neuropathic pain.
288 subunits could be potential drug targets for neuropathic pain.SIGNIFICANCE STATEMENT Neuropathic pain
289 ic cognitive deficits that are comorbid with neuropathic pain.SIGNIFICANCE STATEMENT The medial prefr
290  including chemotherapy (paclitaxel)-induced neuropathic pain.SIGNIFICANCE STATEMENT This work demons
291  therapeutic target against inflammatory and neuropathic pain.SIGNIFICANCE STATEMENT We demonstrate t
292  increased 5-HT2CR in the BLA contributes to neuropathic-pain-related amygdala plasticity by driving
293 e, decreases neuronal activity, and inhibits neuropathic-pain-related behaviors.
294 ategy, 5-HT2CR knockdown in the BLA inhibits neuropathic-pain-related behaviors.SIGNIFICANCE STATEMEN
295 r its anxiolytic-like and ability to relieve neuropathic painful conditions evaluated in CCI and STZ
296 hat VA1/HMO-C viruses, unlike HAstV 1-8, are neuropathic, particularly in immunocompromised patients,
297  body, it was tested whether skin cells from neuropathic patients would display the cellular patholog
298                                Similarly, in neuropathic rats kD emerged weeks after injury, in propo
299 inflammatory (complete Freund's adjuvant) or neuropathic (spared nerve injury) model of persistent pa
300      In humans, CSF spermine was elevated in neuropathic subtypes of MPS (MPS I, II, IIIA, IIIB), but

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