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1     In addition, GI pain can be nociceptive, neuropathic and associated with cancer, but in many case
2 6-mediated light-dependent analgesia both in neuropathic and in acute/tonic inflammatory pain models.
3 ipherally induced nociception and alleviated neuropathic and inflammatory pain.
4 iceptive efficacy and tolerance in models of neuropathic and/or inflammatory pain.
5 ions, including postoperative, inflammatory, neuropathic, and migraine pain, as well as opioid-induce
6                                           WT neuropathic animals showed signs of spontaneous pain and
7                                              Neuropathic breast pain did not differ by anaesthetic te
8     In cohort 3, we assessed the presence of neuropathic characteristics of pain.
9  quarters of patients presented with pain of neuropathic characteristics, which had a length-dependen
10 pain, originating from both inflammatory and neuropathic components, and compounds able to modulate t
11 itudinal, prospective study of patients with neuropathic diabetic foot ulcers (DFU).
12  possible effective treatment option for the neuropathic forms of Gaucher disease.
13  sensitization, attenuating inflammatory and neuropathic hyperalgesia.
14 inals in simulated models of inflammatory or neuropathic hyperexcitability led to a change in the tem
15 deletion of miR-21 in sensory neurons reduce neuropathic hypersensitivity as well as the extent of in
16 g and significantly reduced inflammatory and neuropathic hypersensitivity.
17                 Samples from age-matched non-neuropathic individuals were used as controls.
18       The human ENS expresses risk genes for neuropathic, inflammatory, and extra-intestinal diseases
19 order convey mechanical allodynia induced by neuropathic injuries.
20  Pain sensitivity both acutely and following neuropathic injury was largely unaffected by HCN3 deleti
21 ing a new contributor to the pathogenesis of neuropathic itch and identifying a new candidate therape
22 ines, activity-induced genes, and markers of neuropathic itch.
23 ed target engagement in two animal models of neuropathic lysosomal storage diseases (LSDs), Gaucher's
24                                              Neuropathic lysosomal storage disorders (LSDs) present w
25 h L3 and L4 nerves completely alleviated all neuropathic manifestations.
26 sciatic nerve and the dorsal root ganglia in neuropathic mice.
27 sufficient to produce pain-like behaviors in neuropathic mice.SIGNIFICANCE STATEMENT Mechanical allod
28 of LXR pathways have been identified in many neuropathic models.
29 between eIF2alpha and the MEK/ERK pathway in neuropathic nerves.SIGNIFICANCE STATEMENT In the P0S63de
30 nt relief from nociceptive, inflammatory and neuropathic nociception and offers a much-needed non-opi
31 mice in either development or maintenance of neuropathic nociception in either neuropathic pain model
32 ts with diabetes with neuroischaemic (NI) or neuropathic (NP) foot ulcers.
33 h other causes for ulcers, including venous, neuropathic, or pressure changes.
34  of inflammatory origin (atopic dermatitis), neuropathic origin (brachioradial pruritus), and chronic
35 , with a focus on diabetic osteomyelitis and neuropathic osteoarthropathy.
36 eatment and control groups for patients with neuropathic pain (-0.1 points [95% CI, -0.8 to 0.5 point
37 ry, emotional, and cognitive consequences of neuropathic pain (chronic constriction injury) in a rat
38 positive nociceptors in chemotherapy-induced neuropathic pain (CIPN) caused by paclitaxel treatment.
39                  Although NIBS can alleviate neuropathic pain (including PLP), both disease and treat
40                   Pain creams compounded for neuropathic pain (ketamine, gabapentin, clonidine, and l
41                                              Neuropathic pain (NeuP) arises due to injury of the soma
42                                              Neuropathic pain (NP) is a complex chronic pain state wi
43 icated in neuronal excitation, seizures, and neuropathic pain (NP).
44 s and a collection of TDPs in a rat model of neuropathic pain according to a longitudinal, double-bli
45 ions for therapeutics.SIGNIFICANCE STATEMENT Neuropathic pain affects up to 10% of the population, bu
46                                              Neuropathic pain afflicts millions of individuals and re
47 and peripheral electrical NINMs could reduce neuropathic pain among DPN patients, without reported ad
48 ng contributes to various diseases including neuropathic pain and drug addiction.
49           As a result, attenuation of ocular neuropathic pain and dry eye will take place.
50 ular mechanisms engaged by the S1PR1 axis in neuropathic pain and establish S1PR1 as a target for the
51 ciated with the emergence and maintenance of neuropathic pain and increased pin-prick sensation.
52 ed nerve injury replicates symptoms of human neuropathic pain and induces upregulation of many genes
53                              Its key role in neuropathic pain and its limited cellular and tissue dis
54 first-line treatment in chemotherapy-induced neuropathic pain and may be highly efficacious in neurop
55 es could serve as neuroimaging biomarkers of neuropathic pain and might be used for prediction and mo
56 which are associated with the persistence of neuropathic pain and motor dysfunction.
57 se review of the role of dendritic spines in neuropathic pain and outline the potential for modulatio
58 ession, however, has been largely limited to neuropathic pain and perineural invasion.
59 ess behaviour), post-surgical pain, diabetic neuropathic pain and post-herpetic pain.
60 nize GPR160, identify it as a determinant of neuropathic pain and potential therapeutic target, and p
61  fibre damage in relation to the severity of neuropathic pain and quality of life (QoL) in patients w
62 anglion neurons is associated with radicular/neuropathic pain and radiographic nerve root compression
63 berrant afferent input in the maintenance of neuropathic pain and the potential for targeted chemogen
64 , and led to robust motosensory improvement, neuropathic pain and tissue damage mitigation, and myeli
65 play a critical role in mPFC deactivation in neuropathic pain and underlie the mPFC-specific cognitiv
66                     Sensory problems such as neuropathic pain are common and debilitating symptoms in
67 Here, we show that both basal mechanical and neuropathic pain are controlled by the microRNA-183 (miR
68 ved in axon growth, whereas genes related to neuropathic pain are decreased.
69                    The mechanisms underlying neuropathic pain are poorly understood.
70 Non-opioid therapeutics for the treatment of neuropathic pain are urgently needed to address the ongo
71 P2, and DPP10 are potential drug targets for neuropathic pain because they form a channel complex wit
72  plays a critical role in CeA plasticity and neuropathic pain behaviors in the rat spinal nerve ligat
73 al efficacy of nicotinic agents in relieving neuropathic pain best correlated with their activity on
74  showed that they reduce oxaliplatin-induced neuropathic pain by a mechanism involving the alpha7 sub
75 dings support a model in which PI16 promotes neuropathic pain by mediating a cross-talk between fibro
76 inal cord in response to nerve injury drives neuropathic pain by selectively activating the S1P recep
77                                              Neuropathic pain can be a debilitating condition with bo
78 vel translational circuit for the genesis of neuropathic pain caused by chemotherapy with important i
79                                              Neuropathic pain caused by nerve injury presents with se
80                                              Neuropathic pain caused by peripheral nerve injuries sig
81                                       In the neuropathic pain condition, Homer1a, an activity-depende
82 nociceptor sensitization in inflammatory and neuropathic pain conditions.
83 he daily rhythmicity of pain sensation under neuropathic pain conditions.
84 not MMP-2/-12/-14 and significantly relieved neuropathic pain development in mice.
85  specific proteins during distinct phases of neuropathic pain development produces enhanced antinocic
86 golipid metabolism alterations contribute to neuropathic pain development.
87 onic non-freezing cold injury is a disabling neuropathic pain disorder due to a sensory neuropathy.
88 istent post-surgical pain, fibromyalgia, and neuropathic pain disorders, is highly prevalent but rema
89 ntagonists retained their ability to inhibit neuropathic pain during sustained drug administration, a
90 esting paradigms for determining preclinical neuropathic pain efficacy and point to the MNK inhibitor
91 on mechanical allodynia, a standard test for neuropathic pain efficacy.
92                                              Neuropathic pain encompasses a diverse array of clinical
93                                              Neuropathic pain features were present in 50% (95% CI, 3
94 e-specific knockout of S1pr1 did not develop neuropathic pain following nerve injury, thereby identif
95  spinal nerves may be used to manage chronic neuropathic pain following peripheral nerve injury.
96 erlying cause for the development of chronic neuropathic pain following SCI.
97 type channels in SCI-nociceptors and chronic neuropathic pain following SCI.
98 erexcitable state and contributes to chronic neuropathic pain following SCI.SIGNIFICANCE STATEMENT Ch
99  critical role in the development of chronic neuropathic pain following spinal cord injury (SCI).
100     Our findings reveal a novel mechanism of neuropathic pain formation and highlight MrgprD as a pro
101                                              Neuropathic pain frequently leads to decisions about usi
102 acts as the de novo DNMT and is required for neuropathic pain genesis likely through repressing at le
103 hypersensitivities, DRG DNMT1 contributes to neuropathic pain genesis partially through repression of
104 mary sensory neurons of DRG are critical for neuropathic pain genesis.
105 om molecular discoveries in animal models of neuropathic pain have failed to translate following unsu
106 citatory dorsal horn interneurons facilitate neuropathic pain hypersensitivity.
107 ch as paclitaxel are known to elicit chronic neuropathic pain in cancer patients and seriously compro
108  knowledge of the mechanisms contributing to neuropathic pain in diabetes.
109 venues and that has the potential to predict neuropathic pain in future cohorts.
110 lular determinants of nerve regeneration and neuropathic pain in humans.
111 on in the spinal cord prevented and reversed neuropathic pain in male and female rodents without alte
112 nic pain, and notably in oxaliplatin-induced neuropathic pain in mice.
113 s of colorectal carcinoma, causes peripheral neuropathic pain in patients.
114 t not agonists, attenuated and even reversed neuropathic pain in rodents of both sexes and in two mod
115 B2) agonist, suppresses chemotherapy-induced neuropathic pain in rodents without producing tolerance
116 ding to altered sensory phenotypes including neuropathic pain in SFN.SIGNIFICANCE STATEMENT This work
117                     Symptomatic treatment of neuropathic pain in small fibre neuropathy is often disa
118 vidence suggests that cannabis may alleviate neuropathic pain in some patients, but insufficient evid
119 n a well-established mouse model of diabetic neuropathic pain in vivo film implantation showed effect
120      Pin-prick score of the 25 patients with neuropathic pain increased from 1 to 12 months (Deltamea
121                         We show that chronic neuropathic pain increases PACAP expression at multiple
122       The spared nerve injury (SNI) model of neuropathic pain increases PI16 protein levels in fibrob
123 expression of Cdk5 in a preclinical model of neuropathic pain increases the functional expression of
124 nociceptors in naive mice and at the peak of neuropathic pain induced by paclitaxel treatment.
125 phrine, TNFalpha, and interleukin-6, and the neuropathic pain induced by the cancer chemotherapy pacl
126 Identifying the molecular players underlying neuropathic pain induced structural and functional malad
127 nth is the strongest predictor for 12 months neuropathic pain intensity (1.90+/-2.26 and 3.83+/-1.19,
128 tions, drug discovery, prosthetic design and neuropathic pain investigations.
129                                              Neuropathic pain is a complex, chronic pain state that o
130 ced tactile allodynia.SIGNIFICANCE STATEMENT Neuropathic pain is a current public health challenge.
131                                              Neuropathic pain is a debilitating condition caused by t
132 following SCI.SIGNIFICANCE STATEMENT Chronic neuropathic pain is a major comorbidity of spinal cord i
133                                              Neuropathic pain is a significant public health challeng
134                                              Neuropathic pain is an intractable medical condition wit
135                                              Neuropathic pain is believed to arise from damage to noc
136                                     Treating neuropathic pain is challenging and novel non-opioid-bas
137                                              Neuropathic pain is common in peripheral neuropathy.
138 echanisms responsible for the maintenance of neuropathic pain is imperative for the development of mo
139  a primary dermatological disorder can cause neuropathic pain is still unclear.
140 vealing potential peripheral DRG targets for neuropathic pain management.
141 that DRG DNMT1 may be a potential target for neuropathic pain management.SIGNIFICANCE STATEMENT In th
142 ifth lumbar (L5) nerve injury in rats causes neuropathic pain manifested with thermal and mechanical
143 between altered dendritic spine dynamics and neuropathic pain may serve as a structure-based opportun
144                              Here, we used a neuropathic pain model of perineural HIV envelope glycop
145                                         In a neuropathic pain model of perineural HIV gp120 applicati
146                                         In a neuropathic pain model, LC(:SC) activation reduced hind-
147 r cingulate cortex in a chemotherapy-induced neuropathic pain model.
148 howed significant effects on the CCI-induced neuropathic pain model.
149 tenance of neuropathic nociception in either neuropathic pain model.
150 ute inflammatory pain and paclitaxel-induced neuropathic pain models during cancer chemotherapy.
151 fects in myriad preclinical inflammatory and neuropathic pain models.
152 in the spinal cord in a nerve injury-induced neuropathic pain mouse model.
153 isingly, these striking positive outcomes on neuropathic pain occurred in the absence of any effect o
154             Skin biopsies from patients with neuropathic pain often show changes in epidermal innerva
155 x-specific transcriptome changes, leading to neuropathic pain only in female mice.
156 nged in a sciatic nerve transection model of neuropathic pain or in the Complete Freund's adjuvant mo
157 ical hypersensitivity that characterizes the neuropathic pain phenotype.
158 ting the mechanisms by which HCAR2 regulates neuropathic pain plasticity.
159 arget of rapamycin complex 1 is activated in neuropathic pain pointing to a key role of MNK1-eIF4E-me
160 though it has no major influence on acute or neuropathic pain processing.
161 . x 12 days) suppressed chemotherapy-induced neuropathic pain produced by paclitaxel without producin
162 gonist EHD2-sc-mTNF(R2) in mice with chronic neuropathic pain promoted long-lasting pain recovery.
163 udy therefore reveals a function of TNFR2 in neuropathic pain recovery and demonstrates that both TNF
164                                              Neuropathic pain remains a therapeutic challenge because
165 e underlying mechanism of MrgprD involved in neuropathic pain remains elusive.
166 the involvement of CB(2) from these cells in neuropathic pain remains unresolved.
167                RGMa antibody also attenuated neuropathic pain responses, which was associated with fe
168 olecular level, the beneficial reductions in neuropathic pain resulting from S1PR1 inhibition were dr
169  neuropathy symptom inventory questionnaire, neuropathic pain scale) and QoL (SF-36, pre-R-ODS and ho
170       These findings also support the use of neuropathic pain screening tools in these patients and t
171  questionnaire, and treatment algorithms for neuropathic pain should now be used in the management of
172 y, we report that individuals with orofacial neuropathic pain show altered functional connectivity be
173 triggers pC/EBPbeta in the HIV gp120-induced neuropathic pain state.
174 pathic pain and may be highly efficacious in neuropathic pain states that are refractive to opioid an
175 l horn and contributes to characteristics of neuropathic pain such as mechanical and thermal hypersen
176 ion by MRI and patient-based questionnaires (Neuropathic Pain Symptom Inventory and 36-Short Form Hea
177                                              Neuropathic pain symptoms respond poorly to available th
178 and neuronal plasticity related to radicular/neuropathic pain that may suggest therapeutic avenues an
179                      We explored spontaneous neuropathic pain through on-demand self-administration o
180 s essential in cold allodynia in CCI-induced neuropathic pain through the PKA-TRP-A1 pathway.
181       In this study we used a mouse model of neuropathic pain to dissociate these factors.
182 atform for treating pathologies ranging from neuropathic pain to epilepsy.
183  (eFT508) as an important drug candidate for neuropathic pain treatment.
184  agonist drugs for treating inflammatory and neuropathic pain without the psychoactivity of CB1.
185  predominant target in metastasis; MMP-9, in neuropathic pain), beta-secretase 1 (BACE-1, an aspartic
186 sm (eg, painful cramps, nociceptive pain, or neuropathic pain).
187  month) spinal cord injury (25 patients with neuropathic pain, 19 pain-free patients) and neuroimagin
188  for neuropathic pain.SIGNIFICANCE STATEMENT Neuropathic pain, a type of moderate to severe chronic p
189 itical role in all modes of inflammatory and neuropathic pain, although the role of HCN3 in nocicepti
190 rgic receptor is a potential drug target for neuropathic pain, Alzheimer disease, and prostate cancer
191 ne contribute to the generation of epilepsy, neuropathic pain, and autism spectrum disorders; thus, i
192  in rats and dogs and was active in anxiety, neuropathic pain, and lower urinary tract models.
193 multiple sclerosis, asthma, atherosclerosis, neuropathic pain, and rheumatoid arthritis.
194  implicated in neurodevelopmental disorders, neuropathic pain, and schizophrenia.
195 al syndromes and diseases, including chronic neuropathic pain, autism, and epilepsy.
196          In the rodent nerve injury model of neuropathic pain, BDNF-mediated loss of inhibition (disi
197 al dysrhythmia is a key pathology of chronic neuropathic pain, but few studies have investigated thal
198 ts long-lasting spinal inhibitory control of neuropathic pain, but its mechanism of action is complic
199 ormer is causally connected with the chronic neuropathic pain, but its mechanisms are poorly understo
200 st line analgesics used to treat SCI-induced neuropathic pain, but their efficacy is very limited.
201 dimorphism in the microglial contribution to neuropathic pain, depletion of DRG macrophages reduces n
202 artial sciatic nerve ligation (PSNL)-induced neuropathic pain, however, the cell types that are funct
203  a potential new target for the treatment of neuropathic pain, including chemotherapy (paclitaxel)-in
204 unctional perceptual changes associated with neuropathic pain, including pain aversion to light touch
205 on of various ion channels can be altered in neuropathic pain, including T-type Ca(2+) channels that
206    In the spared nerve injury (SNI) model of neuropathic pain, NPY-saporin decreased mechanical and c
207 steroidal anti-inflammatory drugs, drugs for neuropathic pain, opioids, and cannabinoids, to physical
208                      Patients suffering from neuropathic pain, or nerve damage, experience an inversi
209          Given that Kcna2 is a key player in neuropathic pain, our findings suggest that DRG DNMT1 ma
210 ty in vivo in an experimental mouse model of neuropathic pain, raising the possibility that it might
211 old allodynia and models of inflammatory and neuropathic pain, respectively, following intraperitonea
212 adigms in a rat model of oxaliplatin-induced neuropathic pain, showed the better antihypersensitive p
213 aviors in C57BL/6J male mice were induced by neuropathic pain, unpredictable chronic mild stress, and
214  development and/or maintenance of acute and neuropathic pain, we selectively ablated Y1R-expressing
215          In these well-established models of neuropathic pain, we show that the onset of chronic pain
216 T2 represents a valuable strategy to relieve neuropathic pain, we synthesized novel activators (4a-f)
217 us CARTp signaling in spinal cord attenuated neuropathic pain, whereas exogenous intrathecal CARTp ev
218 iors across sensory modalities and abolished neuropathic pain-induced mechanical (hyper-)sensitivity.
219 re severe dry eye symptoms, ocular pain, and neuropathic pain-like ocular symptoms.
220 e blockage of the mGluR5 resulted in chronic neuropathic pain-like symptoms even in the absence of ne
221 regulation, oocyte development, epilepsy and neuropathic pain.
222  pharmacological target to treat SCI-induced neuropathic pain.
223 r synaptic plasticity in the pathogenesis of neuropathic pain.
224 erves (L3 and L4) would alleviate peripheral neuropathic pain.
225 ion mainly produced by fibroblasts, controls neuropathic pain.
226 microglia contribute to nerve injury-induced neuropathic pain.
227 ury and chemotherapy-induced mouse models of neuropathic pain.
228 cause of lower-limb amputation and disabling neuropathic pain.
229 a promising drug target for the treatment of neuropathic pain.
230 ting a potential role in the pathogenesis of neuropathic pain.
231 in chronic constriction injury (CCI)-induced neuropathic pain.
232 on of pain signalling and the maintenance of neuropathic pain.
233 ntial pharmacological target in migraine and neuropathic pain.
234 an potentially be exploited toward targeting neuropathic pain.
235  TRP-A1 facilitates MrgprD to development of neuropathic pain.
236 ntially damaging stimuli, are key drivers of neuropathic pain.
237  the analgesic action of these drugs against neuropathic pain.
238 TSP/alpha(2)delta-1 interaction to alleviate neuropathic pain.
239 nopioid therapy for the treatment of chronic neuropathic pain.
240 elieving effect against nerve injury-induced neuropathic pain.
241 owing promising efficacy in a mouse model of neuropathic pain.
242 for the control of inflammatory, chronic and neuropathic pain.
243  temporomandibular disorders, and trigeminal neuropathic pain.
244 patients with variable presence of radicular/neuropathic pain.
245    Facilitation of MrgprD by TRP-A1 promotes neuropathic pain.
246  acid receptor type 2 (HCAR2) in 2 models of neuropathic pain.
247 trials, eFT508, may be a new therapeutic for neuropathic pain.
248 normalities in Schwann cells (SCs) may cause neuropathic pain.
249 le of Toll-like receptor 4 (TLR4) in driving neuropathic pain.
250 ht to drive aversion associated with chronic neuropathic pain.
251 id receptor type 2 in the pathophysiology of neuropathic pain.
252 ally-directed Y1R agonists to reduce chronic neuropathic pain.
253 h the cognitive and the sensory component of neuropathic pain.
254 which may contribute to nerve injury-induced neuropathic pain.
255  and treatment algorithms designed to target neuropathic pain.
256 hanical hypersensitivity, a major symptom of neuropathic pain.
257 ependent distribution resulting in disabling neuropathic pain.
258 e nociceptive system is a basic mechanism of neuropathic pain.
259 hanical hypersensitivity, a major symptom of neuropathic pain.
260 tic silencing as a new treatment modality in neuropathic pain.
261 ntion of chronic cancer chemotherapy-induced neuropathic pain.
262 the rat chronic constrictive injury model of neuropathic pain.
263 itivity in peripheral nerve injury models of neuropathic pain.
264 odone in pain-free states, and in a model of neuropathic pain.
265 nhibition of Panx1 may be useful in treating neuropathic pain.
266 n the rat spared nerve injury (SNI) model of neuropathic pain.
267 eurological disorders including epilepsy and neuropathic pain.
268 del of peripheral nerve injury (PNI)-induced neuropathic pain.
269 t and the development of novel therapies for neuropathic pain.
270 as modeling human neurological diseases like neuropathic pain.
271 ovel therapeutic target for the treatment of neuropathic pain.
272 Mice deficient in PI16 are protected against neuropathic pain.
273 lue than common outbred strains for modeling neuropathic pain.
274  can cause acute peripheral pain and chronic neuropathic pain.
275 ymal transition (EMT), loss of sensation and neuropathic pain.
276 ied activity of PB neurons in a rat model of neuropathic pain.
277 ndritic spine dysgenesis and the presence of neuropathic pain.
278 ing of LPA(1) signaling in the PSNL model of neuropathic pain.
279 innings in the initiation and maintenance of neuropathic pain.
280 t an interesting therapeutic alternative for neuropathic pain.
281 that protects against spontaneous and evoked neuropathic pain.
282 sence epilepsy, cardiovascular diseases, and neuropathic pain.
283 phage TLR9 signaling in chemotherapy-induced neuropathic pain.SIGNIFICANCE STATEMENT Chemotherapy-ind
284 subunits could be potential drug targets for neuropathic pain.SIGNIFICANCE STATEMENT Neuropathic pain
285 ic cognitive deficits that are comorbid with neuropathic pain.SIGNIFICANCE STATEMENT The medial prefr
286  including chemotherapy (paclitaxel)-induced neuropathic pain.SIGNIFICANCE STATEMENT This work demons
287  therapeutic target against inflammatory and neuropathic pain.SIGNIFICANCE STATEMENT We demonstrate t
288  increased 5-HT2CR in the BLA contributes to neuropathic-pain-related amygdala plasticity by driving
289 r its anxiolytic-like and ability to relieve neuropathic painful conditions evaluated in CCI and STZ
290 aliplatin triggers alterations in peripheral neuropathic pathways previously linked to IL-8 pathway.
291  body, it was tested whether skin cells from neuropathic patients would display the cellular patholog
292 lt K/BxN transgenic arthritic mice display a neuropathic phenotype, an assertion consistent with the
293 plasticity of the brain in DSP driven by the neuropathic process.
294 ace excessive production and accumulation of neuropathic proteins as the major initiating events.
295  reduced measures of allodynia in a chronic, neuropathic sciatic nerve injury model, but tolerance to
296      In humans, CSF spermine was elevated in neuropathic subtypes of MPS (MPS I, II, IIIA, IIIB), but
297 f large and small nerve fibre function, CCM, neuropathic symptoms (small fibre neuropathy symptom inv
298  loss, which correlates with the severity of neuropathic symptoms and reduced QoL in patients with pa
299 ry [Short Form]; and the Leeds Assessment of Neuropathic Symptoms and Signs [Self-Assessment] scale).
300 l CCM parameters and the severity of painful neuropathic symptoms, depression score and QoL.

 
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