Sensory profiles and immune-related expression patterns of patients with and without neuropathic pain after peripheral nerve lesion

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F65269705%3A_____%2F19%3A00071251" target="_blank" >RIV/65269705:_____/19:00071251 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216224:14110/19:00112744

Výsledek na webu

<a href="https://journals.lww.com/pain/fulltext/2019/10000/Sensory_profiles_and_immune_related_expression.16.aspx" target="_blank" >https://journals.lww.com/pain/fulltext/2019/10000/Sensory_profiles_and_immune_related_expression.16.aspx</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1097/j.pain.0000000000001623" target="_blank" >10.1097/j.pain.0000000000001623</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Sensory profiles and immune-related expression patterns of patients with and without neuropathic pain after peripheral nerve lesion

Popis výsledku v původním jazyce

In this multicenter cross-sectional study, we determined sensory profiles of patients with (NL-1) and without neuropathic pain (NL-0) after nerve lesion and assessed immune-related systemic gene expression. Patients and matched healthy controls filled in questionnaires and underwent neurological examination, neurophysiological studies, quantitative sensory testing, and blood withdrawal. Neuropathic pain was present in 67/95 (71%) patients (NL-1). Tactile hyperalgesia was the most prominent clinical sign in NL-1 patients (P &lt; 0.05). Questionnaires showed an association between neuropathic pain and the presence of depression, anxiety, and catastrophizing (P &lt; 0.05 to P &lt; 0.01). Neuropathic pain was frequently accompanied by other chronic pain (P &lt; 0.05). Quantitative sensory testing showed ipsilateral signs of small and large fiber impairment compared to the respective contralateral side, with elevated thermal and mechanical detection thresholds (P &lt; 0.001 to P &lt; 0.05) and lowered pressure pain threshold (P &lt; 0.05). Also, more loss of function was found in patients with NL-1 compared to NL-0. Pain intensity was associated with mechanical hyperalgesia (P &lt; 0.05 to P &lt; 0.01). However, quantitative sensory testing did not detect or predict neuropathic pain. Gene expression of peptidylglycine α-amidating monooxygenase was higher in NL patients compared with healthy controls (NL-1, P &lt; 0.01; NL-0, P &lt; 0.001). Also, gene expression of tumor necrosis factor-α was higher in NL-1 patients compared with NL-0 (P &lt; 0.05), and interleukin-1ß was higher, but IL-10 was lower in NL-1 patients compared with healthy controls (P &lt; 0.05 each). Our study reveals that nerve lesion presents with small and large nerve fiber dysfunction, which may contribute to the presence and intensity of neuropathic pain and which is associated with a systemic proinflammatory pattern.

Název v anglickém jazyce

Sensory profiles and immune-related expression patterns of patients with and without neuropathic pain after peripheral nerve lesion

Popis výsledku anglicky

In this multicenter cross-sectional study, we determined sensory profiles of patients with (NL-1) and without neuropathic pain (NL-0) after nerve lesion and assessed immune-related systemic gene expression. Patients and matched healthy controls filled in questionnaires and underwent neurological examination, neurophysiological studies, quantitative sensory testing, and blood withdrawal. Neuropathic pain was present in 67/95 (71%) patients (NL-1). Tactile hyperalgesia was the most prominent clinical sign in NL-1 patients (P &lt; 0.05). Questionnaires showed an association between neuropathic pain and the presence of depression, anxiety, and catastrophizing (P &lt; 0.05 to P &lt; 0.01). Neuropathic pain was frequently accompanied by other chronic pain (P &lt; 0.05). Quantitative sensory testing showed ipsilateral signs of small and large fiber impairment compared to the respective contralateral side, with elevated thermal and mechanical detection thresholds (P &lt; 0.001 to P &lt; 0.05) and lowered pressure pain threshold (P &lt; 0.05). Also, more loss of function was found in patients with NL-1 compared to NL-0. Pain intensity was associated with mechanical hyperalgesia (P &lt; 0.05 to P &lt; 0.01). However, quantitative sensory testing did not detect or predict neuropathic pain. Gene expression of peptidylglycine α-amidating monooxygenase was higher in NL patients compared with healthy controls (NL-1, P &lt; 0.01; NL-0, P &lt; 0.001). Also, gene expression of tumor necrosis factor-α was higher in NL-1 patients compared with NL-0 (P &lt; 0.05), and interleukin-1ß was higher, but IL-10 was lower in NL-1 patients compared with healthy controls (P &lt; 0.05 each). Our study reveals that nerve lesion presents with small and large nerve fiber dysfunction, which may contribute to the presence and intensity of neuropathic pain and which is associated with a systemic proinflammatory pattern.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2019

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Pain

ISSN

0304-3959

e-ISSN

—

Svazek periodika

160

Číslo periodika v rámci svazku

10

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

12

Strana od-do

2316-2327

Kód UT WoS článku

000512905700016

EID výsledku v databázi Scopus

2-s2.0-85072747523