ReviewCurrent neuropharmacology2017
The Proteomics of Intrathecal Analgesic agents for Chronic Pain.
Review in Current neuropharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Ziconotide and psychosis: from a case report to a scoping review.Frontiers in molecular neuroscience · 2024Article
- Lumbosacral spinal proteomic changes during PAR4-induced persistent bladder pain.Neuroscience letters · 2024Article
- Cerebrospinal fluid immune cells appear similar across neuropathic and non-neuropathic pain conditions.Wellcome open research · 2023Article
- An Investigation into Proteomic Constituents of Cerebrospinal Fluid in Patients with Chronic Peripheral Neuropathic Pain Medicated with Opioids- a Pilot Study.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Article
- Analgesic effects of the CTK 01512-2 toxin in different models of orofacial pain in rats.Pharmacological reports : PR · 2020Article
- Editorial (Thematic Selection: Spinal Neuropharmacological Agents for the Management of Pain).Current neuropharmacology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic pain remains a challenging clinical problem with a growing socio-economic burden for the state. Its prevalence is high and many of the patients are of work age. Our knowledge regarding the pathophysiology of chronic pain is poor. The consensus view is that the central nervous system plays a key role in the persistence of pain after an initiating event has long ceased. However the specifics of this biological response to an initiating event remains unclear. There is a growing body of evidence to support the concept that a central neuroimmune response is initiated and a number of small peptides have been implicated in this process following cerebrospinal fluid analysis in patients with chronic pain. This central biosynthetic peptide response leads to a process called central sensitization. Therapy is aimed at modulating and even inhibiting this response. However current pharmacological therapeutic options are limited in efficacy with significant deleterious side effect profiles. Proteomic studies extend single molecule analysis by identifying the components of biological networks and pathways and defining their interactions. This tool offers the potential to provide a molecular overview of the biological processes involved in chronic pain. It will also facilitate examination of gene-drug interactions. This technique offers a mechanism of defining the central biological responses that result in chronic pain and this information may facilitate the development of better therapies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.