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The Patient Registry of Intrathecal Ziconotide Management evaluated the long-term effectiveness and safety of intrathecal ziconotide.
Painful diabetic polyneuropathy (DPN) is difficult to manage as treatment response is often varied. The primary aim of this study was to examine differences in pain phenotypes between responders and non-responders to intravenous lidocaine treatment using quantitative sensory testing. The secondary aim was to explore differences in brain structure and functional connectivity with treatment response. Forty-five consecutive patients who received intravenous lidocaine treatment for painful DPN were screened. Twenty-nine patients who met the eligibility criteria (responders n=14 and non-responders n=15) and 26 healthy controls underwent detailed sensory profiling. Subjects also underwent multimodal brain magnetic resonance (MR) imaging. Greater proportion of patients with the irritable (IR) nociceptor phenotype were responders to intravenous lidocaine treatment compared to non-responders . The odd-ratio of responding to intravenous lidocaine was 8.67 times greater (95%CI 1.4:53.8) for the IR nociceptor phenotype. Responders to intravenous lidocaine also had significantly greater mean S1 cortical volume and functional connectivity between the insula cortex and the corticolimbic circuitry. This study provides preliminary evidence for a mechanism-based approach for individualising therapy in patients with painful DPN.
The cytokine, interleukin-23 (IL-23), can be critical for the progression of inflammatory diseases, including arthritis, and is often associated with T lymphocyte biology. We previously showed that certain lymphocyte-independent, inflammatory arthritis and pain models have a similar requirement for tumour necrosis factor (TNF), granulocyte macrophage-colony stimulating factor (GM-CSF), and C-C motif ligand 17 (CCL17). Given this correlation in cytokine requirements, we explored whether IL-23 might interact with this cytokine cluster in the control of arthritic and inflammatory pain.
The autoimmune disease rheumatoid arthritis (RA) affects approximately 1% of the global population. RA is characterized with chronic joint inflammation and often associated with chronic pain. The imbalance of pro-inflammatory and anti-inflammatory macrophages is a feature of RA progression. Glial cells affecting neuronal sensitivity at both peripheral and central levels may also be important for RA progression and associated pain. Genetic variants in the T cell death-associated gene 8 (TDAG8) locus are found to associate with spondyloarthritis. TDAG8 was also found involved in RA disease progression and associated hyperalgesia in the RA mouse model. However, its modulation in RA remains unclear.
Our aim was to investigate the relationship between coexisting cluster headache (CH) and migraine with anxiety and depression during active cluster bouts, and how symptoms change during remission.
There is histological evidence of microstructural changes in the zygomaticotemporal branch of the trigeminal nerve in migraineurs. This raises the possibility that altered trigeminal nerve properties contribute to migraine pathophysiology. Whilst it is not possible to explore the anatomy of small trigeminal nerve branches it is possible to explore the anatomy of the trigeminal root entry zone using magnetic resonance imaging in humans. The aim of this investigation is to assess the microstructure of the trigeminal nerve in vivo to determine if nerve alterations occur in individuals with episodic migraine.
Pain is a source of substantial discomfort. Abnormal activity in both the zona incerta (ZI) and posterior complex of the thalamus (Po) are implicated in neuropathic pain, but their exact roles remain unclear. In particular, the precise cell types and molecular mechanisms of the ZI-Po circuit that regulate nociception are largely uncharacterized. Here, we found that parvalbumin (PV)-positive neuronal projections from the ventral ZI (ZIv) to the Po (ZIv-Po) are critical for promoting nocifensive behaviors, whereas selectively inhibiting ZIv-Po activity reduces nocifensive withdrawal responses. Furthermore, cannabinoid type 1 receptors (CBRs) are expressed specifically at ZIv-Po axon terminals in this circuit, and cannabinoids attenuate nocifensive responses through presynaptic inhibition. Selective inhibition of the ZIv-Po circuit or administration of cannabinoids into the Po are sufficient to ameliorate pathological pain. These findings identify the critical role of the ZIv-Po circuit and its modulation by endocannabinoids in controlling nocifensive behaviors.
The effectiveness of Spinal Cord Stimulation (SCS) as pain-relieving treatment for Failed Back Surgery Syndrome (FBSS) has already been demonstrated. However, potential structural and functional brain alterations resulting from subsensory SCS are less clear. The aim of this study is to test structural volumetric changes in a priori chosen regions of interest related to chronic pain after 1 month and 3 months of high-frequency SCS, in patients with FBSS.
Chronic pain is a significant health problem worldwide with limited pharmacological treatment options. This study evaluated the relative efficacy of four treatment sessions each of four non-pharmacological treatments: (1) hypnotic cognitive therapy (using hypnosis to alter the meaning of pain); (2) standard cognitive therapy; (3) hypnosis focused on pain reduction, and (4) pain education. One hundred seventy-three individuals with chronic pain were randomly assigned to receive four sessions of one of the four treatments. Primary (pain intensity) and secondary outcome measures were administered by assessors unaware of treatment allocation at pre-treatment, post-treatment, and 3-, 6- and 12-month follow-up. Treatment effects were evaluated using ANOVA, a generalized estimating equation approach, or a Fisher Exact Test, depending on the outcome domain examined. All four treatments were associated with medium to large effect size improvements in pain intensity that maintained up to 12 months post-treatment. Pre- to post-treatment improvements were observed across the four treatment conditions on the secondary outcomes of pain interference and depressive symptoms, with some return towards pre-treatment levels at 12-months follow-up. No significant between group differences emerged in omnibus analyses, and few statistically significant between-group differences emerged in the planned pairwise analyses, although the two significant effects that did emerge favored hypnotic cognitive therapy. Future research is needed to determine if the significant differences that emerged are reliable.
Background and aims A considerable research-literature focuses on pain during labor and associations with postpartum persistent pain and depression, with findings pointing in various directions. The aim of this study was to examine the role of labor pain and overall birth experience in the development of pain and depression 8 weeks after delivery. Methods The study sample was drawn from the Akershus Birth Cohort. Data from multiple sources were used, including the hospital's birth record (n = 4,391), questionnaire data from gestational week 17 of pregnancy (n = 3,752), 8 weeks postpartum (n = 2,217), and two questions about pain and birth experience asked within 48 h after delivery (n = 1,221). The Edinburgh Postnatal Depression Scale was used to measure postpartum depression, a single question was used to measure persistent pain 8 weeks postpartum, while pain and birth experience were measured by numeric rating scales. A history of pre-pregnant depression and chronic pain were measured through self-report questions in gestational week 17. A total of 645 women had complete data from all sources. We applied multiple imputation techniques to handle missing responses on the two questions about pain and birth experience. Results The results showed that neither labor pain nor birth experience were associated with persistent pain 8 weeks postpartum, whereas pain before pregnancy (OR 3.70; 95% CI 2.71-5.04) and a history of depression (OR 2.31; 95% CI 1.85-2.88) were statistically significant predictors of persistent pain. A negative birth experience was significantly (OR 1.16; 95% CI 1.04-1.29) associated with postpartum depression, whereas labor pain intensity was not. A history of depression (OR 3.95; 95% CI 2.92-5.34) and pre-pregnancy pain (OR 2.03; 95% CI 1.37-3.01) were important predictors of postpartum depression 8 weeks after delivery. Conclusions and implications Whilst the relationship between labor pain intensity and postpartum pain and depression remain unclear, our results do imply the need to screen for previous depression and chronic pain conditions in pregnant women, as well as consider preventive measures in those who screen positive.