Background: Previous studies have demonstrated that intrathecal synthesis of IgM is observed in multiple sclerosis (MS) and correlates with a worse disease course. These results suggest that IgM participates in the formation of MS lesions.
Objective: The aim of the present study was to assess the potential association between the level of intrathecal synthesis of IgM measured after a clinically isolated syndrome (CIS) and the subsequent formation of brain lesions.
Methods: Fifty seven patients with a CIS and a high risk developing MS were enrolled in a longitudinal study. Examination of cerebrospinal fluid was performed after the CIS and included measures of intrathecal IgM and IgG synthesis. Patients were assessed with the same 1.5 Tesla magnetic resonance imaging (MRI) system at baseline and after a mean follow-up period of 49 months (range 36-60). Spearman Rank correlation was used to assess the potential correlations between levels of intrathecal immunoglobulin synthesis and MRI data.
Results: The level of intrathecal IgM synthesis was correlated with the number of gadolinium-enhancing lesions at baseline (p = 0.01) and with accrual of brain lesions during the follow-up period (p = 0.02). By taking into account brain sub-regions, we demonstrated that the level of intrathecal IgM synthesis was only correlated with the increased number of lesions in the periventricular regions (p = 0.004). The level of intrathecal IgG synthesis was not correlated with any MRI data.
Conclusion: The present longitudinal study demonstrates that the level of intrathecal IgM synthesis measured after a CIS is associated with subsequent lesion accrual during the first years of MS. This result emphasizes the involvement of IgM in plaque formation.
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http://dx.doi.org/10.1177/1352458511424589 | DOI Listing |
J Neurosci
January 2025
Center for Neuroscience and Pain Research, Department of Anesthesiology and Perioperative Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA
Transient receptor potential ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) channels are crucial for detecting and transmitting nociceptive stimuli. Inflammatory pain is associated with sustained increases in TRPA1 and TRPV1 expression in primary sensory neurons. However, the epigenetic mechanisms driving this upregulation remain unknown.
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
Maj Institute of Pharmacology, Polish Academy of Sciences, Department of Neurochemistry, 12 Smetna Str., Krakow 31-343, Poland. Electronic address:
Neuropathic pain is a disorder affecting the somatosensory nervous system. However, this condition is also characterized by significant neuroinflammation, primarily involving CNS-resident non-neuronal cells. A promising target for developing new analgesics is histamine H receptor (HR); thus, we aimed to determine the influence of a novel HR antagonist/inverse agonist, E-98 (1-(7-(4-chlorophenoxy)heptyl)-3-methylpiperidine), on pain symptoms and glia activation in model of neuropathic pain in male mice (chronic constriction injury to the sciatic nerve).
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
College of Veterinary Medicine, Konkuk University, 120, Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea. Electronic address:
Rett syndrome (RTT) is a neurological disorder caused by a mutation in the X-linked methyl-CpG binding protein 2 (MECP2), leading to cognitive and motor skill regression. Therapeutic strategies aimed at increasing brain-derived neurotrophic factor (BDNF) levels have been reported; however, BDNF treatment has limitations, including the inability to penetrate the blood-brain barrier, a short half-life, and potential for adverse effects when administered via intrathecal injection, necessitating novel therapeutic approaches. In this study, we focused on the adenosine A receptor (AR), which modulates BDNF and its downstream pathways, and investigated the therapeutic potential of CGS21680, an AR agonist, through in vitro and in vivo studies using R106W RTT model.
View Article and Find Full Text PDFFluids Barriers CNS
January 2025
Adelaide Spinal Research Group & Centre for Orthopaedics and Trauma Research, Faculty of Health and Medical Sciences, The University of Adelaide, Level 7, Adelaide Health and Medical Sciences Building, North Terrace, Adelaide, SA, 5005, Australia.
Background: Traumatic spinal cord injury (SCI) causes spinal cord swelling and occlusion of the subarachnoid space (SAS). SAS occlusion can change pulsatile cerebrospinal fluid (CSF) dynamics, which could have acute clinical management implications. This study aimed to characterise SAS occlusion and investigate CSF dynamics over 14 days post-SCI in the pig.
View Article and Find Full Text PDFClin J Pain
January 2025
Associate Professor, Department of Anesthesiology and Reanimation, Istanbul Marmara University Hospital, Istanbul, Turkey.
Objectives: After cesarean, optimal analgesia is important for early mobilization, mitigating thromboembolic risks, and mother-infant communication. Our study aims to compare the postoperative analgesic effects of intrathecal morphine (ITM) and Erector Spinae Plane Block (ESPB) in elective cesarean section under spinal anesthesia.
Methods: 82 patients were randomized into ESPB and ITM groups.
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