Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology
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J Neuroimmune Pharmacol · Jun 2013
Case ReportsImproving the diagnosis and treatment of CRPS: insights from a clinical immunologist's personal experience with an underrecognized neuroinflammatory disorder.
Complex regional pain syndrome is a neuroinflammatory condition associated with overactive glial cells that can be challenging to diagnose and treat. Early recognition and treatment are thought to be critical for good outcomes, yet many patients experience a delay in diagnosis and have difficulty accessing expert medical care. While there are no universally effective treatments, there are several promising new therapies, but these are not widely available. Some of the specific barriers to diagnosis and treatment are reviewed, with suggestions as to how they might be eliminated, leading to better care for all patients with CRPS.
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J Neuroimmune Pharmacol · Mar 2013
Simvastatin ameliorates cauda equina compression injury in a rat model of lumbar spinal stenosis.
Lumbar spinal stenosis (LSS) is the leading cause of morbidity and mortality worldwide. LSS pathology is associated with secondary injury caused by inflammation, oxidative damage and cell death. Apart from laminectomy, pharmacological therapy targeting secondary injury is limited. ⋯ Simvastatin hastens the locomotor functional recovery and reduces pain after CEC. These outcomes are mediated through the neuroprotective and anti-inflammatory properties of simvastatin. The data indicate that simvastatin may be a promising drug candidate for LSS treatment in humans.
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J Neuroimmune Pharmacol · Mar 2013
Resolvin E1 inhibits neuropathic pain and spinal cord microglial activation following peripheral nerve injury.
Accumulating evidence indicates that activation of spinal cord microglia plays an important role in the genesis of neuropathic pain. Resolvin E1 (E1) is derived from omega-3 polyunsaturated fatty acid and exhibits potent anti-inflammatory, pro-resolution, and anti-nociceptive effects. We further examined whether RvE1 could reduce neuropathic pain and modulate spinal cord microglial activation. ⋯ Finally, RvE1 blocked lipopolisaccharide-induced microgliosis and TNF-α release in primary micoglial cultures. Our data suggest that RvE1 may attenuate neuropathic pain via inhibiting microglial signaling. Targeting the anti-inflammatory and pro-resolution lipid mediators may offer new options for preventing and treating neuropathic pain.
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J Neuroimmune Pharmacol · Mar 2013
ReviewCytokine modulation is necessary for efficacious treatment of experimental neuropathic pain.
Neuropathic pain originates from a damage or disease affecting the somatosensory system. Its treatment is unsatisfactory as it appears refractory to most analgesics. Animal models of neuropathic pain are now available that help to clarify the underlying mechanisms. ⋯ Novel therapeutic approaches efficacious to reduce painful symptoms, for example treatments with the non specific purinergic antagonist PPADS, the phytoestrogen genistein and a cell stem therapy with murine adult neural stem cells also re-established a balance between pro and antinflammatory mediators in the peripheral and central nervous system. These data suggest a pivotal role of immune system and inflammation in neuropathic pain. The modulation of inflammatory molecules appears to be a common trait accomplished throughout different mechanisms by different drugs that might converge in neuropathic pain modulation.
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J Neuroimmune Pharmacol · Dec 2012
Wnt signaling in the pathogenesis of multiple sclerosis-associated chronic pain.
Many multiple sclerosis (MS) patients develop chronic pain, but the underlying pathological mechanism is unknown. Mice with experimental autoimmune encephalomyelitis (EAE) have been widely used to model MS-related neurological complications, including CNS demyelination, neuroinflammation and motor impairments. Similar to MS patients, EAE mice also develop chronic pain. ⋯ In addition, Wnt5a, a prototypic Wnt ligand for the non-canonical pathway, and its receptor (co-receptor) Ror2 were also up-regulated in the SCDH of the EAE mice. We further found that Wnt5a antagonist Box5 and β-catenin inhibitor indomethacin attenuated mechanical allodynia in the EAE mice. Our data collectively suggest that Wnt signaling pathways are up-regulated in the SCDH of the EAE mice and that aberrant activation of Wnt signaling contributes to the development of EAE-related chronic pain.