Articles: neuralgia.
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The effect of spinal cord stimulation (SCS) using differential target multiplexed programming (DTMP) on proteins involved in the regulation of ion transport in spinal cord (SC) tissue of an animal model of neuropathic pain was evaluated in comparison to low rate (LR) SCS. Rats subjected to the spared nerve injury model (SNI) and implanted with a SCS lead were assigned to DTMP or LR and stimulated for 48 h. A No-SCS group received no stimulation, and a Sham group received no SNI or stimulation. ⋯ DTMP also upregulated postsynaptic proteins involved with elevated intracellular Cl-, while modulating proteins, expressed by astrocytes, that regulate postsynaptic Cl- inhibition. DTMP downregulated K+ regulatory proteins affected by SNI that affect neuronal depolarization, and upregulated proteins that are associated with a decrease of intracellular neuronal K+ and astrocyte uptake of extracellular K+. DTMP treatment modulated the expression of proteins with the potential to facilitate a reversal of dysregulation of ion transport and signaling associated with a model of neuropathic pain.
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T lymphocytes are increasingly implicated in pain signaling. A subset of T lymphocytes, termed TChAT, express the rate-limiting enzyme for acetylcholine (ACh) production, choline acetyltransferase (ChAT), and mediate numerous physiological functions. Given that cholinergic signaling has long been known to modulate pain processing and is the basis for several analgesics used clinically, we asked whether TChAT could be the intersection between T lymphocyte and cholinergic mediation of pain signaling. ⋯ Our experiments demonstrate that cholinergic signaling initiated by T lymphocytes neither dampens nor exacerbates the expression of mechanical or thermal sensitivity in neuropathic mice. Thus, while both cholinergic signaling and T lymphocytes have established roles in modulating pain phenotypes, it is not cholinergic signaling initiated by T lymphocytes that drive this. Our findings will help to narrow in on which aspects of T-cell modulation may prove useful as therapies.
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Observational Study
C2 Nerve Root Preservation during Posterior Fixation for Instability secondary to Congenital Craniovertebral Junction Anomalies: Feasibility Factors and Related Outcomes.
Patients with instability because of congenital craniovertebral anomalies often have complex C1-C2 osseovascular anomalies. C2 nerve root sacrifice has been described to address such difficult anatomy during posterior C1-C2 fixation and has its own downsides. Its preservation as a recent alternative poses greater surgical challenge, and the considerations differ from other causes of craniovertebral junctional instability; the pertaining outcomes have been scarcely studied. The objective of this study was to prospectively determine the feasibility and outcomes related to C2 nerve root preservation in patients with congenital atlantoaxial dislocation (CAAD) after posterior C1-C2 fixation. ⋯ In most patients with CAAD, C2 nerve root preservation is feasible despite an aberrant bony and vascular anatomy. A few patients after nerve root preservation develop related symptoms that are conservatively manageable, with no significant adverse consequences. Given the controversy in the literature on C2 nerve sacrifice-related outcomes, we favor an attempt at C2 nerve root preservation.
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Curr Pain Headache Rep · Jan 2022
ReviewTitle: Novel Analgesic Potential of ß2-Agonists for Neuropathic Pain via ß2-Agonist Action.
Multimodal therapies are often employed to treat chronic pain, and ß2-agonists are a potential drug class that shows promise. The primary aim of this paper is to discuss the role of ß2-agonists as an adjunctive therapy for chronic pain based on the current literature. ⋯ Recent studies in mouse models have shown that the ß2-adrenergic system plays an essential role in the analgesic properties of antidepressant drugs used to treat neuropathic pain and that the adrenergic relies on an intact endogenous opioid system to be effective. Studies also show that ß2-agonism alone is adequate to exert anti-allodynic effects in a mouse model. This paper summarized the basic physiology and pharmacology of the sympathetic nervous system and specifically the ß2-adrenergic system and summarized current literature in its involvement in the treatment of chronic neuropathic pain.