Articles: neuropathic-pain.
-
Protein kinase M ζ is well known for its role in maintaining memory and pain. Previously, we revealed that the activation of protein kinase M ζ in the anterior cingulate cortex plays a role in sustaining neuropathic pain. ⋯ We also reveal that the inhibition of protein kinase M ζ through zeta inhibitory peptide treatment is enough to reduce mechanical allodynia responses in mice with one-month-old nerve injuries. However, the zeta inhibitory peptide treatment was only effective for a limited time.
-
Journal of pain research · Jan 2018
Ovine model of neuropathic pain for assessing mechanisms of spinal cord stimulation therapy via dorsal horn recordings, von Frey filaments, and gait analysis.
It is becoming increasingly important to understand the mechanisms of spinal cord stimulation (SCS) in alleviating neuropathic pain as novel stimulation paradigms arise. ⋯ To our knowledge, this is the first reported large animal model of chronic neuropathic pain which facilitates the study of both acute and chronic SCS using complementary behavioral and electrophysiologic measures. As demonstrated by our successful establishment of these techniques, an ovine model of neuropathic pain is suitable for testing the mechanisms of SCS.
-
Journal of pain research · Jan 2018
The effects of transcranial direct current stimulation on metabolite changes at the anterior cingulate cortex in neuropathic pain: a pilot study.
Neuropathic pain (NP) in individuals with spinal cord injury (SCI) is both common and highly refractory to treatment. Primary motor cortex stimulation can relieve pain by interrupting the transmission of noxious information of descending pain modulatory systems including the anterior cingulate cortex (ACC). Previous research has shown that transcranial direct current stimulation (tDCS) can produce pain relief in individuals with NP. However, the underlying mechanisms for these effects are not yet understood. Research findings suggest the possibility that changes in brain metabolite concentrations produced by tDCS might explain some of these effects. For example, previous research has shown that SCI-related NP is associated with elevated levels of glutamine combined glutamate (Glx) per creatine (Glx/Cr). In addition, decreased N-acetylaspartate (NAA) has been observed in the ACC in individuals with chronic pain. ⋯ The findings suggest the possibility that tDCS's beneficial effects on neuropathic pain may be due, at least in part, to the changes it produces in Glx/Cr and NAA/Cr levels in the ACC. Additional research with larger samples sizes and a control group to evaluate this possibility is warranted.
-
The aim of the study was to compare characteristics of pain in terms of neuropathic pain (NeP) and to assess the association between the neuropathic component and quality of life (QoL) in patients with systemic sclerosis (SSc) and rheumatoid arthritis (RA). ⋯ The NeP component was similar between patients with SSc and RA. However, NeP was associated with a heavier burden of disease in patients with RA.
-
Clinical studies show that anxiety and chronic pain are concomitant. The neural basis for the comorbidity is unclear. The prefrontal cortex (PFC) has been recognized as a critical area for affective disorders and chronic pain modulation. ⋯ Inhibition of serotonin transporter effectively alleviated anxiety-like behaviors following sub-chronic (15 days) treatment with systemic citalopram (10 mg/kg/day, intraperitoneally). Moreover, the anxiety-like behaviors in the SNI rats were also suppressed by direct mPFC application of serotonin. Taken together, we conclude that the plasticity of serotonin transmission in the mPFC likely contribute to the promotion of anxiety state associated with neuropathic pain.