Articles: neuralgia.
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Trigeminal neuropathic pain has been modeled in rodents through the constriction of the infraorbital nerve (CCI-ION). Sensory alterations, including spontaneous pain, and thermal and mechanical hyperalgesia are well characterized, but there is a notable lack of evidence about the affective pain component in this model. Evaluation of the emotional component of pain in rats has been proposed as a way to optimize potential translational value of non-clinical studies. ⋯ Amphetamine caused a marked increase in 50 kHz USV emission in CCI-ION rats. In addition, TH expression was lower in constricted animals and c-Fos analysis revealed an increase in neuronal activation. Taken together, these data indicate that CCI-ION causes a reduction in the emission of environmental-induced appetitive calls concomitantly with facial mechanical hyperalgesia and that both changes may be related to a reduction in the mesolimbic dopaminergic activity.
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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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Clinical Trial
Characterization of Hyperacute Neuropathic Pain after Spinal Cord Injury: A Prospective Study.
There is currently a lack of information regarding neuropathic pain in the very early stages of spinal cord injury (SCI). In the present study, neuropathic pain was assessed using the Douleur Neuropathique 4 Questions (DN4) for the patient's worst pain within the first 5 days of injury (i.e., hyperacute) and on follow-up at 3, 6, and 12 months. Within the hyperacute time frame (i.e., 5 days), at- and below-level neuropathic pain were reported as the worst pain in 23% (n = 18) and 5% (n = 4) of individuals with SCI, respectively. ⋯ This may lead to an underestimation of the incidence of neuropathic pain during the very early, hyperacute time points post-injury. TRIAL REGISTRATION: ClinicalTrials.gov (Identifier: NCT01279811) PERSPECTIVE: This article presents distinct pain phenotypes of hyperacute and late presenting neuropathic pain after spinal cord injury and highlights the challenges of pain assessments in the acute phase after injury. This information may be relevant to clinical trial design and broaden our understanding of neuropathic pain mechanisms after spinal cord injury.
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Neuropathic pain arises as a direct consequence of a lesion or disease affecting the somatosensory system. A number of preclinical studies have provided evidence for the involvement of cytokines, predominantly secreted by a variety of immune cells and by glial cells from the nervous system, in neuropathic pain conditions. Clinical trials and the use of anti-cytokine drugs in different neuropathic aetiologies support the relevance of cytokines as treatment targets. However, the use of such drugs, in particularly biotherapies, can provoke notable adverse effects. Moreover, it is challenging to select one given cytokine as a target, among the various neuropathic pain conditions. It could thus be of interest to target other proteins, such as growth factors, in order to act more widely on the neuroinflammation network. Thus, platelet-rich plasma (PRP), an autologous blood concentrate, is known to contain a natural concentration of growth factors and immune system messengers and is widely used in the clinical setting for tissue regeneration and repair. ⋯ Preclinical and clinical studies highlight the idea of a cytokine imbalance in the development and maintenance of neuropathic pain. Clinical trials with anticytokine drugs are encouraging but are limited by a 'cytokine candidate approach' and adverse effect of biotherapies. PRP, containing various growth factors, is a new therapeutic used in regenerative medicine. Growth factors can be also considered as modulators of cytokine balance. Here, we emphasize a potential therapeutic effect of PRP on cytokine imbalance in neuropathic pain. We also underline the clinical interest of the use of PRP, not only for its therapeutic effect but also for its safety of use.
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Analysis of Potential Hub Genes for Neuropathic Pain Based on Differential Expression in Rat Models.
Neuropathic pain (NP) is a type of intractable chronic pain with complicated etiology. The exact molecular mechanism underlying NP remains unclear. In this study, we searched for molecular biomarkers of NP. ⋯ The results of this study form a basis for further research into the mechanism of NP development and are expected to aid in the development of novel therapeutic strategies.