Our findings suggest that vision can influence pathologic pain, and preliminarily suggest that prism adaptation has a direction-specific and reproducible effect on not only pathologic pain but also other CRPS pathologic features. Thus, prism adaptation may be a viable cognitive treatment for CRPS.

Nerve injury can trigger affective disturbances in mice that appear much later than sensory hypersensitivity.

Spatial perception is achieved by integrating multisensory information. Using visual subjective body midline (vSM) judgments in patients with unilateral limb pain (complex regional pain syndrome [CRPS]), we found that their vSM deviated toward the affected side; however, deafferentation of the affected limb caused a transient pain decrease and a transient shift of the vSM deviation toward the unaffected side. Our results indicate that the persistent pain state in CRPS distorts visuospatial perception.

GASTROINTESTINAL IMAGINGG iven the extensive use of medical cross-sectional imaging, the incidental detection of adrenal lesions has concomitantly increased, occurring in approximately 5%-8% of patients undergoing CT (1-5). Although most incidental adrenal lesions are benign adenomas, the most common clinical dilemma has been the differentiation between adenomas and metastases, particularly among patients with a history of extra-adrenal malignancy (1-3). Because the presence of metastasis can affect treatment strategies and patient prognosis, accurate and noninvasive discrimination between the two entities is critical.Adrenal adenomas have two key CT imaging features: (a) low unenhanced attenuation reflecting intracytoplasmic fat content and (b) maximized contrast enhancement during the portal venous phase followed by rapid washout during the delayed phase (5)(6)(7)(8)(9)(10)(11)(12). Approximately 70% of adenomas can be diagnosed as lipid-rich adenoma based on unenhanced attenuation (10 HU) (5-8), whereas most lipid-poor adenomas (.10 HU) can be diagnosed based on the high washout rate calculated at multiphasic adrenal CT (7-12

Pro-inflammatory cytokines have been shown to be involved in the genesis, persistence, and severity of neuropathic pain following nerve injury. The transcription factor, nuclear factor-kappa B (NF-kappaB), plays a pivotal role in regulating pro-inflammatory cytokine gene expression. To elucidate the role of NF-kappaB in the pathogenesis of neuropathic pain, using a gene-based approach of NF-kappaB decoy, we tested whether the activated NF-kappaB affected pain behavior via the expression of inflammatory mediators. Single endoneurial injections of NF-kappaB decoy, at the site of nerve lesion, significantly alleviated thermal hyperalgesia for up to 2 weeks and suppressed the expression of mRNA of the inflammatory cytokines, iNOS, and adhesion molecules at the site of nerve injury. This finding suggests that a perineural inflammatory cascade, that involves NF-kappaB, is involved in the pathogenesis of neuropathic pain.

No abstract

Optic nerve (ON) injury in adult mammals causes retinal ganglion cell (RGC) death and subsequent visual loss. Recovery of vision requires both rescuing axotomized RGCs and inducing their axonal regeneration. Axotomized RGCs are significantly rescued by overexpression of bcl-2, an anti-apoptotic gene. However, whether bcl-2 affects axonal regeneration is controversial. In neonatal bcl-2 transgenic mice (bcl-2 mice), optic tract regeneration after tectal lesion was promoted (Chen et al., 1997), whereas ON regeneration after ON crush was not (Lodovichi et al., 2001). These conflicting results may be attributable to different environments between tectum and ON. We tested here whether bcl-2 overexpression enhances in vivo RGC axonal regeneration in adult mice through a permissive environment in the peripheral nerve (PN) graft. Four weeks after PN transplantation to the proximal ON stump, we assessed the number of surviving and regenerating RGCs by retrograde labeling. Although the survival rate in bcl-2 mice was significantly enhanced compared with that in wild-type (wt) mice, the regeneration rate was not enhanced. In both bcl-2 and wt mice, RT97 immunostaining of the PN-grafted retinas revealed some RGC axons regrowing intraretinally but repulsed at the optic disk. To circumvent this repulsive barrier, we directly transplanted the PN graft to the partially injured retina and compared regeneration rates between these mice. Here again the regeneration rate in bcl-2 mice did not exceed that in wt mice. These findings indicate that bcl-2 overexpression enhances survival but not axonal regeneration of adult RGCs even within a permissive environment.

No abstract