Metastatic prostate adenocarcinoma presenting with pulmonary symptoms: a case report and review of the literature.

INTRODUCTION: Prostate cancer has a high tendency to spread to bone. Pulmonary metastasis and generalized lymphadenopathy commonly develop after pelvic and bone involvement have already occurred. Few patients with prostate cancer present initially with symptomatic metastatic lung lesions and lymphadenopathy without any other concomitant distant dissemination. CASE PRESENTATION: We report a case of a 73-year-old white male who sought medical help for symptoms of cough, hemoptysis, and dyspnea. A chest X-ray was done revealing multiple "cannon ball" infiltrates involving all segments of the lung parenchyma. Fine-needle aspiration cytology under computed tomography guidance of a subpleural lesion revealed adenocarcinomatous cells. Despite the absence of any detectable osseous lesions and with the presence of multiple hilar, mediastinal, para-aortic, and pelvic lymphadenopathy, the patient had a complete work-up in search for the primary adenocarcinoma. His prostate specific antigen was 146 ng/ml and a prostatic biopsy done, revealing an acinar prostatic adenocarcinoma. A tru-cut biopsy of a lung lesion under computed tomography guidance showed a metastatic prostatic adenocarcinoma positive for prostate specific antigen stain. CONCLUSION: This case sheds light on an unusual metastatic pattern of prostatic adenocarcinoma. It also emphasizes the importance of including prostate cancer in the differential diagnosis of men with adenocarcinoma of unknown origin.

Spinal pathways involved in supraspinal modulation of neuropathic manifestations in rats.

Controversial results have been recently reported on the role of supraspinal centers in the modulation of nociceptive behavior in animal models of mononeuropathy. Our aim was to investigate the role of the various spinal pathways in the modulation of the neuropathic manifestations. Several groups of rats were subjected to selective spinal-tract lesions, either 2-3 weeks before or 2-3 weeks after the induction of mononeuropathy following the chronic constriction injury (CCI) or the spared nerve injury (SNI) models. Tactile and cold allodynias were assessed by Von Frey filaments and the acetone drops test, respectively. Thermal hyperalgesia was assessed by the paw withdrawal and the hot plate tests. The effects of unilateral and bilateral lesions of the dorso-lateral funiculus (DLF), the anterolateral column (ALC) or hemisection were tested over a period of 4-8 weeks. All spinal tract lesions produced reversible, but significant decrease of allodynia and hyperalgesia over a period of 1-3 weeks. The most pronounced effects were observed with bilateral lesions. The stronger attenuation was observed on thermal hyperalgesia, assessed by the paw withdrawal test, while cold allodynia was the least affected. Spinal lesions performed before the induction of neuropathy did not produce significant alterations in the temporal development of neuropathic manifestations. The present results allow the conclusion that all spinal tracts can be involved in the rostral transmission and the descending modulation of neuropathic manifestations. The recovery of symptoms following spinal lesions provides illustration on the plasticity of the neural network involved in the processing of the neuropathic syndromes.

Continuous perfusion with morphine of the orbitofrontal cortex reduces allodynia and hyperalgesia in a rat model for mononeuropathy.

Recent imaging reports demonstrate the activation of the orbitofrontal cortical (OFC) area during acute and chronic pain. The aim of this study was to compare the effects of chronic perfusion of this area with morphine on nociception in control rats and in rats subjected to mononeuropathy. Chronic perfusion of morphine, using miniosmotic pumps, produced significant and naloxone-reversible depression of tactile and cold allodynias and thermal hyperalgesia, observed in neuropathic rats, while it produced significant elevation and naloxone insensitive increase of acute nociceptive thresholds in control rats. The observed results support the idea that this area is a component of a flexible cerebral network involved in pain processing and perception.