Neural circuits that are positioned to regulate rat distal colon function were identified by immunohistochemical detection of pseudorabies virus (PRV) and corticotropin‐releasing factor (CRF). The distribution of PRV‐immunoreactive neurons was examined in spinal cord and brain at increasing times (72–118 hours) after distal colon injection. At 72–80 hours, PRV‐labeling was confined to the spinal cord, in the parasympathetic preganglionic column in the lumbosacral spinal cord and in the intermediolateral column of the thoracic spinal cord. At longer survival times (88 hours), PRV‐immunolabeled neurons in the lumbosacral spinal cord were also distributed in superficial layers of the dorsal horn, the dorsal commissure, and around the central canal. Trans‐synaptic labeling was identified in the medullary raphe nuclei, parapyramidal region, A5, Barrington's nucleus, A7, and the dorsal cap of the paraventricular nucleus of the hypothalamus after longer survival times (88–91 hours). Substantial labeling of the locus coeruleus, periaqueductal gray and forebrain regions occurred at later survival times (≥96 hours). In dual‐labeled sections, CRF terminal labeling surrounded PRV‐labeled neurons in the parasympathetic preganglionic column of the lumbosacral spinal cord. Additionally, many neurons in Barrington's nucleus, but not other CRF‐containing nuclei, were double labeled for CRF and PRV. These results, taken with previous studies, support a convergence in transneuronal labeling from different pelvic viscera that may be related to coordination of overall pelvic visceral functions. Importantly, they provide an anatomic substrate for an impact of CRF from Barrington's nucleus in normal and pathophysiological functions of the distal colon. J. Comp. Neurol. 417:399–414, 2000. © 2000 Wiley‐Liss, Inc.

Neural circuits that are positioned to regulate rat distal colon function were identified by immunohistochemical detection of pseudorabies virus (PRV) and corticotropin-releasing factor (CRF). The distribution of PRV-immunoreactive neurons was examined in spinal cord and brain at increasing times (72-118 hours) after distal colon injection. At 72-80 hours, PRV-labeling was confined to the spinal cord, in the parasympathetic preganglionic column in the lumbosacral spinal cord and in the intermediolateral column of the thoracic spinal cord. At longer survival times (88 hours), PRV-immunolabeled neurons in the lumbosacral spinal cord were also distributed in superficial layers of the dorsal horn, the dorsal commissure, and around the central canal. Trans-synaptic labeling was identified in the medullary raphe nuclei, parapyramidal region, A5, Barrington's nucleus, A7, and the dorsal cap of the paraventricular nucleus of the hypothalamus after longer survival times (88-91 hours). Substantial labeling of the locus coeruleus, periaqueductal gray and forebrain regions occurred at later survival times (> or = 96 hours). In dual-labeled sections, CRF terminal labeling surrounded PRV-labeled neurons in the parasympathetic preganglionic column of the lumbosacral spinal cord. Additionally, many neurons in Barrington's nucleus, but not other CRF-containing nuclei, were double labeled for CRF and PRV. These results, taken with previous studies, support a convergence in transneuronal labeling from different pelvic viscera that may be related to coordination of overall pelvic visceral functions. Importantly, they provide an anatomic substrate for an impact of CRF from Barrington's nucleus in normal and pathophysiological functions of the distal colon.

A 65-year-old man presented with long-standing rheumatoid arthritis (RA), severe fatigue and mild arthritis of metacarpophalaneal joints. Physical examination revealed S3, II/IV decrescendo diastolic murmur and 2+ LL oedema. Anticyclic citrullinated peptide antibodies were >250 units. Echocardiogram showed an 8 cm pericardial mass with no atrial or ventricular collapse and mild to moderate aortic regurgitation. Cardiac MRI defined the mass as a heterogeneous entity attached to the right, anterior and inferior heart borders, with compression on right cardiac structures and the left ventricle. CT-guided biopsy demonstrated fibrinous material without granulomas or infection. Fatigue did not improve on immunosuppression with low-dose prednisone and leflunamide. Cardiac tamponade was confirmed by heart catheterisation and the mass was surgically excised with partial pericardiectomy. The patient had a dramatic improvement and, 4 years later, he remains asymptomatic cardiac wise. This case highlights the clinical significance of pericardial disease in RA and its response to therapy.

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Introduction: Rheumatoid arthritis (RA) can affect the heart via either inflammatory or ischemic processes. Pericardial disease is common in RA patients (30-50%) but is usually subclinical and not hemodynamically significant unless accompanied by infiltrative cardiomyopathy which carries a poor prognosis. Case report: A 65 year-old Caucasian male presented with long standing RA, severe fatigue and mild arthritis of MCP joints. Physical examination indicated S3, II/VI decrescendo diastolic murmur, and 2+ LL edema. ESR was normal but anti-CCP antibodies were > 250 units. On echocardiogram, a large pericardial mass was detected without atrial nor ventricular collapse and mild-moderate aortic regurgitation. Cardiac MRI defined the mass as a heterogeneous entity attached to the right, anterior, and inferior borders of the heart with compression of the right atrium, left and right ventricles, and the tricuspid valve. CT guided biopsy demonstrated fibrinous material without granulomas nor infection. Fatigue was initially attributed to uncontrolled RA and low dose prednisone and Leflunamide were started. 3 months later, he developed frank heart failure with NYHA class IIIb functional impairment. Cardiac Tamponade was confirmed by heart catheterization demonstrating typical 4-chamber pressure equalization. The mass was surgically excised with partial pericardiectomy. The patient had a dramatic improvement and 4 years later, he remains asymptomatic. Discussion: Our patient presented with uncontrolled RA and a pericardial mass that was not hemodynamically significant per the initial echocardiogram. Despite intensifying immunosuppression, his fatigue progressed with signs of congestive heart failure. Tamponade physiology was diagnosed invasively and the mass was resected with excellent recovery. Microscopically, the lesion consisted of a fibrous and exudative material. The patient likely had multiple asymptomatic episodes of pericarditis, gradually leading to this condition. We demonstrate with this case that RA pericardial disease can cause hemodynamic compromise while sparing myocardium and valves and that surgery is associated with very good prognosis. Physicians should be vigilant about a cardiac cause of fatigue in RA patients.