Reversal of morphine and stimulus-produced analgesia by subtotal spinal cord lesions.

This study examined the hypothesis that descending inhibitory pathways from brain stem to spinal cord mediate the analgesic effect of both electrical brain stimulation and morphine. In the first set of experiments, the effect of subtotal midthoracic spinal cord lesions on the analgesic effect of electrical stimulation in the periaqueductal gray matter of the rat was examined. In the second, the effect of similar cord lesions on the analgesic effect of intraperitoneal morphine was studied. In both cases, a lesion of the dorsal part of the lateral funiculus (DLF) reduced or abolished the analgesia of the hindlimbs. Analgesia of the forelimbs was unaffected. Lesions of the dorsal columns, which include the corticospinal tract, or lesions of the ventral part of the lateral funiculus had no effect on analgesia. It is concluded that an inhibitory pathway, which descends in the dorsal part of the lateral funiculus and which probably originates in the nucleus raphe magnus of the medulla, mediates the descending control found in both morphine and stimulus-produced analgesia.

Progressive renal failure due to renal infiltration by BK polyomavirus and leukaemic cells: which is the culprit?

Renal infiltration with leukaemic cells is a common finding in patients suffering with chronic lymphocytic leukaemia (CLL) but rarely does it lead to significant renal dysfunction. Similarly, BK nephropathy is a recognized cause of graft failure in renal transplant recipients but rarely causes significant disease in native kidneys. In the few reports where leukaemic infiltration of the kidney has led to significant renal impairment, the pathological process causing renal dysfunction is not identified on biopsy. In these cases, it is unclear whether BK polyomavirus (BKV) nephropathy has been excluded. We describe a case of dual pathologies in a patient with Binet stage C CLL and deteriorating renal function where renal biopsy reveals leukaemic infiltration of the kidney occurring alongside BKV nephropathy. The relative importance of each pathology in relation to the rapid decline to end-stage renal failure remains unclear, but the presence of both pathologies appears to impart a poor prognosis. Additionally, we describe the novel histological finding of loss of tubular integrity resulting in tubular infiltration and occlusion by leukaemic cells. It is possible that the patient with advanced CLL is at particular risk of BK activation, and the presence of BK nephropathy may compromise tubular integrity allowing leukaemic cell infiltration and obstruction of tubules. This case bares remarkable resemblance to the first and only other report of its kind in the literature. It is not clear how available immunocytochemistry for polyoma infection is outside transplant centres, and it is possible that BK nephropathy is being under-diagnosed in patients with CLL in the context of declining renal function. At present, the combination of BKV nephropathy and leukaemic infiltration represents a management conundrum and the prognosis is poor. Further research is required in order to better understand the pathological process and therefore develop management strategies.