Cerebellar spongiform degeneration is accompanied by metabolic, cellular, and motor disruption in male rats with portacaval anastomosis.

The episodes of cerebral dysfunction, known as encephalopathy, are usually coincident with liver failure. The primary metabolic marker of liver diseases is the increase in blood ammonium, which promotes neuronal damage. In the present project, we used an experimental model of hepatic encephalopathy in male rats by portacaval anastomosis (PCA) surgery. Sham rats had a false operation. After 13 weeks of surgery, the most distinctive finding was vacuolar/spongiform neurodegeneration exclusively in the molecular layer of the cerebellum. This cerebellar damage was further characterized by metabolic, histopathological, and behavioral approaches. The results were as follows: (a) Cellular alterations, namely loss of Purkinje cells, morphological changes, such as swelling of astrocytes and Bergmann glia, and activation of microglia; (b) Cytotoxic edema, shown by an increase in aquaporin-4 and N-acetylaspartate and a reduction in taurine and choline-derivate osmolytes; (c) Metabolic adjustments, noted by the elevation of circulating ammonium, enhanced presence of glutamine synthetase, and increase in glutamine and creatine/phosphocreatine; (d) Inflammasome activation, detected by the elevation of the marker NLRP3 and microglial activation; (e) Locomotor deficits in PCA rats as assessed by the Rotarod and open field tests. These results lead us to suggest that metabolic disturbances associated with PCA can generate the cerebellar damage that is similar to morphophysiological modifications observed in amyloidogenic disorders. In conclusion, we have characterized a distinctive cerebellar multi-disruption accompanied by high levels of ammonium and associated with spongiform neurodegeneration in a model of hepatic hypofunctioning.

Neurophysiological Intraoperative Monitoring in the Elderly.

INTRODUCTION: Intraoperative neurophysiological monitoring (IONM) is widely used to prevent nervous system injury during surgeries in elderly patients. However, there are no studies that describe the characteristics and changes in neurophysiological tests during the IONM of patients aged 60 years and older. The study aims to describe and compare IONM changes during surgeries in adult patients aged 18 to 59 years with those aged 60 years and older. METHODS: We performed a comparative retrospective study of patients aged 18 to 59 years versus those 60 aged years and older who underwent IONM during 2013 to 2018 in Mexico City. Sociodemographic characteristics were recorded and compared. Intraoperative neurophysiological monitoring techniques, their changes, and surgical procedures for both groups were analyzed and compared using descriptive statistics, Mann-Whitney U, Fisher, and χ2 tests. The sensitivity, specificity, and positive and negative predictive values were calculated. RESULTS: In total, 195 patients were analyzed: 104 patients, 68.63 ± 6.54 years old (elderly group) and 91 patients, 42.3 ± 10.5 years old (younger group). No differences were found in the rates of signal change during IONM between the group of elderly patients and the younger group. The sensitivity, specificity, and positive and negative predictive values were 80%, 99%, 80%, and 99%, respectively. CONCLUSIONS: Elderly patients have a similar rate of changes in IONM signals compared with younger patients during heterogeneous surgeries guided by IONM.