Objectives:To study the clinical profile and outcome of Japanese Encephalitis(JE) Methods: Prospective study was done in Vijayanagara Institute Medical Sciences hospital, Bellary, Karnataka. 233 patients below 12 years of age presented with acute encephalitic picture during the epidemic period formed the subjects and were worked up according to a predesigned protocol. CSF and serum samples were tested for JE specific IgM antibodies. Patients were followed up for 4 months to over one year. Results: The predominant age group was 5 to 12 years. Fever (94.84%), seizures (73.39%) and altered sensorium(91.84%) were the important presenting symptoms. Onset of illness was acute in 28.32% and subacute in 38.62% .CSF showed lymphocytosis and 45.06% had cell count of 6-50/cmm and in majority it was <200/cmm. 55.36% patients were positive for JE. Mortality was 22.74%. Deeper level of coma , respiratory irregularities and meningeal signs were associated with mortality. 147 patients survived the acute attack. Of that 40.85% completely recovered. Speech disturbance (47.61%), motor deficits (36.73%), behavioural disturbance (14.96%), involuntary movements (12.24%) and seizures (1.36%) were the morbidities. The deficits found to be gradually improving. Motor deficits and speech disturbances were found in 25.68% and 22.01% respectively at one year follow up. Conclusions:The characteristic clinical features of JE include fever, seizure, altered sensorium, aphasia, relative absence of cranial nerve involvement and irregular and rapidly changing motor and tone abnormality. Deeper level of coma, respiratory abnormalities and meningeal signs were associated with mortality. Speech disturbance and motor deficits were frequently encountered sequelae.

Background and Aim: Depression and anxiety are the most prominent neuropsychiatric disease and have been considered as the most burdensome diseases of society. The hippocampus and prefrontal cortex have a prominent role in stress-induced neurological disorders. Chronic unpredictable stress exposed rats are a perfect model in understanding comorbid depression and anxiety disorders. The inflammatory response occurring in the body has been linked to C-reactive protein (CRP) in many diseased conditions. The present research primarily focus on the possible correlation of Cortisol, CRP level and neuronal assay in different regions of hippocampus, dentate gyrus (DG), and prefrontal cortex. Materials and Methods: The control group of rats (n=6) was not exposed to any stress. Whereas, the experimental stress group (n=6) of rats was exposed to various stressors for 15 days. After the experimentation procedures, the blood samples were collected and brain dissection was done. The neurons in the prefrontal cortex, the DG along with various hippocampal regions was counted. Statistical analysis was performed using student's t-test and p<0.05 was expressed as statistically significant. Results: Animals exposed to chronic unpredictable stressors showed a significant (p<0.0001) decrease in the neuronal count in prefrontal cortex and hippocampus. A significant rise in the serum cortisol (p<0.0001) and CRP (p<0.001) was witnessed in the stressed group. Conclusion: Our results demonstrate that chronic unpredictable stress exposure has affected neurogenesis in prefrontal cortex and hippocampal regions. Decreased neurogenesis was well in coordinance with the increase in cortisol and CRP. The chronic unpredictable stress-induced inflammatory response correlated to various brain regions might provoke insights into a variety of new drugs targeting neurogenesis.

Background In recent years, increased stress in human life has a dual effect on brain and body physiology. Chronic stress takes a toll on physiology as well as on quality of life, ultimately leading to affective disorders. Rodent models are indispensable tools for studying the etiology and progress of depression. C-reactive protein has been proposed as a novel inflammatory marker. Methods Rats were divided into control and experimental stress groups (n = 6 each). The experimental group consisted of rats that were exposed to a set of chronic unpredictable stressors for 15 days. At the end of the 15th day, the animals were anesthetized, and blood samples were collected through cardiac puncture. Then the blood samples were analyzed for selected biochemical and oxidative stress parameters. Results Serum glutamic oxaloacetic transaminase (p < 0.0001), serum glutamic pyruvic transaminase (p < 0.001), serum malondialdehyde (p < 0.0001), total antioxidant level (p < 0.0001), and serum cortisol (p < 0.0001) were significantly increased in the stressed group when compared with the control group. C-reactive protein significantly (p < 0.0001) increased in the stressed group when compared with the control group. Conclusion Our results demonstrate that chronic unpredictable stress ameliorated depression-like behavior, which might have caused the dysregulation of the hypothalamic-pituitary-adrenal axis, causing the imbalance in the biochemical and oxidative parameters increasing the inflammatory markers. The inflammation-induced model of the chronic unpredictable stress model of comorbid depression might provide a variety of new targets for antidepressant therapies.