In vivo study of experimental pneumococcal meningitis using magnetic resonance imaging

<p>Abstract</p> <p>Background</p> <p>Magnetic Resonance Imaging (MRI) methods were evaluated as a tool for the study of experimental meningitis. The identification and characterisation of pathophysiological parameters that vary during the course of the disease could be used as markers for future studies of new treatment strategies.</p> <p>Methods</p> <p>Rats infected intracisternally with <it>S. pneumoniae </it>(n = 29) or saline (n = 13) were randomized for imaging at 6, 12, 24, 30, 36, 42 or 48 hours after infection. T1W, T2W, quantitative diffusion, and post contrast T1W images were acquired at 4.7 T. Dynamic MRI (dMRI) was used to evaluate blood-brain-barrier (BBB) permeability and to obtain a measure of cerebral and muscle perfusion. Clinical- and motor scores, bacterial counts in CSF and blood, and WBC counts in CSF were measured.</p> <p>Results</p> <p>MR images and dMRI revealed the development of a highly significant increase in BBB permeability (P < 0.002) and ventricle size (P < 0.0001) among infected rats. Clinical disease severity was closely related to ventricle expansion (P = 0.024).</p> <p>Changes in brain water distribution, assessed by ADC, and categorization of brain 'perfusion' by cortex ΔSI_(bolus)were subject to increased inter-rat variation as the disease progressed, but without overall differences compared to uninfected rats (P > 0.05). Areas of well-'perfused' muscle decreased with the progression of infection indicative of septicaemia (P = 0.05).</p> <p>Conclusion</p> <p>The evolution of bacterial meningitis was successfully followed <it>in-vivo </it>with MRI. Increasing BBB-breakdown and ventricle size was observed in rats with meningitis whereas changes in brain water distribution were heterogeneous. MRI will be a valuable technique for future studies aiming at evaluating or optimizing adjunctive treatments</p

Hydrocephalus induces dynamic spatiotemporal regulation of aquaporin-4 expression in the rat brain

<p>Abstract</p> <p>Background</p> <p>The water channel protein aquaporin-4 (AQP4) is reported to be of possible major importance for accessory cerebrospinal fluid (CSF) circulation pathways. We hypothesized that changes in AQP4 expression in specific brain regions correspond to the severity and duration of hydrocephalus.</p> <p>Methods</p> <p>Hydrocephalus was induced in adult rats (~8 weeks) by intracisternal kaolin injection and evaluated after two days, one week and two weeks. Using magnetic resonance imaging (MRI) we quantified lateral ventricular volume, water diffusion and blood-brain barrier properties in hydrocephalic and control animals. The brains were analysed for AQP4 density by western blotting and localisation by immunohistochemistry. Double fluorescence labelling was used to study cell specific origin of AQP4.</p> <p>Results</p> <p>Lateral ventricular volume was significantly increased over control at all time points after induction and the periventricular apparent diffusion coefficient (ADC) value significantly increased after one and two weeks of hydrocephalus. Relative AQP4 density was significantly decreased in both cortex and periventricular region after two days and normalized after one week. After two weeks, periventricular AQP4 expression was significantly increased. Relative periventricular AQP4 density was significantly correlated to lateral ventricular volume. AQP4 immunohistochemical analysis demonstrated the morphological expression pattern of AQP4 in hydrocephalus in astrocytes and ventricular ependyma. AQP4 co-localized with astrocytic glial fibrillary acidic protein (GFAP) in glia limitans. In vascular structures, AQP4 co-localized to astroglia but not to microglia or endothelial cells.</p> <p>Conclusions</p> <p>AQP4 levels are significantly altered in a time and region dependent manner in kaolin-induced hydrocephalus. The presented data suggest that AQP4 could play an important neurodefensive role, and may be a promising future pharmaceutical target in hydrocephalus and CSF disorders.</p

Study of experimental pneumococcal meningitis using magnetic resonance imaging-0

<p><b>Copyright information:</b></p><p>Taken from "study of experimental pneumococcal meningitis using magnetic resonance imaging"</p><p>http://www.biomedcentral.com/1471-2342/8/1</p><p>BMC Medical Imaging 2008;8():1-1.</p><p>Published online 14 Jan 2008</p><p>PMCID:PMC2253532.</p><p></p>ters from 6 to 48 hours after inoculation in infected (n = 29, open circles and solid median line) and control rats (n = 13, black circles and dashed median line). Graph (a) and (b) show median and interquartile range of bacterial counts and WBC counts. Graph (c) and (d) show the steady worsening of clinical disease and deteriorating motor performance among infected animals. The ventricle-brain ratio (VBR) in (e) was subject to marked development among infected rats from 30 hours after infection and all infected rats had increased VBR from 36 hours onwards (P < 0.0001). The number of enhancing cortical voxels (f), indicative of BBB breakdown, was significantly increased among meningitis rats (6 to 48 hours, P = 0.0019). Graphs (g) and (h) illustrate comparable ADC values in cortex and basal ganglia among infected rats with increased variation around the mean values from the control group until 36 hours after infection (P > 0.05). Graph (i) shows decreased areas of high ΔSImuscle (no. of voxels) in infected rats presented as a fraction of the value in corresponding control animals at time point (P = 0.05). Graphs (j), (k) and (l) show the total number of voxels (enhancing + non-enhancing) in each ΔSIcategory (P > 0.05)

Study of experimental pneumococcal meningitis using magnetic resonance imaging-3

<p><b>Copyright information:</b></p><p>Taken from "study of experimental pneumococcal meningitis using magnetic resonance imaging"</p><p>http://www.biomedcentral.com/1471-2342/8/1</p><p>BMC Medical Imaging 2008;8():1-1.</p><p>Published online 14 Jan 2008</p><p>PMCID:PMC2253532.</p><p></p>ters from 6 to 48 hours after inoculation in infected (n = 29, open circles and solid median line) and control rats (n = 13, black circles and dashed median line). Graph (a) and (b) show median and interquartile range of bacterial counts and WBC counts. Graph (c) and (d) show the steady worsening of clinical disease and deteriorating motor performance among infected animals. The ventricle-brain ratio (VBR) in (e) was subject to marked development among infected rats from 30 hours after infection and all infected rats had increased VBR from 36 hours onwards (P < 0.0001). The number of enhancing cortical voxels (f), indicative of BBB breakdown, was significantly increased among meningitis rats (6 to 48 hours, P = 0.0019). Graphs (g) and (h) illustrate comparable ADC values in cortex and basal ganglia among infected rats with increased variation around the mean values from the control group until 36 hours after infection (P > 0.05). Graph (i) shows decreased areas of high ΔSImuscle (no. of voxels) in infected rats presented as a fraction of the value in corresponding control animals at time point (P = 0.05). Graphs (j), (k) and (l) show the total number of voxels (enhancing + non-enhancing) in each ΔSIcategory (P > 0.05)