Symptomatic spinal extramedullary mass lesion secondary to chronic overdrainage of ventricular fluid--case report.
(49/402)
A 69-year-old man presented with progressive nuchal pain and spastic gait 2 years after undergoing ventriculoperitoneal (VP) shunting for a pineal astrocytoma with obstructive hydrocephalus. The neurological manifestations were compatible with radiculomyelopathy caused by an upper cervical lesion. Magnetic resonance imaging showed an enhanced extramedullary mass lesion tightly constricting the upper cervical spinal cord. The pressure of the shunt system was 150 mmH2O, and lumbar puncture revealed normal cerebrospinal fluid (CSF) pressure of 170 mmH2O. After removal of the shunt system, the clinical symptoms and neuroradiological findings markedly improved. This symptomatic spinal mass lesion was thought to be formed secondary to chronic depletion of ventricular CSF through the VP shunt. (+info)
Subcortical low intensity on MR images of meningitis, viral encephalitis, and leptomeningeal metastasis.
(50/402)
BACKGROUND AND PURPOSE: Subcortical low-intensity lesion on T2-weighted images is an uncommon manifestation of ischemia, multiple sclerosis, and Sturge-Weber disease. This study was performed to determine whether subcortical low signal intensity is an MR feature of meningitis, viral encephalitis, or leptomeningeal metastasis and to investigate a cause of subcortical low intensity. METHODS: We retrospectively reviewed MR images of 117 patients with meningitis, encephalitis (viral or unknown), or leptomeningeal metastasis for the presence of subcortical low intensity, meningeal enhancement, signal intensity change of cortex, and change in subcortical low intensity on follow-up images. Diffusion-weighted (DW) images and apparent diffusion coefficient (ADC) maps were obtained in 55 patients. Subcortical low-intensity lesions were also quantitatively analyzed on T2-weighted, fluid-attenuated inversion recovery (FLAIR), and DW images. RESULTS: Subcortical low intensity was found in nine (23.7%) of 38 patients with encephalitis (viral, 31; unknown origin, 7), five (24%) of 21 with leptomeningeal metastasis, and five (9%) of 58 with meningitis. Leptomeningeal enhancement was observed in 100% and cortical hyperintensity in 14 (74%) of 19 patients with subcortical low intensity. Leptomeningeal enhancement was seen in 46 (47%) and cortical hyperintensity in 33 (34%) of 98 patients without subcortical low intensity. Subcortical low intensity disappeared or decreased in extent on follow-up MR images in all seven patients who underwent follow-up. ADC of subcortical low-intensity lesions was lower than that of the contralateral area and decreased by 9.3 +/- 11.4%. CONCLUSION: Subcortical low intensity was uncommonly found in meningitis, viral encephalitis, and leptomeningeal metastasis. It is a nonspecific MR sign of various meningeal and cortical diseases. Although the cause of subcortical low intensity remains uncertain, free radical formation may play a role as a causative factor. (+info)
Use of IMiD3, a thalidomide analog, as an adjunct to therapy for experimental tuberculous meningitis.
(51/402)
Tuberculous meningitis (TBM), the most severe form of Mycobacterium tuberculosis infection in humans, is associated with significant morbidity and mortality despite successful treatment with antituberculous drugs. This is due to the irreversible brain damage subsequent to the local inflammatory response of the host to M. tuberculosis. Corticosteroids have been used in conjunction with antituberculous therapy in an attempt to modulate the inflammatory response, but this strategy has been of limited success. Therefore, we examined whether combining antituberculous drugs with the immunomodulatory drug thalidomide or with a new thalidomide analog, immunomodulatory drug 3 (IMiD3), would be effective in reducing morbidity and mortality in an experimental rabbit model of TBM. Intracisternal inoculation of 5 x 10(4) CFU of Mycobacterium bovis Ravenel in rabbits induced progressive subacute meningitis characterized by high cerebrospinal fluid (CSF) leukocytosis, protein influx, release of tumor necrosis factor (TNF), substantial meningeal inflammation, and mortality by day 28. Treatment with antituberculous drugs or with antituberculous drugs plus thalidomide improved the clinical course of disease somewhat and increased survival to about 50%. In contrast, treatment with antituberculous drugs in combination with IMiD3 limited pathological neurologic changes and resulted in marked improvement (73%) in survival. IMiD3 treatment was also associated with reduced leukocytosis in the CSF and significantly lower levels of TNF in CSF and plasma. Histologically, the meningeal inflammation in animals treated with antituberculous drugs plus IMiD3 was considerably attenuated compared to that of the other treatment groups. These results suggest a potential role for IMiD3 in the management of TBM in patients. (+info)
Role of the chemokine SDF-1 as the meningeal attractant for embryonic cerebellar neurons.
(52/402)
Migration of neuronal precursor cells from the external germinal layer (EGL) to the internal granular layer (IGL) is a crucial process in the development of the mammalian cerebellar cortex. These cells make up the only precursor population known to migrate away from the surface of the brain. We studied the role of the chemokine stromal-derived factor 1 (SDF-1) in the cerebellar tissue of rats and knockout mice and found (i) that it functions as an attractive guidance cue for neuronal migration and (ii) that its secretion from non-neuronal meningeal tissue is important for controlling the migration of embryonic EGL cells. (+info)
Interaction of Neisseria meningitidis with human meningeal cells induces the secretion of a distinct group of chemotactic, proinflammatory, and growth-factor cytokines.
(53/402)
The interactions of Neisseria meningitidis with cells of the leptomeninges are pivotal events in the progression of bacterial leptomeningitis. An in vitro model based on the culture of human meningioma cells was used to investigate the role of the leptomeninges in the inflammatory response. Following challenge with meningococci, meningioma cells secreted specifically the proinflammatory cytokine interleukin-6 (IL-6), the CXC chemokine IL-8, the CC chemokines monocyte chemoattractant protein 1 (MCP-1) and regulated-upon-activation, normal-T-cell expressed and secreted protein (RANTES), and the cytokine growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF). A temporal pattern of cytokine production was observed, with early secretion of IL-6, IL-8, and MCP-1 followed by later increases in RANTES and GM-CSF levels. IL-6 was induced equally by the interactions of piliated and nonpiliated meningococci, whereas lipopolysaccharide (LPS) had a minimal effect, suggesting that other, possibly secreted, bacterial components were responsible. Induction of IL-8 and MCP-1 also did not require adherence of bacteria to meningeal cells, but LPS was implicated. In contrast, efficient stimulation of RANTES by intact meningococci required pilus-mediated adherence, which served to deliver increased local concentrations of LPS onto the surface of meningeal cells. Secretion of GM-CSF was induced by pilus-mediated interactions but did not involve LPS. In addition, capsule expression had a specific inhibitory effect on GM-CSF secretion, which was not observed with IL-6, IL-8, MCP-1, or RANTES. Thus, the data demonstrate that cells of the leptomeninges are not inert but are active participants in the innate host response during leptomeningitis and that there is a complex relationship between expression of meningococcal components and cytokine induction. (+info)
Hypertrophic granulomatous cranial pachymeningitis causing progressive blindness in a chronic dialysis patient.
(54/402)
A patient on chronic haemodialysis because of renal failure developed progressive visual field loss and eventual blindness. A postmortem examination indicated that the blindness was caused by granulomatous thickening of the pachymeninges which constricted the optic nerves as they passed through the optic foramina. Exhaustive bacteriological and histopathological studies failed to identify a specific cause for this hypertrophic cranial pachymeningitis. (+info)
Matrix metalloproteinases limit functional recovery after spinal cord injury by modulation of early vascular events.
(55/402)
Inflammation in general and proteinases generated as a result are likely mediators of early secondary pathogenesis after spinal cord injury. We report that matrix metalloproteinase-9 (MMP-9) plays an important role in blood-spinal cord barrier dysfunction, inflammation, and locomotor recovery. MMP-9 was present in the meninges and neurons of the uninjured cord. MMP-9 increased rapidly after a moderate contusion spinal cord injury, reaching a maximum at 24 hr, becoming markedly reduced by 72 hr, and not detectable at 7 d after injury. It was seen in glia, macrophages, neutrophils, and vascular elements in the injured spinal cord at 24 hr after injury. The natural tissue inhibitors of MMPs were unchanged over this time course. MMP-9-null mice exhibited significantly less disruption of the blood-spinal cord barrier, attenuation of neutrophil infiltration, and significant locomotor recovery compared with wild-type mice. Similar findings were observed in mice treated with a hydroxamic acid MMP inhibitor from 3 hr to 3 d after injury, compared with the vehicle controls. Moreover, the area of residual white matter at the lesion epicenter was significantly greater in the inhibitor-treated group. This study provides evidence that MMP-9 plays a key role in abnormal vascular permeability and inflammation within the first 3 d after spinal cord injury, and that blockade of MMPs during this critical period attenuates these vascular events and leads to improved locomotor recovery. Our findings suggest that early inhibition of MMPs may be an efficacious strategy for the spinal cord-injured patient. (+info)
Pretreatment cognitive performance predicts survival in patients with leptomeningeal disease.
(56/402)
BACKGROUND: Leptomeningeal disease (LMD) involves the spread of malignant cells from solid tumors to the cerebrospinal fluid or to the leptomeninges. LMD has a very poor prognosis and it is difficult to diagnose and follow with traditional diagnostic tools. The purposes of this study were to characterize cognitive functioning of LMD patients before treatment and to determine if measurement of cognitive functioning could be used to predict survival time. METHODS: Thirty-seven subjects with LMD were administered the Mattis Dementia Rating Scale (DRS) before they received treatment and statistical analyses were performed. RESULTS: The Conceptualization subtest of the DRS was the most sensitive to disease course. It was the only individual subtest to predict survival and it was the most impaired subtest across individual subjects. These results support earlier findings of a frontal-subcortical pattern of dysfunction in LMD patients. Cognitive performance at time of LMD diagnosis predicts survival time. Age and clinical status, two factors often correlated with survival in the cancer literature, did not predict survival time for our LMD population. In addition, there were no correlations between survival time and previous medical history or demographic factors. CONCLUSIONS: Neuropsychological assessment appears to be a valuable tool both for tracking disease course over time and for predicting survival of patients. (+info)