Subject(s)
Acquired Immunodeficiency Syndrome/drug therapy , Antiretroviral Therapy, Highly Active/adverse effects , Brain Diseases/chemically induced , Cognition Disorders/chemically induced , Depressive Disorder/chemically induced , Peripheral Nervous System Diseases/chemically induced , Brain Diseases/diagnosis , Cognition Disorders/diagnosis , Depressive Disorder/diagnosis , Diagnosis, Differential , Humans , Neuropsychological Tests , Peripheral Nervous System Diseases/diagnosisABSTRACT
Seventy-nine cytokines, chemokines, and growth factors were measured by protein array analysis in the cerebrospinal fluid of patients with meningitis and controls. Several factors were found to be regulated, which have not been studied in the CNS before, e.g., macrophage inflammatory protein-1delta (CCL15) and neutrophil-activating peptide-2 (CXCL7). In pneumococcal meningitis, other new observations were an increase of macrophage migration inhibitory factor, monocyte chemoattractant protein-2 (CCL8), pulmonary and activation-regulated chemokine (CCL18), and macrophage inflammatory protein-3alpha (CCL20), and a sustained upregulation of several growth factors. In viral meningitis, new findings were an elevation of CCL8, thrombopoietin, and vascular endothelial growth factor.
Subject(s)
Meningitis, Bacterial/cerebrospinal fluid , Meningitis, Viral/cerebrospinal fluid , Protein Array Analysis/methods , Chemokines/cerebrospinal fluid , Cytokines/cerebrospinal fluid , Growth Substances/cerebrospinal fluid , Humans , Retrospective StudiesABSTRACT
Human herpesvirus 6 (HHV-6), the causative agent of exanthema subitum in childhood, can also induce meningoencephalitis in immunocompromised individuals. In contrast, HHV-6 encephalitis in immunocompetent patients is rare, and the clinical syndrome not well defined. We report a case of meningoencephalitis caused by HHV-6 type B in an otherwise healthy woman.
Subject(s)
Ganciclovir/therapeutic use , Herpesvirus 6, Human/physiology , Immunocompetence , Meningoencephalitis/drug therapy , Meningoencephalitis/virology , Roseolovirus Infections/virology , Adult , Antiviral Agents/therapeutic use , Female , Herpesvirus 6, Human/isolation & purification , Humans , Meningoencephalitis/diagnosis , Roseolovirus Infections/diagnosis , Roseolovirus Infections/drug therapyABSTRACT
Thrombosis of the deep venous system presenting with bilateral thalamic infarction or edema is a common finding, but unilateral venous thrombosis presenting with unilateral thalamic edema is extremely rare. We report a case of a patient with this unusual condition presenting with nonspecific clinical signs and symptoms. CT and MR imaging revealed a unilateral thalamostriate lesion. The imaging sign that was most helpful in establishing the diagnosis, however, was the MR finding of a thrombus in a single internal cerebral vein.
Subject(s)
Brain Edema/complications , Cerebral Veins , Thalamic Diseases/complications , Venous Thrombosis/complications , Adult , Brain Edema/diagnosis , Cerebral Veins/diagnostic imaging , Cerebral Veins/pathology , Female , Humans , Magnetic Resonance Imaging , Thalamic Diseases/diagnosis , Tomography, X-Ray Computed , Venous Thrombosis/diagnosisABSTRACT
Fas (CD95) and Fas ligand (FasL, CD95L) have been implicated to be involved in the acute inflammatory response by attracting neutrophils and regulating their survival. Increased levels of soluble Fas and FasL are found in cerebrospinal fluid (CSF) samples of patients with bacterial meningitis but not in controls. Functional FasL (gld)- or Fas (lpr)-deficient mice were used to assess their role in the pathophysiology of pneumococcal meningitis. Induction of meningitis in wild-type (WT) mice caused an increase in CSF white blood cell (WBC) count, intracranial pressure (ICP), and vessel permeability, paralleled by a worse clinical status at 24 h. The inflammatory response was accompanied by elevated levels of IL-1beta, MMP-2, and MMP-9 in the brain. Neither gld- nor lpr-mice showed significant differences in the above-mentioned pneumococci-induced pathophysiological alterations. These results indicate that Fas and FasL are not essential in the regulation of the acute inflammatory response during pneumococcal meningitis.
Subject(s)
Inflammation/physiopathology , Membrane Glycoproteins/deficiency , Meningitis, Pneumococcal/physiopathology , fas Receptor/metabolism , Animals , Brain/metabolism , Brain/microbiology , Brain/pathology , Disease Models, Animal , Fas Ligand Protein , Humans , Inflammation/metabolism , Membrane Glycoproteins/cerebrospinal fluid , Meningitis, Pneumococcal/immunology , Mice , Mice, Mutant Strains , Rats , Reverse Transcriptase Polymerase Chain Reaction , fas Receptor/cerebrospinal fluidABSTRACT
The CX(3)C chemokine fractalkine is suggested to play an important role in inflammatory brain diseases, for example, because of its chemotactic properties. To investigate the release of soluble fractalkine in HIV-induced brain diseases fractalkine levels were determined in cerebrospinal fluid (CSF) and serum samples of HIV-infected patients with (n = 10) and without (n = 23) HIV-induced CNS complications, using semiquantitative Western blot analysis. Fractalkine CSF levels were significantly elevated (p < 0.05) in HIV-infected patients with CNS diseases compared with those without, and compared with HIV-negative controls (n = 23). Fractalkine serum concentrations did not differ between the two groups of HIV-infected patients, but were significantly elevated (p < 0.05) in HIV-infected patients with CNS complications compared with HIV-negative controls. Levels of fractalkine did not correlate with the CSF and serum HIV load and other CSF parameters. In one patient with HIV-associated dementia and myelopathy CSF fractalkine levels decreased on initiation of antiretroviral therapy and subsequent clinical improvement. In conclusion, intrathecal fractalkine release was observed in the majority of patients with HIV infection. The highest levels of soluble fractalkine were detected in CSF (and serum) samples of patients with HIV-induced CNS disorders. These results suggest a dysregulation of brain soluble fractalkine release during HIV infection.
