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 21,692 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report presents the first case described in the English literature of dual infection with Cryptococcus neoformans and Streptococcus pneumoniae in the cerebrospinal fluid of an AIDS patient. The patient was a 32-year-old, HIV-positive South African woman who had been diagnosed with disseminated tuberculosis 5 months prior to the index admission. Her chief complaints at presentation were abdominal pain, chronic diarrhea, and vaginal discharge, suggesting a diagnosis of pneumonia and pelvic inflammatory disease. Persistence of confusion led to a lumbar puncture; gram-positive and budding yeasts were observed and subsequent India-ink staining revealed capsulated yeast typical of C. neoformans. S. pneumoniae and C. neoformans were cultured 24 and 48 hours, respectively, after incubation. The woman died within 24 hours of hospital admission, precluding further investigation. It is presumed that this woman already had disseminated cryptococci at the earlier presentation, but was incorrectly diagnosed as having tuberculosis. The finding of pneumococci, in the absence of inflammatory cells in cerebrospinal fluid, suggests the terminal event was fulminant pneumococcal meningitis in the setting of chronic cryptococcal meningitis. This case supports the importance of performing both the Gram- and India-ink stains and cryptococcal antigen test on cerebrospinal fluid specimens from immunocompromised patients, even when biochemical and cellular parameters are normal.
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PMID:Meningitis due to a combined infection with Cryptococcus neoformans and Streptococcus pneumoniae in an AIDS patient. 957 Jun 64

Aeromonas hydrophila is rarely reported as a causative organism of meningitis in humans. A 39-year-old man with alcoholic liver cirrhosis was admitted with a 2-day history of fever, chills, and confusion. Laboratory data revealed leukocytosis with granulocytosis, marked impairment of renal and liver function, and an elevated serum ammonia level. A. hydrophila was isolated from both blood and cerebrospinal fluid samples. Skin and soft-tissue lesions, consisting of bullae and necrotizing fasciitis, were found in the lower left leg 2 days after admission. Cultures of the bullous fluid, subcutaneous tissue, and fascia all yielded A. hydrophila. Pathologic examination revealed extensive necrosis. Although the patient was appropriately managed with antibiotics, debridement, and fasciotomies, his clinical status rapidly deteriorated, resulting in death 3 days after admission.
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PMID:Aeromonas hydrophila sepsis presenting as meningitis and necrotizing fasciitis in a man with alcoholic liver cirrhosis. 970 Feb 48

A 67-year-old woman with a diagnosis of polymyalgia rheumatica presented initially with periods of confusion and incontinence. A CT scan of the brain was normal and she was treated with tapering doses of corticosteroids and clinical improvement. After a brief period off steroids, the patient presented with a progressive dementia, left-sided clumsiness, gait disturbances and left hemispatial neglect. An MRI at this time demonstrated a large area of edema over the right parietal lobe and intense cortical enhancement. A chest CT demonstrated multiple nodules. Biopsies of the lung and brain failed to identify any infectious organisms or malignant tissue. The leptomeningeal biopsy revealed multiple granulomatous areas with central necrosis and hystiocytic cells consistent with idiopathic hypertrophic pachy-meningitis.
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PMID:A 67-year-old woman with polymyalgia rheumatica and left hemispatial neglect. 978 Aug 54

This preliminary report deals with a polyetiological and pathophysiologically multifacted encephalopathy that is fairly common and yet in need of identification as a clinical (but not nosological) entity: Mixed-Type Encephalopathy (MTE). MTE is a mostly acute condition, characterized by change of mentation (confusion, delirium, etc.) with little or no neurological deficit but with impressive diffuse EEG slowing. A variety of medical conditions lead to MTE, especially at an age above 50 years, but status-post-surgery (leaving aside cranial neurosurgery, but also cardiac surgery in view of common embolic cerebral pathology) may also result in MTE, especially with the use of general anesthesia. An attempt is made to analyze the plethora of contributory factors and underlying pathophysiological mechanisms. All types of classical brain pathology such as strokes, meningitis-encephalitis and typical metabolic encephalopathies (hepatic, renal, etc.) and others must be excluded from the diagnosis of MTE. Special emphasis is being placed on behavioral and EEG criteria in the early state of impaired consciousness with subdivision into 4 types: obtundation, somnolence, morbid lethargy and delirium. Cases of MTE are best picked up by an interdepartmental consultation (liaison) service making use of neurological consultations and EEG assessment. The value of the latter cannot be overestimated in these cases, especially in view of the very limited contributions of neuroimaging methods. The prognosis tends to be good. Severe and fatal developments are usually due to intervening cerebral hypoxia or anoxia. In such a development, epileptic manifestations, which are usually absent or mild in MTE, can become quite prominent. A thorough multi-institutional and international study of MTE is already in the planning stage. It is hoped that preventive measures can minimize the cerebral complications.
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PMID:Mixed-type encephalopathies: preliminary considerations. 989 Nov 86

Aseptic herpetic meningitis is a clinical syndrome characterized by fever, headaches, confusion, and a combination of meningeal signs. The spinal fluid findings consist of an increase in mononuclear cells (mononuclear pleocytosis), increased protein concentration, and normal glucose concentrations. Aseptic herpetic meningitis is thought to be caused by a viral infection, although the specific virus is usually not demonstrated. The condition is self-limited and requires no treatment.
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PMID:Aseptic herpetic meningitis: an uncommon genital herpes sequelae. 1041 72

Diagnostic confusion often exists between tuberculous meningitis and other meningoencephalitides. Newer diagnostic tests are unlikely to be available in many countries for some time. This study examines which clinical features and simple laboratory tests can differentiate tuberculous meningitis from other infections. Two hundred and thirty two children (110 tuberculous meningitis, 94 non-tuberculous meningitis, 28 indeterminate) with suspected meningitis and cerebrospinal fluid (CSF) pleocytosis were enrolled. Tuberculous meningitis was defined as positive CSF mycobacterial culture or acid fast bacilli stain, or basal enhancement or tuberculoma on computed tomography (CT) scan with clinical response to antituberculous treatment. Non-tuberculous meningitis was defined as positive CSF bacterial culture or Gram stain, or clinical response without antituberculous treatment. Thirty clinical/laboratory features of patients with tuberculous meningitis and non-tuberculous meningitis were compared by univariate and multiple logistic regression analysis. Five features were independently predictive of the diagnosis of tuberculous meningitis (p < 0.007): prodromal stage >/= 7 days, optic atrophy on fundal examination, focal deficit, abnormal movements, and CSF leucocytes < 50% polymorphs. When validated on another set of 128 patients, if at least one feature was present, sensitivity was 98.4% and, if three or more were present, specificity was 98.3%. This simple rule would be useful to physicians working in regions where tuberculosis is prevalent.
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PMID:A diagnostic rule for tuberculous meningitis. 1045 94

The first succinct description of otogenic meningitis related to the common cavity deformity of the inner ear was made from a post mortem study of 150 years ago. Since then there has been much confusion with less severe malformations of the cochlea, but these patients can now be treated by cochlear implant. It is therefore necessary that an accurate appraisal of the state of the cochlea is made beforehand by computed tomography and by Magnetic Resonance Imaging.
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PMID:The common cavity deformity of the ear. A precursor of meningitis but now being implanted. 1058 75

West Nile Virus (WNV) is a mosquito-borne flavivirus, which has been known to cause human infection in Africa, the Middle East, and southwestern Asia. It has also been isolated in Australia and sporadically in Europe but never in the Americas. Clinical features include acute fever, severe myalgias, headache, conjunctivitis, lymphadenopathy, and a roseolar rash. Rarely is encephalitis or meningitis seen. During the month of August 1999, a cluster of 5 patients with fever, confusion, and weakness were admitted to the intensive care unit of the same hospital in New York City. Ultimately 4 of the 5 developed flaccid paralysis and required ventilatory support. Three patients with less-severe cases presented shortly thereafter. With the assistance of the New York City and New York State health departments and the Centers for Disease Control and Prevention, these were documented as the first cases of WNV infection on this continent.
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PMID:The West Nile Virus outbreak of 1999 in New York: the Flushing Hospital experience. 1072 21

Glioblastoma multiforme (GBM) is the commonest primary malignant neoplasm of the CNS. Usually, patients present with seizures and headache but in the elderly, confusion and generalised cognitive decline are more frequently the initial features. Multiple cranial nerve lesions as a manifestation of leptomeningeal meningitis is a rare presentation of GBM. The diagnosis is not often suggestive on either brain computed tomography (CT) or magnetic resonance imaging (MRI) and is usually confirmed by cerebrospinal fluid (CSF) cytology or histology. We describe the case of an 80-year-old man, who presented with multiple cranial nerve palsies and confusion secondary to leptomeningeal gliomatosis, in whom GBM was detected along the intra-ventricular lining of the left lateral ventricle at ventriculoscopy, in the absence of a distinct parenchymal lesion.
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PMID:Leptomeningeal glioblastoma presenting with multiple cranial neuropathies and confusion. 1115 9

Tuberculous meningitis is characterized by cerebral tissue destruction. Monocytes, pivotal in immune responses to Mycobacterium tuberculosis, secrete matrix metalloproteinase-9 (MMP-9), which facilitates leukocyte migration across the blood-brain barrier, but may cause cerebral injury. In vitro, human monocytic (THP-1) cells infected by live, virulent M. tuberculosis secreted MMP-9 in a dose-dependent manner. At 24 h, MMP-9 concentrations increased 10-fold to 239 +/- 75 ng/ml (p = 0.001 vs controls). MMP-9 mRNA became detectable at 24--48 h. In contrast, tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) gene expression and secretion were similar to constitutive levels from controls at 24 h and increased just 5-fold by 48 h. In vivo investigation revealed MMP-9 concentration per leukocyte in cerebrospinal fluid (CSF) from tuberculous meningitis patients (n = 23; median (range), 3.19 (0.19--31.00) ng/ml/cell) to be higher than that in bacterial (n = 12; 0.23 (0.01--18.37) ng/ml/cell) or viral meningitis (n = 20; 0.20 (0.04--31.00) ng/ml/cell; p < 0.01). TIMP-1, which was constitutively secreted into CSF, was not elevated in tuberculous compared with bacterial meningitis or controls. Thus, a phenotype in which MMP-9 activity is relatively unrestricted by TIMP-1 developed both in vitro and in vivo. This is functionally significant, since MMP-9 concentrations per CSF leukocyte (but not TIMP-1 concentrations) were elevated in fatal tuberculous meningitis and in patients with signs of cerebral tissue damage (unconsciousness, confusion, or neurological deficit; p < 0.05). However, MMP-9 activity was unrelated to the severity of systemic illness. In summary, M. tuberculosis-infected monocytic cells develop a matrix-degrading phenotype, which was observed in vivo and relates to clinical signs reflecting cerebral injury in tuberculous meningitis.
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PMID:Identification of a matrix-degrading phenotype in human tuberculosis in vitro and in vivo. 1123 75


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