Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The proton magnetic resonance (1H-NMR) spectra were obtained from 38 cerebrospinal fluid (CSF) samples from 34 patients with various central nervous system (CNS) diseases and the H2O signals were reduced by the presaturation method. A doublet signal for CH3 protons of lactate, as well as a singlet one for alpha-CH proton of glucose, were clearly detected in all the spectra obtained. The relative lactate concentration values were calculated on the basis of the glucose concentrations which had been measured by a routine laboratory method in the hospital and the ratios of the peak heights (lactate CH3/glucose alpha-CH). In the CSF samples examined, the relative lactate values semi-quantitatively determined in this way were clearly elevated in cerebral infarction and bacterial meningitis, but not in other disorders including viral meningitis. On the other hand, one CSF component whose enhancement was found only in a sample from a hepatic encephalitis patient was identified as glutamine from the double quantum filtered-shift correlation spectrum. These results suggest that 1H-NMR spectroscopy of CSF can become a powerful aid in biochemical diagnosis of CNS diseases.
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PMID:Proton magnetic resonance spectroscopy of cerebrospinal fluid as an aid in neurological diagnosis. 814 94

The diagnostic value of cerebrospinal fluid (CSF) ferritin was assessed in 30 patients with meningeal reaction (viral meningitis 10; bacterial meningitis 6; meningism 14) and in 37 patients with cerebrovascular disease (cerebral infarction 29; transient ischaemic attacks 4; cerebral haemorrhage 4). The control group comprised 13 subjects with minor neurological disorders. CSF-ferritin levels were not significantly different in the various subgroups, most patients having values within the normal reference interval (2-7 micrograms/l). A clearly elevated CSF-ferritin was seen in one patient with bacterial meningitis and in one patient with intraventricular bleeding. In patients with meningeal reaction, CSF-ferritin was significantly correlated to CSF-protein. Patients with cerebrovascular disease displayed significant correlations between CSF-albumin and CSF-IgG and between CSF-ferritin, CSF-albumin and CSF-IgG. The present study indicates that measurement of CSF-ferritin is of no practical clinical relevance in the evaluation of patients with meningeal reaction and cerebrovascular disease.
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PMID:Cerebrospinal fluid ferritin in patients with meningitis and cerebral infarction or bleeding. 822 69

To evaluate significance of superoxide dismutase in neurological diseases, we measured cerebrospinal fluid (CSF) levels of copper-zinc superoxide dismutase (Cu/Zn SOD) and manganese superoxide dismutase (Mn SOD) using enzyme immunoassay methods in 181 neurological patients and 43 controls. The mean level of Cu/Zn SOD in CSF of controls was 54.4 +/- 28.7 ng/ml, and that of Mn SOD 8.1 +/- 2.5 ng/ml, although other methods have reported that Mn SOD is undetectable in CSF. Cu/Zn SOD or Mn SOD showed no statistical difference in age or sex of the controls. The elevation of both SOD levels was marked in acute diseases such as cerebrovascular diseases (CVD), bacterial meningitis and encephalitis, but mild in aseptic meningitis. The elevation of Cu/Zn SOD level was more prominent than that of Mn SOD in CVD, whereas vice versa in bacterial meningitis and encephalitis. In neurodegenerative diseases and cervical spondylosis, only Mn SOD level was significantly elevated. To examine the source of CSF SOD, we compared it with CSF levels of neuron-specific enolase (NSE) and S-100b protein (S-100b) in cerebral infarction and bacterial meningitis. Both SOD levels were correlated with NSE and S-100b levels in patients with cerebral infarction, but in bacterial meningitis no significant relationship was found among SOD levels, NSE and S-100b levels. This means that elevations of SODs in CSF may be due to not only damage of the nervous tissues but also the other mechanisms, as induction of SOD in the lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Superoxide dismutase in cerebrospinal fluid in patients with neurological diseases]. 833 70

We described a 4-month-old boy with cerebral infarction due to streptococcal meningitis. He complained of cough and high fever for 2 days. On the next day he admitted to our hospital because of bad humor, drowsiness, and vomiting associated with high fever, respiratory failure and loss of consciousness. On admission, he had opisthotonic posturing, anisocoria and elevated deep tendon reflexes with left side dominance. The cerebrospinal fluid showed increased cells (564/mm3), protein (295 mg/dl), and decreased sugar (1 mg/dl). Streptococcus pneumoniae was detected in the cerebrospinal fluid. Despite intensive treatment by antibiotics, glycerol, and dexamethasone, general condition was worsened, MRI showed a high intense area along the territory of bilateral anterior cerebral arteries and left middle cerebral artery 3-D time-of-flight MRA revealed a decreased signal of these arteries, confirming cerebral infarction. Recanalization of the arteries were observed 17 days after the first MRA examination. Since complication of cerebral infarction influences the prognosis of meningitis, repetitive MRA is very beneficial in patients with bacterial meningitis in order to evaluate the vascular lesion.
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PMID:[Usefulness of MRA in an infant with cerebral infarction due to streptococcal meningitis]. 894 Aug 80

We report two cases of pneumococcal meningitis with paranasal sinusitis followed by cerebrovascular disease. Both cases were occupational divers, and had past histories of head trauma and paranasal sinusitis. Despite the combined therapy with antibiotics and dexamethasone, they developed cerebrovascular complications. Case 1 developed cerebral infarction and hemorrhage on day 13, and in case 2 cerebral infarction occurred on day 15. In both cases, serum levels of TNF-alpha and IL-6 were elevated in the early stage of the illness (12 pg/ml and 21.3 pg/ml in case 1, and 50 pg/ml and 7,570 pg/ml in case 2, respectively). In case 2, TNF-alpha, IL-1 beta and IL-6 levels in the cerebrospinal fluid were also elevated on day 4 (25 pg/ml, 320 pg/ml and 6,870 pg/ml, respectively). Thrombocytosis was observed in both cases before the onset of the cerebrovascular complications. These cytokines may play significant roles in thrombocytosis leading to cerebrovascular complications in pneumococcal meningitis. Although the use of steroids as adjunctive therapy for bacterial meningitis has been found to be beneficial, the dosage of dexamethasone administered in our cases may not be enough to suppress the synthesis and release of the cytokines. Therefore, administration of large doses of glucocorticoid should be recommended before the treatment with antibiotics.
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PMID:[Two cases of severe bacterial meningitis with paranasal sinusitis followed by cerebrovascular disease--pathophysiology and treatment of cerebrovascular disease]. 897 33

Treatment of bacterial meningitis depends on its severity. The signs, symptoms, and laboratory values of 51 patients with bacterial meningitis admitting to the Department of Pediatrics at Sendai City Hospital from January 1985 to December 1994 were analyzed in order to evaluate their prognostic value. The overall mortality rate was 3.9%. The incidence of neurological deficit on discharge was 31.4%. According to their prognoses, patients were divided into two groups: those who recovered with no detectable disabilities (good prognosis) and those who died or were left with neurological deficits (poor prognosis). An analysis of these groups using Fisher's exact probability test revealed that the following risk factors were associated with poor prognosis: 1) duration of fever (including the periods of relapse) for more than 10 days ; 2) abnormal findings on brain imaging, such as cerebral infarction, cerebral hemorrhage, cerebral abscess and subdural effusion: 3 initial serum CRP value above 16 mg/dl; 4) initial CSF glucose value below 12 mg/dl; and 5) initial CSF LDH value above 220 IU/l. Streptococcus pneumoniae infection carried the worst prognosis: the causal organism of both the two fetal cases was S. pneumoniae. The incidence of poor prognosis was also high in S. pneumoniae meningitis (60.0%), compared to those by Hemophilus influenzae (46.7%) and group B streptococcus (25.0%). In the cases in which causal agents were not detected, this incidence was as low as 10 percent, showing significant difference from cases in which causal agents were identified. In order to improve the prognosis of bacterial meningitis, factors associated with poor prognosis should be recognized at early stages of the illness.
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PMID:[Factors associated with the prognosis of bacterial meningitis in children]. 924 88

Neonatal cerebral infarction in term infants has many possible causes, including bacterial meningitis, inherited or acquired coagulopathies, trauma, and hypoxia-ischemia. However, a specific cause often cannot be identified. Neurologic symptoms in the neonatal period are often subtle and nonspecific, even in infants with large infarctions involving an entire cerebral artery distribution. The most common presenting symptom is focal motor seizures of the contralateral limbs. Cranial magnetic resonance imaging, especially with diffusion-weighting, is the most sensitive imaging modality, although ultrasonography with Doppler imaging of cerebral blood flow is useful in the neonate who is too ill to transport. Neurodevelopmental outcome is often surprisingly good, with many infants making a complete recovery of motor function. The effect of neonatal stroke on cognitive function, especially language acquisition and emotional and social development, has not been fully established.
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PMID:Neonatal cerebral infarction. 1120 17

Infective endocarditis involves the brain in 20-40% of cases. The neurologic syndrome often is the presenting feature. The most frequent neurologic complication is cerebral ischemia. In these patients and those with intracranial hemorrhage, a heart murmur as well as systemic signs of inflammation point to endocarditis. The encephalopathy in endocarditis is mostly due to cerebral infarction. In bacterial meningitis and brain abscess an uncommon isolate arouses suspicion. The most important therapy is antibiotic treatment. Valve replacement improves outcome; in the acute phase of endocarditis, however, it is only necessary in a third of the patients. Neurologic complications interfere with the timing of the valve replacement. If it is urgently required, its risk is reasonable within 3 days after cerebral ischemia; if possible 2-4 weeks should be waited. Cases of successful valve replacement within 4 weeks after intracranial hemorrhage have been reported, but it is recommended to postpone it for 4-6 weeks. There are no data available for the other neurologic complications. Even today patients with endocarditis challenge the diagnostic and therapeutic capacity of various disciplines.
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PMID:[Neurological complications of infective endocarditis]. 1503 58

A 59-year-old woman presented with bacterial meningitis causing arterial narrowing in the very late stage. She initially underwent transsphenoidal surgery for massive non-functioning pituitary adenoma resulting in gross total removal. The postoperative course was uneventful, and she was discharged 12 days after surgery. Fourteen months later, she presented with bacterial meningitis due to streptococcus. Administration of multiple antibiotics resulted in normalization of cerebrospinal fluid findings. Forty days after meningitis onset, she suddenly suffered motor weakness of the right extremities. Magnetic resonance (MR) angiography revealed multiple intracranial arterial narrowings. Despite intensive treatment, no improvement of arterial narrowing was seen, and she suffered cerebral infarction. Six months after the onset of meningitis, MR angiography still showed multiple arterial narrowings, and MR plaque imaging of the stenotic vessel disclosed thickened arterial wall. This case illustrates the complex time course of arteritis caused by severe bacterial meningitis, and the intractability to treatment.
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PMID:Cerebral arteritis with extremely late onset secondary to bacterial meningitis - case report - . 2151 55

Cerebrovascular complications of bacterial meningitis may include vasculitis, vasospasm or vasoconstriction, delayed cerebral infarction, venous and arterial thrombosis, intracranial aneurysm formation. The role of invasive endovascular therapies has not been well studied for infectious vasospasm, which can lead to dire neurologic consequences. We present 2 patients who were diagnosed with bacterial meningitis. Brain MRI showed areas of acute ischemia. Neurologic worsening was seen in both patients despite aggressive medical management. Follow-up imaging demonstrated significant narrowing of the intracranial vessels with associated new scattered infarcts. Both patients underwent targeted intra-arterial vasodilator infusion with angiographically improved vessel caliber and distal flow. The neurological exam subsequently stabilized in both cases. Follow-up radiographic images demonstrated no further ischemia in one of the 2 patients. Vasculopathy and vasospasm causing delayed ischemic neurologic deficit is a rare, but severe complication of acute meningitis. It can be a significant predictor of poor prognosis, and the disease may progress despite aggressive medical therapy. Although frequently used in subarachnoid hemorrhage-related vasospasm, to our knowledge, this is the first report of endovascular vasodilator treatment as adjunctive intervention in patients with meningitis associated vasculopathy.
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PMID:Intra-arterial vasodilator therapy for parainfectious cerebral vasospasm. 2465 38


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