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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acquired central auditory disorders not due to a tumour are unusual. The well-known conditions such as hypoxic encephalopathy, erythroblastosis, bacterial meningitis and trauma are reviewed. Recent experimental and clinical studies contribute to progress in the understanding of the pathogenesis and etiology of these conditions. The pattern of presbyacusis and cortical deafness is discussed also. AIDS must be considered as a new cause of acquired central auditory dysfunction.
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PMID:[Non-neoplastic central hearing loss--a review]. 174 76

We report the results of treatment of intractable seizures with lorazepam in seven neonates. All of the patients were part of a prospective study, who failed to respond to 40 mg/k of phenobarbital. Lorazepam was given intravenously at 0.05 mg/k and repeated up to a total dose of 0.15 mg/k if necessary. The diagnosis of seizures and the efficacy of treatment was assessed clinically and by EEG during the administration of lorazepam in three patients and on clinical grounds in four patients. Six patients were full term and one was premature; there were five males and two females. Four patients had hypoxic-ischemic encephalopathy, two had intracranial hemorrhage, and one had bacterial meningitis. Two patients received one dose of lorazepam, three received two doses, and two received three doses. Six patients responded with a complete cessation of seizures within three minutes of their last dose; the remaining patient (who received two doses) had a reduction in seizures. No patients developed apnea or hypotension during or immediately after the infusion of lorazepam and no other adverse effects were observed. Four patients remained seizure-free for the rest of the neonatal period and no other anticonvulsant medications were added. Seizures recurred in one patient at 16 hours; subsequent intermittent seizures were managed with additional phenobarbital. In another patient, seizures recurred at 12 hours and subsequent intermittent seizures were managed with phenytoin. In one patient, seizures continued with reduction of frequency and duration. We conclude that lorazepam may be effective in the treatment of neonatal seizures refractory to phenobarbital and that further treatment with intravenous phenytoin may be unnecessary under these circumstances.
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PMID:Lorazepam in the treatment of refractory neonatal seizures. 194 Jan 33

The examination of cerebrospinal fluid has provided useful information for diagnosis of CNS infections. The progress of analytical technology has brought the possibility to detect very small amounts of chemical substances. I thought that new information from brain should be obtained by using modern analytical technology for several substances in CSF. Free amino acid pattern, glutamine, homocarnosine, glutamic acid decarboxylase (GAD), neuron specific enolase (NSE) and 2',5'-oligoadenylic acid synthetase (2-5 A) in CSF have been examined for information of brain injury and dysfunctions. The results are as follows. 1) The individual difference and constancy of free amino acid pattern in CSF were found in children without any neurological diseases. 2) The levels of free amino acids in CSF increased in the acute phase of bacterial meningitis. 3) High levels of glutamine in CSF of children with acute bacterial meningitis were normalized during the recovery phase. 4) A marked imbalance of free amino acids in CSF was found in children with Lennox-Gastaut syndrome. 5) A decrease of homocarnosine levels in CSF was related with the degree of unconsciousness in children suffering from neurological diseases. 6) High GAD activities in CSF were observed in the acute phase of aseptic meningitis and after intrathecal injection of methotrexate for the therapy against meningeal leukemia. 7) High NSE activities in CSF were found in the acute phase of bacterial meningitis, intracranial hemorrhage, encephalopathy and encephalitis. 8) High 2-5A activities CSF were measured in the acute phase of mumps meningitis with subsequent decreases during the recovery phase. These results suggest that several substances in CSF are useful as markers of brain injury and dysfunction.
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PMID:[Cerebrospinal fluid as informative source of the brain]. 201 95

A retrospective study was performed to determine the clinical and pathologic features, etiology, and outcome of children with the reversal sign. The reversal sign, a striking CT finding, probably represents a diffuse, anoxic/ischemic cerebral injury. CT features of the reversal sign are diffusely decreased density of cerebral cortical gray and white matter with a decreased or lost gray/white matter interface, or reversal of the gray/white matter densities and relatively increased density of the thalami, brainstem, and cerebellum. Twenty children with the reversal sign were retrospectively analyzed. We divided the patients into three groups: (1) acute reversal, (2) intermediate group, and (3) chronic reversal. There were nine cases of trauma (seven of child abuse); nine hypoxia/anoxia incidents (birth asphyxia, drowning, status epilepticus); one bacterial meningitis; and one degenerative encephalitis. All acute- and intermediate-group patients had respiratory problems requiring ventilator support and intensive care. In five of seven patients who died, autopsy findings were consistent with anoxic/ischemic encephalopathy. Surviving patients have profound neurologic deficits with severe developmental delay. The CT reversal sign carries a poor prognosis and indicates irreversible brain damage.
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PMID:Reversal sign on CT: effect of anoxic/ischemic cerebral injury in children. 210 31

A retrospective study was performed to determine the clinical and pathologic features, etiology, and outcome of children with the reversal sign. The reversal sign, a striking CT finding, probably represents a diffuse, anoxic/ischemic cerebral injury. CT features of the reversal sign are diffusely decreased density of cerebral cortical gray and white matter with a decreased or lost gray/white matter interface, or reversal of the gray/white matter densities and relatively increased density of the thalami, brainstem, and cerebellum. Twenty children with the reversal sign were retrospectively analyzed. We divided the patients into three groups: (1) acute reversal, (2) intermediate group, and (3) chronic reversal. There were nine cases of trauma (seven of child abuse); nine hypoxia/anoxia incidents (birth asphyxia, drowning, status epilepticus); one bacterial meningitis; and one degenerative encephalitis. All acute- and intermediate-group patients had respiratory problems requiring ventilator support and intensive care. In five of seven patients who died, autopsy findings were consistent with anoxic/ischemic encephalopathy. Surviving patients have profound neurologic deficits with severe developmental delay. The CT reversal sign carries a poor prognosis and indicates irreversible brain damage.
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PMID:Reversal sign on CT: effect of anoxic/ischemic cerebral injury in children. 251 81

The metabolic basis of the encephalopathy associated with acute bacterial meningitis is unknown. The presence of cerebrospinal fluid lactic acidosis and hypoglycorrhachia suggests that intracellular acidosis or cellular energy depletion may play a role. Phosphorus magnetic resonance spectroscopy allows for the noninvasive determination of intracellular pH and relative amounts of phosphate-containing metabolites in humans. In seven normal volunteers, the intracellular pH of a mixed volume of gray and white matter was 7.00 +/- 0.04 (mean +/- SD). The apparent relative intensities of resonances from adenosine triphosphate, phosphocreatine, phosphodiesters and phosphomonoesters, and inorganic phosphate were measured. An encephalopathic patient with pneumococcal meningitis who had severe cerebrospinal fluid lactic acidosis was studied. Brain intracellular pH and relative phosphate metabolite concentrations were normal. Intracellular acidosis and bioenergetic compromise are therefore not causes of encephalopathy in this disease. This also demonstrates that the human brain can maintain tight control of intracellular pH even in the presence of marked extracellular metabolic acidosis.
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PMID:Brain phosphorus magnetic resonance spectroscopy in acute bacterial meningitis. 277 14

We reviewed retrospectively the clinical records, autopsy protocols and central nervous system tissue sections of 50 patients who underwent orthotopic liver transplantation for end-stage liver disease between 12/83 and 8/93. The postoperative survival period ranged from hours (6), weeks (17), months (17), to years (10). All patients received immunosuppressive drugs from the immediate postoperative period to the time of their death (cyclosporine, steroids; occasionally azathioprine, OKT3, FK506). Nineteen patients had neurological manifestations (hepatic encephalopathy) prior to surgery. Post-transplant neurologic signs and symptoms included: hepatic encephalopathy/altered mental status (11), focal or generalized seizures (9) and stroke (2). In the majority of cases (37) the cause of death was septicemia and/or bleeding diathesis. The neuropathologic findings present in 36 patients could be classified into 3 distinct categories: metabolic disorders: hepatic/anoxic encephalopathy, central pontine myelinolysis (15); cerebrovascular disease: subarachnoid and/or intracerebral hemorrhage, bland or hemorrhagic infarction (23); and infection: bacterial meningitis/cerebritis, multifocal fungal microabscesses, presumptive viral meningitis/encephalomyelitis (10). In conclusion, 72% of 50 patients who came to autopsy after liver transplantation were found to have neuropathologic abnormalities; these abnormalities were predominantly infections and vascular diseases.
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PMID:Neuropathology of liver transplantation. 760 96

We studied seizures that occur during the acute phase of aseptic and bacterial meningitis in childhood. Of the 108 children with aseptic meningitis, five had seizures (4.7%). Four patients developed them within 24 hours of the onset of the initial symptom (fever in 3 cases), and three had repeated seizures on the first day. One case had SIADH complication, but another neurologic abnormalities were not observed. On the 18 children with bacterial meningitis, three cases (16.7%) had seizure, which occurred on the second day of illness. Disturbance of consciousness and cerebral hypertension were observed in 2 cases each, and abnormal cerebral CT findings in all the three. The NSE level in the cerebrospinal fluid was elevated in 2 cases. Thus, seizures occurring in the acute phase of aseptic meningitis may reflect transient cerebral functional abnormality accompanying fever or SIADH, whereas those in bacterial meningitis may result from neural tissue damage due to encephalopathy or angitis. In aseptic and bacterial meningitis, the presence of seizures in the acute phase was not correlated with the neurological outcome.
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PMID:[Seizures in the acute phase of aseptic and bacterial meningitis]. 984 13

We investigated the concentrations of ciliary neurotrophic factor (CNTF) in cerebrospinal fluid (CSF) from children with inflammatory diseases of the central nervous system. We studied 6 children with acute disseminated encephalomyelitis (ADEM), 14 with acute encephalitis/encephalopathy, 17 with bacterial meningitis, and 24 with aseptic meningitis. We found that CNTF was undetectable in the CSF of all children with acute encephalitis/encephalopathy during the acute and convalescent stages, those with aseptic meningitis, and the 25 control subjects. In children with ADEM, CNTF was undetectable during the acute stage, but its concentration was elevated in all six at the convalescent stage. In children with bacterial meningitis, the CNTF concentration was slightly elevated in two of the 17 during the acute stage and another two at the convalescent stage. Our results suggest that CNTF is part of the regulatory system for oligodendrocyte functions, such as remyelination, in ADEM.
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PMID:Elevated cerebrospinal fluid level of ciliary neurotrophic factor in acute disseminated encephalomyelitis. 1098 Mar 11

The diagnostic approach to the compromised host with CNS infection depends on an analysis of the patient's clinical manifestations of CNS disease, the acuteness or subacuteness of the clinical presentation, and an analysis of the type of immune defect compromising the patient's host defenses. Most patients with CNS infections may be grouped into those with meningeal signs, or those with mass lesions. Other common manifestations of CNS infection include encephalopathy, seizures, or a stroke-like presentation. Most pathogens have a predictable clinical presentation that differs from that of the normal host. CNS Aspergillus infections present either as mass lesions (e.g., brain abscess), or as cerebral infarcts, but rarely as meningitis. Cryptococcus neoformans, in contrast, usually presents as a meningitis but not as a cerebral mass lesion even when cryptococcal elements are present. Aspergillus and Cryptococcus CNS infections are manifestations of impaired host defenses, and rarely occur in immunocompetent hosts. In contrast, the clinical presentation of Nocardia infections in the CNS is the same in normal and compromised hosts, although more frequent in compromised hosts. The acuteness of the clinical presentation coupled with the CNS symptomatology further adds to limit differential diagnostic possibilities. Excluding stroke-like presentations, CNS mass lesions tend to present subacutely or chronically. Meningitis and encephalitis tend to present more acutely, which is of some assistance in limiting differential diagnostic possibilities. The analysis of the type of immune defect predicts the range of possible pathogens likely to be responsible for the patient's CNS signs and symptoms. Patients with diseases and disorders that decrease B-lymphocyte function are particularly susceptible to meningitis caused by encapsulated bacterial pathogens. The presentation of bacterial meningitis is essentially the same in normal and compromised hosts with impaired B-lymphocyte immunity. Compromised hosts with impaired T-lymphocyte or macrophage function are prone to develop CNS infections caused by intracellular pathogens. The most common intracellular pathogens are the fungi, particularly Aspergillus, other bacteria (e.g., Nocardia), viruses (i.e., HSV, JC, CMV, HHV-6), and parasites (e.g., T. gondii). The clinical syndromic approach is most accurate when combining the rapidity of clinical presentation and the expression of CNS infection with the defect in host defenses. The presence of extra-CNS sites of involvement also may be helpful in the diagnosis. A patient with impaired cellular immunity with mass lesions in the lungs and brain that have appeared subacutely or chronically should suggest Nocardia or Aspergillus rather than cryptococcosis or toxoplasmosis. Patients with T-lymphocyte defects presenting with meningitis generally have meningitis caused by Listeria or Cryptococcus rather than toxoplasmosis or CMV infection. The disorders that impair host defenses, and the therapeutic modalities used to treat these disorders, may have CNS manifestations that mimic infections of the CNS clinically. Clinicians must be ever vigilant to rule out the mimics of CNS infections caused by noninfectious etiologies. Although the syndromic approach is useful in limiting diagnostic possibilities, a specific diagnosis still is essential in compromised hosts in order to describe effective therapy. Bacterial meningitis, cryptococcal meningitis, and tuberculosis easily are diagnosed accurately from stain, culture, or serology of the CSF. In contrast, patients with CNS mass lesions usually require a tissue biopsy to arrive at a specific etiologic diagnosis. In a compromised host with impaired cellular immunity in which the differential diagnosis of a CNS mass lesion is between TB, lymphoma, and toxoplasmosis, a trial of empiric therapy is warranted. Antitoxoplasmosis therapy may be initiated empirically and usually results in clinical improvement after 2 to 3 weeks of therapy. The nonresponse to antitoxoplasmosis therapy in such a patient would warrant an empiric trial of antituberculous therapy. Lack of response to anti-Toxoplasma and antituberculous therapy should suggest a noninfectious etiology (e.g., CNS lymphoma). Fortunately, most infections in compromised hosts are similar in their clinical presentation to those in the normal host, particularly in the case of meningitis. The compromised host is different than the normal host in the distribution of pathogens, which is determined by the nature of the host defense defect. In compromised hosts, differential diagnostic possibilities are more extensive and the likelihood of noninfectious explanations for CNS symptomatology is greater. (ABSTRACT TRUNCATED)
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PMID:Central nervous system infections in the compromised host: a diagnostic approach. 1144 10


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