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

Tuberculous meningitis (TBM) remains a common serious neurological emergency especially in the developing world. Elevated intracranial pressure (ICP) is often a feature of severe TBM and is associated with high morbidity and mortality. The pathology associated with TBM, such as cerebral edema, hydrocephalus, tuberculoma(s), and infarcts related to arthritis, contribute to increase in intracranial volume and, therefore, elevated ICP. The three types of edema (vasogenic, cytotoxic, and interstitial) may contribute to cerebral edema. The molecular mechanisms underlying the events that ultimately lead to brain damage and cerebral edema during infection are complex. Similarly to bacterial meningitis, cerebral blood flow autoregulation is probably impaired in TBM, and the mechanisms are unclear. Although no universal guidelines are available to institute ICP monitoring in patients with severe TBM, it is be prudent to monitor patients at risk for increases in ICP. Such an approach helps to detect the secondary brain insults, allowing for a more informed approach to treatment. Treatment of elevated ICP involves a multipronged approach. The first step should be to identify focal brain lesions and hydrocephalus (which require surgical intervention) by brain imaging. Cerebral edema is treated with hyperosmolar agents. Mannitol is currently the most commonly used agent. It appears that use of hypertonic saline as an osmotic agent in infection-related cerebral edema has certain advantages. However, this needs to be established by well-designed trials. Use of steroids reduces not only cerebral edema but also the production of cytokines and other chemicals involved in the immunopathogenesis of TBM. Fever associated with TBM should be aggressively treated, because fever can worsen the impact of elevated ICP. Hyponatremia may complicate TBM and requires appropriate correction because it can aggravate cerebral edema.
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PMID:Management of intracranial pressure in tuberculous meningitis. 1615 82

Bacterial meningitis is a medical emergency and is optimally managed in an intensive care environment. Despite the use of antibiotics, the prognosis of this disease is poor because of central nervous system complications such as brain edema formation, cerebrovascular alterations, intracranial hemorrhage, and hydrocephalus. Effective adjunctive therapies are still missing. Experimental studies with animal models have provided new insights into the pathophysiology during the acute phase of bacterial meningitis. In recent years, knockout mice have become a powerful tool to investigate the role of particular genes and have also been applied in bacterial meningitis research. The use of these mice offered new insights into the role of different cytokines, proteases, and oxidants involved in the inflammatory cascade. Translating this knowledge into new therapies will provide new treatment strategies for this serious disease in the future.
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PMID:Development of adjunctive therapies for bacterial meningitis and lessons from knockout mice. 1615 83

Between January 1999 and December 2003, 81 cases of single pathogen-related culture-proven Gram-negative adult bacterial meningitis were identified at Chang Gung Memorial Hospital-Kaohsiung. Of these 81 cases, Acinetobacter infection was found in 13 cases. Clinical and laboratory data of these Acinetobacter meningitis patients were studied and were compared with those of other 68 non-Acinetobacter Gram-negative bacterial meningitis (GNBM) patients. Of the 13 implicated Acinetobacter strains, A. baumannii was the most common (12), and the other was A. lwoffii (1). Eleven of these 13 cases were due to a post-neurosurgical infection. The results of the antibiotic susceptibility test of the 13 Acinetobacter strains from cerebrospinal fluid included ceftriaxone, (1/13, 8%), ciprofloaxin (6/13, 46%), ceftazidime (6/13, 46%), cefepime (7/13, 54%), ampicillin-subtactam (7/13, 54%), imipenem (12/13, 92%) and meropenem (12/13, 92%). One strain with pan-drug resistant A. baumannii (PDRAB) emerged in 2003. A statistically significant difference between Acinetobacter meningitis and non-Acinetobacter GNBM included hydrocephalus and ceftazidime-resistance. A mortality rate was 30% (4/13), and 7 of the other 9 survivals had severe neurologic deficits. The emergence of Acinetobacter infections in adult post-neurosurgical infections, multiple antibiotic resistant characteristics, and the emergence of PDRAB strain remained a challenge of the initial management of this specific meningitis. Use of carbapenem, especially meropenem, could be considered as one of the initial empiric antibiotics chosen for the management of adult post-neurosurgical meningitis.
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PMID:Adult Acinetobacter meningitis and its comparison with non-Acinetobacter gram-negative bacterial meningitis. 1625 15

Aquaporin-4 (AQP4) is expressed in astrocytes throughout the central nervous system, particularly at the blood-brain and brain-cerebrospinal fluid barriers. Phenotype analysis of transgenic mice lacking AQP4 has provided compelling evidence for involvement of AQP4 in cerebral water balance, astrocyte migration, and neural signal transduction. AQP4-null mice have reduced brain swelling and improved neurological outcome in models of (cellular) cytotoxic cerebral edema including water intoxication, focal cerebral ischemia, and bacterial meningitis. However, brain swelling and clinical outcome are worse in AQP4-null mice in models of vasogenic (fluid leak) edema including cortical freeze-injury, brain tumor, brain abscess and hydrocephalus, probably due to impaired AQP4-dependent brain water clearance. AQP4 deficiency or knock-down slows astrocyte migration in response to a chemotactic stimulus in vitro, and AQP4 deletion impairs glial scar progression following injury in vivo. AQP4-null mice also manifest reduced sound- and light-evoked potentials, and increased threshold and prolonged duration of induced seizures. Impaired K+ reuptake by astrocytes in AQP4 deficiency may account for the neural signal transduction phenotype. Based on these findings, we propose modulation of AQP4 expression or function as a novel therapeutic strategy for a variety of cerebral disorders including stroke, tumor, infection, hydrocephalus, epilepsy, and traumatic brain injury.
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PMID:Three distinct roles of aquaporin-4 in brain function revealed by knockout mice. 1656 96

A 40-year-old woman presented with a right petroclival meningioma compressing the brainstem and manifesting as a 6-month history of headache and gait difficulty. The patient underwent subtotal removal of the tumor via an anterior transpetrosal approach. The postoperative course was complicated by cerebrospinal fluid rhinorrhea, bacterial meningitis, and acute hemorrhagic rectal ulcer. The patient was discharged home in good condition after prolonged medical treatment. Four months after the surgery, the patient noted recurrence of gait difficulty. Magnetic resonance (MR) imaging of the brain showed enlargement of the ventricles and no residual brainstem compression. A ventriculoperitoneal shunt was placed, but the symptoms were unchanged. The shunt was removed 2 months later because of infection. The patient's gait gradually deteriorated, although repeat brain MR imaging showed no significant increase in ventricular size. Ten months after the initial surgery she became paraplegic. MR imaging of the thoracic spine revealed a large arachnoid cyst extending from C-6 to T-6. The patient underwent T2-4 laminectomy, partial removal of the cyst wall, and duraplasty, but no clinical improvement was observed. Preexisting long-tract signs and coincidental hydrocephalus confused the neurological findings and delayed detection of the spinal lesion in this case. Neurosurgeons should be alert to the possibilities of insidious spinal lesion if the patient has progressive neurological disorder which does not match the known cranial lesion.
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PMID:Spinal arachnoid cyst causing paraplegia following skull base surgery. 1679 54

Cranial sonography plays an important role in the initial evaluation of infants with suspected bacterial meningitis and in monitoring for complications of the disease. Echogenic widening of the brain sulci, meningeal thickening and hyperemia suggest the diagnosis in an at-risk population. Sonography can identify the presence of extra-axial fluid collections, and color Doppler sonography can be very helpful in differentiating benign enlargement of subarachnoid spaces from subdural effusions. Intraventricular debris and stranding, and an irregular and echogenic ependyma are highly suggestive findings associated with ventriculitis. Sonography can play an important role in the detection of postinfectious hydrocephalus, in the determination of the level of obstruction, and in the evaluation of intracranial compliance. Focal or diffuse parenchymal involvement can represent parenchymal involvement by cerebritis, infarction, secondary hemorrhage or early abscess.
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PMID:Sonographic findings in bacterial meningitis in neonates and young infants. 1761 50

Bacterial meningitis and viral encephalitis are life-threatening infections with high mortality rates. Patients who survive these infections often remain permanently disabled. Potential neurologic complications requiring careful attention include impaired consciousness, elevated intracranial pressure, hydrocephalus, stroke, and seizures. Systemic complications are also common and are frequently the immediate cause of death. Critical care of these patients should focus not only on treatment of the underlying infection and its immediate complications but also on minimizing secondary brain injury. Given the increasing complexity of the diagnostic and therapeutic modalities available in managing central nervous system infections, the involvement of neurocritical care units and neurointensivists may be particularly helpful in improving outcomes.
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PMID:Neurocritical care of patients with central nervous system infections. 1761 51

Ventriculoperitoneal (VP) shunt surgery is the most used technique for the treatment of hydrocephalus. This procedure is associated with a large amount of complications. Bowel perforation caused by a peritoneal shunt catheter is one of these complications, sometimes fatal, and is usually difficult to recognize, except when protrusion of the peritoneal catheter through a natural orifice occurs. This report presents the case of a 2-year-old boy who had undergone a VP shunt and later presented with protrusion of the peritoneal catheter through his mouth. The shunt device was removed and an external shunt procedure was achieved, using the original ventricular catheter kept in place. The diagnosis of bacterial meningitis was retained and an antibiotic therapy was started. The evolution was fatal in 15 days secondary to a bacterial ventriculitis. Through the reported cases of bowel perforation, many risk factors were individualized, such as age, congenital etiology of the hydrocephalus, silicon allergy or the length of the peritoneal catheter. Bowel perforation is a serious complication of VP shunt surgery, leading sometimes to a fatal outcome.
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PMID:Transoral protrusion of a peritoneal catheter: a rare complication of ventriculoperitoneal shunt. 1823 Sep 35

We report a very unusual case of meningoencephalitis due to Listeria monocytogenes in a 7-month-old immunocompetent boy. Cerebrospinal fluid (CSF) culture was initially negative, but was positive on the seventh day. The disease was complicated by seizures and hydrocephalus managed with temporary ventriculostomy. The infant was discharged without obvious neurological sequelae after 30 days and developed without neurological or developmental sequelae at two years of age. Listeria is difficult to isolate and is not susceptible to third-generation cephalosporins commonly used for the empirical treatment of bacterial meningitis.
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PMID:A case of Listeria meningoencephalitis complicated by hydrocephalus in an immunocompetent infant. 1846 93

Bacterial meningitis and viral encephalitis are life-threatening infections with high mortality rates. Patients who survive these infections often remain permanently disabled. Potential neurologic complications requiring careful attention include impaired consciousness, elevated intracranial pressure (ICP), hydrocephalus, stroke, and seizures. Systemic complications are also common and are frequently the immediate cause of death. The importance of emergent administration of appropriate antimicrobial therapy cannot be overstated, but critical care of these patients should focus not only on treatment of the underlying infection and its immediate complications but also on minimizing secondary brain injury. Given the increasing complexity of the diagnostic and therapeutic modalities available to manage central nervous system (CNS) infections, the involvement of neurocritical care units and neurointensivists may be particularly helpful in improving outcomes. It is our opinion that ICP measurement should be strongly considered in selected patients with CNS infections, particularly those who are comatose. Treatments for intracranial hypertension, specifically in the setting of CNS infection, are described in this paper. For bacterial meningitis, intravenous dexamethasone should be administered, beginning concomitantly with the initial dose of antibiotics, at least until Streptococcus pneumoniae can be excluded as a pathogen. Clinicians should maintain a high index of suspicion for nonconvulsive seizures. Deterioration in neurologic status should also prompt early use of CT or magnetic resonance angiography and venography to exclude cerebrovascular complications.
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PMID:Neurocritical care of patients with central nervous system infections. 1857 24


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