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

Colloid cyst is a relatively rare benign tumor which is usually found in the third ventricle. A patient who had a "colloid cyst" in his right lateral ventricle was experienced. A 33-year-old man had suffered from intermittent attacks of headache and vomiting for five months. On July 22, 1974, he was hospitalized to our clinic because of headache, memory and gait disturbance. At the time of admission his consciousness was clear but he had slight memory disturbance and urinary incontinence. Incipient papilledma was noted and the deep tendon reflexes of the lower extrimities were slightly accentuated. Lumbar puncture revealed a clear CSF and its pressure was within normal limit and the protein was 59 mg/dl. The plain skull films showed no abnormal findings. EEG showed an asymmetry of alpha-wave, and paroxysmal high voltage of slow wave was found in the right frontal area. Right cerebral angiography demonstrated an unrolling of the pericallosal arteries suggesting dilatation of the lateral ventricles. On the 9th hospital day, he suddenly began to complain of severe headache and became drowsy. Mannitol and hydrocortisone were injected intravenously without producing any remarkable effects. A ventricular drainage was done, and the patient recovered rapidly. A conray ventriculography revealed a round filling defect in the right lateral ventricle. A transventricular approach through a short linear incision in the right frontal cortex was preformed on the 25th hospital day. A cyst containing colloid substance, about 5x4 cm in size, was found to be attached to the medial wall of the right lateral ventricle anterior to the foramen of Monro. This cyst was almost completely removed. Histological findings revealed inner lining of epithelial cells, He died on the 25th postoperative day from bacterial meningitis. Autopsy confirmed the cyst to have originated from the right lateral ventricle. A review of the literature was made and the pathogenesis and diagnosis of this disease and the mechanism of development of the symptoms were discussed.
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PMID:["Colloid cyst" of the lateral ventricle--report of a case (author's transl)]. 98 73

In recent years the treatment of bacterial meningitis has been modified on the basis of a better understanding of its physiopathological mechanisms. It has been shown, for example, that the inflammatory reaction is the primary cause of brain damage in bacterial meningitis. Inflammation and consequent brain damage are greatest in the first hours of antibiotic treatment when rapid and massive bacteriolysis takes place. In effect, the bacterial components activate metabolic pathways and cellular elements leading to the release of inflammation mediators: cytokines (TNF, IL-I) neutrophil degranulation products, complement components and clotting factors. Initially these substances make the blood-fluid and blood-brain barriers permeable. The result is cerebral oedema, excessive fluid pressure, congestion of the cerebral blood vessels and finally endocranial hypertension, reduced cerebral flow, cerebral hypoxia and brain damage. This sequence of events can be stopped by a multifactorial therapy that is not only aetiological (antibiotic) but also treats the inflammation, oedema (Dexamethasone, Mannitol) and symptoms. In this study 129 patients with non-tubercular bacterial meningitis were treated as described. All patients were administered Ceftriaxone (100 mg/kg per diem) Dexamethasone (0.2-0.3 mg/kg/per diem), Mannitol, fluid restriction and--where necessary--intensive symptomatic therapy (against shock, convulsions, fever). Both the antibiotic and the corticosteroid were also administered intrathecally at the time of the first lumbar puncture at intake. Of these 129 patients, 7 died very soon after admission as they had arrived in a moribund condition. Duration of therapy was 3-6 days in 90% of these cases. There were no recurrences.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rational basis of modern therapy of bacterial meningitis. Review of the literature and our clinical experience of 122 pediatric cases. 180 76

The authors report a case and treatment of multiple brain abscesses located in the cerebrum and cerebellum combined with subdural empyema. In conjunction with the case report, the authors review the literature on the pathogenesis of brain abscesses and discuss therapeutic strategies concerning the topic. In the case presented, the primary infection persisted in the lung causing subclinical bronchitis. The hemoculture showed evidence of Streptococcus mitis infection. Although the etiological role of this bacterium in meningitis is known, it rarely causes bacterial meningitis without underlying predisposing factors. In their case, the patient was free of the most common predisposing factors such as congenital heart disease or immunodeficiency. Following the 2 month period of latency, a rapid onset of the symptoms of intracranial inflammation could be observed: fever, headache, meningeal symptoms, focal neurological symptoms and coma. They were not able to identify any bacteria in the cerebrospinal fluid; the Streptocossus mitis could be cultivated only from the haemoculture. The cytological analysis of the cerebrospinal fluid showed typical signs of bacterial infection and the cranial Computed Tomography revealed multiple cerebral abscesses. Neurosurgical intervention was not recommended because of the number, localization and size of the focal lesions. The therapy consisted of intravenous administration of 24 x 10(6) IU/die Penicillin and 4 g/die ceftriaxon. For supportive therapy, Mannitol B, 3 mg/die clonazepam and 300 mg/die phenytoin were administered. Corticosteroids were not used during the course of therapy. Two years later the 55 year old female is symptom free and doing well.
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PMID:[Non-invasive management of multiple brain abscesses. Case report and review of the literature]. 1053 93

Acute bacterial meningitis (ABM) in children is associated with a high rate of acute complications and mortality, particularly in the developing countries. Most of the deaths occur during first 48 hours of hospitalization. Coma, raised intracranial pressure (ICP), seizures, shock have been identified as significant predictors of death and morbidity. This article reviews issues in critical care with reference to our experience of managing 88 children with ABM in PICU. Attention should first be directed toward basic ABCs of life-support. Children with Glasgow Coma Scale (GSC) score < 8 need intubation and supplemental oxygen. Antibiotics should be started, even without LP (contraindicated if focal neuro-deficit, papilledema, or signs of raised ICP). Raised ICP is present in most of patients; GCS < 8 and high blood pressure are good guides. Mannitol (0.25 gm/Kg) should be used in such patients. If there are signs of (impending) herniation short-term hyperventilation is recommended; prolonged hyperventilation (> 1 hour) must be avoided. Any evidence of poor perfusion, hypovolemia and/or hypotension needs aggressive treatment with normal saline boluses and inotropes, if necessary, to maintain normal blood pressure. Empiric fluid restriction is not justified. Seizures may be controlled with intravenous diazepam or lorazepam. Refractory status epilepticus may be treated with continuous diazepam (0.01-0.06) mg/kg/min) or midazolam infusion. Ventilatory support may be needed early for associated pneumonia, poor respiratory effort and/or coma, and occasionally to reduce work of breathing in shock. Provision of critical care to children with ABM may reduce the mortality significantly as experienced by us.
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PMID:Bacterial meningitis in children: critical care needs. 1156 52

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