Cases reported "Brain Edema"

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1/203. Abrupt exacerbation of acute subdural hematoma mimicking benign acute epidural hematoma on computed tomography--case report.

    A 75-year-old male was hit by a car, when riding a bicycle. The diagnosis of acute epidural hematoma was made based on computed tomography (CT) findings of lentiform hematoma in the left temporal region. On admission he had only moderate occipitalgia and amnesia of the accident, so conservative therapy was administered. Thirty-three hours later, he suddenly developed severe headache, vomiting, and anisocoria just after a positional change. CT revealed typical acute subdural hematoma (ASDH), which was confirmed by emergent decompressive craniectomy. He was vegetative postoperatively and died of pneumonia one month later. Emergent surgical exploration is recommended for this type of ASDH even if the symptoms are mild due to aged atrophic brain.
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2/203. Bilateral sphenoid wing metastases of prostate cancer presenting with extensive brain edema.

    A 76-year-old man insidiously developed diffuse neurological symptoms: cognitive decline, dysphagia, dysphasia and mental disturbance. Computed tomography of the cranium revealed widespread bilateral brain edema and symmetrical bilateral sphenoid wing hyperostosis. Adjacent to the hyperostosis that resembled skull base meningiomas, two separate parenchymatous temporal lobe lesions enhancing with contrast medium were observed. The patient had earlier been diagnosed to have prostatic carcinoma. dexamethasone therapy resulted in discontinuation of the neurological symptoms. The diagnosis of metastasized adenocarcinoma of the prostate was confirmed histologically on autopsy after a sudden death from pneumonia. Intracranial metastases of prostate cancer may have a predilection site at the sphenoid wing, and can mimic a skull base meningioma. Intracranial spread of prostatic adenocarcinoma should be considered in elderly men as a treatable cause of gradual neurological deterioration, especially if cranial malignancy or hyperostosis is found.
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3/203. Aggravation of brainstem symptoms caused by a large superior cerebellar artery aneurysm after embolization by Guglielmi detachable coils--case report.

    An 81-year-old male presented with right oculomotor nerve paresis and left hemiparesis caused by a mass effect of a large superior cerebellar artery aneurysm. Endovascular treatment was performed using Guglielmi detachable coils. The patient subsequently suffered aggravation of the mass effect 3 weeks after the embolization. Bilateral vertebral artery occlusion was performed, which decreased the cerebral edema surrounding the aneurysm, but his neurological symptoms did not improve. Parent artery occlusion is recommended as the first choice of treatment for an unclippable large or giant aneurysm causing a mass effect on the brainstem.
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4/203. Edema associated with calcified lesions in neurocysticercosis.

    OBJECTIVE: To determine serial MRI and CT abnormalities around calcified cysts due to cysticercosis in previously treated patients during periods of seizure activity. BACKGROUND: Some patients with calcified lesions due to cysticercosis have seizures. How and why seizures occur in this setting are unknown. methods: Three patients with known, treated cysticercosis were studied prospectively by serial MRI and CT before, during, and after seizure activity. RESULTS: All three patients demonstrated edema surrounding calcified lesions. Two of three patients had repeated episodes involving the same calcified lesions, and their symptoms corresponded to the location of the lesion. Enhancement was present in the lesions demonstrating edema, but was also present surrounding other nonsymptomatic calcified lesions. CONCLUSIONS: Perilesional edema surrounding calcified lesions due to cysticercosis occurs in some patients at the time of seizure activity. Repeated seizure episodes tend to be associated with the same lesions. Although the mechanisms involved are unknown, long-term antiseizure medication is likely indicated in these patients. Current evidence does not support the use of specific antiparasitic treatment in these patients.
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5/203. MRI features of intracerebral hemorrhage within 2 hours from symptom onset.

    BACKGROUND AND PURPOSE: MRI has been increasingly used in the evaluation of acute stroke patients. However, MRI must be able to detect early hemorrhage to be the only imaging screen used before treatment such as thrombolysis. Susceptibility-weighted imaging, an echo-planar T2* sequence, can show intracerebral hemorrhage (ICH) in patients imaged between 2.5 and 5 hours from symptom onset. It is unknown whether MRI can detect ICH earlier than 2.5 hours. We describe 5 patients with ICH who had MRI between 23 and 120 minutes from symptom onset and propose diagnostic patterns of evolution of hyperacute ICH on MRI. methods: As part of our acute imaging protocol, all patients with acute stroke within 24 hours from symptom onset were imaged with a set of sequences that included susceptibility-weighted imaging, diffusion- and perfusion-weighted imaging, T1- and T2-weighted imaging, fluid-attenuated inversion recovery (FLAIR), and MR angiography using echo-planar techniques. Five patients with ICH had MRI between 23 and 120 minutes from the onset of symptoms. RESULTS: ICH was identified in all patients. Distinctive patterns of hyperacute ICH and absence of signs of ischemic stroke were the hallmark features of this diagnosis. The hyperacute hematoma appears to be composed of 3 distinct areas: (1) center: isointense to hyperintense heterogeneous signal on susceptibility-weighted and T2-weighted imaging; (2) periphery: hypointense (susceptibility effect) on susceptibility-weighted and T2-weighted imaging; and (3) rim: hypointense on T1-weighted imaging and hyperintense on T2-weighted imaging, representing vasogenic edema encasing the hematoma. CONCLUSIONS: MRI is able to detect hyperacute ICH and show a pattern of evolution of the hematoma within 2 hours from the onset of symptoms.
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6/203. Fatal toxic effect of bleomycin on brain tissue after intracystic chemotherapy for a craniopharyngioma: case report.

    OBJECTIVE AND IMPORTANCE: Craniopharyngiomas are benign neoplasms of epithelial origin that arise from the remnants of Rathke's pouch and are located in the sellar, parasellar, and third ventricular regions. Despite major advances in microsurgical techniques, total removal of these tumors is associated with a high risk of death, long-term endocrinological dependence, cognitive dysfunction, and behavioral disorders. For patients with monocystic craniopharyngiomas, encouraging postoperative survival rates and high rates of cyst regression after intracavitary administration of bleomycin have been reported. Moreover, only a few side effects have been reported for this treatment method. We report a patient with a cystic craniopharyngioma who was treated using intracavitary bleomycin administration and died as a result of the direct toxic effects of bleomycin on deep brain structures and the brainstem. CLINICAL PRESENTATION AND INTERVENTION: A 47-year-old woman with a cystic craniopharyngioma underwent stereotactic insertion of a catheter attached to a subcutaneous reservoir. Five months after the procedure, positive-contrast computed tomographic cystography was performed to confirm the absence of fluid leakage. Daily intracavitary injections of bleomycin were administered through the reservoir into the cyst, until a total dose of 56 mg had been administered in 8 days. After the treatment, the cystic cavity regressed but the patient exhibited neurological deterioration; magnetic resonance imaging scans revealed diffuse edema in the diencephalon and brainstem. The patient died 45 days after completion of the treatment. CONCLUSION: Intracavitary administration of bleomycin is not a treatment protocol without risks or side effects, even if there is no fluid leakage into the cerebrospinal fluid. Although this is known to be an effective treatment for cystic craniopharyngiomas, previous reports cannot be used to establish a standard treatment method, and more research is needed to yield a safer effective protocol.
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7/203. coccidioidomycosis meningitis with massive dural and cerebral venous thrombosis and tissue arthroconidia.

    To our knowledge we report the first case of meningitis from coccidioides immitis associated with massive dural and cerebral venous thrombosis and with mycelial forms of the organism in brain tissue. The patient was a 43-year-old man with late-stage acquired immunodeficiency syndrome (AIDS) whose premortem and postmortem cultures confirmed C immitis as the only central nervous system pathogenic organism. death was attributable to multiple hemorrhagic venous infarctions with cerebral edema and herniation. Although phlebitis has been noted parenthetically to occur in C immitis meningitis in the past, it has been overshadowed by the arteritic complications of the disease. This patient's severe C immitis ventriculitis with adjacent venulitis appeared to be the cause of the widespread venous thrombosis. AIDS-related coagulation defects may have contributed to his thrombotic tendency.
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8/203. Acute cerebellar ataxia of a patient with SLE.

    We described a 28-year-old woman with systemic lupus erythematosus (SLE) presented with digestive tract, skin and renal symptoms and afterwards developed acute cerebellar ataxia, a paresis of the right inferior rectus muscle, left abducens paralysis and left facial palsy which seemed to be consistent with a brainstem lesion visible on magnetic resonance imaging (MRI). This lesion disappeared within 9 days of corticosteroid treatment. It is suggested that this lesion is focal edema induced by acute changes in the blood brain barrier secondary to a vasculopathy. Other causes, including local infarction, are unlikely.
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9/203. Risks of intravenous administration of hypotonic fluids for pediatric patients in ED and prehospital settings: let's remove the handle from the pump.

    Fluid resuscitation of infants and children is a common management problem in prehospital and emergency department care. We present two cases of children who received 5% dextrose in water as the initial resuscitation fluid. Bolus administration of hypotonic fluid contributed to fatal outcomes in these cases. Recommendations are made for eliminating hypotonic fluids as stock items in both the prehospital and emergency department settings.
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10/203. flushing in relation to a possible rise in intracranial pressure: documentation of an unusual clinical sign. Report of five cases.

    This report documents clinical features in five children who developed transient reddening of the skin (epidermal flushing) in association with acute elevations in intracranial pressure (ICP). Four boys and one girl (ages 9-15 years) deteriorated acutely secondary to intracranial hypertension ranging from 30 to 80 mm Hg in the four documented cases. Two patients suffered from ventriculoperitoneal shunt malfunctions, one had diffuse cerebral edema secondary to traumatic brain injury, one was found to have pneumococcal meningitis and hydrocephalus, and one suffered an intraventricular hemorrhage and hydrocephalus intraoperatively. All patients were noted to have developed epidermal flushing involving either the upper chest, face, or arms during their period of neurological deterioration. The response was transient, typically lasting 5 to 15 minutes, and dissipated quickly. The flushing reaction is postulated to be a centrally mediated response to sudden elevations in ICP. Several potential mechanisms are discussed. flushing has clinical importance because it may indicate significant elevations in ICP when it is associated with neurological deterioration. Because of its transient nature, the importance of epidermal flushing is often unrecognized; its presence confirms the need for urgent treatment.
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