Cases reported "Cerebral Hemorrhage"

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11/113. Scleroderma cerebritis, an unusual manifestation of progressive systemic sclerosis.

    A 42-year-old female with scleroderma experienced two exacerbations in which behavioral changes were the main clinical features. On both occasions she presented with paranoid delusions, perceptual aberrations, and disorientation. After treatment with corticosteroids, the patient's mental status returned to normal, and her electroencephalogram showed an increase in alpha wave frequency, which is consistent with a resolving delirium. Unlike systemic lupus erythematosus, scleroderma rarely involves the central nervous system. This case illustrates an unusual manifestation of progressive systemic sclerosis, primary cerebral involvement which presented as an acute organic brain syndrome. connective tissue diseases, notably systemic lupus erythematosus, often present neuropsychiatric symptoms. Despite the fact that there appears to be a clinical and pathological continuum among the connective tissue diseases, an organic psychosis rarely occurs in progressive systemic sclerosis (scleroderma. Described here is a patient with scleroderma in whom behavioral abnormalities were the main features of two exacerbations of the disease.
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12/113. Familial amyloidotic polyneuropathy (ATTR Val30Met) with widespread cerebral amyloid angiopathy and lethal cerebral hemorrhage.

    We report an autopsy case of familial amyloidotic polyneuropathy (FAP) with cerebral hemorrhage. A 38-year-old woman with a typical FAP pedigree started developing severe diarrhea and sensori-motor polyneuropathy at the age of 28 years; autonomic nervous system, heart and renal dysfunction manifested themselves in the following years. Genetic analysis revealed a single amino acid substitution at codon 30 of transthyretin (ATTR Val30Met). Ten years after her initial symptoms, the patient died of a sudden convulsive attack and respiratory failure. autopsy revealed lethal cerebral hemorrhages and uremic lungs. Histochemical and immunohistochemical analyses revealed TTR-derived amyloid protein in every tissue examined, particularly in glomeruli and peripheral vessels. Severe meningo-cerebrovascular amyloidosis was also detected. Because uremia causes oxidative damage to the vascular system and amyloid formation is closely associated with oxidative stress, it is possible that uremic endothelial damage facilitated an unusual cerebral amyloid deposition. In typical FAP (ATTR Val30Met), cerebral amyloid angiopathy does not usually have clinical manifestations. However, cerebral amyloid angiopathy should be considered to explain FAP symptoms when some risk factors such as uremic vascular damage are accompanying features.
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13/113. Respiratory failure in the neurological patient: the diagnosis of neurogenic pulmonary edema.

    Neurogenic pulmonary edema (NPE) is a potential complication of a central nervous system (CNS) insult such as intracranial hemorrhage, uncontrolled generalized seizures, head trauma, tumors, and neurosurgical procedures. The proposed etiology is massive sympathetic discharge following a CNS event. The pathogenesis is not completely understood. However, there are two theories on how NPE occurs: the blast theory and the permeability defect theory. There is evidence for both theories, and NPE is probably the result of a combination of the two. The treatment is mainly supportive with the use of mechanical ventilation and alpha-adrenergic blocking agents while managing increased intracranial pressure. A thorough understanding of the pathophysiological mechanisms behind the development of NPE aids in the management of these patients to prevent further complications.
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14/113. Hemorrhage in cerebral metastasis from angiosarcoma of the heart: case report.

    The purpose of this article is to describe the clinical and pathological features of metastatic angiosarcoma in the central nervous system. Only a few cases of cerebral metastasis from angiosarcoma of the heart have been recorded in the literature; particularly related to intracerebral hemorrhage. A case of secondary cerebral angiosarcoma of the heart in a 33 years old man is presented. The initial symptoms were headache, vomiting, lethargy and aphasia. There was a mass in the left temporal lobe with hemorrhage and edema on the computerized tomography (CT). After 24 hours the neurological status worsened and another CT scan showed rebleeding on the tumor area. He underwent an emergency craniotomy but died two days after. Considering the longer survival of sarcoma patients with new modalities of treatment, the incidence of brain metastasis may increase, demanding a better preventive and more aggressive approach. Besides, due to the hemorrhagic nature of such lesions, we suggest the immediate surgery to prevent a fast and lethal evolution because rebleeding.
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15/113. Intratumoral hemorrhage from a posterior fossa tumor after cardiac valve surgery--case report.

    A 53-year-old woman suffered intracranial hemorrhage from a cerebellar tumor several days after aortic valve replacement. Surgical intervention was not performed because the patient refused blood infusion for religious reasons (Jehovah's Witness). Instead, the anticoagulation therapy was interrupted for a week, and the patient was conservatively treated with administration of mannitol and steroid. The anticoagulation therapy was restarted 7 days after the hemorrhage. The intratumoral hemorrhage did not recur, and no systemic embolism occurred. The tumor was treated with gamma knife radiosurgery 6 weeks after the hemorrhage, under the radiological diagnosis of meningioma. Anticoagulation therapy is routinely used for patients following cardiac surgery to decrease the risk of thromboembolic complications, but also increases the risk of hemorrhagic events which often involve the central nervous system. Temporary discontinuation of anticoagulation therapy is an option for intratumoral hemorrhage in patients with replacement heart valves, and patients with known brain tumors should be informed about the risk of intracranial hemorrhage before cardiac surgery.
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16/113. endocarditis and hemorrhagic stroke caused by cunninghamella bertholletiae infection after kidney transplantation.

    cunninghamella bertholletiae is a saprophytic fungus found in soil. infection with this organism is extremely rare, occurring almost exclusively in immunosuppressed hosts. There have been only three previous cases of infection with this fungus reported in solid-organ recipients. We report an unusual case of disseminated cunninghamella infection in a woman who had received a renal transplant. A 48-year-old woman received a living-related kidney transplant for focal segmental glomerulonephritis. She was treated with plasmapheresis and muromonab-cd3 (OKT3) for two episodes of rejection. Because of recurrent focal segmental glomerulonephritis with diuretic-resistant edema, she underwent transplant nephrectomy, was restarted on hemodialysis, and had her immunosuppression stopped. Shortly thereafter, the patient presented with pulmonary infiltrates and hemorrhagic stroke with a rapidly fatal course. autopsy revealed widely disseminated C bertholletiae involving the central nervous system, lungs, and heart. This is the first reported case of endocarditis caused by this organism. diagnosis of this fungal infection is often difficult. Because the few patients who have survived this infection seemed to have been diagnosed early, it is important for clinicians caring for transplant patients to be aware of this invasive infection. Successful treatment requires prompt diagnosis and high-dose amphotericin b.
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17/113. Primary angiitis of the central nervous system and silent cortical hemorrhages.

    Primary angiitis of the CNS is histopathologically characterized by ischemic lesions and small petechial hemorrhages. Unlike CT or conventional MR imaging, gradient-echo MR imaging depicts these chronic petechial hemorrhages. We herein report the case of biopsy-proved primary angiitis of the CNS in a 42-year-old man; whom gradient-echo MR imaging revealed multiple petechial hemorrhages in the cortical-subcortical brain regions. The identification of petechial hemorrhages by gradient-echo MR imaging promises to be a valuable surrogate marker supporting the diagnosis of primary angiitis of the CNS.
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18/113. Cardiac arrhythmias in acute central nervous system disease. Successful management with stellate ganglion block.

    Cardiac rhythm disturbances and ECG wave-form abnormalities have been described with CNS disease or injury in experimental animals and in man. Unilateral sympathetic stimulation has been shown to produce similar changes in ventricular repolarization and reduce the fibrillation threshold. A patient with a ruptured congenital aneurysm of the basilar artery developed an accelerating ventricular tachycardia associated with an episode of active intracranial bleeding. The rhythm disturbance proved refractory to all modalities of chemotherapy, including lidocaine, phenytoin, atropine, procainamide, digoxin, and propranolol. The ECG showed a repolarization abnormality similar to that described with left stellate ganglion stimulation. Left stellate ganglion block was carried out with 15 ml of 1% lidocaine. An effect on the tachyarrhythmia was noted in five minutes. By 15 minutes, the rhythm disturbance was abolished. The repolarization abnormalities improved over a period of hours. Successful management with left stellate ganglion block suggests that this form of therapy may have clinical application in arrhythmias associated with CNS disease.
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19/113. Nonketotic hyperglycemic hyperosmolar coma. Report of neurosurgical cases with a review of mechanisms and treatment.

    Seventy-eight critically ill patients who died while on the neurosurgical service were studied retrospectively to establish the prevalence of nonketotic hyperglycemic hyperosmolar coma (NHHC). All the patients had been comatose before death, and all underwent necropsy. Criteria for the diagnosis of NHHC included moderate-to-severe hyperglycemia with glucosuria, absence of significant acetonuria, hyperosmolarity with dehydration, and neurological dysfunction. This study revealed seven cases of unequivocal NHHC (9%), and six of hyperosmolarity but with incomplete records. Five of the seven confirmed cases of NHHC demonstrated no evidence of cerebral edema transtentorial herniation, or brain-stem damage, and showed central nervous system (CNS) lesions compatible with survival. Fatal complications of this syndrome, such as acute renal failure, terminal arrhythmias, and vascular accidents, both cerebral and systemic, were common in this series. The mechanism of coma in NHHC is believed related to shifts of free water from the cerebral extravascular space to the hypertonic intravascular space, with subsequent intracellular dehydration, accumulation of metabolic products of glucose, and brain shrinkage. It is uncertain whether injury to specific areas in the CNS is a predisposing factor to the development of NHHC. Factors documented to be significant in its development include nonspecific stress to primary illnesses, hyperosmolar tube feedings, dehydration, diabetes and mannitol, Dilantin, or steroid administration.
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20/113. Intravascular lymphomatosis.

    Intravascular lymphomatosis (IVL) is a rare angiotrophic large cell lymphoma producing vascular occlusion of arterioles, capillaries, and venules. Antigenic phenotyping shows that these lymphomas are mostly of B cell type, and less commonly T cell or Ki-1 lymphomas. The central nervous system and skin are the two most commonly affected organs; patients usually present with progressive encephalopathy with mental status changes and focal neurological deficits and skin petechia, purpura, plaques, and discolouration. Other involved organs include adrenal glands, lungs, heart, spleen, liver, pancreas, genital tract, and kidneys. bone marrow, blood, cerebrospinal fluid, and lymph nodes are typically spared. fever of unknown origin is another common presentation. Only one case of IVL presenting with disseminated intravascular coagulation and anasarca (generalised oedema) has been reported in the literature. This report describes a postmortem case of a patient with IVL who initially presented with disseminated intravascular coagulation complicated by intracerebral haemorrhage.
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