Cases reported "Pseudotumor Cerebri"

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1/8. cerebral amyloid angiopathy (CAA) with presentation as a brain inflammatory pseudo-tumour.

    cerebral amyloid angiopathy (CAA) is frequent but often asymptomatic. It can induce lobar haemorrhage, rapidly progressive dementia or recurrent transient neurological symptoms, other presentations being less frequent. We report 3 patients in their sixties presenting with a space occupying lesion which was the first manifestation of CAA. They were operated with a diagnosis of cerebral tumour. In all three cases, macroscopy was similar, the lesions were superficial in the cerebral cortex and the preoperative diagnoses were glioblastoma, meningioma and cavernoma. Histologically, the lesions consisted of a large inflammatory granuloma with numerous lipophages and siderophages surrounding capillaries with prominent endothelial cells. Vessels in the near cortex and meninges and within the granuloma harboured heavy amyloid deposits immunolabelled by anti-P component, anti-protein beta A4 with a A40 predominance and anti-apolipoprotein E. Adjacent cerebral cortex showed reactive gliosis and rare senile plaques. amyloidosis is rarely considered among diagnoses of space occupying lesions. In our three cases, CT scan and MRI changes were related to the presence of an inflammatory granuloma around foci of haemorrhage and amyloid laden vessels.
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2/8. Microvascular changes in the retrobulbar optic nerve in idiopathic intracranial hypertension.

    PURPOSE: To examine the microvascular changes in the retrobulbar optic nerve in idiopathic intracranial hypertension (PTC). methods: Both optic nerves from a 29-year-old man with a two year history of PTC were examined histologically and morphometrically. A semi-automated image analysis system and paraphenylenediamine (PPD) stain were employed to resolve sufficiently the microvascular images for counts and measurement. RESULTS: There were 150 vessels distributed in the optic nerves which revealed the following: The average lumen of the vessels in outer sectors were larger than those of the inner sector vessels (168.17 microns 2 vs. 46.99 microns 2; p = 0.0338; OD; and 251.96 microns 2 vs. 130.02 microns 2; p = 0.029; OS) while in the normal control optic nerve the outer and inner area lumens were reversed in size-differential, but this did not show a statistical difference. The thickness of the PTC optic nerve vessel walls in the outer sectors was also greater than that of the walls in the inner sectors (4.95 microns vs. 2.67 microns; p = 0.013; OD and 5.25 microns vs. 3.34 microns; p = 0.019; OS); the same measurements in the normal optic nerve showed a reversed ratio, which was opposite that of the experimental group and but not statistically different. CONCLUSION: This pattern of microvascular changes is consistent with the selective axonal loss in the peripheral area of each optic nerve as much more severe than that in the inner sectors.
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3/8. pseudotumor cerebri complicating measles: a case report and literature review.

    A previously healthy 8-year-old girl patient was referred with the complaints of severe headache associated with nausea and vomiting. Three weeks prior to her admission, she had measles manifested with fever and typical skin eruptions. Fundoscopic examination revealed bilateral swollen optic discs with tortuous blood vessels. Other physical examinations were unremarkable, except for photophobia. Lumbar puncture demonstrated a cerebrospinal fluid opening pressure of 30 cm H(2)O, no cells, normal levels of glucose and protein. serum measles immunoglobulin m level was elevated (183 AU). Our further investigations revealed that the patient had pseudotumor cerebri (PTC) following measles infection.
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4/8. Lumboperitoneal shunting as a cause of visual loss in benign intracranial hypertension.

    The causes of visual loss in benign intracranial hypertension are related to long standing papilloedema, ischaemic optic neuropathy or haemorrhage into a subretinal neovascular membrane. decompression procedures generally preserve or improve visual acuity but surgical treatment with subtemporal decompression may lead to visual impairment. Such a deficit has been recorded in the past as occurring with ventriculography. Postulated mechanisms have included brain herniation, spasm of vessels supplying the visual cortices or retinal vascular disturbance. To our knowledge treatment with lumboperitoneal shunting has not previously been reported as leading to further significant visual loss in this condition. This report describes such an occurrence in a patient. Retinal vascular disturbance is postulated on the basis of several normal CT scans, normal CSF pressure measured after surgery and visual evoked responses suggesting retinal or optic nerve damage.
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5/8. Relationship between intracranial hypertension and ultrasonic patterns of the common carotid artery and the internal jugular vein.

    The Doppler technique has only been used in neurological practice to evidence local vessel pathology such as occlusion or stenosis. Both common carotid artery and internal jugular vein flows can change not only because of pathological processes of the vessels but also because of impedance of their distribution territory. In this report we analyze the relationship between flow velocity, one of the parameters of blood flow, and intracranial impedance variations which occur in cerebral concussion, tumors and acute vascular cerebral pathology. During our observations we noticed that the diastolic wave of the velocity curve of the common carotid artery is a very important signal of the flow variations in the internal carotid artery and, in turn, of variations in cerebral flow. We studied the behaviour of the common carotid artery velocity curve in our patients both during clinical disease development and during the action of mannitol in the acute phases of the disease. We found that the ultrasonic patterns during antiedema action were similar to the ones obtained during the recovery period. We were able to note some differences and some similarities of the curve morphology in relation to generalized or focal causes of cerebral edema. This may be very important considering that at present no non-invasive and therefore repeatable technique is available for monitoring cerebral blood flow in intracranial hypertension.
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6/8. Benign intracranial hypertension vs. intracranial arteriovenous malformation: a possible CT dilemma.

    A nine-year-old boy, presenting only with signs of increased ICP, underwent computerized tomography. This examination demonstrated no abnormalities in the precontrast scan. Following C. E., it showed scattered areas of blood-like density in both hemispheres, as well as a presumedly abnormal vessel in the left occipital region and dilated vein of Galen, sinus rectus, and tentorial veins. The presumptive diagnosis of left occipital AVM was not confirmed by angiography, which also ruled out obstructions of the intracranial sinuses. The possible mechanism responsible for this atypical CT picture is briefly discussed in the light of pertinent literature. It is suggested that careful consideration should be given to the indications for angiography in similar cases, in the presence of a "hypervascular" aspect of the postcontrast CT scan, particularly if a considerable amount of contrast medium has been used.
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7/8. Disappearing opticociliary shunt vessels and pseudotumor cerebri.

    In two patients opticociliary venous shunts occurred in association with pseudotumor cerebri. One patient underwent bilateral optic nerve sheath fenestrations, after which her papilledema resolved, and the opticociliary venous shunts were noted to be markedly decreased in caliber.
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8/8. Management of visual loss after optic nerve sheath decompression in patients with pseudotumor cerebri.

    PURPOSE: To determine the appropriate management of patients with pseudotumor cerebri with early, progressive visual loss after optic nerve sheath decompression (ONSD). methods: The records of all patients with pseudotumor cerebri who underwent ONSD were reviewed retrospectively. patients who showed visual loss within 1 month of surgery were studied. RESULTS: Five patients with pseudotumor cerebri, including two with renal failure and hypertension, had visual loss within 1 month of ONSD. The first patient had an abrupt decrease in vision 6 days after ONSD. In this patient, a vessel on the nerve sheath bled into the surgical site. At the time of ONSD, this patient had a visual acuity of 20/20 1 day after surgery. Six days later, visual acuity decreased to 20/200. After high-dose intravenous corticosteroids failed to improve vision, emergency lumboperitoneal shunt resulted in full visual recovery. An apparent infectious optic neuropathy developed in the second patient 3 days after surgery. After 72 hours of intravenous antibiotics, visual acuity improved from 20/600 to 20/15. The other three patients had gradual visual loss after ONSD, which stabilized after lumboperitoneal shunts. CONCLUSIONS: Avoidance of bleeding during ONSD may prevent fibrous occlusion of the surgical site. patients with no identifiable cause for visual loss after ONSD, who do not respond to intravenous corticosteroids, should be evaluated for emergency lumboperitoneal shunting. Postoperative infectious optic neuropathy should be considered in the differential diagnosis of abrupt visual loss after ONSD.
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