Cases reported "Intracranial Hypertension"

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1/104. Endovascular recanalization with balloon angioplasty and stenting of an occluded occipital sinus for treatment of intracranial venous hypertension: technical case report.

    OBJECTIVE AND IMPORTANCE: Dural sinus thrombosis can lead to intracranial venous hypertension and can be complicated by intracranial hemorrhage. We present a case report of a patient who underwent endovascular recanalization and stenting of a thrombosed occipital sinus. CLINICAL PRESENTATION: A 13-year-old patient with a history of chronic sinus thrombosis refractory to anticoagulant therapy presented with acute onset of aphasia and hemiparesis. Computed tomography and magnetic resonance imaging revealed hydrocephalus and cerebral edema. Angiography delineated multiple dural arteriovenous fistulae and persistent occlusion of the posterior sagittal, occipital, and bilateral transverse dural sinuses with retrograde cortical venous drainage. INTERVENTION: After embolization of the dural arteriovenous fistulae, a transvenous approach was used to recanalize and perform balloon angioplasty of the right internal jugular vein and the occipital and left transverse sinuses, resulting in subsequent clinical improvement. The patient's condition deteriorated 3 days later with reocclusion of both balloon-dilated sinuses. Repeat angioplasty and then deployment of an endovascular stent in the occipital sinus were performed, and reestablishment of venous outflow was achieved, resulting in a decrease of intracranial venous pressure from 41 to 14 mm Hg and neurological improvement. At the 3-month follow-up examination, the stented occipital sinus remained patent and served as the only conduit for extracranial venous outflow; the patient remained neurologically intact at the 12-month follow-up examination. CONCLUSION: This is the first report of mechanical recanalization, balloon angioplasty, and stent deployment in the occipital sinus to provide sustained venous outflow for the treatment of venous hypertension with retrograde cortical venous drainage in a patient with dural pansinus thrombosis refractory to anticoagulant therapy.
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2/104. Diffuse calvarial meningioma. Case report and review of the literature.

    An extremely unusual calvarial meningioma in a 77-year-old woman is reported. The meningioma spread widely and symmetrically within the calvaria and grew extracranially within the scalp as well as intracranially. Reactive dural hyperplasia induced narrowing of the intracranial space and occlusion of the superior sagittal sinus, resulting in intracranial hypertension. After external decompression, the patient's symptoms markedly resolved. The authors review the literature on calvarial meningioma, discuss its pathogenesis, and propose mechanisms responsible for the patient's intracranial hypertension.
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3/104. Acquired dural fistulae in benign intracranial hypertension: a short case report.

    Venous sinus thrombosis has been regarded as a known cause of intracranial hypertension. We report a case of long-standing raised intracranial hypertension (ICT) that presented with deteriorating vision in both eyes. Magnetic resonance (MR) imaging of the brain and cerebral angiography showed blockage of superior saggital sinus and sigmoid sinuses with bilateral dural arteriovenous fistulae (DAVF) formation.
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4/104. ovarian hyperstimulation syndrome and benign intracranial hypertension in pregnancy after in-vitro fertilization and embryo transfer: case report.

    ovarian hyperstimulation syndrome (OHSS) is a dangerous and sometimes life-threatening complication of ovulation induction with exogenous gonadotrophins. While many complications of severe OHSS are recognized we have only identified one review detailing neurological problems. This report concerns a 32-year-old patient with bilateral tubal blockage who achieved her first pregnancy following in-vitro fertilization (IVF) and embryo transfer. Shortly after embryo transfer she developed clinical signs of moderate OHSS with symptoms which were later diagnosed as benign intracranial hypertension (BIH). The BIH was treated effectively using repeated lumbar puncture and diuretics. Spontaneous labour and delivery occurred at 40 weeks' gestation. There was no neurological sequel and no recurrence of the BIH 2 years after the pregnancy. The possible link between OHSS and BIH is discussed as well as the risks of further pregnancy.
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5/104. Idiopathic intracranial hypertension: a case report with optic nerve histopathology.

    We present the clinical and pathologic findings in an atypical case of idiopathic intracranial hypertension. A 51-year-old man had headaches, visual deterioration, papilloedema, and deafness. neuroimaging was normal, and cerebrospinal fluid pressure monitoring confirmed increased intracranial pressure. The patient was treated with a ventriculo-peritoneal shunt. Histopathology revealed grossly atrophic optic nerves with almost complete axonal loss. The prelaminar portion of the optic nerves was thickened by gliosis and hyalinized capillaries, which have not been described previously.
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6/104. Divergence paralysis & intracranial hypertension due to neurobrucellosis. A case report.

    CASE REPORT: A 22 year old female presented with sudden onset of uncrossed diplopia at distance, intracranial hypertension, esotropia and was evaluated. Microbiological tests of CSF and sera showed for brucellosis and the patient received therapy for this and her intracranial hypertension. The papilledema, headache, esotropia and diplopia all disappeared after therapy. CONCLUSIONS: Diagnostic tests for brucella must be considered for patients who have divergence palsy and papilledema, especially those living in endemic areas.
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7/104. Visual loss in idiopathic intracranial hypertension after resolution of papilledema.

    PURPOSE: To demonstrate that progressive visual field loss may occur after resolution of papilledema in patients with idiopathic intracranial hypertension and persistently elevated intracranial pressure. methods: A patient with idiopathic intracranial hypertension was evaluated with serial Humphrey automated static perimetry after initial treatment and resolution of papilledema. RESULTS: The patient developed recurrent headache and elevated cerebrospinal fluid pressure. optic nerve head appearance did not change. Automated perimetry demonstrated reproducible, worsening visual field loss; mean deviation decreased 11 dB in each eye. Visual field defects resolved after optic nerve sheath fenestration. CONCLUSIONS: Increased intracranial pressure caused visual field loss after resolution of papilledema. optic nerve sheath fenestration improved visual function in this patient.
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8/104. subarachnoid hemorrhage following permissive hypercapnia in a patient with severe acute asthma.

    In this article, we describe a case of a subarachnoid hemorrhage (SAH) in an acute severe asthma patient following mechanical hypoventilation. A 49-year-old man was admitted to an intensive care Unit with an acute exacerbation of asthma. After 3 days of mechanical ventilation (hypercapnia and normoxaemia), it was noted that his right pupil was fixed, dilated, and unreactive to light. Computed tomography (CT) scan showed localized SAH within the basilar cisterns and diffuse cerebral swelling. On the fourth day, a new CT scan showed hemorrhage resorption and a cerebral swelling decrease. In the following days, the patient's condition continued improving with no detectable neurological deficits. A review of similar published reports showed that all patients performed respiratory acidosis, normoxaemia, and hypercapnia. The most frequent neurological sign was mydriasis, and all subjects showed cerebral edema. Since normoxaemic hypercapnia has been associated with absence, or less cerebral edema, we considered additional factors to explain cerebral edema and intracranial hypertension causes. Thus, intrathoracic pressures due to patient's efforts by forcibly exhaling, or during mechanical ventilation, would further increase intracranial pressure by limiting cerebral venous drainage. This case emphasizes the fact that patients with acute severe asthma who have developed profoundly hypercarbic without hypoxia before or during mechanical ventilation, may have raised critical intracranial pressure.
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9/104. Extrinsic cerebral venous sinus obstruction resulting in intracranial hypertension.

    We report the case of a 70-year-old man reporting with headache and visual disturbances who was being treated for prostate cancer. Investigations showed him to have intracranial hypertension caused by venous sinus obstruction. patients with metastatic disease and raised intracranial pressure in the absence of focal signs should be considered as possible cases of venous outflow obstruction.
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10/104. Cryptococcal meningitis in the immunocompromised host: intracranial hypertension and other complications.

    cryptococcosis as a complication of the immunocompromised host has dramatically increased in frequency since the start of the AIDS epidemic. This trend has heightened awareness of the complications of cryptococcal meningitis; of these, intracranial hypertension is common, severe, and life-threatening, as exemplified by three cases in our institutions presented here in detail. An aggressive approach to management of this complication has not been the standard of care, but neurosurgical interventional studies combined with physiologic observations suggest early intervention may reduce the devastating morbidity and mortality.
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