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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 39-year-old woman presented with a 2-month history of repeated severe headache, nausea and diplopia. On admission she was obese with bilateral papilledma and abducens weakness. Mass lesion and sinus thrombosis were ruled out by brain CT and angiography. CSF pressure was normal initially. CSF pressure fluctuated with menstrual cycle, sometimes showing over 600 mmH2O with worsening of the symptoms. She was diagnosed as benign intracranial hypertension (BIH). Diuretics did not improve the symptoms, and visual disturbances ensued and deteriorated. A spinal subarachnoid space-peritoneal shunt was inserted to control CSF pressure, showing rapid improvement of headache and diplopia but visual disturbances remained almost unchanged. Optic nerve sheath fenestration was performed without improvement of visual deterioration. We postulated multiple factors such as obesity, menstrual abnormality, iron deficiency anemia and analgesic drugs played important roles to produce BIH in this case. Careful quantitative perimetry should be done to decide a suitable time for surgical treatment in BIH.
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PMID:[A case of benign intracranial hypertension with fluctuated symptoms and CSF pressure synchronized with menstrual cycle]. 149 Mar 15

Idiopathic intracranial hypertension is a diagnosis most frequently made in young, overweight women. The chief hazard to the patient is permanent visual loss due to chronic papilledema. After the diagnosis has been clearly established using lumbar puncture and imaging techniques, the neurologist is involved in helping to lower the intracranial pressure, control the headaches, and encourage weight loss. Careful vision monitoring is essential and should be done in collaboration with an ophthalmologist. Visual fields, fundus photographs, intraocular pressure measurement, and visual acuity should be performed at each follow-up visit. The use of visual evoked response and repeated measurement of intracranial pressure by lumbar puncture do not provide data that help to guide therapeutic decisions. Indications for surgery are loss of visual field or decline in visual acuity in the fact of medical therapy, persistent headache, or the inability to perform visual-function studies. Optic nerve sheath fenestration and lumbar peritoneal shunt both appear to be effective surgical means to reduce the pressure on the optic disc. A neurologist and an ophthalmologist working together provide the evidence on which to base rational decisions in the care of the patient with idiopathic intracranial hypertension.
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PMID:The rational management of idiopathic intracranial hypertension. 267 6

Five patients with serious ocular complications of benign intracranial hypertension are described. Optic nerve sheath fenestration resulted in resolution of papilloedema with, in three instances, improvement in vision. Benign intracranial hypertension may not always be benign for vision and fenestration operations may prevent or reverse visual deterioration by an effect on the optic nerve rather than by reducing intra-cranial pressure.
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PMID:Benign intracranial hypertension: visual loss and optic nerve sheath fenestration. 395 37

Optic nerve disease has been reported in patients with renal failure. A toxic aetiology has been postulated. The incidence of this complication of renal failure has not been determined. We observed 60 patients with renal failure on dialysis for 24 months to determine the incidence of optic neuropathy. Four patients developed typical acute ischaemic optic neuropathy. Their case notes were reviewed in order to determine the pathogenesis. Each patient had long-standing renal failure and its sequelae of anaemia and hypertension. The immediate causes of ischaemia were hypotension in 1, severe anaemia in 1, and generalised atherosclerosis in 2 patients.
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PMID:Optic neuropathy in uraemic patients on dialysis. 832 6

Intracranial hypertension is not a definitive diagnosis, but rather a syndrome that may result from a number of neurologic and systemic disorders. Intracranial hypertension refers to prolonged elevation of intracranial pressure, generally above 200 mm H2O. This condition may be recognized by the various clinical signs and symptoms that are manifest in most patients, including headache, papilledema, transient visual obscurations, diplopia, ocular motor disorders, tinnitus, nausea, vomiting, and mental irregularities, as well as dysfunctions of the circulatory and respiratory systems. Thorough medical testing as well as a comprehensive ocular evaluation is indicated in these cases. Intracranial hypertension most commonly results from mass lesions, tension hydrocephalus, and pseudotumor cerebri. Other causes include disorders of venous outflow, such as dural sinus thromboses or arteriovenous malformations, and various encephalopathies. Management for intracranial hypertension may involve medical treatment, drug therapy, or surgical intervention. Typically, diuretics are used initially. Corticosteroids may be used as well, although they are not the first choice for treatment. Cerebrospinal fluid shunting procedures may be necessary if medical treatment fails. Optic nerve sheath decompression may also be attempted when chronic papilledema threatens visual function. It is important that the primary care optometrist recognize the manifestations of intracranial hypertension in order to make necessary referrals for management of the underlying etiologies.
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PMID:Intracranial hypertension. 897 12

Optic nerve fenestration is carried out in cases of severe benign intracranial hypertension. This study aimed to monitor the optic nerve sheath appearances and orbital changes that occur following this procedure. The eight patients were all female with an average age of 37.3 years and a range of 20-58 years. The duration of symptoms was 2-6 years. Symptoms included headaches, diplopia and visual obscurations. Examination revealed severe papilledema. All investigations, including MRI, biochemical and immunological tests, were negative. Patients had fenestration of a 2 mm x 3 mm segment of the medial aspect of the optic nerve sheath. Imaging was obtained with a 1 T MRI machine using a head coil. Coronal, axial and sagittal 3 mm contiguous sections using STIR sequences with TR 4900 ms, IT 150 ms and TE 60 ms were obtained. Five patients showed clinical improvement. The post-operative MRI findings in four of these included a decreased volume of cerebrospinal fluid (CSF) around the optic nerve sheaths and a localized collection of fluid within the orbit. There were no MRI changes in the three patients with no clinical improvement. Decreased CSF volume around the optic nerve and a fluid collection within the orbit may indicate a favorable outcome in optic nerve fenestration.
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PMID:The MRI appearance of the optic nerve sheath following fenestration for benign intracranial hypertension. 972 37

Papilledema from benign intracranial hypertension can cause severe loss of visual acuity and visual field, with an optic neuropathy. We report a study of 5 patients with benign intracranial hypertension, and severe visual loss (visual field loss and visual acuity reduced to 1/10 or less) not improved by medical therapy (acetazolamide). We performed unilateral orbital decompression of the optic nerve sheath. No major operative complication was noted. Follow-up ranged from 11 months to 23 months, with an average of sixteen months. Visual function improvement was noted within 3 months after operation in 4 patients (for 2 eyes on the surgical side improvement of 2/10 and 5/10, for 3 eyes on the opposite surgical side average improvement of 4.6/10). The other patient showed improvement, but no significant. Optic nerve sheath decompression in benign intracranial hypertension seems to be a safe procedure and a therapeutic option in the management of raised intracranial pressure complicated by optic neuropathy with severe visual loss.
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PMID:[Intra-orbital decompression of the optic nerve by opening the peri-optic meninges in the treatment of severe optic neuropathies complicating benign intracranial hypertension]. 1044 51

Optic nerve sheath decompression is a surgical procedure only used in optic neuropathy complicating idiopathic intracranial hypertension. We describe this technique and compare it with the classic technique of cerebrospinal liquid derivation. Several points contrast optic nerve sheath decompression and cerebrospinal fluid derivation: there is no biomaterial, it is limited to the orbital area, and intracranial pressure remains unchanged. The complications are different, yet analysis of the literature shows the same efficacy in terms of visual function. We recommend a practical management of optic neuropathy complicating idiopathic intracranial hypertension, depending on the functional severity and the therapeutic efficacy. The surgical indication should only concern serious optic neuropathy not responding to medical therapy, with the choice of the surgical technique belonging to the surgeon.
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PMID:[Optic nerve sheath decompression in optic neuropathy complicating idiopathic intracranial hypertension: a new focus]. 1266 May 96

Optic nerve sheath decompression (ONSD) maintains a role in the management of visual loss complicating papilloedema in selected patients primarily with idiopathic intracranial hypertension. The evidence base for this intervention is reviewed and audit data on visual outcomes for patients with acute, chronic, and atrophic forms of papilloedema are contrasted. Optic canal decompression has a role in the management of compressive optic neuropathies complicating mass lesions arising from paranasal sinuses and intracranially and can be achieved by transethmoidal, transbasal, and open craniotomy routes. The evidence base supporting this intervention in traumatic optic neuropathy and in primary bone disease causing canal stenosis (in particular fibrous dysplasia) is reviewed where the indications are more controversial.
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PMID:Optic nerve disorders: role of canal and nerve sheath decompression surgery. 1553 2

The aim of this study was to evaluate the accuracy of previously reported neuroimaging signs in establishing or excluding the diagnosis of idiopathic intracranial hypertension (IIH). In a retrospective study, 30 patients with confirmed IIH and 56 controls were evaluated with brain magnetic resonance imaging. All examinations were evaluated in a blinded fashion by three neuroradiologists for the presence or absence of the 'traditional' signs of IIH: empty sella turcica, deformation of the pituitary, slit-like ventricles, 'tight' subarachnoid spaces, flattening of the posterior globe, protrusion of the optic nerve, enhancement of the optic nerve head, distension of the optic nerve sheath and vertical tortuosity of the optic nerve. Optic nerve protrusion and enhancement, slit-like ventricles and tight cerebrospinal fluid spaces were not significantly associated with IIH (P>0.05). Posterior globe flattening, optic nerve sheath distension, optic nerve tortuosity, pituitary deformity and empty sella turcica were significantly associated with IIH (P<0.05). However, most of these are not helpful in a clinical setting, with the exception of posterior globe flattening. This is the only sign that, if present, strongly suggests the diagnosis of IIH (specificity 100%, 95% CI 93.6% to 100%; sensitivity 43.5%, 95% CI 27.3% to 60.8%; positive likelihood ratio 49.7). The majority of the reported signs for IIH on cross-sectional imaging are not helpful in establishing or excluding the diagnosis of IIH, and are of no value in the clinical setting. Flattening of the posterior aspect of the globe is the only sign that, if present, is suggestive of the diagnosis of IIH.
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PMID:Idiopathic intracranial hypertension: the validity of cross-sectional neuroimaging signs. 1670 59


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