“Benign” Intracranial Hypertension

Boddie, H. G.; Banna, M.; Bradley, Walter G.

doi:10.1093/brain/97.1.313

Cited by 119 publications

(13 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…'-3 It may result in serious sequelae; in a cumulative series of 1020 cases, 29% developed visual loss and 3% became blind. 4 The risk of recurrence has been reported as 8%-12% over a decade.5 6 A proportion of patients, particularly those associated with chronic middle ear infection, arise from dural venous sinus thrombosis.7 In a series of 16 patients in which sinography was performed, five patients (31 %) had sinus occlusion, of whom only two had otitis.8 BIH has also been described in association with polycythaemia rubra vera,9 essential thrombocythaemia,'0 myeloma," and protein C deficiency,"2 all conditions associated with a prothrombotic state. It is not known whether intracranial thrombosis was present in most of these cases.…”

mentioning

confidence: 99%

Potentially prothrombotic abnormalities of coagulation in benign intracranial hypertension.

Sussman

Leach

Greaves

et al. 1997

Journal of Neurology, Neurosurgery & Psychiatry

View full text Add to dashboard Cite

Objective-Benign intracranial hypertension (BIH) may be caused by intracranial venous sinus thrombosis. Cerebral angiograms may, however, be normal in patients with BIH that are associated with conditions with an increased risk of venous thrombosis. This raises the possibility that unrecognised non-occlusive venous thrombus might impede CSF drainage. This study therefore examined the strength of the association between risk factors for thrombosis and BIH. Methods-The incidence of prothrombotic abnormalities among a mixed prospectively and retrospectively investigated cohort of 38 patients with BIH, was compared with healthy obese subjects, and patients with other neurological diseases. Prothrombotic abnormalities investigated included anticardiolipin antibodies, lupus anticoagulant, antithrombin III, proteins C and S, plasma fibrinogen, kaolin cephalin clotting time, prothrombin time, and full blood counts. Results-Evidence for the presence of an antiphospholipid antibody was found in 32% of cases. Cases of familial deficiency of antithrombin III, thrombocytosis, and polycythaemia were also noted. Additionally, an increased concentration of plasma fibrinogen was found in 26%. A coagulation abnormality was more often detectable in those subjects with normal or low body mass index and in those tested within six months of onset. Conclusion-There is a thrombotic pathogenesis in some cases of BIH.

show abstract

mentioning

confidence: 99%

Potentially prothrombotic abnormalities of coagulation in benign intracranial hypertension.

Sussman

Leach

Greaves

et al. 1997

Journal of Neurology, Neurosurgery & Psychiatry

View full text Add to dashboard Cite

show abstract

“…Sixth cranial nerve palsy is known to occur in 10 to 40% of patients in most series of IIH,2-4 and third or fourth nerve palsy has been described occasionally 5,6. However, concurrent third, fourth, and sixth nerve palsies in one patient has not been reported previously.…”

Section: Discussionmentioning

confidence: 89%

A Case of Multiple Cranial Nerve Palsies as the Initial Ophthalmic Presentation of Antiphospholipid Syndrome

Shin

Lee

2006

Korean J Ophthalmol

View full text Add to dashboard Cite

PurposeTo report a case of third, fourth, and six cranial nerve palsies with antiphospholipid syndrome (APS).MethodsMedical records of a 16 year old female diagnosed with idiopathic intracranial hypertension (IIH) in primary APS were reviewed.ResultsA 16 year old female presented with headache and diplopia. Ocular examinations revealed marked bilateral disc edema. She was unable to depress, adduct, and abduct in left eye and had limited abduction in the right eye. Cerebrospinal fluid had a normal composition and a pressure of 400 mmH2O. Lupus anticoagulant and IgG anticardiolipin antibody were positive. There was no clinical evidence of other autoimmune disease. Brain magnetic resonance (MR) imaging, MR angiography, and conventional angiogram with venous phase were normal. She was diagnosed with bilateral sixth, and left third and fourth cranial nerve palsies secondary to idiopathic intracranial hypertension in primary APS.ConclusionsTo our knowledge this is the first reported case of concurrent third, fourth, and sixth cranial nerve palsies in a patient with primary APS.

show abstract

“…Benign intracranial hypertension is generally a self-limiting condition in which signs and symptoms often resolve, with or without treatment, within 12 months of diagnosis (Johnston & Paterson 1974, Boddie et al 1974). The term 'benign' is, however, inappropriate when applied to the visual status.…”

Section: Discussionmentioning

confidence: 99%

“…The term 'benign' is, however, inappropriate when applied to the visual status. Irreversible optic nerve damage, with significantly impaired visual acuities and visual field loss, occurs in 8-24% of patients (Boddie et al 1974, Corbett et al 1982. Visual loss occurs from damage to the retinal axons at the optic disc and may be insidious or rapid.…”

Section: Discussionmentioning

confidence: 99%