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• W2474294659 abstract "Idiopathic intracranial hypertension (IIH), also known as pseudotumour cerebri, is a syndrome of increased intracranial hypertension of unknown cause found predominantly in women of childbearing age and associated with an increased body mass index or a history of recent weight gain.1Friedman D.I. Jacobson D.M. Idiopathic intracranial hypertension.J Neuroophthalmol. 2004; 24: 138-145Crossref PubMed Scopus (182) Google Scholar The modified Dandy criteria for diagnosing IIH include (i) an imaging study confirming the absence of radiographic hydrocephalus or mass lesion, (ii) elevated cerebrospinal fluid (CSF) opening pressure (OP) upon lumbar puncture (LP) with normal CSF contents, and (iii) an intact neurologic examination with the exception of visual disturbances, sixth cranial nerve palsy, and papilledema.2Friedman D.I. Jacobson D.M. Diagnostic criteria for idiopathic intracranial hypertension.Neurology. 2002; 59: 1492-1495Crossref PubMed Scopus (808) Google Scholar The principal morbidity of IIH is vision loss secondary to chronic papilledema. Most patients have visual field defects on presentation. Visual field loss in IIH usually follows a chronic and slowly progressive course with most patients responding to weight loss and medical management.3Galgano M.A. Deshaies E.M. An update on the management of pseudotumor cerebri.Clin Neurol Neurosurg. 2013; 115: 252-259Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar However, about 2.9% of IIH patients present with rapidly progressive and sometimes irreversible vision loss.4Thambisetty M. Lavin P.J. Newman N.J. Biousse V. Fulminant idiopathic intracranial hypertension.Neurology. 2007; 68: 229-232Crossref PubMed Scopus (171) Google Scholar This subtype has been termed “fulminant IIH” and is thought to require immediate surgical intervention. We present a case of fulminant IIH that responded adequately to medical treatment alone. A 34-year-old white female patient presented to the clinic with a 3-week history of headaches, binocular diplopia, and blurry vision. Her medical history was significant for polycystic ovarian syndrome and borderline hypertension. She had no history of migraine. Her body mass index was 34.9 kg/m2. Her surgical history included only appendectomy. She was taking no medications and had no drug allergies. Headaches started 3 weeks before while traveling in Canada. She first thought that they were “sinus headaches,” but as they worsened, she visited a local emergency department (ED). She reported being diagnosed with an “ear infection” and given antibiotics. Symptoms, however, did not improve, and she started experiencing blurry vision and binocular diplopia. She revisited the ED and was diagnosed with migraine. After returning to the United States, she sought further evaluation at another ED. Symptoms had not improved, and she continued having bi-frontal throbbing headache and visual disturbances. Best-corrected visual acuity (BCVA) measured in the ED was 20/70 OD and 20/100 OS. A noncontrast head computed tomography (CT) showed no evidence of acute intracranial hemorrhage, mass, hydrocephalus, or stroke. The sella, however, was slightly enlarged and partially empty. She was diagnosed with migraine and discharged on sumatriptan. She was instructed to follow-up with ophthalmology for her vision complaints. The next day, she saw a local optometrist, who noted bilateral optic disc edema. She then was referred to neurology for further evaluation and management. A repeat noncontrast head CT again showed no intracranial abnormalities. CT angiographies of the head and neck were unremarkable and were negative for venous sinus thrombosis. LP showed an elevated OP of 55 cm H2O with normal CSF contents. Magnetic resonance imaging of the brain with and without contrast showed a partially empty sella as well as cerebellar tonsil ectopia. She was diagnosed with IIH, started on acetazolamide 1 g/day, and referred to our neuro-ophthalmology clinic. On neuro-ophthalmology examination, BCVA was 20/70 OD and 20/80 OS. Automated visual field testing showed an enlarged blind spot in the right eye with an inferior arcuate defect and an enlarged blind spot in the left eye with a nasal step. Mean deviations (MD) were −11.25 and −9.25, respectively (Fig. 1). Ishihara colour plates were 14/14 bilaterally. Pupils were symmetric in light and dark, and there was no relative afferent pupillary defect. She had a small esophoria in primary gaze, but extraocular movements were full. Slit-lamp finding was unremarkable. On funduscopic examination, she had Frisen grade 4–5 disc edema bilaterally with flame-shaped hemorrhages and cotton wool spots (Fig. 2). Treatment options were discussed with the patient, including optic nerve sheath fenestration. Because she was only on acetazolamide day 2, the patient insisted upon medical treatment alone despite adequate understanding of the risk and our bias toward surgical intervention for fulminant IIH. She was advised to report further vision loss immediately.Fig. 2Fundus photograph. Frisen grade 4 disc edema with cotton wool spots and flame-shaped hemorrhages in both eyes.View Large Image Figure ViewerDownload Hi-res image Download (PPT) The patient returned a week later and reported marked improvement in headaches and visual symptoms. She also had lost 10 pounds. LP had been repeated by neurology and still showed an elevated OP of 39.5 cm H2O. Acetazolamide was increased to 1.5 g/day. On examination, BCVA was now 20/40 OD and 20/70 OS. Automated visual fields were also improved with MD of −7.00 and −3.72, respectively. Disc edema had decreased to grade 3–4, and there were no hemorrhages or cotton wool spots. Spectral domain optic nerve optical coherence tomography (OCT) showed a mean retinal nerve fibre layer (RNFL) of 221 μm OD and 207 μm OS (Fig. 3). She was advised to continue medical therapy and was given a 3-week follow-up appointment. On her 3-week follow-up examination, BCVA was 20/30 OD and 20/50 OS. Two weeks before, LP had been repeated by neurology and OP was still elevated at 32 cm H2O. Automated visual fields showed continued improvement with MD of −3.96 OD and −2.49 OS and only unspecific scatter. OCT mean RNFL was now 103 μm OD and 106 μm OS, with some thinning of the temporal RNFL (Fig. 4). Disc edema had decreased to a grade 1 bilaterally, but some temporal pallor was noted (Fig. 5). She was encouraged to pursue further weight loss and continue acetazolamide at 1.5 g/day.Fig. 5Fundus photograph. Disc edema grade 1 bilaterally with some temporal pallor.View Large Image Figure ViewerDownload Hi-res image Download (PPT) Fulminant IIH has been described in up to 2.9% of all IIH cases. It has been defined as those cases having acute onset of symptoms and signs of intracranial hypertension with less than 4 weeks between onset of symptoms and severe vision loss (rapid worsening vision over a few days). Thambisetty et al. described 16 patients with fulminant IIH in whom surgical treatment was required to lower ICP.4Thambisetty M. Lavin P.J. Newman N.J. Biousse V. Fulminant idiopathic intracranial hypertension.Neurology. 2007; 68: 229-232Crossref PubMed Scopus (171) Google Scholar The mean first lumbar puncture opening pressure was 54.1 cm H2O (range 29–60 cm H2O). Acetazolamide 1–2 g/day was started in all patients. Surgical treatment included optic nerve sheath fenestration in 5 cases, lumboperitoneal shunt in 9, and ventriculoperitoneal shunt in the remaining 2. The median delay between neuro-ophthalmology consultation and surgery was 3 days, but a wide range of a few hours to 37 days was reported. Visual function improved in 14 cases (87.5%), but 8 patients (50%) remained legally blind. Unfortunately, visual fields remained severely altered in all cases. This study emphasized the need for aggressive and rapid treatment of fulminant IIH. Our patient met all fulminant IIH criteria as described by Thambisetty et al., but insisted upon being treated medically with acetazolamide alone. She was advised to report further vision loss, and a close follow-up appointment was recommended. Fortunately, visual acuity, visual fields, and disc edema markedly improved on her follow-up appointment, and medical therapy alone was continued. Although no macular OCT was done, our patient’s favourable outcome raises the possibility that vision loss was mainly secondary to macular edema rather than ischemic optic neuropathy. The patient also had 3 serial LPs. However, it is impossible to determine how much they contributed to the improvement in disc edema and visual symptoms. The normal rate of CSF production is approximately 20 mL/hour, and it typically takes only 6 hours after LP to restore the drained fluid.5Oresković D. Klarica M. The formation of cerebrospinal fluid: nearly a hundred years of interpretations and misinterpretations.Brain Res Rev. 2010; 64: 241-262Crossref PubMed Scopus (229) Google Scholar This factor is one of the reasons why serial LPs are not advocated in the treatment of IIH and should only be used as a temporizing measure. In conclusion, fulminant IIH presents with rapidly progressive and sometimes irreversible vision loss. Although many authors have suggested that these patients with fulminant IIH must have surgery, some of these patients either refuse or cannot safely undergo surgery or general anaesthesia. It is also important to evaluate the presence of concomitant macular edema as it might represent the main cause of vision loss in some of our fulminant IIH patients. The current fulminant IIH diagnostic criteria do not take into account this last variable. It might be interesting to incorporate central macular thickness into fulminant IIH diagnostic criteria as a possible alternate explanation for severe and rapidly progressive vision loss. Lastly, we believe that our case supports the possibility that certain patients, possibly those with significant macular edema, can be treated with medical therapy and close observation. The authors have no proprietary or commercial interest in any materials discussed in this article." @default.
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• W2474294659 title "Fulminant idiopathic intracranial hypertension managed with oral acetazolamide" @default.
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