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ABSTRACT: Concomitant chorioretinal folds with disc edema can be seen in cases of thyroid eye disease presenting with compressive optic neuropathy and may portend optic nerve ischemia. We describe an unusual case of a 64-year-old man who developed partial vision loss after orbital decompression.

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PURPOSE: Terson syndrome presents with retinal and vitreous hemorrhages in patients with a subarachnoid hemorrhage or after acutely elevated intracranial pressure. The source of this hemorrhage has been debated and may originate either from direct extension of intracranial hemorrhage or more likely from the peripapillary retinal vessels. OBSERVATIONS: A 39-year-old woman presenting with nausea, vomiting, floaters and papilledema with normal neuroimaging was diagnosed ultimately with pseudotumor cerebri syndrome. She had a right vitreous hemorrhage and bilateral subretinal and intraretinal hemorrhages which were consistent with Terson like syndrome. Her symptoms resolved with acetazolamide over one month and the retinal and vitreous hemorrhages significantly improved over two months. CONCLUSIONS AND IMPORTANCE: This case with initial presentation of pseudotumor cerebri syndrome causing a Terson like syndrome may help elucidate the mechanism behind the etiology of these hemorrhages from leaking peripapillary vessels.

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PURPOSE: To determine whether patients with Type B orbital blowout fractures (soft-tissue distortion disproportionate to bone-fragment displacement) repaired within 7 days of injury have statistically greater postoperative vertical binocular fusion than similar patients who undergo later surgery. METHODS: Prospective and retrospective surgical case series. Inclusion criteria were orbital floor (with or without medial wall) blowout fracture repair, preoperative coronal orbital CT scans, and patient age of at least 12 years at time of postoperative binocular visual field. RESULTS: Twenty-five patients met inclusion criteria. Ten patients (group 1) had surgery within 7 days of injury, and 15 patients (group 2) had surgery more than 7 days after injury. The total cohort had a median postoperative vertical binocular fusion of 90°. Group 1 had postoperative vertical binocular fusion averaging 100°. Nine of 10 patients (90%) were above and 1 of 10 (10%) were below the median for the entire cohort. Group 2 had postoperative vertical binocular fusion averaging 70°. Three of 15 patients (20%) were above and 12 of 15 patients (80%) were below the median for the entire cohort. The difference between the average postoperative vertical binocular fusion of the 2 groups was statistically significant by two-tailed unpaired t test with p value 0.0022. CONCLUSIONS: Patients with Type B orbital blowout fractures (soft-tissue distortion disproportionate to bone-fragment displacement) have statistically greater average postoperative vertical binocular fusion if repaired within 7 days of injury than similar patients who undergo later surgery.

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Cerebral venous sinus thrombosis (CVST) is a rare and potentially life-threatening cause of stroke. In the past few decades, the incidence and patient demographics have changed because of many factors, including the widespread use of oral contraceptives, improved detection of prothrombotic conditions, and advancement of imaging technology. The presentation of CVST is varied and can include ocular signs and symptoms. We present 2 cases of oral contraceptive-induced CVST in 18-year-old women, whose main presenting findings were ophthalmologic.

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A 73-year-old woman underwent routine enucleation for a blind, painful eye related to end-stage diabetic retinopathy and neovascular glaucoma. A large cystoid space, in continuity with the optic nerve stump, formed around the implant in the first few weeks following surgery. Aspirated contents were positive for ß-2 transferrin, confirming cerebrospinal fluid origin. Multiple comorbidities delayed surgical intervention, but the condition was ultimately managed with exposure of the patent optic nerve sheath at the compartment's base, temporary control of cerebrospinal fluid leakage with pulmonary hyperventilation and topical fibrin glue, dissection and vascular-clip ligation of the nerve stump, and capping with a dermis-fat graft. To the authors' knowledge, this postenucleation entity has not been previously described, and asymptomatic idiopathic intracranial hypertension may have been an underlying factor.

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BACKGROUND: Expert interpretation of modern noninvasive neuroimaging such as computed tomographic angiography (CTA) or MRA should detect nearly all aneurysms responsible for an isolated third nerve palsy. Whether a catheter angiogram should still be obtained in cases with negative CTA or MRA remains debated and mostly relies on whether the noninvasive study was correctly performed and interpreted. The aim of our study was to review the diagnostic strategies used to evaluate patients with isolated aneurysmal third nerve palsy at a large academic center. METHODS: Retrospective review of all cases with posterior communicating artery (PCom A) aneurysmal third nerve palsies seen at our institution since 2001. RESULTS: We identified 417 cases with third nerve palsy, aneurysm, or subarachnoid hemorrhage, among which 17 presented with an acute isolated painful third nerve palsy related to an ipsilateral PCom A aneurysm (mean age: 52 years; range: 33-83 years). Patients were classified into 3 groups based on the results of the noninvasive imaging obtained at initial presentation. Group I included 4 cases with subarachnoid hemorrhage on initial noncontrast head CT initially obtained in an emergency department for evaluation of their isolated third nerve palsy. Group II included 5 cases with isolated third nerve palsy and normal noncontrast head CT at presentation, immediately correctly diagnosed with a PCom A aneurysm at the referring institution. Group III included the 8 remaining cases who all had aneurysms that were missed on noninvasive studies at outside institutions. Review of these outside studies at our institution showed a PCom A aneurysm, confirming misinterpretation of these tests by the outside radiologists, rather than inadequate technique. Absence of specific training in neuroradiology and inaccurate clinical information provided to the interpreting radiologist were associated with test misinterpretation at the outside institutions. The average size of PCom A aneurysms causing an isolated third nerve palsy across all 3 groups was 7.3 mm and was similar in each group. CONCLUSION: Our study suggests that aside from an accurate history, the training and experience of the interpreting radiologist is probably the most important factor in determining the reliability of a noninvasive scan in patients with isolated third nerve palsies.

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PURPOSE: To delineate the disease course and prognosis of patients with mass lesions of the fourth nerve presumed to be schwannomas. DESIGN: Nonrandomized retrospective case series. PARTICIPANTS: Thirty-seven consecutive cases of presumed trochlear nerve schwannoma from 9 tertiary university neuro-ophthalmology centers. METHODS: Cases were collected, and their clinical characteristics on presentation and follow-up are described. Inclusion criteria were brain magnetic resonance imaging (MRI) with a lesion suggestive of a schwannoma along the course of the fourth nerve. Exclusion criteria were other causes of fourth nerve palsy, such as congenital, traumatic or microvascular; normal (or lack of) initial brain MRI; lack of adequate clinical information; and disappearance of the lesion on subsequent follow-up brain MRI. MAIN OUTCOME MEASURES: Demographics of patients, presence of neurofibromatosis, symptoms on presentation, vertical deviation, lesion size (on presentation and follow-up), length of follow-up, and outcomes of treatment for lesions or diplopia. RESULTS: Seven patients were excluded and of the 30 patients included in our series, patients were predominantly male (77%) with a mean age of 51 years (range 9-102 years). In contrast with prior case reports, almost all of our cases had a fourth nerve palsy on presentation (29/30), often isolated. Mean follow-up was 3.1 years (range 0.2 months to 11.1 years). There was no significant difference between initial and follow-up lesion size (4.4 vs. 5 mm) for patients who did not receive treatment of lesions (P = 0.36). Only 3 patients underwent neurosurgical resection and an additional patient received gamma-knife radiotherapy. The majority of patients (24/30) did not pursue strabismus surgery for vertical diplopia. CONCLUSIONS: Patients with isolated fourth nerve palsy and small lesions of the fourth nerve have a good prognosis and should be followed with serial MRI scans without neurosurgical intervention unless they develop signs of brain stem compression. Most patients with diplopia and benign fourth nerve lesions typical of trochlear nerve schwannoma can adapt with either prism spectacles or no treatment at all, although strabismus surgery can be successful.

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OBJECTIVE: Protective properties of high-density lipoproteins (HDL) may include reverse cholesterol transport and suppression of oxidation and inflammation. These were investigated in vivo, as were the effects of HDL on the characteristics of atherosclerotic lesions. METHODS AND RESULTS: Male apolipoprotein E knockout (apoE-/-) and apoE-/- mice expressing human apolipoprotein AI (hAI/apoE-/-) were studied up to 20 weeks after commencing a high-fat diet. Plasma HDL cholesterol was twice as high in hAI/apoE-/- mice. Over time, aortic root lesion area remained less in hAI/apoE-/- mice, although plaques became complex. In advanced lesions, plaque lipid was higher in apoE-/- mice, whereas plaque collagen and alpha actin were increased in hAI/apoE-/- mice. In nonlesional aorta, mRNA abundance for pro-inflammatory proteins (vascular cell adhesion molecule [VCAM]-1, intercellular adhesion molecule-1 [ICAM-1], monocyte chemoattractant protein-1 [MCP-1]) increased between 4 and 16 weeks in apoE-/- (but not wild-type) mice, and were not reduced by elevated HDL. Autoantibodies to malondialdehyde low-density lipoprotein (LDL) increased progressively in apoE-/- mice, with similar results in hAI/apoE-/- mice. CONCLUSIONS: HDL retarded plaque size progression despite greatly elevated plasma cholesterol. This effect was over a wide range of lesion severity. Expression of hAI reduced plaque lipid and increased the proportion of plaque occupied by collagen and smooth muscle cells, but did not affect indicators of inflammation or LDL oxidation.

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OBJECTIVE: To test the non-lipid-lowering effects of simvastatin on the response to injury in normolipidemic and hyperlipidemic mice. METHODS AND RESULTS: Wild-type (WT) mice (n = 40) and hyperlipidemic apolipoprotein-E-deficient (apoE(-/-)) mice (n = 40) received normal chow or chow containing simvastatin 100 mg/kg/day prior to bilateral femoral artery wire injury. Intimal hyperplasia and plasma cholesterol concentration were quantified after 4 weeks. Plasma cholesterol in WT mice treated or untreated with simvastatin was similar (100.9 +/- 6.6 vs. 94.3 +/- 17.5 mg/dl). Simvastatin did not affect intimal hyperplasia. In apoE(-/-) mice, intimal hyperplasia was increased 2.3-fold relative to WT mice (17090 +/- 4998 vs. 39490 +/- 16190; p < 0.001). In apoE(-/- )mice, simvastatin caused a paradoxical increase in plasma cholesterol (1094 +/- 60.3 vs. 658 +/- 66.8 mg/dl; p < 0.001), confirmed by FPLC. This was associated with a further increase in intimal area (39490 +/- 16190 vs. 55420 +/- 22590 mm(2); p < 0.01). CONCLUSIONS: (1). Simvastatin had no effect on plasma cholesterol or the response to arterial injury in normolipidemic WT mice; (2). hyperlipidemia was associated with markedly increased intimal hyperplasia, and (3). simvastatin treatment of apoE(-/-) mice caused paradoxical hyperlipidemia and increased intimal hyperplasia.

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