Hemodialysis graft-induced intracranial hypertension

Intracranial hypertension is rarely associated with peripheral hemodialysis shunts, presumably in association with central venous stenosis.1,2 Hemodialysis Reliable Outflow (HeRO) grafts (CryoLife, Inc., Kennesaw, GA) are designed to bypass preexisting central venous stenosis by connecting the brachial artery with the venous circulation through the ipsilateral internal jugular vein (IJV) (figure, C and D).3 We report a case of intracranial hypertension immediately after placement of a HeR

Pituitary apoplexy: re-evaluation of risk factors for bleeding into pituitary adenomas and impact on outcome

Objective: To assess frequency, symptoms and outcome of pituitary apoplexy (PA) among pituitary adenoma patients, to gain better insight into risk factors for bleeding into pituitary adenoma, and to estimate the sequelae of PA by means of a matched control group. Method: By reviewing charts of 574 patients with pituitary adenoma we analysed incidence, symptoms and outcome of PA, and potential risk factors for developing PA by means of a control group (patients with pituitary adenoma without PA). Results: 42 suffered from PA; all had macroadenomas. 30/217 male (14%) and 12/179 female (7%) macroadenoma patients, 32/194 patients with clinically non-functioning (16.5%) and 10/202 with clinically active (5.0%) macroadenoma were affected. Antithrombotic therapy predisposed patients to PA (p = 0.026), diabetes mellitus and hypertension did not (p = 1.00). Patients with PA and pituitary adenoma patients without PA had similar frequencies of hypopituitarism (45 vs. 48%, p > 0.05) and visual field defects (38 vs. 55%, p > 0.05), but ophthalmoplegia was significantly more common (76 vs. 5%, p < 0.001) in patients with PA. Nearly all patients were treated by surgery; most recovered from ophthalmoplegia whereas visual function improved only moderately. Endocrine outcome was worse in patients with PA compared to patients without PA. Conclusions: Male gender and characteristics of the adenoma itself (especially tumour size and tumour type) rather than patient's cardiovascular risk factors such as diabetes and hypertension seem to predispose to PA; antithrombotic therapy may also be important

Painful Horner Syndrome as a Harbinger of Silent Carotid Dissection

A painful Horner's syndrome should alert clinicians to the possibilty of a silent carotid dissectio

Hypertensive eye disease

Hypertensive eye disease includes a spectrum of pathological changes, the most well known being hypertensive retinopathy. Other commonly involved parts of the eye in hypertension include the choroid and optic nerve, sometimes referred to as hypertensive choroidopathy and hypertensive optic neuropathy. Together, hypertensive eye disease develops in response to acute and/or chronic elevation of blood pressure. Major advances in research over the past three decades have greatly enhanced our understanding of the epidemiology, systemic associations and clinical implications of hypertensive eye disease, particularly hypertensive retinopathy. Traditionally diagnosed via a clinical funduscopic examination, but increasingly documented on digital retinal fundus photographs, hypertensive retinopathy has long been considered a marker of systemic target organ damage (for example, kidney disease) elsewhere in the body. Epidemiological studies indicate that hypertensive retinopathy signs are commonly seen in the general adult population, are associated with subclinical measures of vascular disease and predict risk of incident clinical cardiovascular events. New technologies, including development of non-invasive optical coherence tomography angiography, artificial intelligence and mobile ocular imaging instruments, have allowed further assessment and understanding of the ocular manifestations of hypertension and increase the potential that ocular imaging could be used for hypertension management and cardiovascular risk stratification

Intra-arterial Thrombolysis for Central Retinal Artery Occlusion: Two Cases Report

Central retinal artery occlusion (CRAO) causes severe visual loss in affected eye and vision does not recover in more than 90% of the patients. It is believed that it occurs by occlusion of the central retinal artery with small emboli from atherosclerotic plaque of internal cerebral artery. Retina is a part of the brain, thus basically CRAO is corresponding to acute occlusion of intracerebral artery and retinal ischemia is to cerebral stroke. Therefore, intra-arterial thrombolysis (IAT) has been considered as a treatment method in CRAO. Recently, we treated 2 patients diagnosed as CRAO and could achieve complete recanalization on fundus fluorescein angiogram with IAT. Of them, one recovered visual acuity to 20/25. We report our 2 CRAO cases treated with IAT and discuss technical aspects for IAT and management of patient. To the best of our knowledge, this is the first Korean report of IAT for CRAO

Mitochondrial oxidative phosphorylation in autosomal dominant optic atrophy

<p>Abstract</p> <p>Background</p> <p>Autosomal dominant optic atrophy (ADOA), a form of progressive bilateral blindness due to loss of retinal ganglion cells and optic nerve deterioration, arises predominantly from mutations in the nuclear gene for the mitochondrial GTPase, OPA1. OPA1 localizes to mitochondrial cristae in the inner membrane where electron transport chain complexes are enriched. While OPA1 has been characterized for its role in mitochondrial cristae structure and organelle fusion, possible effects of OPA1 on mitochondrial function have not been determined.</p> <p>Results</p> <p>Mitochondria from six ADOA patients bearing <it>OPA1 </it>mutations and ten ADOA patients with unidentified gene mutations were studied for respiratory capacity and electron transport complex function. Results suggest that the nuclear DNA mutations that give rise to ADOA in our patient population do not alter mitochondrial electron transport.</p> <p>Conclusion</p> <p>We conclude that the pathophysiology of ADOA likely stems from the role of OPA1 in mitochondrial structure or fusion and not from OPA1 support of oxidative phosphorylation.</p

Abducens Nerve Palsy Complicated by Inferior Petrosal Sinus Septic Thrombosis Due to Mastoiditis

We present a very rare case of a 29-month-old boy with acute onset right abducens nerve palsy complicated by inferior petrosal sinus septic thrombosis due to mastoiditis without petrous apicitis. Four months after mastoidectomy, the patient fully recovered from an esotropia of 30 prism diopters and an abduction limitation (-4) in his right eye

Meta-analysis of treatment outcomes for patients with m.11778G>A MT-ND4 Leber hereditary optic neuropathy

Our aim was to assess the visual outcomes of patients with Leber hereditary optic neuropathy (LHON) harboring the m.11778G&gt;A MT-ND4 mutation who had no treatment (natural history) or received idebenone or lenadogene nolparvovec. Efficacy outcomes included clinically relevant recovery (CRR) from nadir and final best-corrected visual acuity (BCVA). For the natural history and idebenone groups, we performed a systematic review of the literature and available clinical/regulatory reports. For the lenadogene nolparvovec group, all data from phase 3 studies were included. The overall effect and its 95 % confidence interval (CI) were estimated using a random effects model. For each meta-analysis, patients had a mean age of approximately 30 years at vision loss and were mostly (≥78 %) men. The CRR from nadir [95 % CI] at eye level was 17 % [7 %; 30 %] (n=316 eyes), 31 % [24 %; 40 %] (n=313) and 59 % [54 %; 64 %] (n=348) in untreated, idebenone-treated and lenadogene nolparvovec-treated patients, respectively. This gradient of efficacy was also observed with CRR at the patient level and final BCVA. There was a gradient of efficacy in all assessed visual outcomes, more marked for CRR than for final BCVA, with lenadogene nolparvovec gene therapy superior to idebenone treatment, and both superior to the natural history of the disease