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- Neurosyphilis in a Man with Human Immunodeficiency Virus. [JOURNAL ARTICLE]
- J Clin Aesthet Dermatol 2014 Aug; 7(8):35-40.
The authors describe a 33-year-old man with human immunodeficiency virus who developed erythematous macules on the palms and soles with subsequent headaches, papilledema, and iritis. They review the salient characteristics of neurosyphilis with a focus on human immunodeficiency virus-positive individuals. The incidence of syphilis has increased since the year 2000 in African Americans, Hispanics, and men who have sex with men. Treponema pallidum is the causative agent of this disease-a fastidious, slowly growing, microaerophilic spirochete. Sexual contact is the most common mode of transmission. The rapid plasma reagin, Venereal Disease Research Laboratory assay, and fluorescent treponemal antibody absorption assay are commonly used to diagnose syphilis. The mainstay treatment is penicillin. Special considerations exist in the natural history and management of syphilis in the setting of human immunodeficiency virus.
- Steroid-induced recurrent myocardial ischemia. [JOURNAL ARTICLE]
- Rev Port Cardiol 2014 Aug 22.
We report the case of a female patient under oral prednisolone therapy due to a diagnosis of idiopathic intracranial hypertension with papilledema. Unfortunately, short-term treatment with prednisolone caused an unusual complication in the patient, i.e., recurrent myocardial ischemia. Possible mechanisms leading to this complication were evaluated in the light of current knowledge.
- [Congenital optic disc anomalies--own observations]. [English Abstract, Journal Article]
- Klin Oczna 2014; 116(1):64-9.
The aim of this article is to present a clinical picture of congenital optic nerve anomalies, which occur quite frequently in the general population, may cause low vision and visual field defects. These abnormalities can coexist with central nervous system defects or the other ocular abnormalities. Some of them may be misdiagnosed as papilloedema during the episode of intracranial fluid pressure elevation or glaucomatous neuropathy. Diagnosing the congenital nerve optic disc defects coexisting with multiorgans anomalies requires multidisciplinary medical care especially in babies. developmental optic disc anomalies, congenital eye abnormalities, differential diagnosis.
- Optical coherence tomography in papilledema: what am I missing? [Journal Article]
- J Neuroophthalmol 2014 Sep.:S10-7.
Grading of papilledema severity is subjective and based on monocular fundus features of the optic nerve. Interobserver agreement on grading the severity of papilledema is poor among expert observers, even using well-defined criteria such as the Frisen scale, which is a non-continuous ordinal scale of grading. Furthermore, non-expert clinicians often find it difficult to properly view and interpret features of the optic nerve using ophthalmoscopy, which can lead to failure to diagnose papilledema in non-ophthalmologic care settings. This may delay treatment, which can result in vision loss. Distinguishing papilledema from pseudopapilledema can also be difficult when surface drusen are not easily identified. Once papilledema is diagnosed, it is often difficult to determine whether a reduction in optic nerve edema is due solely to improvement in the status of the nerve or whether this represents concomitant loss of axons and viable retinal ganglion cells, leading to a poor visual outcome. Timely advancement of treatment would occur if loss of neurons could be diagnosed at an earlier stage of evaluation while optic disc edema is still present. This review will critically assess the role of optical coherence tomography (OCT) in solving these problems by providing an advanced imaging approach for diagnosis of papilledema and evaluating its severity on a continuous scale and evaluating the causes of visual loss in the setting of a swollen nerve.The published literature (PubMed) was reviewed from 2000 to 2014 on the use of OCT for diagnosing papilledema, differentiating it from pseudopapilledema, providing a continuous scale of its severity and in evaluating causes of visual loss.Recent evidence shows that OCT analysis of the retinal nerve fiber layer and retinal ganglion cell layer in papilledema can be associated with misleading artifacts due to layer segmentation failures. Newer 3D algorithms using neighboring locations help to overcome these problems. Disc volume appears to be a promising continuous measure of papilledema that is robust and has less associated artifacts. Buried optic disc drusen can be identified using enhanced depth OCT imaging, but recent studies have shown poor ability to differentiate papilledema from pseudopapilledema using OCT when the degree of disc evaluation is similar. Analysis of the retinal ganglion cell layer shows promise of early detection of vision loss due to neuronal injury. Subretinal fluid is easily identified with OCT and can help to identify a potentially reversible component of vision loss. Newer OCT imaging methods will allow the definition of capillaries and flow within them in and around the optic nerve head.Currently, the most useful OCT derived features relevant to papilledema are disc volume, subretinal fluid, buried disc drusen, and thickness of the retinal ganglion cell layer.
- Literature Commentary. [JOURNAL ARTICLE]
- J Neuroophthalmol 2014 Sep; 34(3):306-310.
Acetazolamide is commonly used to treat idiopathic intracranial hypertension (IIH), but there is insufficient information to establish an evidence base for its use.To determine whether acetazolamide is beneficial in improving vision when added to a low-sodium weight-reduction diet in patients with IIH and mild visual loss.A multicenter, randomized, double-masked, placebo-controlled study of acetazolamide in 165 participants with IIH and mild visual loss who received a low-sodium weight-reduction diet. Participants were enrolled at 38 academic and private practice sites in North America from March 2010 to November 2012 and followed up for 6 months (last visit in June 2013). All participants met the modified Dandy criteria for IIH and had a perimetric mean deviation (PMD) between -2 and -7 dB. The mean age was 29 years, and all but 4 participants were women.Low-sodium weight-reduction diet plus the maximally tolerated dosage of acetazolamide (up to 4 g/d) or matching placebo for 6 months.The planned primary outcome variable was the change in PMD from baseline to Month 6 in the most affected eye, as measured using a Humphrey field analyzer. PMD is a measure of global visual field loss (mean deviation from age-corrected normal values), with a range of 2 to -32 dB; larger negative values indicate greater vision loss. Secondary outcome variables included changes in papilledema grade, quality of life (Visual Function Questionnaire 25 [VFQ-25] and 36-Item Short Form Health Survey), headache disability, and weight at Month 6.The mean improvement in PMD was greater with acetazolamide (1.43 dB, from -3.53 at baseline to -2.10 dB at Month 6; n = 86) than with placebo (0.71 dB, from -3.53 to -2.82 dB; n = 79); the difference was 0.71 dB (95% confidence interval [CI]: 0-1.43 dB; P = 0.050). Mean improvements in papilledema grade (acetazolamide: -1.31, from 2.76 to 1.45; placebo: -0.61, from 2.76 to 2.15; treatment effect: -0.70; 95% CI: -0.99 to -0.41; P < 0.001) and vision-related quality of life as measured by the National Eye Institute VFQ-25 (acetazolamide: 8.33, from 82.97 to 91.30; placebo: 1.98, from 82.97 to 84.95; treatment effect: 6.35; 95% CI: 2.22-10.47; P = 0.003) and its 10-item neuro-ophthalmic supplement (acetazolamide: 9.82, from 75.45 to 85.27; placebo: 1.59, from 75.45 to 77.04; treatment effect: 8.23; 95% CI: 3.89-12.56; P < 0.001) were also observed with acetazolamide. Participants assigned to acetazolamide also experienced a reduction in weight (acetazolamide: -7.50 kg, from 107.72 to 100.22 kg; placebo: -3.45 kg, from 107.72 to 104.27 kg; treatment effect: -4.05 kg; 95% CI: -6.27 to -1.83 kg; P < 0.001).In patients with IIH and mild visual loss, the use of acetazolamide with a low-sodium weight-reduction diet compared with a diet alone resulted in modest improvement in visual field function. The clinical importance of this improvement remains to be determined.
- Mercury Poisoning as a Cause of Intracranial Hypertension. [JOURNAL ARTICLE]
- J Child Neurol 2014 Aug 13.
Mercury poisoning is a rare but fatal toxicologic emergency. Neurologic manifestations involving the central nervous system are seen usually with chronic mercury intoxication. The most commonly seen complaints are headache, tremor, impaired cognitive skills, weakness, muscle atrophy, and paresthesia. Here, we present a male patient who was chronically exposed to elemental mercury and had papilledema and intracranial hypertension without parenchymal lesion in the central nervous system. A 12-year-old male patient was referred to our emergency room because of severe fatigue, generalized muscle pain and weakness, which was present for a month. Physical examination revealed painful extremities, decreased motor strength and the lack of deep tendon reflexes in lower extremities. He had mixed type polyneuropathy in his electromyography. Whole blood and 24-hour urinary mercury concentrations were high. A chelation therapy with succimer (dimercaptosuccinic acid) was started on the fourth day of his admission. On the seventh day of his admission, he developed headache and nausea, and bilateral papilledema and intracranial hypertension were detected on physical examination. Acetazolamide was started and after 1 month of treatment, the fundi examination was normal. The patient stayed in the hospital for 35 days and was then discharged with acetazolamide, vitamin B6, gabapentin, and followed as an outpatient. His clinical findings were relieving day by day. Although headache is the most common symptom in mercury poisoning, the clinician should evaluate the fundus in terms of intracranial hypertension.
- Anterior ischemic optic neuropathy in association with optic nervehead drusen. [Journal Article]
- Indian J Ophthalmol 2014 Jul; 62(7):829-31.
Optic nerve head drusen (ONHD) are incidental ophthalmologic finding in the optic nerve. Patients with ONHD are often asymptomatic, but sometimes present with transient visual obscuration's (TVO), the reported incidence of which is 8.6%. Optic nerve head drusen are of two types: Superficial; visible and deep. The deep-buried drusen mimic papilledema. Because of the varied presentation deep-buried drusen pose a diagnostic challenge to the ophthalmologists. In young patients, they are mistaken for papilledema as it is clinically difficult to detect a buried drusen in the optic nerve head, but are seen on the surface with aging as the retinal nerve fiber layer thins out. They are observed as pale yellow lesions more often located towards the poles. Clinical examination aided with diagnostic tests like computed tomography (CT) orbits and ultrasound B scan can help establish the diagnosis. Herein, we report a rare case of optic nerve head drusen in a young lady, who presented with loss of vision and clinical evaluation and investigations suggested ONHD with anterior ischemic optic neuropathy.
- Papilledema and idiopathic intracranial hypertension. [Journal Article]
- Continuum (Minneap Minn) 2014 Aug; 20(4 Neuro-ophthalmology):857-76.
Papilledema is one of the most concerning physical examination findings in neurology: it has a broad differential diagnosis of intracranial (and occasionally spinal) pathology associated with increased intracranial pressure. Papilledema impairs axoplasmic flow within the optic nerves and compresses the optic nerves externally; it may lead to profound visual loss. Thus, detection of papilledema and assessment of visual function are essential to patient management. This article reviews the treatment of papilledema-related visual loss in pseudotumor cerebri syndrome, one of the most common causes of papilledema encountered by neurologists.Results from the Idiopathic Intracranial Hypertension Trial (IIHTT), the first randomized, double-masked, placebo-controlled trial for the treatment of patients with mild visual loss from idiopathic intracranial hypertension, were published in April 2014. The IIHTT provides the first evidence-based treatment recommendations, showing the benefit of acetazolamide and weight loss for improving visual status in patients with mild visual field loss from idiopathic intracranial hypertension.A detailed ophthalmic examination, including perimetry, is critical to the evaluation, treatment, and assessment of treatment response in patients with papilledema.
- Headache and the pseudotumor cerebri syndrome. [Journal Article]
- Curr Pain Headache Rep 2014 Sep; 18(9):446.
Pseudotumor cerebri syndrome (PTCS) refers to the primary and secondary disorders that cause elevated intracranial pressure without an intracranial mass lesion, ventriculomegaly, or central nervous system infection or malignancy. Headache is the most frequent symptom of PTCS, but there is considerable overlap between the headache features of raised intracranial pressure and the headache features of primary headache disorders. We review headache subtypes that occur in PTCS, non-headache features that help distinguish PTCS from other headache types, changes to the diagnostic criteria for PTCS with and without papilledema, and headache treatment strategies as they apply to PTCS.