RESUMO
AIMS: To determine the degree to which optical coherence tomography (OCT) can distinguish differences in retinal nerve fibre layer (RNFL) thickness between eyes with mild papilloedema, pseudopapilloedema, and normal findings. METHODS: 13 patients with mild papilloedema, 11 patients with congenitally crowded optic nerves, and 17 normal subjects underwent neuro-ophthalmic examination, automated visual field testing, and fundus photography. Spinal fluid pressure measurements were obtained in a subgroup of five patients with pseudopapilloedema and 11 patients with mild papilloedema. Circular OCT scans using a diameter of 3.38 mm surrounding the optic disc were performed in each eye of patients and subjects. Fundus photographs were analysed by two observers who diagnosed crowding or papilloedema and graded amounts of swelling. Findings were assessed by descriptive statistics and variance analysis. RESULTS: RNFL thickness was greater in the superior and inferior quadrants and showed a high degree of correlation between each group of patients and subjects. A statistically significant difference was found in mean RNFL thickness between both groups of patients with optic disc swelling and normal subjects. However, there was not a statistical difference in mean nerve fibre layer thickness between patients with papilloedema and those with congenitally crowded optic nerves. CONCLUSIONS: OCT demonstrates measurable differences in nerve fibre layer thickness between normal subjects and patients with either papilloedema or pseudopapilloedema. However, OCT does not appear to differentiate between those individuals with congenitally crowded optic nerves and those with mild papilloedema caused by increased intracranial pressure.
Assuntos
Lasers , Fibras Nervosas/patologia , Nervo Óptico/patologia , Papiledema/patologia , Retina/patologia , Tomografia de Coerência Óptica , Adolescente , Adulto , Estudos de Casos e Controles , Criança , Humanos , Oftalmoscopia , Campos VisuaisRESUMO
During 1992 and 1993 an epidemic of optic and peripheral neuropathy affected over 50,000 Cubans. This occurred in the unique setting of a communist country which had a widespread health care network and wherein sudden changes in the economy affected most of the population. Although nutritional factors appeared to play a key role in the pathogenesis of the epidemic neuropathy, viral, toxic, and genetic factors were investigated by Cuban and North American scientists. The authors, representing different disciplines and different groups that visited Cuba during the epidemic, review and reflect on the clinical and laboratory findings which became available through their own experience and through reviewing the literature. The recent Cuban epidemic is compared to similar outbreaks of optic and peripheral neuropathy which have occurred in the past.
Assuntos
Surtos de Doenças , Doenças do Nervo Óptico/epidemiologia , Consumo de Bebidas Alcoólicas/efeitos adversos , Cuba/epidemiologia , Humanos , Distúrbios Nutricionais/complicações , Doenças do Nervo Óptico/diagnóstico , Doenças do Nervo Óptico/etiologia , Doenças do Sistema Nervoso Periférico/diagnóstico , Doenças do Sistema Nervoso Periférico/epidemiologia , Doenças do Sistema Nervoso Periférico/etiologia , Política , Saúde Pública , Fatores de Risco , Fumar/efeitos adversosRESUMO
OBJECTIVE: To investigate the potential role of mitochondrial DNA (mtDNA) mutations in the recent outbreak in Cuba of optic neuropathy and peripheral neuropathy (COPN). DESIGN AND METHODS: Historical features were reviewed and neuro-ophthalmologic examinations were performed on a sample of COPN patients (n = 9) and Cuban patients with other forms of optic neuropathy (n = 2). Molecular genetic methods were then used to test for the presence of 9 mtDNA mutations that were previously associated with Leber's hereditary optic neuropathy (LHON). RESULTS: Two (22%) of 9 COPN patients harbored an LHON-associated mtDNA mutation at nucleotide position 9438 and a novel mutation at nucleotide position 9738 in the cytochrome c oxidase subunit III gene. None of the Cuban patients harbored any of the 8 other LHON-associated mtDNA mutations. Detailed sequence analysis revealed that the Cuban patients could be divided into 7 distinct mtDNA haplotypes and that the 2 COPN patients with mtDNA mutations in the cytochrome c oxidase subunit III gene were not members of the same maternal lineage. CONCLUSIONS: The pathogenesis of epidemic COPN is likely complex and multifactorial. Our preliminary results in a small sample of Cuban patients suggest that mtDNA mutations may play a role in some cases. mtDNA mutations may render an individual genetically susceptible to a variety of factors that impair oxidative phosphorylation, including nutritional deficiency, tobacco, alcohol, and other toxins.
Assuntos
DNA Mitocondrial , Mutação/genética , Doenças do Nervo Óptico/genética , Doenças do Sistema Nervoso Periférico/genética , Adulto , Cuba/epidemiologia , Surtos de Doenças , Complexo IV da Cadeia de Transporte de Elétrons/genética , Feminino , Haplótipos , Humanos , Masculino , Pessoa de Meia-Idade , Atrofias Ópticas Hereditárias/epidemiologia , Atrofias Ópticas Hereditárias/genética , Doenças do Nervo Óptico/epidemiologia , Doenças do Sistema Nervoso Periférico/epidemiologia , Doenças do Sistema Nervoso Periférico/etiologia , Reação em Cadeia da PolimeraseRESUMO
From late 1991 to mid-1993, cases of optic neuropathy of unknown etiology, which first appeared in unusual numbers in a western province of Cuba, spread and multiplied throughout the island. The dominant symptoms changed, becoming increasingly those of peripheral neuropathy. Incidence rates peaked in April 1993. An estimated 50,000 cases were reported. The majority were adult men and women (aged about 25-65), with comparatively few children or elderly people being affected. The cause has yet to be delineated. However, food shortages and radical changes in diet resulting from the longstanding US trade embargo and the recent loss of Eastern Europe as Cuba's trading partner have compromised nutritional status, especially B-vitamin sufficiency, and appear to be related to the neuropathic illnesses. In April 1993, the Cuban government began distributing vitamin supplements to every citizen. Causal hypotheses include tobacco-alcohol or "nutritional" amblyopia; cyanide toxicity from cassava; toxic legumes introduced as supplements to scarce flour; other toxins, for example pesticides, or a "blue mold" on tobacco; enterovirus; and a hereditary enzyme deficiency in affected persons. None of these factors appears to be present in all cases, but it is generally believed that an interaction of some toxin or toxins, in combination with nutritional deficiency, is likely to be the major cause.
Assuntos
Abastecimento de Alimentos , Estado Nutricional , Doenças do Nervo Óptico/epidemiologia , Doenças do Sistema Nervoso Periférico/epidemiologia , Adulto , Idoso , Deficiência de Vitaminas/complicações , Cuba , Dieta , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Doenças do Nervo Óptico/etiologia , Doenças do Sistema Nervoso Periférico/etiologiaRESUMO
PURPOSE: The purpose of this study is to examine changes in color Doppler imaging parameters before and after optic nerve sheath decompression (ONSD) for chronic papilledema caused by pseudotumor cerebri (PTC). METHODS: Color Doppler imaging was performed within 48 hours before surgery and within 48 hours after the procedure using a color Doppler unit with a 7.5-MHz phased linear transducer. Pulsed Doppler spectrum analyses were recorded digitally on videotape from the ophthalmic, central retinal, and short posterior ciliary arteries, using a 0.4 x 0.6-mm sample volume. RESULTS: Blood flow velocities in the ophthalmic, short posterior ciliary, and central retinal arteries of 24 eyes were significantly decreased compared with a healthy age-matched group. Eyes with visual acuities worse than 20/30 before surgery had significantly decreased velocities in the ophthalmic, short posterior ciliary, and retinal arteries, whereas in eyes with visual acuities better than 20/30, only the short posterior ciliary and central retinal arteries demonstrated decreased velocities. In addition, Gosling's pulsatility index was increased for the central retinal artery but not the ophthalmic or short posterior ciliary arteries. Thirteen eyes improving in visual acuity and field after ONSD demonstrated significant improvement in all color Doppler imaging parameters for the short posterior ciliary arteries. The ophthalmic artery diastolic velocity also increased significantly but the central retinal artery parameters did not change. The eyes that remained stable or worsened did not demonstrate significant postoperative changes. CONCLUSION: These results suggest that some of the visual loss from chronic papilledema may be due to ischemia, and worsening visual acuity correlates with greater impairment of the retrobulbar circulation. One of the mechanisms by which ONSD improves visual function may be reversal of this ischemic process.