Análise da camada de fibras nervosas da retina em usuários crônicos do tabaco e álcool

Impairment of color spatial vision in chronic alcoholism measured by psychophysical methods.

“…At more advanced stages of chronic alcoholism, whether attributable to long-term exposure to ethanol or large quantities of daily ethanol intake, or because of the association between alcoholism and severe forms of malnutrition and vitamin deficiency, color vision dysfunction appears to be associated with decreased visual acuity, contrast sensitivity losses, visual field central defects, and anatomical signs of retinal damage, such as degeneration of the papillomacular nerve fiber bundle and atrophy of the temporal optic disk (Plant & Perry, 1990;Sadun et al, 1994;de Lima, Carvalho, Campos, Dantas, 2006). Such deleterious effect are possible if retinal ganglion cell loss related to chronic alcoholism (see below) progresses from preferential damage to P and K ganglion cells involved with color vision in the first stages of the disease to include the several ganglion cell classes involved in achromatic vision in later stages (Silveira et al, 2004;Silveira et al, 2008 Rodrigues et al (2007) are underlined.…”

“…Retinoscopy has provided evidence for ganglion cell degeneration as a possible pathophysiological mechanism to explain the visual dysfunction symptoms observed in several metabolic neuropathies, such as heredodegenerative diseases (e.g., Leber's hereditary optic neuropathy), nutritional deficiencies (e.g., vitamin B9 [folic acid] and vitamin B12 [cobalamin] deficiencies), and toxic conditions (e.g., those associated with exposure to ethambutol, cyanide, ethanol, and tobacco, among many other toxicants; Plant & Perry, 1990; Sadun et al, 1994; de Lima et al, 2006; Orssaud, Roche, & Dufier, 2007). Impairment of mitochondrial function attributable to genetic mutations, endogenous toxicity secondary to vitamin deficiency, or toxic exposure to exogenous agents has been considered a common pathway leading to neuronal degeneration in these diseases (Sadum, 2002a, b; Carelli, Ross-Cisneros, & Sadun, 2004; Sadun & Carelli, 2006; Orssau et al, 2007).…”

Impairment of color spatial vision in chronic alcoholism measured by psychophysical methods

“…At more advanced stages of chronic alcoholism, whether attributable to long-term exposure to ethanol or large quantities of daily ethanol intake, or because of the association between alcoholism and severe forms of malnutrition and vitamin deficiency, color vision dysfunction appears to be associated with decreased visual acuity, contrast sensitivity losses, visual field central defects, and anatomical signs of retinal damage, such as degeneration of the papillomacular nerve fiber bundle and atrophy of the temporal optic disk (Plant & Perry, 1990;Sadun et al, 1994;de Lima, Carvalho, Campos, Dantas, 2006). Such deleterious effect are possible if retinal ganglion cell loss related to chronic alcoholism (see below) progresses from preferential damage to P and K ganglion cells involved with color vision in the first stages of the disease to include the several ganglion cell classes involved in achromatic vision in later stages (Silveira et al, 2004;Silveira et al, 2008 Comparison with previous studies Acquired color vision losses have frequently been observed among chronic alcoholics (Cruz-Coke & Varela, 1965;Reynolds, 1979;Mergler et al, 1988;Braun & Richer, 1993;Kapitany et al, 1993;Shimozono, Townsend, Ilsen, & Bright, 1998).…”

“…All of the means corresponding to color discrimination thresholds at different locations in the color space for all alcoholic groups were within the tolerance limits of the statistical norms of the age-matched control groups, with the exception of Ellipses 1 and 4 for the oldest age group. Values for individual alcoholic subjects are shown in Table 2. heredodegenerative diseases (e.g., Leber's hereditary optic neuropathy), nutritional deficiencies (e.g., vitamin B9 [folic acid] and vitamin B12 [cobalamin] deficiencies), and toxic conditions (e.g., those associated with exposure to ethambutol, cyanide, ethanol, and tobacco, among many other toxicants; Plant & Perry, 1990;Sadun et al, 1994;de Lima et al, 2006;Orssaud, Roche, & Dufier, 2007). Impairment of mitochondrial function attributable to genetic mutations, endogenous toxicity secondary to vitamin deficiency, or toxic exposure to exogenous agents has been considered a common pathway leading to neuronal degeneration in these diseases (Sadum, 2002a, b;Carelli, Ross-Cisneros, & Sadun, 2004;Sadun & Carelli, 2006;Orssau et al, 2007).…”

Effects of chronic alcoholism in the sensitivity to luminance contrast in vertical sinusoidal gratings

“…Among the changes in visual perception associated with alcohol use, we highlight: (i) neurodegenerative alterations in visual pathways and retinal layers integrated into the functional decline of rods and cones (Lima et al 2006); (ii) alterations in cortical receptive fields of single cells and hypercomplex selective visual spatial orientation (Medina, Krahe, & Ramoa, 2005); and (iii) alterations in visual processing of chromatic and achromatic stimuli (Castro et al 2009;Chen, Xia, Li, & Zhou, 2010;Rosenbloom et al, 2004;Wegner, Günthner, & Fahle, 2001).…”