1/12. carbon monoxide poisoning causes optic neuropathy.PURPOSE: To describe the electrophysiological and psychophysical effects of carbon monoxide (CO) poisoning on visual function. methods: Three patients are presented who suffered CO poisoning, two due to suicide attempts and one in the course of a road traffic accident. After a full ocular examination, Goldmann visual fields, flash and pattern visual evoked potentials (VEPs) and flash and pattern electroretinograms (ERGs) were tested. RESULTS: electrophysiology showed reduced or absent N95 components of the pattern ERG and delayed, reduced VEPs. A positive-negative-positive (PNP) VEP waveform was seen in two cases. In one case, where presentation occurred at an early stage, visual and electrophysiological function was improved with hydroxycobalamine. CONCLUSIONS: The combination of ERG and VEP findings suggest that CO poisoning can cause a toxic optic neuropathy that may have a similar aetiological mechanism to that in tobacco amblyopia. Early treatment with hydroxycobalamine may be of some benefit.- - - - - - - - - - ranking = 1keywords = tobacco (Clic here for more details about this article) |
2/12. Acquired mitochondrial impairment as a cause of optic nerve disease.BACKGROUND: blindness from an optic neuropathy recently occurred as an epidemic affecting 50,000 patients in cuba (CEON) and had clinical features reminiscent of both tobacco-alcohol amblyopia (TAA) and Leber's hereditary optic neuropathy (Leber's; LHON). Selective damage to the papillomacular bundle was characteristic, and many patients also developed a peripheral neuropathy. Identified risk factors included vitamin deficiencies as well as exposure to methanol and cyanide. In all 3 syndromes, there is evidence that singular or combined insults to mitochondrial oxidative phosphorylation are associated with a clinically characteristic optic neuropathy. PURPOSE: First, to test the hypothesis that a common pathophysiologic mechanism involving impairment of mitochondria function and, consequently, axonal transport underlies both genetic optic nerve diseases such as Leber's and acquired toxic and nutritional deficiency optic neuropathies. According to this hypothesis, ATP depletion below a certain threshold leads to a blockage of orthograde axonal transport of mitochondria, which, in turn, leads to total ATP depletion and subsequent cell death. Second, to address several related questions, including (1) How does impaired energy production lead to optic neuropathy, particularly since it seems to relatively spare other metabolically active tissues, such as liver and heart? (2) Within the nervous system, why is the optic nerve, and most particularly the papillomacular bundle, so highly sensitive? Although there have been previous publications on the clinical features of the Cuban epidemic of blindness, the present hypothesis and the subsequent questions have not been previously addressed. methods: patients in cuba with epidemic optic neuropathy were personally evaluated through a comprehensive neuro-ophthalmologic examination. In addition, serum, lymphocytes for dna analysis, cerebrospinal fluid (CSF), sural nerves, and eyes with attached optic nerves were obtained from Cuban patients, as well as from Leber's patients, for study. Finally, we developed an animal model to match the low serum folic acid and high serum formate levels found in the CEON patients, by administering to rats low doses of methanol after several months of a folic acid-deficient diet. Optic nerves and other tissues obtained from these rats were analyzed and compared with those from the Cuban patients. RESULTS: patients from the Cuban epidemic of optic neuropathy with clinical evidence of a selective loss of the papillomacular bundle did much better once their nutritional status was corrected and exposure to toxins ceased. patients with CEON often demonstrated low levels of folic acid and high levels of formate in their blood. Histopathologic studies demonstrated losses of the longest fibers (in the sural nerve) and those of smallest caliber (papillomacular bundle) in the optic nerve, with intra-axonal accumulations just anterior to the lamina cribrosa. Our animal model duplicated the serologic changes (low folic acid, high formate) as well as these histopathologic changes. Furthermore, ultrastructural examination of rat tissues demonstrated mitochondrial changes that further matched those seen on ultrastructural examination of tissues from patients with Leber's. CONCLUSION: mitochondria can be impaired either genetically (as in Leber's) or through acquired insults (such as nutritional or toxic factors). Either may challenge energy production in all cells of the body. While this challenge may be met through certain compensatory mechanisms (such as in the size, shape, or number of the mitochondria), there exists in neurons a threshold which, once passed, leads to catastrophic changes. This threshold may be that point at which mitochondrial derangement leads to such ATP depletion that axonal transport is compromised, and decreased mitochondrial transport results in even further ATP depletion. neurons are singularly dependent on the axonal transport of mitochondria. (- - - - - - - - - - ranking = 1keywords = tobacco (Clic here for more details about this article) |
3/12. Chiasmopathy?A 57-year-old man presented with progressive visual loss in both eyes, bitemporal field defect, and a history of poor nutrition, alcohol abuse, and excessive cigar smoking. magnetic resonance imaging was normal. The visual acuity and field defect improved with supplementation with vitamins and reduction of alcohol and tobacco consumption. A diagnosis of toxic optic neuropathy was made. The authors discuss the differential diagnosis of bitemporal/pseudobitemporal field defects and the diagnosis and treatment of toxic optic neuropathy.- - - - - - - - - - ranking = 1keywords = tobacco (Clic here for more details about this article) |
4/12. Optic neuropathy from folic acid deficiency without alcohol abuse.A 47-year-old woman with a 2-month history of bilateral progressive visual loss was found to have a bilateral retrobulbar optic neuropathy. Her serum vitamin B(12) concentration and hemoglobin level were normal, but her serum folic acid concentration was decreased. The patient had a minimal alcohol intake and moderate tobacco use that had been unchanged for over 20 years; however, she had markedly altered her diet 4 years earlier in the setting of clinical depression. After treatment with oral folic acid and diet modification without change in her tobacco or alcohol use, the patient's visual function returned to normal. This case supports the role of folic acid deficiency as an important cause of some cases of nutritional optic neuropathy.- - - - - - - - - - ranking = 2keywords = tobacco (Clic here for more details about this article) |
5/12. Visual functions and trace element metabolism in tobacco-toxic optic neuropathy.Visual functions and nutrition metabolic characteristics were studied in 8 subjects (16 eyes) with tobacco-toxic optic neuropathy (TTON). Their visual functions tested by psychophysical and electrophysiologic methods showed that 1: 1. central vision diminished in 16 eyes, 2. dyschromatopsias were found in 14 tested eyes, 3. bilateral symmetrical central or cecocentral scotomas were the visual field characteristics in all cases, 4. PVEP were severe abnormal in 3 spatial frequencies in all cases and 56.3% of 15' checkboard PVEP showed flat responses, which indicated the impairment of optic nerve dominated by the central field. However, the preserved visual responses could be obtained by FVEP test in 14 tested eyes even though their visual acuity were between the range of 0.02-0.2 and flat PVEP responses. The II and III wave latencies of primary stage were more prolonged than those of control group (P < 0.01), which further indicated the preferential demyelination corresponding to the papillomacular bundles, 5. ERG showed slightly attenuated amplitudes in 5 of 8 tested eyes, which indicated the secondary and mild retinal lesion. On the other hand, TTON occurred on a background of long-term, heavy smoking, drinking, emaciation and malnutrition bodies with low serum zinc level.- - - - - - - - - - ranking = 5keywords = tobacco (Clic here for more details about this article) |
6/12. Optic neuropathy in a patient with vitamin B12 deficiency: a case report.A 19-year-old man presented with blurring of vision for 2 weeks. He also complained of anorexia with weight loss during the past 4 months. Eight years ago, his small bowel from midportion of the jejunum, ileum, ascending colon and transverse colon were resected because of gangrene. He gave no history of exposure to tobacco, alcohol or other toxins. The bone marrow aspiration showed hypocellular with panhypoplasia. serum vitamin B12 level was low while serum and red cell folate were within normal limits. His visual acuity was 5/200 in both eyes with centrocecal scotomas in both eyes. Other neurologic and ophthalmic examinations were found to be normal. The patient was given intramuscular injections of 1,000 micrograms of cyanocobalamin. Four months later, his visual acuity improved, serum vitamin B12 level and the bone marrow returned to be normal. This is a frank case of optic neuropathy in a patient with vitamin B12 deficiency due to a massive small bowel resection.- - - - - - - - - - ranking = 1keywords = tobacco (Clic here for more details about this article) |
7/12. The perils of Pauline: visual loss in a tippler.A 31-year-old alcoholic woman who smoked had subacute visual loss. She was treated for tobacco-alcohol amblyopia with subsequent improvement in vision.- - - - - - - - - - ranking = 1keywords = tobacco (Clic here for more details about this article) |
8/12. serum cobalamin and folate in the optic neuropathy associated with tobacco smoking.The concentrations of vitamin B12 in the sera from 77 patients diagnosed as suffering from the toxic optic neuropathy associated with tobacco smoking were compared with control levels and with serum folic acid concentrations from the same patients. Of these, 17 patients had associated pernicious anaemia. serum vitamin B12 levels were significantly lower, whereas the folic acid concentrations showed great variation. Folic acid levels in the serum tended to be high when the vitamin B12 level was low (r = 0.29). The results suggest that the role of folic acid in the genesis of the optic neuropathy is not marked. However persistently low levels of folic acid occurred in one subject and significant clinical improvement resulted only from specific therapy.- - - - - - - - - - ranking = 5keywords = tobacco (Clic here for more details about this article) |
9/12. Fundus changes in acute malnutritional optic neuropathy.A peculiar dilation and tortuosity of small retinal vessels within the arcuate areas of the retinal nerve fiber layer occurred in a series of patients with acute malnutritional optic neuropathy ("tobacco-alcohol amblyopia"). These evanescent vascular abnormalities may be caused by arteriovenous shunting. They seem to be specific indicators of the early phase of this disease.- - - - - - - - - - ranking = 1keywords = tobacco (Clic here for more details about this article) |
10/12. food shortages and an epidemic of optic and peripheral neuropathy in cuba.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.- - - - - - - - - - ranking = 2keywords = tobacco (Clic here for more details about this article) |
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