Toxic and nutritional optic neuropathy
Toxic and nutritional optic neuropathy is a group of medical disorders defined by visual impairment due to optic nerve damage secondary to a toxic substance and/or nutritional deficiency.
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Both toxic and nutritional factors can play a role, acting synergistically.
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both toxic and nutritional factors play a role, acting synergistically
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These disorders are acquired mitochondrial optic neuropathies because all risk factors impact mitochondrial oxidative phosphorylation.
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All of the above risk factors impact mitochondrial oxidative phosphorylation. Thus, the toxic and nutritional optic neuropathies are actually acquired mitochondrial optic neuropathies
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The clinical picture is similar to congenital mitochondrial optic neuropathies like Leber's hereditary optic neuropathy and Kjer's optic neuropathy.
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The clinical picture that they produce is akin to that of the congenital mitochondrial optic neuropathies, e.g., Leber's hereditary optic neuropathy and Kjer's optic neuropathy
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Vision loss is bilateral, symmetric, painless, gradual, and progressive.
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Vision loss in toxic and nutritional optic neuropathy is bilateral, symmetric, painless, gradual, and progressive
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Dyschromatopsia (change in color vision) is often the first symptom.
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Dyschromatopsia , a change in color vision, is often the first symptom
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Red colors may appear less bright or vivid; others have general loss of color perception.
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Some patients notice that certain colors, particularly red, are less bright or vivid; others have a general loss of color perception
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Loss of visual acuity may start with a blur or haze at the point of fixation, followed by progressive decline.
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Loss of visual acuity may start with a blur or haze at the point of fixation, followed by a progressive decline
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Vision loss can extend to total blindness, but loss beyond 20/400 is rare except in methanol ingestion.
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The degree of vision loss can extend to total blindness, but a loss beyond 20/400 is rare, except in the case of methanol ingestion
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Peripheral vision is usually spared; loss pattern typically involves a central or cecocentral scotoma.
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Peripheral vision is usually spared since the pattern of loss typically involves a central or cecocentral scotoma
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Pupils usually demonstrate a normal response to light and near stimulation.
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the pupils usually demonstrate a normal response to light and near stimulation
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In practically blind patients, pupils will be dilated with weak or absent response to light.
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In those who are practically blind, the pupils will be dilated with a weak or absent response to light
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The optic disc may appear normal, swollen, or hyperemic in early stages; disc hemorrhages may be present with hyperemia.
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The optic disc may appear normal, swollen, or hyperemic in early stages. With hyperemia , disc hemorrhages may also be present
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Continued damage results in optic atrophy, classically seen as temporal pallor of the optic disc.
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Continued damage to the optic nerve results in the development of optic atrophy , classically seen as temporal pallor of the optic disc
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Diagnosis is usually established by a detailed medical history and careful eye examination.
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The diagnosis of toxic or nutritional optic neuropathy is usually established by a detailed medical history and careful eye examination
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If medical history clearly points to a cause, neuroimaging to rule out compressive or infiltrative lesion is optional.
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If the medical history clearly points to a cause, neuroimaging to rule out a compressive or infiltrative lesion is optional
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If medical history is atypical or does not clearly point to a cause, neuroimaging is required to rule out other causes and confirm diagnosis.
source quote
if the medical history is atypical or does not clearly point to a cause, neuroimaging is required to rule out other causes and confirm the diagnosis
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An MRI scan is obtained in most cases requiring neuroimaging.
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In most cases of suspected toxic or nutritional optic neuropathy that require neuroimaging, an MRI scan is obtained
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Further testing (e.g., blood testing for methanol or vitamin B12 levels) can be performed to elucidate a specific toxin or nutritional deficiency.
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Further testing, guided by the medical history and physical examination, can be performed to elucidate a specific toxin or nutritional deficiency as a cause of the optic neuropathy. Examples include blood testing for methanol levels or vitamin B 12 levels
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Treatment is dictated by the cause of the disorder.
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Treatment of toxic and nutritional optic neuropathy is dictated by the cause of the disorder
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Toxic optic neuropathy is treated by identification and removal of the offending agent.
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Toxic optic neuropathy is treated by identification and removal of the offending agent
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Nutritional optic neuropathy is treated with improved nutrition, including a well-balanced diet with protein and green leafy vegetables.
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Nutritional optic neuropathy is treated with improved nutrition. A well-balanced diet with plenty of protein and green leafy vegetables
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Vitamin supplementation (thiamine, vitamin B12, folic acid, multivitamins) and reduction of smoking and/or drinking are mainstay of treatment.
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vitamin supplementation (thiamine, vitamin B 12 , folic acid, multivitamins), and reduction of smoking and/or drinking are the mainstay of treatment
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Methanol ingestion can cause vision loss beyond 20/400, which is otherwise rare.
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a loss beyond 20/400 is rare, except in the case of methanol ingestion
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Individuals who consume excessive amounts of alcohol and use tobacco are at greater risk due to malnourishment.
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Those individuals who consume excessive amounts of alcohol and use tobacco are at greater risk because they tend to be malnourished
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Those with pernicious anemia are at risk due to impaired ability to absorb vitamin B12.
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Those with pernicious anemia are also at risk due to an impaired ability to absorb vitamin B 12 from the intestinal tract
Prognosis is variable and dependent upon the affected individual, treatment compliance, and degree of vision loss at diagnosis. Vision generally recovers to normal over several days to weeks, though it may take months for full restoration and there is always the risk of permanent vision loss. Visual acuity usually recovers before color vision.
| Toxic and nutritional optic neuropathy | |
|---|---|
| Specialty | Ophthalmology |
Toxic and nutritional optic neuropathy is a group of medical disorders defined by visual impairment due to optic nerve damage secondary to a toxic substance and/or nutritional deficiency. The causes of these disorders are various, but they are linked by shared signs and symptoms. In several of these disorders, both toxic and nutritional factors play a role, acting synergistically.
Vision loss in toxic and nutritional optic neuropathy is bilateral, symmetric, painless, gradual, and progressive. Dyschromatopsia, a change in color vision, is often the first symptom. Some patients notice that certain colors, particularly red, are less bright or vivid; others have a general loss of color perception. Loss of visual acuity may start with a blur or haze at the point of fixation, followed by a progressive decline. The degree of vision loss can extend to total blindness, but a loss beyond 20/400 is rare, except in the case of methanol ingestion. Peripheral vision is usually spared since the pattern of loss typically involves a central or cecocentral scotoma, a visual field defect at or surrounding the point of fixation. This pattern can be revealed via visual field testing. [citation needed]
Upon examination, the pupils usually demonstrate a normal response to light and near stimulation. In those who are practically blind, the pupils will be dilated with a weak or absent response to light. The optic disc may appear normal, swollen, or hyperemic in early stages. With hyperemia, disc hemorrhages may also be present. Continued damage to the optic nerve results in the development of optic atrophy, classically seen as temporal pallor of the optic disc.[citation needed]
Toxic optic neuropathy
There are several causes of toxic optic neuropathy.[1] Among these are: ingestion of methanol (wood alcohol), ethylene glycol (automotive antifreeze), disulfiram (used to treat chronic alcoholism), (amebicidal medications), ethambutol and isoniazid (tuberculosis treatment), and antibiotics such as linezolid and chloramphenicol as well as chloroquine and the related hydroxychloroquine (for lupus and rheumatoid arthritis) where it is known as chloroquine retinopathy. Tobacco is also a major cause of toxic optic neuropathy.[citation needed]
Nutritional optic neuropathy
The predominant cause of nutritional optic neuropathy is thought to be deficiency of B-complex vitamins, particularly thiamine[2] (vitamin B1), cyanocobalamin (vitamin B12) and recently copper.[3] Deficiency of pyridoxine (vitamin B6), niacin (vitamin B3), riboflavin (vitamin B2), and/or folic acid also seems to play a role. Those individuals who consume excessive amounts of alcohol and use tobacco are at greater risk because they tend to be malnourished. Those with pernicious anemia are also at risk due to an impaired ability to absorb vitamin B12 from the intestinal tract.[citation needed]
All of the above risk factors impact mitochondrial oxidative phosphorylation. Thus, the toxic and nutritional optic neuropathies are actually acquired mitochondrial optic neuropathies. The clinical picture that they produce is akin to that of the congenital mitochondrial optic neuropathies, e.g., Leber's hereditary optic neuropathy and Kjer's optic neuropathy.[citation needed]
The diagnosis of toxic or nutritional optic neuropathy is usually established by a detailed medical history and careful eye examination. If the medical history clearly points to a cause, neuroimaging to rule out a compressive or infiltrative lesion is optional. However, if the medical history is atypical or does not clearly point to a cause, neuroimaging is required to rule out other causes and confirm the diagnosis. In most cases of suspected toxic or nutritional optic neuropathy that require neuroimaging, an MRI scan is obtained. Further testing, guided by the medical history and physical examination, can be performed to elucidate a specific toxin or nutritional deficiency as a cause of the optic neuropathy. Examples include blood testing for methanol levels or vitamin B12 levels.[citation needed]
Treatment of toxic and nutritional optic neuropathy is dictated by the cause of the disorder.[citation needed]
- Toxic optic neuropathy is treated by identification and removal of the offending agent. Depending upon the individual affected, the nature of the agent, total exposure prior to removal, and degree of vision loss at the time of diagnosis, the prognosis is variable.
- Nutritional optic neuropathy is treated with improved nutrition. A well-balanced diet with plenty of protein and green leafy vegetables, vitamin supplementation (thiamine, vitamin B12, folic acid, multivitamins), and reduction of smoking and/or drinking are the mainstay of treatment. Again, prognosis is variable and dependent upon the affected individual, treatment compliance, and degree of vision loss at diagnosis.
In both toxic and nutritional neuropathy, vision generally recovers to normal over several days to weeks, though it may take months for full restoration and there is always the risk of permanent vision loss. Visual acuity usually recovers before color vision.[citation needed]
In industrialized nations, toxic and nutritional optic neuropathy is relatively uncommon and is primarily associated with specific medications, occupational exposures, or tobacco and alcohol use disorder. However, in developing nations, nutritional optic neuropathy is much more common, especially in regions afflicted by shortage. All genders and all races are equally affected, and all ages are susceptible.[citation needed]
- ↑ Neil R. Miller; William Fletcher Hoyt (2005). Walsh and Hoyt's clinical neuro-ophthalmology. Lippincott Williams & Wilkins. pp. 447–. ISBN 978-0-7817-4811-7. Retrieved 6 February 2011.
- ↑ Spinazzi, Marco; Angelini, Corrado; Patrini, Cesare (2010). "Subacute sensory ataxia and optic neuropathy with thiamine deficiency". Nature Reviews Neurology. 6 (5): 288–93. doi:10.1038/nrneurol.2010.16. PMID 20308997.
- ↑ Spinazzi, Marco; De Lazzari, Franca; Tavolato, Bruno; Angelini, Corrado; Manara, Renzo; Armani, Mario (2007). "Myelo-optico-neuropathy in copper deficiency occurring after partial gastrectomy". Journal of Neurology. 254 (8): 1012–7. doi:10.1007/s00415-006-0479-2. PMID 17415508.
- Glaser, JS (1999). "Nutritional and toxic optic neuropathies". In Glaser, JS (ed.). Neuro-ophthalmology (3rd ed.). Philadelphia: Lippincott Williams & Wilkins. pp. 181–6.
- Lessell, S (2000). "Nutritional deficiency and toxic optic neuropathies". In Albert, DM; Jakobiec, FA (eds.). Principles and Practice of Ophthalmology (2nd ed.). Philadelphia: W.B. Saunders Company. pp. 4169–76.
- Sadun, A. A (2002). "Mitochondrial optic neuropathies". Journal of Neurology, Neurosurgery, and Psychiatry. 72 (4): 423–5. doi:10.1136/jnnp.72.4.423. PMC 1737836. PMID 11909893.