STUDY - Technical - New Dacian's Medicine
Eye and
Vision Disorders (5)
Translation Draft
Let's move on to optic neuropathies!
Anterior ischemic optic neuropathy (NOIA) is due to insufficient blood flow through the posterior ciliary arteries that vascularize the optic disc. It produces a sudden, painless monocular loss of vision, although sometimes patients describe the appearance of visual premonitoring shadows. The optical disc is swollen and surrounded by clifellive hemorrhages in the layer of nerve fibers.
NOIA is divided into two forms: artheritic and non-arteritic (most common). No specific cause could be identified and there is no treatment, although diabetes and hypertension are common risk factors. Approximately 5% of patients, especially those over 65 years of age, develop the arteritic form of NOIA in combination with giant (temporal) cell arteritis.
Patients with noIA arteritic should be identified as a matter of urgency so that glucocorticoid treatment can be started immediately in order to prevent the other eye's cetacean. Symptoms of rheumatic polymyalgia may be present, and VSH is usually increased.
In patients with vision loss due to an alleged arterial NOIA, temporal artery biopsy is useful for confirming the diagnosis, but steroid treatment should be done without waiting for the biopsy result. Diagnosis of arterial NOIA is difficult to sustain in the presence of a normal VSH and a negative temporal artery biopsy, but such cases are rare.
Posterior ischemic optic neuropathy (NOIP) is a rare cause of acute vision loss. It is induced by the association of severe anemia with hypertension, causing infarction of the retrobulbar optic nerve. Cases have been reported due to massive bleeding from surgery, exsanguinating trauma, gastrointestinal bleeding and renal dialysis. The bottom of the eye usually has normal appearance, though, if the process extends quite a lot to the previous level, it can cause swelling of the optic disc. In some patients, vision can be saved by prompt blood transfusions and by correction of hypotension.
Optical neuritis is a common inflammatory condition of the optic nerve. In a recent study on the treatment of optic neuritis, the average age of patients was 32 years, 77% were women, 92% had eye pain (especially eye movements) and 35% had swelling of the optic disc. In most patients, demyelination was retrobulbar, and the bottom of the eye looked normal on initial examination, although over the following months, the pallor of the optic disc appeared slowly.
Many patients with optic neuritis eventually develop multiple sclerosis, but for some patients, optic neuritis remains an isolated process. In principle, after a single episode of optic neuritis, all patients experience a gradual recovery of vision, even without treatment. This rule is so certain that the absence of substantial improvement in vision after a first attack of optic neuritis calls the initial diagnosis into question.
Treatment of optic neuritis with glucocorticoids is controversial. The optical neuritis study demonstrated that patients treated with conventional doses of oral steroids did not perform better than placebo-treated patients. Surprisingly, patients treated with oral prednisone had an increased rate of recurrence of optic neuritis. These results show that the treatment of optic neuritis with oral glucocorticoids is of no use, but may even increase the risk of further attacks.
High doses of intravenous methylprednisolone followed by oral prednisone led to a slightly faster recovery of visual function, but the final visual acuity after 6 months was not significantly different from that of patients treated with placebo.
Remarkably, intravenous glucocorticoid therapy has been associated with a low rate of multiple sclerosis in a 2-year clinical trial, especially in the subgroup of patients with multiple demyelination outbreaks evidenced by the MRI examination. However, at the end of the third year of the monitoring period, there were no differences between patients treated with intravenous glucocorticoids and those treated with placebo in the rate of occurrence of multiple sclerosis. Furthermore, venous steroids did not reduce the likelihood of subsequent attacks of optic neuritis.
To recap: the study authors recommend that MRI be performed in patients with optic neuritis. If two or more outbreaks of demyelination are detected or if vision loss is severe, they recommend intravenous steroid treatment. The possible benefits of intravenous steroid treatment are: 1. a slightly faster recovery of visual function and 2. a potential reduction in the risk of developing subsequent neurological manifestations of multiple sclerosis.
Critics of this treatment point out the following: 1. the effect on vision is the same, finally, 2. the evidence involving the reduction of the risk of multiple sclerosis is based on data obtained in a small number of patients and 3. protection against multiple sclerosis is temporary and is no longer evident after 3 years of treatment.
In the case of unilateral optic neuritis, the decision to perform the MRI examination or to proceed with intravenous steroid treatment should be based on clinical judgment and thorough discussion with the patient. In the case of simultaneous bilateral optic neuritis, the arguments in favor of intravenous steroid treatment are somewhat stronger.
Leber hereditary optic neuropathy is a condition of young men, characterized by the installation over several weeks of severe loss of central, painless vision in one eye, followed by several weeks or months of the appearance of the same process in the other eye. In the acute phase, the optic papilla appears moderately hyperemic, with telangiectasis of the superficial capillaries, but without signs of hemorrhage to the fluoroscein angiography.
Eventually optical atrophy occurs and there is no treatment. The hereditary name occurs because it has been discovered that the condition is produced by a punctate mutation in a mitochondrial gene, and then other mutations responsible for this condition are discovered, most of them in the mitochondrial genes that encode the proteins involved in the transfer of electrons. Mitochondrial mutations that cause the condition are transmitted maternally to all children, but only some male children develop symptoms (this curious predilection for the male sex is a mystery).
Toxic optic neuropathy can cause acute vision loss, with bilateral swelling of the optic disc and central or cecocentral scotomas. Such cases have been reported following the use of embutanol, methyl alcohol (counterfeit alcoholic beverages), ethylene glycol (antifreeze) and carbon monoxide. In toxic optic neuropathy, vision loss can also occur gradually and cause optical atrophy without an acute phase of edema of the optic papilla.
Many substances have been criminalised as causes of toxic optic neuropathy, but for most of them, the evidence supporting this association is inconsistent. I will present a short and partial list of potentially harmful drugs or toxins: disulfiram, etclorvinol, chloramphenicol, amiodarone, anti-CD3 monoclonal antibody, ciprofloxacin, digital, streptomycin, lead, arsenic, taly, D-penicillamide, isoniazide, emetin and sulfonamides. The carendiseases, induced by malabsorption or alcoholism, can lead to insidious loss of vision. in any patient with unexplained bilateral central scotomas and optical pallor, concentrations of thiamine, vitamin B12 and folate should be checked.
Papillary edema involves bilateral swelling of the optic disc due to intracranial hypertension. Headache is a symptom of accompanying frequently, but not invariably. For all other forms of swelling of the optic disc, e.g. those due to optic neuritis or ischemic optic neuropathy, the name 'optic disc oedema' should be used. This convention is arbitrary, but it helps to avoid confusion.
Often, the differentiation of the papilloma from other forms of edema of the optic disc is difficult only with the help of the examination of the bottom of the eye. Transient vision darkenings are a classic symptom of papillary edema. It can occur in one eye or simultaneously in both eyes. It usually takes a few seconds, but can persist for minutes if the papillomademe is fulminant. Darkness occurs as a result of sudden posture changes or spontaneously occurs. When darkness is prolonged or spontaneous, the papillomademe is even more dangerous. Visual acuity is not affected by papiloedema unless it is severe, long-lasting or accompanied by macular edema and macular bleeding.
Visual field assessment tests reveal extensive blind spots and peripheral constriction. In persistent papiloedema, the peripheral field defect evolves gradually, while the optic nerve atrophies. In this case, the reduction of swelling of the optic disc is an ominous sign, an indicator of nerve death, rather than an encouraging sign of remission of the papiloedema.
Assessment of papillomadis requires computer-tomographic examination (CT) or MRI to rule out a brain tumor. If no brain tumour is detected, mri angiography is practiced in selected cases to investigate the possibility of a dural venous sinus occlusion or arteriovenous shunt.
If neuroradiological examinations are normal, the pressure at the opening of the subarachnoid space by lumbar puncture should be measured to confirm that its value is increased. If this pressure is increased without any explanation, the diagnosis of cerebral pseudotumor (idiopathic intracranial hypertension) is excluded. Most patients are young, female and obese.
Treatment with carbonic anhydrase inhibitors such as acetazolamide reduces intracranial pressure by decreasing the production of cerebrospinal fluid. Weight loss is extremely important, but frequently to no avail. If treatment with acetazolamide and weight loss do not work and the visual field defect evolves, when necessary, the lumboperitoneal shunt or windowing of the optic nerve's eye should be practiced without delay in order to prevent blindness.
And so, I proved another day of posting...
Let's move on to optic neuropathies!
Anterior ischemic optic neuropathy (NOIA) is due to insufficient blood flow through the posterior ciliary arteries that vascularize the optic disc. It produces a sudden, painless monocular loss of vision, although sometimes patients describe the appearance of visual premonitoring shadows. The optical disc is swollen and surrounded by clifellive hemorrhages in the layer of nerve fibers.
NOIA is divided into two forms: artheritic and non-arteritic (most common). No specific cause could be identified and there is no treatment, although diabetes and hypertension are common risk factors. Approximately 5% of patients, especially those over 65 years of age, develop the arteritic form of NOIA in combination with giant (temporal) cell arteritis.
Patients with noIA arteritic should be identified as a matter of urgency so that glucocorticoid treatment can be started immediately in order to prevent the other eye's cetacean. Symptoms of rheumatic polymyalgia may be present, and VSH is usually increased.
In patients with vision loss due to an alleged arterial NOIA, temporal artery biopsy is useful for confirming the diagnosis, but steroid treatment should be done without waiting for the biopsy result. Diagnosis of arterial NOIA is difficult to sustain in the presence of a normal VSH and a negative temporal artery biopsy, but such cases are rare.
Posterior ischemic optic neuropathy (NOIP) is a rare cause of acute vision loss. It is induced by the association of severe anemia with hypertension, causing infarction of the retrobulbar optic nerve. Cases have been reported due to massive bleeding from surgery, exsanguinating trauma, gastrointestinal bleeding and renal dialysis. The bottom of the eye usually has normal appearance, though, if the process extends quite a lot to the previous level, it can cause swelling of the optic disc. In some patients, vision can be saved by prompt blood transfusions and by correction of hypotension.
Optical neuritis is a common inflammatory condition of the optic nerve. In a recent study on the treatment of optic neuritis, the average age of patients was 32 years, 77% were women, 92% had eye pain (especially eye movements) and 35% had swelling of the optic disc. In most patients, demyelination was retrobulbar, and the bottom of the eye looked normal on initial examination, although over the following months, the pallor of the optic disc appeared slowly.
Many patients with optic neuritis eventually develop multiple sclerosis, but for some patients, optic neuritis remains an isolated process. In principle, after a single episode of optic neuritis, all patients experience a gradual recovery of vision, even without treatment. This rule is so certain that the absence of substantial improvement in vision after a first attack of optic neuritis calls the initial diagnosis into question.
Treatment of optic neuritis with glucocorticoids is controversial. The optical neuritis study demonstrated that patients treated with conventional doses of oral steroids did not perform better than placebo-treated patients. Surprisingly, patients treated with oral prednisone had an increased rate of recurrence of optic neuritis. These results show that the treatment of optic neuritis with oral glucocorticoids is of no use, but may even increase the risk of further attacks.
High doses of intravenous methylprednisolone followed by oral prednisone led to a slightly faster recovery of visual function, but the final visual acuity after 6 months was not significantly different from that of patients treated with placebo.
Remarkably, intravenous glucocorticoid therapy has been associated with a low rate of multiple sclerosis in a 2-year clinical trial, especially in the subgroup of patients with multiple demyelination outbreaks evidenced by the MRI examination. However, at the end of the third year of the monitoring period, there were no differences between patients treated with intravenous glucocorticoids and those treated with placebo in the rate of occurrence of multiple sclerosis. Furthermore, venous steroids did not reduce the likelihood of subsequent attacks of optic neuritis.
To recap: the study authors recommend that MRI be performed in patients with optic neuritis. If two or more outbreaks of demyelination are detected or if vision loss is severe, they recommend intravenous steroid treatment. The possible benefits of intravenous steroid treatment are: 1. a slightly faster recovery of visual function and 2. a potential reduction in the risk of developing subsequent neurological manifestations of multiple sclerosis.
Critics of this treatment point out the following: 1. the effect on vision is the same, finally, 2. the evidence involving the reduction of the risk of multiple sclerosis is based on data obtained in a small number of patients and 3. protection against multiple sclerosis is temporary and is no longer evident after 3 years of treatment.
In the case of unilateral optic neuritis, the decision to perform the MRI examination or to proceed with intravenous steroid treatment should be based on clinical judgment and thorough discussion with the patient. In the case of simultaneous bilateral optic neuritis, the arguments in favor of intravenous steroid treatment are somewhat stronger.
Leber hereditary optic neuropathy is a condition of young men, characterized by the installation over several weeks of severe loss of central, painless vision in one eye, followed by several weeks or months of the appearance of the same process in the other eye. In the acute phase, the optic papilla appears moderately hyperemic, with telangiectasis of the superficial capillaries, but without signs of hemorrhage to the fluoroscein angiography.
Eventually optical atrophy occurs and there is no treatment. The hereditary name occurs because it has been discovered that the condition is produced by a punctate mutation in a mitochondrial gene, and then other mutations responsible for this condition are discovered, most of them in the mitochondrial genes that encode the proteins involved in the transfer of electrons. Mitochondrial mutations that cause the condition are transmitted maternally to all children, but only some male children develop symptoms (this curious predilection for the male sex is a mystery).
Toxic optic neuropathy can cause acute vision loss, with bilateral swelling of the optic disc and central or cecocentral scotomas. Such cases have been reported following the use of embutanol, methyl alcohol (counterfeit alcoholic beverages), ethylene glycol (antifreeze) and carbon monoxide. In toxic optic neuropathy, vision loss can also occur gradually and cause optical atrophy without an acute phase of edema of the optic papilla.
Many substances have been criminalised as causes of toxic optic neuropathy, but for most of them, the evidence supporting this association is inconsistent. I will present a short and partial list of potentially harmful drugs or toxins: disulfiram, etclorvinol, chloramphenicol, amiodarone, anti-CD3 monoclonal antibody, ciprofloxacin, digital, streptomycin, lead, arsenic, taly, D-penicillamide, isoniazide, emetin and sulfonamides. The carendiseases, induced by malabsorption or alcoholism, can lead to insidious loss of vision. in any patient with unexplained bilateral central scotomas and optical pallor, concentrations of thiamine, vitamin B12 and folate should be checked.
Papillary edema involves bilateral swelling of the optic disc due to intracranial hypertension. Headache is a symptom of accompanying frequently, but not invariably. For all other forms of swelling of the optic disc, e.g. those due to optic neuritis or ischemic optic neuropathy, the name 'optic disc oedema' should be used. This convention is arbitrary, but it helps to avoid confusion.
Often, the differentiation of the papilloma from other forms of edema of the optic disc is difficult only with the help of the examination of the bottom of the eye. Transient vision darkenings are a classic symptom of papillary edema. It can occur in one eye or simultaneously in both eyes. It usually takes a few seconds, but can persist for minutes if the papillomademe is fulminant. Darkness occurs as a result of sudden posture changes or spontaneously occurs. When darkness is prolonged or spontaneous, the papillomademe is even more dangerous. Visual acuity is not affected by papiloedema unless it is severe, long-lasting or accompanied by macular edema and macular bleeding.
Visual field assessment tests reveal extensive blind spots and peripheral constriction. In persistent papiloedema, the peripheral field defect evolves gradually, while the optic nerve atrophies. In this case, the reduction of swelling of the optic disc is an ominous sign, an indicator of nerve death, rather than an encouraging sign of remission of the papiloedema.
Assessment of papillomadis requires computer-tomographic examination (CT) or MRI to rule out a brain tumor. If no brain tumour is detected, mri angiography is practiced in selected cases to investigate the possibility of a dural venous sinus occlusion or arteriovenous shunt.
If neuroradiological examinations are normal, the pressure at the opening of the subarachnoid space by lumbar puncture should be measured to confirm that its value is increased. If this pressure is increased without any explanation, the diagnosis of cerebral pseudotumor (idiopathic intracranial hypertension) is excluded. Most patients are young, female and obese.
Treatment with carbonic anhydrase inhibitors such as acetazolamide reduces intracranial pressure by decreasing the production of cerebrospinal fluid. Weight loss is extremely important, but frequently to no avail. If treatment with acetazolamide and weight loss do not work and the visual field defect evolves, when necessary, the lumboperitoneal shunt or windowing of the optic nerve's eye should be practiced without delay in order to prevent blindness.
And so, I proved another day of posting...
Happy birthday to all
those associated with the holy name of Gheorghe!!
Dorin, Merticaru