STUDY - Technical - New Dacian's Medicine
Eye and
Vision Disorders (2)
Translation Draft
Christ has risen!
I'm going to start fasting today with eye movements and alignment. Testing of eye movements is done by asking the patient to follow with both eyes open a small target, such as a pen flashlight, moved in the cardinal fields of vision. Normal eye movements are smooth, symmetrical, complete and sustained in all directions, without nystagmus.
The jerky movements or rapid eye refixation movements are evaluated by having the patient look forward and then between two stationary targets. The eyeballs must move quickly and accurately in a single motion towards the target. Eye alignment can be evaluated by holding a pen flashlight directly in front of the patient about one meter away. if the eyes look straight, the corneal bright reflex will be centered in the middle of each pupil.
For more precise eye alignment testing, the coating test is useful. The patient is instructed to focus his gaze on a small target located at a distance. One eye suddenly covers and the other eye is observed. If the uncovered eye moves so it can fix the target, it's not well aligned.
If it does not move, the first eye is discovered and the test is repeated on the second eye. If neither eye moves, it means that the eyes are orthotropicly aligned. if the eyes look orthotropic when the head is straight, but the patient accuses diplopia, the cover test should be performed with the head tilted or turned towards the direction that causes the patient's diplopia.
Through exercise, the examiner can detect ocular deviation (heterotropy) of up to 1-2 degrees with the help of the coating test. Deviations can be measured by placing prisms in front of the misaligned eye thus determining the power necessary to neutralize the movement of the eye in order to fix the target, caused by the covering of the other eye.
With regard to stereoscopic vision, stereoacuity is determined by presenting targets with retinal discrepancy, separately at the level of each eye, using polarized images. In the cabinet the most commonly used tests measure a range of thresholds from 800 to 40 seconds of arc. If a patient obtains this level of stereoacuity in tests, we can be sure that the eyes are orthotropicly aligned and the vision is intact in both eyes. Randomly punctuated stereograms do not give indications of deep monocular vision and are an excellent screening test for strabismus and amblyopia in children.
Let me move on to the chromatic view now. The retina contains three categories of cones with visual pigments with maximum different spectral sensitivity: red (560 nm), green (530 nm) and blue (430 nm). The red and green pigments of the cones are encoded on the X chromosome, the blue pigment on chromosome 7.
Blue pigment mutations are extremely rare. Mutations of red and green pigments produce congenital X-linked acromotopsia in 8% of men. Affected individuals are not really achromatic, but differ from normal subjects in the way they perceive colors and how they combine monochromatic primary radiation to obtain a given color.
Abnormal tricomatas have three types of cones, but a mutation in a pigment (usually red or green) causes a change in maximum spectral sensitivity, altering the proportion of primary colors needed to obtain a color. Dicromats have only two types of cones and therefore will form colors only on the basis of two primary colors.
Abnormal tricomations and dicromats have a visual acuity of 6/6, but the discrimination of shades is affected. Ishihara colored plates can be used to detect red-green discromatopia. Test plates include a hidden number, visible only to subjects who confuse colors due to red-green discromatopsia. because discromatopsias are almost entirely X-linked, screening is only worth in the case of male children.
Ishihara plaques are often used to test patients with acquired colored vision disorders. Although they were not designed for this purpose, there is no other simpler and more convenient method for routine quantitative testing of colored vision. Acquired defects of colored vision are often the result of diseases of the macula or optic nerve.
For example, patients with a history of optic neuritis often experience a decrease in color perception long after their visual acuity has returned to normal. Colorful vision disorders may also be caused by bilateral strokes affecting the ventral portion of the occipital lobe (cerebral acromatopsia).
These patients may perceive only shades of grey and may also have difficulty recognizing faces (prosopagnosia). Infarctions of the dominant occipital lobe sometimes cause visual anomie for colors. Affected patients can distinguish and differentiate colors, but they can't name them.
In the case of the field of vision, vision can be damaged by damage to the visual system anywhere between the eyeballs and the occipital lobes. The site of the lesion can be located with considerable precision mapping the visual field deficit by assessing the perception of the examiner's fingers and then linking it with the topographical anatomy of the visual path.
More quantitative information can be obtained by the usual perimetric examination of visual fields. At kinetic perimetry, the patient looks at a tangent screen or hemispheric vessel (Goldmann perimeter), while the examiner moves a small bright target from the periphery to the center. These manual methods have largely been replaced by computerized perimeters (Humphrey, Octopus) that exhibit a variable intensity target in fixed positions in the field of vision.
By automatically printing light thresholds, these static perimeters provide a sensitive method for detecting scotoms from the field of vision. They are also useful for serial evaluation of visual function in chronic diseases such as glaucoma or cerebral pseudotumors. The essence of the visual field analysis is to decide whether the lesion is located previously, at the level or posterior to the optical chiasma. if the scotoma is limited to one eye, it is probably due to a lesion previously located of chiasma, affecting either the optic nerve or the retina. Retinal lesions produce scotomas that correspond optically to their location in the bottom of the eye. For example, a supero-nasal retinal detachment leads to amputation of the lower temporal field. Macular damage produces a central scotom.
Optical nerve disorders produce characteristic patterns of visual field defects. Glaucoma selectively destroys the axons that penetrate through the supero-temporal or infero-temporal poles of the optical disc by producing arched scotoams in the form of a Turkish yatagan, which start from the blind point, describe an arc and end in a straight line at the level of the horizontal meridian. This defective type of field of vision reflects the arrangement of the nerve fiber layer in the temporal retina.
The excellent visual acuity of man is obtained by removing all retinal elements from the fovea, except photoreceptors, in order to minimize the absorption and scattering of light. To avoid passing over the fovea, the axons of cells in the temporal retina must follow an indirect path arching around the fovea to reach the level of the optical disc.
The arched or layer of nerve fibers also occur as a result of optic neuritis, ischemic neuropathy, optical disc geodes and retinal artery branch occlusion. Damage to the entire upper or lower pole of the optical disc causes an altitudinal field amputation, which follows the horizontal meridian.
This visual field defect pattern is typical for ischemic optic neuropathy, but it can also occur due to retinal vessel occlusion, advanced glaucoma and optic neuritis. About half of the fibers of the optic nerve originate in the ganglion cells serving the macola. Damage to the papillomal fibers produces a cecocentral scotom that comprises the blind spot and the macula.
If the lesion is irreversible, eventually, paleness appears in the temporal portion of the optic disc. Time pallor following a cecocentral scotom may occur in optic neuritis, nutritional optic neuropathy, toxic optic neuropathy, leber hereditary optic neuropathy and compressive optic neuropathy.
It is important to note that in most normal subjects the temporal part of the optic disc is slightly paler than the nasal part. Therefore, it can sometimes be difficult to decide whether the visible temporal pallor on the examination of the bottom of the eye represents a pathological change. The paleness of the nasal edge of the optic disc is a less equivocal sign of optical atrophy.
At the level of the optic chiasma, the fibers of the ganglion cells in the nasal level cross by passing into the controlled optic tract. For unknown reasons, cross-fibres are damaged by compression to a greater extent than cross-breeding fibres. Consequently, tumor lesions in the selare region produce temporal hemianopsia in each eye.
Tumors located previously compared to the optic chiasma, e.g. the meningiomas of the selarum selarum produce a junctional scocom, characterized by optic neuropathy in each eye and amputation of the upper temporal field in the other eye. Symmetrical compressions of the optic chiasma due to pituitary adenoma, meningioma, craniopharyngeal, glioma or aneurysm cause bitemporal hemianopsia.
The insidious evolution of bitemporal hemianopsia often goes unnoticed by the patient and will escape medical examination if the eyes are not treated separately. accurate localization of a postchiasmatic lesion is difficult, since lesions at any point along the optic tract, lateral genicular body, optical radiation or visual cortex can produce eponymous hemianopsia, i.e. a defect of temporal hemifield in the controlled eye and a defect pair of nasal hemifield in the ipsilateral eye.
Unilateral postchiasmatic lesions leave the visual acuity of each eye intact, although the patient can only read the letters in the left or right half of the optotype. Optical radiation lesions tend to cause incongruous visual field defects in each eye. The lesions of optical radiation in the temporal lobe (Meyer's loop) produce a eponymous hemianopsia in the upper quadrant, while optical radiation in the parietal lobe produces an eponymous hemianopsia in the lower quadrant.
Injuries to the primary visual cortex give rise to a congruent, dense hemianopsia. The occlusion of the posterior cerebral artery that vascularizes the occipital lobe is a common cause of total homonymous hemianopsia. Some patients with hemianopsia following an occipital stroke have the macula intact, because the macular representation at the tip of the occipital lobe is vascularized by collateral in the middle cerebral artery. The destruction of both occipital lobes produces cortical cetate. This situation can be differentiated from the bilateral prechiasmatic visual defect, in that the pupil responses and the bottom of the eye remain normal.
Tomorrow we'll continue with the patient's approach...
Christ has risen!
I'm going to start fasting today with eye movements and alignment. Testing of eye movements is done by asking the patient to follow with both eyes open a small target, such as a pen flashlight, moved in the cardinal fields of vision. Normal eye movements are smooth, symmetrical, complete and sustained in all directions, without nystagmus.
The jerky movements or rapid eye refixation movements are evaluated by having the patient look forward and then between two stationary targets. The eyeballs must move quickly and accurately in a single motion towards the target. Eye alignment can be evaluated by holding a pen flashlight directly in front of the patient about one meter away. if the eyes look straight, the corneal bright reflex will be centered in the middle of each pupil.
For more precise eye alignment testing, the coating test is useful. The patient is instructed to focus his gaze on a small target located at a distance. One eye suddenly covers and the other eye is observed. If the uncovered eye moves so it can fix the target, it's not well aligned.
If it does not move, the first eye is discovered and the test is repeated on the second eye. If neither eye moves, it means that the eyes are orthotropicly aligned. if the eyes look orthotropic when the head is straight, but the patient accuses diplopia, the cover test should be performed with the head tilted or turned towards the direction that causes the patient's diplopia.
Through exercise, the examiner can detect ocular deviation (heterotropy) of up to 1-2 degrees with the help of the coating test. Deviations can be measured by placing prisms in front of the misaligned eye thus determining the power necessary to neutralize the movement of the eye in order to fix the target, caused by the covering of the other eye.
With regard to stereoscopic vision, stereoacuity is determined by presenting targets with retinal discrepancy, separately at the level of each eye, using polarized images. In the cabinet the most commonly used tests measure a range of thresholds from 800 to 40 seconds of arc. If a patient obtains this level of stereoacuity in tests, we can be sure that the eyes are orthotropicly aligned and the vision is intact in both eyes. Randomly punctuated stereograms do not give indications of deep monocular vision and are an excellent screening test for strabismus and amblyopia in children.
Let me move on to the chromatic view now. The retina contains three categories of cones with visual pigments with maximum different spectral sensitivity: red (560 nm), green (530 nm) and blue (430 nm). The red and green pigments of the cones are encoded on the X chromosome, the blue pigment on chromosome 7.
Blue pigment mutations are extremely rare. Mutations of red and green pigments produce congenital X-linked acromotopsia in 8% of men. Affected individuals are not really achromatic, but differ from normal subjects in the way they perceive colors and how they combine monochromatic primary radiation to obtain a given color.
Abnormal tricomatas have three types of cones, but a mutation in a pigment (usually red or green) causes a change in maximum spectral sensitivity, altering the proportion of primary colors needed to obtain a color. Dicromats have only two types of cones and therefore will form colors only on the basis of two primary colors.
Abnormal tricomations and dicromats have a visual acuity of 6/6, but the discrimination of shades is affected. Ishihara colored plates can be used to detect red-green discromatopia. Test plates include a hidden number, visible only to subjects who confuse colors due to red-green discromatopsia. because discromatopsias are almost entirely X-linked, screening is only worth in the case of male children.
Ishihara plaques are often used to test patients with acquired colored vision disorders. Although they were not designed for this purpose, there is no other simpler and more convenient method for routine quantitative testing of colored vision. Acquired defects of colored vision are often the result of diseases of the macula or optic nerve.
For example, patients with a history of optic neuritis often experience a decrease in color perception long after their visual acuity has returned to normal. Colorful vision disorders may also be caused by bilateral strokes affecting the ventral portion of the occipital lobe (cerebral acromatopsia).
These patients may perceive only shades of grey and may also have difficulty recognizing faces (prosopagnosia). Infarctions of the dominant occipital lobe sometimes cause visual anomie for colors. Affected patients can distinguish and differentiate colors, but they can't name them.
In the case of the field of vision, vision can be damaged by damage to the visual system anywhere between the eyeballs and the occipital lobes. The site of the lesion can be located with considerable precision mapping the visual field deficit by assessing the perception of the examiner's fingers and then linking it with the topographical anatomy of the visual path.
More quantitative information can be obtained by the usual perimetric examination of visual fields. At kinetic perimetry, the patient looks at a tangent screen or hemispheric vessel (Goldmann perimeter), while the examiner moves a small bright target from the periphery to the center. These manual methods have largely been replaced by computerized perimeters (Humphrey, Octopus) that exhibit a variable intensity target in fixed positions in the field of vision.
By automatically printing light thresholds, these static perimeters provide a sensitive method for detecting scotoms from the field of vision. They are also useful for serial evaluation of visual function in chronic diseases such as glaucoma or cerebral pseudotumors. The essence of the visual field analysis is to decide whether the lesion is located previously, at the level or posterior to the optical chiasma. if the scotoma is limited to one eye, it is probably due to a lesion previously located of chiasma, affecting either the optic nerve or the retina. Retinal lesions produce scotomas that correspond optically to their location in the bottom of the eye. For example, a supero-nasal retinal detachment leads to amputation of the lower temporal field. Macular damage produces a central scotom.
Optical nerve disorders produce characteristic patterns of visual field defects. Glaucoma selectively destroys the axons that penetrate through the supero-temporal or infero-temporal poles of the optical disc by producing arched scotoams in the form of a Turkish yatagan, which start from the blind point, describe an arc and end in a straight line at the level of the horizontal meridian. This defective type of field of vision reflects the arrangement of the nerve fiber layer in the temporal retina.
The excellent visual acuity of man is obtained by removing all retinal elements from the fovea, except photoreceptors, in order to minimize the absorption and scattering of light. To avoid passing over the fovea, the axons of cells in the temporal retina must follow an indirect path arching around the fovea to reach the level of the optical disc.
The arched or layer of nerve fibers also occur as a result of optic neuritis, ischemic neuropathy, optical disc geodes and retinal artery branch occlusion. Damage to the entire upper or lower pole of the optical disc causes an altitudinal field amputation, which follows the horizontal meridian.
This visual field defect pattern is typical for ischemic optic neuropathy, but it can also occur due to retinal vessel occlusion, advanced glaucoma and optic neuritis. About half of the fibers of the optic nerve originate in the ganglion cells serving the macola. Damage to the papillomal fibers produces a cecocentral scotom that comprises the blind spot and the macula.
If the lesion is irreversible, eventually, paleness appears in the temporal portion of the optic disc. Time pallor following a cecocentral scotom may occur in optic neuritis, nutritional optic neuropathy, toxic optic neuropathy, leber hereditary optic neuropathy and compressive optic neuropathy.
It is important to note that in most normal subjects the temporal part of the optic disc is slightly paler than the nasal part. Therefore, it can sometimes be difficult to decide whether the visible temporal pallor on the examination of the bottom of the eye represents a pathological change. The paleness of the nasal edge of the optic disc is a less equivocal sign of optical atrophy.
At the level of the optic chiasma, the fibers of the ganglion cells in the nasal level cross by passing into the controlled optic tract. For unknown reasons, cross-fibres are damaged by compression to a greater extent than cross-breeding fibres. Consequently, tumor lesions in the selare region produce temporal hemianopsia in each eye.
Tumors located previously compared to the optic chiasma, e.g. the meningiomas of the selarum selarum produce a junctional scocom, characterized by optic neuropathy in each eye and amputation of the upper temporal field in the other eye. Symmetrical compressions of the optic chiasma due to pituitary adenoma, meningioma, craniopharyngeal, glioma or aneurysm cause bitemporal hemianopsia.
The insidious evolution of bitemporal hemianopsia often goes unnoticed by the patient and will escape medical examination if the eyes are not treated separately. accurate localization of a postchiasmatic lesion is difficult, since lesions at any point along the optic tract, lateral genicular body, optical radiation or visual cortex can produce eponymous hemianopsia, i.e. a defect of temporal hemifield in the controlled eye and a defect pair of nasal hemifield in the ipsilateral eye.
Unilateral postchiasmatic lesions leave the visual acuity of each eye intact, although the patient can only read the letters in the left or right half of the optotype. Optical radiation lesions tend to cause incongruous visual field defects in each eye. The lesions of optical radiation in the temporal lobe (Meyer's loop) produce a eponymous hemianopsia in the upper quadrant, while optical radiation in the parietal lobe produces an eponymous hemianopsia in the lower quadrant.
Injuries to the primary visual cortex give rise to a congruent, dense hemianopsia. The occlusion of the posterior cerebral artery that vascularizes the occipital lobe is a common cause of total homonymous hemianopsia. Some patients with hemianopsia following an occipital stroke have the macula intact, because the macular representation at the tip of the occipital lobe is vascularized by collateral in the middle cerebral artery. The destruction of both occipital lobes produces cortical cetate. This situation can be differentiated from the bilateral prechiasmatic visual defect, in that the pupil responses and the bottom of the eye remain normal.
Tomorrow we'll continue with the patient's approach...
Understanding, love and
gratitude! Christ has risen!
Dorin, Merticaru