STUDY - Technical - New Dacian's Medicine
Eye and
Vision Disorders (6)
Translation Draft
Let's get on with it!
The hyaline bodies of the optic disc are refractory deposits at the point of formation of the optic nerve and are not correlated with the hyaline bodies of the retina, which occur in age-related macular degeneration. Hyaline bodies of the optical disc are very common in individuals of North European origin, with an incidence of 3-4 in thousand.
The diagnosis is evident when they are visible as bright particles on the surface of the optical disc. However, in many patients, hyaline bodies are hidden below the surface causing the appearance of the optical disc with sharp edges, which easily leads to confusion with the papillomademe.
Recognition of pseudopapiloedema due to the hyaline bodies of the optical disc is important in the sense of avoiding a useless examination for papiloedema. Ultrasound and CT are sensitive methods of detecting the deep hyaline bodies of the optic disc because they contain calcium. In most patients, the hyaline bodies of the optical disc are a random, harmless discovery, although they can produce visual obtulations.
At perimetry, they produce enlarged blind spots and arced scotoms following damage to the optical disc. As you get older, hyaline bodies tend to become superficial as optic atrophy develops. Hemorrhages, the choroidal neovascular membrane and anterior ischemic optic neuropathy occur more likely in patients with hyaline bodies of the optic disc. No treatment for hyaline bodies is known.
Vitreous body degeneration occurs in all patients of advanced age, producing chronic and acute visual symptoms. In the vitreous body, opacities are produced that annoyingly overshadow the retina. As the eye moves, these "floating" opacities move synchronously, with a slight latency due to the inertia of vitreous humor.
The traction exerted by the vitreous body on the retina produces mechanical stimulation which results in the perception of bright lights. This photopsy is short-lived and is limited to one eye, as opposed to bilateral, prolonged scintillations of cortical migraine. Vitreous body contractions can lead to its sudden separation from the retina, heralded by an alarming abundance of floating opacity and photopsy.
This process, known as vitreous body detachment, is a common degenerative phenomenon in the elderly. It is not harmful unless it harms the retina. Careful examination of the bottom of the eye after dilation is mandatory in any patient who accuses floating opacity and photopsy, in order to detect possible ruptures or peripheral holes.
If such lesions are detected, the application of the laser or cryotherapy may prevent the detachment of the retina. Sometimes a rupture perforates a retinal vessel, causing hemorrhages in the vitreous body and sudden loss of vision. On the ophthalmoscope exam, the bottom of the eye is covered with dark red blood.
It is necessary to ultrasound the interior of the eyeball, in order to detect a possible rupture or detachment of the retina. If the bleeding does not spontaneously recover, the vitreous body can be surgically removed. Hemorrhages in the vitreous body also occur due to fragile neoformation vessels that proliferate on the surface of the retina in diabetes, sickle cell disease and other ischemic eye conditions.
Retinal detachment produces symptoms such as floating opacity, bright lights and a scotom in the peripheral field of vision corresponding to detachment. If the detachment includes the fovea, there is a related pupil defect and the visual acuity is diminished. In most eyes, retinal detachment begins with a hole, fissure or rupture at the periphery of the retina (regmatogenic retinal detachment). Patients with thinned peripheral retina (reticular degeneration) are particularly vulnerable to this process.
Once a gap has occurred in the retina, the liquefied vitreous can penetrate freely into the subretinal space, separating the retina from the pigment epithelium. The association of the traction exerted by the vitreous body on the surface of the retina with the penetration of fluid behind the retina inevitably leads to retinal detachment. Patients with a history of myopia, trauma or previous cataract surgery are at the highest risk of retinal detachment. The diagnosis is confirmed by the ophthalmoscopy of the dilated eye.
Classical migraine usually occurs with a visual aura that lasts about 20 minutes. In a typical attack, a small visual field defect moves toward the periphery, leaving a transient scotom behind. The expandable limit of the migraine scotoma has a sparky, dancing or zigzag edge, similar to the bastions of a fortress, hence the term "spectrum of fortifications". The way patients describe the spectra of fortifications varies greatly and can be confused with fleeting amaurosis.
Spectres of migraine fortifications usually last longer and are perceived in both eyes, while fleeting amaurosis is shorter in duration and occurs only in one eye. Migraine phenomena remain visible in the dark or with eyes closed. They are generally limited to either the right or left visual hemifields, but sometimes both fields are involved simultaneously. Patients usually have a long history of stereotypical attacks. After the return of visual symptoms, headache occurs in most patients.
Transient ischemic attacks due to vertebro-basilary insufficiency cause acute homonymous visual symptoms. Many patients misdescribe the symptoms in either the left or right eye, when in fact they appear in the right or left hemifield in both eyes. Disruption of blood flow to the visual cortex causes sudden blurring or darkening of vision, sometimes with bright lights or other positive phenomena that mimic migraine.
Cortical ischemic attacks have a shorter duration than migraine, occur in the elderly and are not followed by headache. Signs of ischemia of the brain stem may be associated, such as diplopia, vertigo, paresthesia, weakness or dysarcria.
Stroke occurs when disruption of blood flow from the posterior cerebral artery to the visual cortex is prolonged. The only information obtained from the examination is represented by an eponymous visual field defect, which suddenly stops at the level of the vertical meridian. Vascular accident of the occipital lobe is usually due to thrombotic occlusion of the vertebro-bazilary system, embolisms or dissection. Lobar haemorrhages, tumors, abscesses and arteriovenous malformations are other common causes of cortical hemianopsian vision loss.
Artificial (functional, non-organic) loss of vision is accused of hysterics or simulants. The latter comprise the vast majority, they are in search of sympathy, special treatment or financial gain, by simulating loss of vision. Diagnosis is suspected when history is atypical, physical examination data are absent or contradictory, tests provide inconsistent data and a secondary reason can be identified. In our litigious society, attempts to obtain fraudulent rewards have given rise to an epidemic of artificial vision loss.
Let me move on to chronic vision loss now! Cataracts are the opacification of the lens to a sufficient extent to diminish vision. Most cataracts evolve slowly as a result of the aging process, leading to progressive impairment of vision. Cataracts occur more quickly in patients with a history of eye trauma, uveitis or diabetes mellitus.
Cataracts are found in a number of genetic diseases, such as myotonic dystrophy, neurofibromatosis type 2 and galactosemia. Radiation therapy and glucocorticoid treatment may have the adverse effect of inducing cataracts. Cataracts associated with radiotherapy or glucocorticoid therapy have a typical subcapsular posterior localization.
Cataracts can be detected by observing a deficient red reflex when viewing with the ophthalmoscope the light reflected from the bottom of the eye or when examining the dilated eye with the slit lamp.
The only treatment of cataracts is surgical extraction of the opaque lens. The operation is generally performed under local retrobulbar anesthesia in the ambulatory. Remarkable technical innovations have made it possible to suction cataracts with the lens capsule intact (extracapsular cataract extraction).
Subsequently, in the empty capsule of the lens in the rear chamber, a plastic or silicone intraocular lens is inserted, which replaces the natural lens, leading to the rapid recovery of vision. More than 95% of patients who have undergone cataract extraction interventions eventually opacity, producing a secondary vision defect. to restore clarity, a new opening is applied in the lens capsule using the laser.
Glaucoma is an insidious, slowly evolutionary optic neuropathy, usually associated with chronic increase in intraocular pressure. The mechanism by which increased intraocular pressure damages the optic nerve is not yet understood. Axons entering the infero-temporal and super-temporal dials of the optic papilla are damaged first, producing typical defects of nerve fiber beam or arcuated scoames in perimetry tests. As nerve fibers are destroyed, the neural edge of the optic papilla contracts and the physiological excavation at the optical disc increases.
This process is colloquially called pathological "excavation". The excavation-papil diameter is expressed by a ratio (e.g. 0,2/1). The excavate/papilla ratio varies widely in normal subjects, making it difficult to diagnose glaucoma by simply observing an unusually large or deep excavation in the optic papillae. Careful study of prospective serial examinations is useful.
In patients with physiological excavation, a large excavation remains stable, while in patients with glaucoma, it expands continuously over the years. Detection of visual field defects in routine perimetry also contributes to the diagnosis of glaucoma. Finally, most patients with glaucoma have elevated intraocular pressure levels.
However, a surprising number of patients with typical glaucomaous excavations and typical field of vision defects have intraocular pressures that apparently never exceed the 20 mmHg limit (so-called low intraocular tension glaucoma).
In acute closed-angle glaucoma, the eye is red and painful due to sudden and severe increase in intraocular pressure. Such cases are only found in a small proportion of glaucoma patients. most patients with glaucoma have open angles of the anterior chamber, which do not block. The cause of increased intraocular pressure from open-angle glaucoma is unknown.
Because increased intraocular pressure occurs gradually and is less important than in closed-angle glaucoma, the patient does not experience pain or eye congestion. The central field of vision and acuity of the fovea are spared until the final stage of the disease is reached. For these reasons, severe and irreversible damage may occur before the patient or doctor recognizes the diagnosis: Screening patients for glaucoma by observing the excavate/papillratio ratio at ophthalmoscopy and by measuring intraocular pressure (using a Schiotz, Tonopen or Goldmann tonometer) is vital.
Treatment of glaucoma consists of local administration of adrenergic agonists (epinephrine, dipivefrin or apraclonidine), cholinergic agonists (pilocarpine) and beta blockers (betaxolol, carteolol, levobunolol, metipranolol and timolol). Sometimes, systemic absorption of beta blocker from the eye drop may be sufficient to produce bradycardia, hypotension, cardiac block, brohospasm, impotence or depression.
Carbonic anhydrase inhibitors are used topically or orally to reduce intraocular pressure by reducing the production of aqueous humor. Laser treatment of the traberculation network at the angle of the anterior chamber improves the drainage of the watery humor from the eye. If medical or laser treatment fails to stop the progression of the optic nerve injury following glaucoma, a filter (trabeculectomy) should be surgically constructed to allow controlled drainage of the aqueous humor in the eye.
Let's get on with it!
The hyaline bodies of the optic disc are refractory deposits at the point of formation of the optic nerve and are not correlated with the hyaline bodies of the retina, which occur in age-related macular degeneration. Hyaline bodies of the optical disc are very common in individuals of North European origin, with an incidence of 3-4 in thousand.
The diagnosis is evident when they are visible as bright particles on the surface of the optical disc. However, in many patients, hyaline bodies are hidden below the surface causing the appearance of the optical disc with sharp edges, which easily leads to confusion with the papillomademe.
Recognition of pseudopapiloedema due to the hyaline bodies of the optical disc is important in the sense of avoiding a useless examination for papiloedema. Ultrasound and CT are sensitive methods of detecting the deep hyaline bodies of the optic disc because they contain calcium. In most patients, the hyaline bodies of the optical disc are a random, harmless discovery, although they can produce visual obtulations.
At perimetry, they produce enlarged blind spots and arced scotoms following damage to the optical disc. As you get older, hyaline bodies tend to become superficial as optic atrophy develops. Hemorrhages, the choroidal neovascular membrane and anterior ischemic optic neuropathy occur more likely in patients with hyaline bodies of the optic disc. No treatment for hyaline bodies is known.
Vitreous body degeneration occurs in all patients of advanced age, producing chronic and acute visual symptoms. In the vitreous body, opacities are produced that annoyingly overshadow the retina. As the eye moves, these "floating" opacities move synchronously, with a slight latency due to the inertia of vitreous humor.
The traction exerted by the vitreous body on the retina produces mechanical stimulation which results in the perception of bright lights. This photopsy is short-lived and is limited to one eye, as opposed to bilateral, prolonged scintillations of cortical migraine. Vitreous body contractions can lead to its sudden separation from the retina, heralded by an alarming abundance of floating opacity and photopsy.
This process, known as vitreous body detachment, is a common degenerative phenomenon in the elderly. It is not harmful unless it harms the retina. Careful examination of the bottom of the eye after dilation is mandatory in any patient who accuses floating opacity and photopsy, in order to detect possible ruptures or peripheral holes.
If such lesions are detected, the application of the laser or cryotherapy may prevent the detachment of the retina. Sometimes a rupture perforates a retinal vessel, causing hemorrhages in the vitreous body and sudden loss of vision. On the ophthalmoscope exam, the bottom of the eye is covered with dark red blood.
It is necessary to ultrasound the interior of the eyeball, in order to detect a possible rupture or detachment of the retina. If the bleeding does not spontaneously recover, the vitreous body can be surgically removed. Hemorrhages in the vitreous body also occur due to fragile neoformation vessels that proliferate on the surface of the retina in diabetes, sickle cell disease and other ischemic eye conditions.
Retinal detachment produces symptoms such as floating opacity, bright lights and a scotom in the peripheral field of vision corresponding to detachment. If the detachment includes the fovea, there is a related pupil defect and the visual acuity is diminished. In most eyes, retinal detachment begins with a hole, fissure or rupture at the periphery of the retina (regmatogenic retinal detachment). Patients with thinned peripheral retina (reticular degeneration) are particularly vulnerable to this process.
Once a gap has occurred in the retina, the liquefied vitreous can penetrate freely into the subretinal space, separating the retina from the pigment epithelium. The association of the traction exerted by the vitreous body on the surface of the retina with the penetration of fluid behind the retina inevitably leads to retinal detachment. Patients with a history of myopia, trauma or previous cataract surgery are at the highest risk of retinal detachment. The diagnosis is confirmed by the ophthalmoscopy of the dilated eye.
Classical migraine usually occurs with a visual aura that lasts about 20 minutes. In a typical attack, a small visual field defect moves toward the periphery, leaving a transient scotom behind. The expandable limit of the migraine scotoma has a sparky, dancing or zigzag edge, similar to the bastions of a fortress, hence the term "spectrum of fortifications". The way patients describe the spectra of fortifications varies greatly and can be confused with fleeting amaurosis.
Spectres of migraine fortifications usually last longer and are perceived in both eyes, while fleeting amaurosis is shorter in duration and occurs only in one eye. Migraine phenomena remain visible in the dark or with eyes closed. They are generally limited to either the right or left visual hemifields, but sometimes both fields are involved simultaneously. Patients usually have a long history of stereotypical attacks. After the return of visual symptoms, headache occurs in most patients.
Transient ischemic attacks due to vertebro-basilary insufficiency cause acute homonymous visual symptoms. Many patients misdescribe the symptoms in either the left or right eye, when in fact they appear in the right or left hemifield in both eyes. Disruption of blood flow to the visual cortex causes sudden blurring or darkening of vision, sometimes with bright lights or other positive phenomena that mimic migraine.
Cortical ischemic attacks have a shorter duration than migraine, occur in the elderly and are not followed by headache. Signs of ischemia of the brain stem may be associated, such as diplopia, vertigo, paresthesia, weakness or dysarcria.
Stroke occurs when disruption of blood flow from the posterior cerebral artery to the visual cortex is prolonged. The only information obtained from the examination is represented by an eponymous visual field defect, which suddenly stops at the level of the vertical meridian. Vascular accident of the occipital lobe is usually due to thrombotic occlusion of the vertebro-bazilary system, embolisms or dissection. Lobar haemorrhages, tumors, abscesses and arteriovenous malformations are other common causes of cortical hemianopsian vision loss.
Artificial (functional, non-organic) loss of vision is accused of hysterics or simulants. The latter comprise the vast majority, they are in search of sympathy, special treatment or financial gain, by simulating loss of vision. Diagnosis is suspected when history is atypical, physical examination data are absent or contradictory, tests provide inconsistent data and a secondary reason can be identified. In our litigious society, attempts to obtain fraudulent rewards have given rise to an epidemic of artificial vision loss.
Let me move on to chronic vision loss now! Cataracts are the opacification of the lens to a sufficient extent to diminish vision. Most cataracts evolve slowly as a result of the aging process, leading to progressive impairment of vision. Cataracts occur more quickly in patients with a history of eye trauma, uveitis or diabetes mellitus.
Cataracts are found in a number of genetic diseases, such as myotonic dystrophy, neurofibromatosis type 2 and galactosemia. Radiation therapy and glucocorticoid treatment may have the adverse effect of inducing cataracts. Cataracts associated with radiotherapy or glucocorticoid therapy have a typical subcapsular posterior localization.
Cataracts can be detected by observing a deficient red reflex when viewing with the ophthalmoscope the light reflected from the bottom of the eye or when examining the dilated eye with the slit lamp.
The only treatment of cataracts is surgical extraction of the opaque lens. The operation is generally performed under local retrobulbar anesthesia in the ambulatory. Remarkable technical innovations have made it possible to suction cataracts with the lens capsule intact (extracapsular cataract extraction).
Subsequently, in the empty capsule of the lens in the rear chamber, a plastic or silicone intraocular lens is inserted, which replaces the natural lens, leading to the rapid recovery of vision. More than 95% of patients who have undergone cataract extraction interventions eventually opacity, producing a secondary vision defect. to restore clarity, a new opening is applied in the lens capsule using the laser.
Glaucoma is an insidious, slowly evolutionary optic neuropathy, usually associated with chronic increase in intraocular pressure. The mechanism by which increased intraocular pressure damages the optic nerve is not yet understood. Axons entering the infero-temporal and super-temporal dials of the optic papilla are damaged first, producing typical defects of nerve fiber beam or arcuated scoames in perimetry tests. As nerve fibers are destroyed, the neural edge of the optic papilla contracts and the physiological excavation at the optical disc increases.
This process is colloquially called pathological "excavation". The excavation-papil diameter is expressed by a ratio (e.g. 0,2/1). The excavate/papilla ratio varies widely in normal subjects, making it difficult to diagnose glaucoma by simply observing an unusually large or deep excavation in the optic papillae. Careful study of prospective serial examinations is useful.
In patients with physiological excavation, a large excavation remains stable, while in patients with glaucoma, it expands continuously over the years. Detection of visual field defects in routine perimetry also contributes to the diagnosis of glaucoma. Finally, most patients with glaucoma have elevated intraocular pressure levels.
However, a surprising number of patients with typical glaucomaous excavations and typical field of vision defects have intraocular pressures that apparently never exceed the 20 mmHg limit (so-called low intraocular tension glaucoma).
In acute closed-angle glaucoma, the eye is red and painful due to sudden and severe increase in intraocular pressure. Such cases are only found in a small proportion of glaucoma patients. most patients with glaucoma have open angles of the anterior chamber, which do not block. The cause of increased intraocular pressure from open-angle glaucoma is unknown.
Because increased intraocular pressure occurs gradually and is less important than in closed-angle glaucoma, the patient does not experience pain or eye congestion. The central field of vision and acuity of the fovea are spared until the final stage of the disease is reached. For these reasons, severe and irreversible damage may occur before the patient or doctor recognizes the diagnosis: Screening patients for glaucoma by observing the excavate/papillratio ratio at ophthalmoscopy and by measuring intraocular pressure (using a Schiotz, Tonopen or Goldmann tonometer) is vital.
Treatment of glaucoma consists of local administration of adrenergic agonists (epinephrine, dipivefrin or apraclonidine), cholinergic agonists (pilocarpine) and beta blockers (betaxolol, carteolol, levobunolol, metipranolol and timolol). Sometimes, systemic absorption of beta blocker from the eye drop may be sufficient to produce bradycardia, hypotension, cardiac block, brohospasm, impotence or depression.
Carbonic anhydrase inhibitors are used topically or orally to reduce intraocular pressure by reducing the production of aqueous humor. Laser treatment of the traberculation network at the angle of the anterior chamber improves the drainage of the watery humor from the eye. If medical or laser treatment fails to stop the progression of the optic nerve injury following glaucoma, a filter (trabeculectomy) should be surgically constructed to allow controlled drainage of the aqueous humor in the eye.
Have a good day!
Dorin, Merticaru