STUDY - Technical - New Dacian's Medicine
Eye and
Vision Disorders (1)
Translation Draft
I'll start with a few "things" about the human visual system. The visual analyzer is an extremely effective means of rapidly receiving information from the environment in order to guide behavior (estimated that more than 70% of all human perceptions of the environment are visual information).
The act of vision begins by capturing focused images of the cornea and the lens on a light-sensitive membrane located at the back of the eyeball, called the retina. Basically, the retina belongs to the encephalus, being located on the periphery in order to serve as a transformer for the conversion of light energy into neural signals.
Light is absorbed by photopigments in the two classes of receptors: cells with canes (approximately 100 million) and cells with cones (approximately 5 million). Bastons operate under dark or scotopic lighting conditions. Cones are active in photopic conditions or in daylight conditions, they specialize in color perception and high spatial resolution. Most cones are located in the macula, that part of the retina that serves the 10 central degrees of the field of vision.
In the middle of the macula there is a small depression called the fovea, which contains exclusively cones and which confers maximum visual acuity. Photoreceptors hyperpolarize under the action of light, activating the bipolar, amacrine and horizontal cells in the internal nuclear layer.
After processing the response of photoreceptors by this retinal circuit complex, the flow of sensory information finally converges to a common pathway: ganglion cells. These cells transform the projected visual image on the retina into a continuous train of variable action potentials, which propagate along the primary optical pathway to the visual centers of the brain.
In each retina there are a million ganglion cells and so a million fibers of each optic nerve. The axons of ganglion cells located along the inner surface of the retina, in the layer of nerve fibers, leave the eye at the level of the optic disc and reach through the optic nerve to the encephalic centers. Most fibers make synapses with cells in the lateral genicular body, a talamic relay station. Cells in the lateral genicular body are also projected into the primary visual cortex.
This massive retinogeniculocortical sensory pathway is the neural substrate of visual perception. Although the lateral genicular body is the main relay station for retinal aferences, separate classes of ganglion cells are projected into other subcortical visual nuclei involved in different functions.
The pupil reflex is mediated by the aferences to the preectal olivarial nucles in the mesencephalus. These pretectal nuclei send eferences to the Edinger-Westphal ipsilateral and contralateral nuclei of the oculomotor nuclear complex. Cells in the Edinger-Westphal cells irritate the sphincter of the iris parasympathetically via an intermediate neuron in the ciliary ganglia.
Circadian rhythms are timed by a retinal projection to the suprachiasmatic nucleus. Visual orientation and ovulation movements are served by retinal adhesions to the upper colic. Eye stabilization and optokinetic reflexes are governed by a group of small retinal fibers, known generically as the optical accessor system of the brain stem. Finally, there is a large retinal projection of considerable size to the pulvinar, a large visual talamic nucleus with obscure function.
The eyeballs rotate continuously in the orbits in order to place and maintain the object of visual interest at the fovea level. This activity, called foveation or the act of looking, is governed by a very complex efferent motor system. Each eye is set in motion by six extrinsic muscles, innervated by cranial nerves originating in the oculomotor (III), trochlear (IV) and abducens (VI) monsters.
Activity at the level of these ocular motor nuclei is coordinated by the pontine and mesencephalic mechanisms that perform fine movements, jerky movements of the eyeballs and fixation of the gaze during head and body movements. Large regions of the frontal and parietooccipital cortex control these centers of eye movements in the brain stem through supranuclear descending nerve fibers.
Visual function can be affected in many ways. Eye globes proemin in the head, exposed to trauma, noxiousness and infections. Vision can be damaged by intrinsic eye diseases such as glaucoma, cataracts or retinal detachment.
Many neurological diseases produce eye symptoms because large areas of the cortex, thalamus and brain stem are involved in visual perception or movement of the eyeballs. In genetic disorders eye manifestations are common and often help the clinician in identifying a rare syndrome. Finally, the eyes are frequently affected by acquired systemic diseases.
The eye is a specialized organ, requiring unique optical instruments for proper examination. The slit lamp and ophthalmone provide a very good, amplified image of the transparent structures of the eyeball, representing the only means of direct inspection of blood vessels in the eye of a subject of life.
There are doctors who fail to acquire the skill required to use these tools and therefore feel unable to deal with patients with eye conditions. While it may be obvious that a particular patient requires the specialized care of an ophthalmologist, the initial assessment of eye symptoms is the responsibility of all physicians, and the assessment of visual acuity, pupils, eye movements, visual fields and the bottom of the eye remains an integral part of any complete physical examination.
Let's move on to clinical visual function evaluation! And, I'm going to start with the refraction cap. The approach of a patient with diminished vision consists in the first step in the investigation of a possible refractive defect.
In emetropy, light rays/radiation are focused directly on the retina. In myopia, the eyeball is too long, and the light rays are focused at a point in front of the retina. Nearby objects can be clearly seen, but remote objects require divergent lenses to be placed in front of the eye.
In hypermetropy, the eyeball is too short and therefore convergent lenses are used to compensate for the refractive power of the eye.
In astigmatism, the surface of the cornea is not perfectly spherical, requiring for correction cylindrical lenses. Towards the middle age, presbiopia develops, as the lens becomes unable to increase its refractive power to accommodate nearby objects.
To compensate for presbiopia, the emetropic patient should use reading glasses. The patient who already wears eyeglasses for remote correction usually switched to bifocal lenses. The only exception is the myopia, which can clearly see up close by simply removing the glasses for remote correction.
Refractive vices usually develop slowly and remain stable after adolescence, except in unusual situations. For example, the acute onset of diabetes mellitus can suddenly cause myopia, due to fluid inhibition and swelling of the lens, induced by hyperglycaemia. Testing vision through a punctuform orifice is a useful method for rapid detection of refractive defects. If visual acuity is better through a point hole than with the naked eye, the patient needs a serious research of refraction.
Another landmark is visual acuity. The Snellen map is used to test visual acuity at a distance of 6 meters. For convenience, a scale version of the Snellen map, called the Rosenbaum table, is used, 36 centimeters from the patient. All subjects should be able to read the 6/6 meter line with each eye using the appropriate refraction correction. Patients who need reading glasses should wear these glasses for the accuracy of the examination.
If the acuity of 6/ 6 is not present in each eye, the vision defect must be explained. In the case of a flash of less than 6/ 240, the ability to count fingers, to detect hand movements or to perceive bright light should be assessed. The degree of generally accepted cetate is defined as the best corrected acuity of 6/ 60 or less in the healthy eye, or a binocular field of vision narrowed to 20 degrees or less. Motor vehicle laws vary from state to state, but most require a corrected acuity of 6/12 in at least one eye. Patients with eponymous hemianopsia cannot drive.
Pupils should be individually tested in low light, with the patient staring at a distant target. If the pupils react promptly to light, there is no need to check the response for closeness, as isolated loss of contraction (myosis) for accommodation does not occur.
For this reason, the abbreviation PERRLA (Equal, Round and Reactive To Light and Accommodation) implies unnecessary effort in the last stage. However, if the response to light is weak or absent, it is important to test the response for closeness. Dissociation between adaptation to light and adaptation for close vision occurred in neurosyphilis (Argyll Robertson pupil), lesions of the dorsal mesencephalus (obstructive hydrocephalus, tumors of the pineal region) and after aberrant regeneration (oculomotor nerve paralysis, atonic pupil Adie).
An eye that does not perceive light does not show a pupillary response to direct light stimulation. If the retina or optic nerve are only partially damaged, the direct pupil response will be weaker than the consensual pupil response evoked by stimulating the other eye with a bright light. This relatively related pupil defect (Marcus Gunn pupil) can be evoked by the alternating light test. It is an extremely useful sign in retrobulbar optic neuritis and other disorders of the optic nerve, in which it may be the only objective sign of the disease. Fine inequality of pupil sizes, up to 0.5 mm, is quite common in normal subjects.
The diagnosis of essential or physiological anisocoria is safe as long as the relative pupil asymmetry remains constant under conditions of variable ambient illumination. Anisocoria that amplifies in low light indicates a sympathetic paralysis of the dilator muscle of the iris. Myosis triad, ipsilateral palpebral ptosis and anhydrosis form Horner syndrome, although anhydrosis is often absent.
Strokes in the brain stem, carotid dissection or neoplasms affecting the sympathetic chain are occasionally identified as causes of Horner syndrome, but most cases are idiopathic. Anisocoria that amplifies in bright light suggests parasympathetic paralysis.
The first cause to be suspected is oculomotor nerve paralysis. This possibility is excluded if the eye movements are complete and the patient does not have ptosis or diplopia. Acute pupil dilation (midriasis) can occur as a result of damage to the ciliary ganglion in the orbit. The usual mechanisms are by infection (herpes zoster, influenza), trauma (closed, penetrating, surgical) or ischemia (diabetes, temporal arteritis).
After denervation of the holy iris, the pupil does not respond correctly to light, but the adaptation for close-up vision is often relatively intact. If the nearby stimulus is removed, the pupil expands again very slowly compared to the normal pupil, hence the term tonic pupil.
In Adie syndrome, the tonic pupil is associated with weak or absent tendinous reflexes in the lower extremities. This benign condition, which occurs predominantly in healthy young women, is thought to represent moderate disautonomy. Tonic pupils are also associated with Shy-Drager syndrome, segmental hypohidrosis, diabetes and amyloidosis. Occasionally a tonic pupil is discovered by chance in an otherwise completely normal and asymptomatic patient.
The diagnosis is confirmed by the application of a diluted pilocarpine drop to each eye. Hypersensitivity of denervation produces pupillary constriction to a tonic pupil, while the normal pupil shows no reaction. Pharmacological dilation following accidental or deliberate instillation of anticholinergic agents (atropine drop, scopolamine) in the eye may also produce pupil mydriasis. In this situation, normal concentration pilocarpine (1%) does not cause constriction.
Both pupils are equally influenced by systemic medication. They are myotic in the case of the use of narcotics (morphine, heroin) and mydriatic in the case of the use of anticholinergics (scopolamine). Parasympathetic agents (pilocarpine, demecarium bromide) used to treat glaucoma, produce myosis.
In any patient with an unexplained pupillary abnormality, slot examination helps to exclude a surgical trauma of the iris, an occult foreign body, a perforation injury, intraocular inflammation, adhesions (sinechia), closed-angle glaucoma and rupture of the iris sphincter following closed trauma.
Ready for today! Prepare your sight for tomorrow's Light Holidays!
I'll start with a few "things" about the human visual system. The visual analyzer is an extremely effective means of rapidly receiving information from the environment in order to guide behavior (estimated that more than 70% of all human perceptions of the environment are visual information).
The act of vision begins by capturing focused images of the cornea and the lens on a light-sensitive membrane located at the back of the eyeball, called the retina. Basically, the retina belongs to the encephalus, being located on the periphery in order to serve as a transformer for the conversion of light energy into neural signals.
Light is absorbed by photopigments in the two classes of receptors: cells with canes (approximately 100 million) and cells with cones (approximately 5 million). Bastons operate under dark or scotopic lighting conditions. Cones are active in photopic conditions or in daylight conditions, they specialize in color perception and high spatial resolution. Most cones are located in the macula, that part of the retina that serves the 10 central degrees of the field of vision.
In the middle of the macula there is a small depression called the fovea, which contains exclusively cones and which confers maximum visual acuity. Photoreceptors hyperpolarize under the action of light, activating the bipolar, amacrine and horizontal cells in the internal nuclear layer.
After processing the response of photoreceptors by this retinal circuit complex, the flow of sensory information finally converges to a common pathway: ganglion cells. These cells transform the projected visual image on the retina into a continuous train of variable action potentials, which propagate along the primary optical pathway to the visual centers of the brain.
In each retina there are a million ganglion cells and so a million fibers of each optic nerve. The axons of ganglion cells located along the inner surface of the retina, in the layer of nerve fibers, leave the eye at the level of the optic disc and reach through the optic nerve to the encephalic centers. Most fibers make synapses with cells in the lateral genicular body, a talamic relay station. Cells in the lateral genicular body are also projected into the primary visual cortex.
This massive retinogeniculocortical sensory pathway is the neural substrate of visual perception. Although the lateral genicular body is the main relay station for retinal aferences, separate classes of ganglion cells are projected into other subcortical visual nuclei involved in different functions.
The pupil reflex is mediated by the aferences to the preectal olivarial nucles in the mesencephalus. These pretectal nuclei send eferences to the Edinger-Westphal ipsilateral and contralateral nuclei of the oculomotor nuclear complex. Cells in the Edinger-Westphal cells irritate the sphincter of the iris parasympathetically via an intermediate neuron in the ciliary ganglia.
Circadian rhythms are timed by a retinal projection to the suprachiasmatic nucleus. Visual orientation and ovulation movements are served by retinal adhesions to the upper colic. Eye stabilization and optokinetic reflexes are governed by a group of small retinal fibers, known generically as the optical accessor system of the brain stem. Finally, there is a large retinal projection of considerable size to the pulvinar, a large visual talamic nucleus with obscure function.
The eyeballs rotate continuously in the orbits in order to place and maintain the object of visual interest at the fovea level. This activity, called foveation or the act of looking, is governed by a very complex efferent motor system. Each eye is set in motion by six extrinsic muscles, innervated by cranial nerves originating in the oculomotor (III), trochlear (IV) and abducens (VI) monsters.
Activity at the level of these ocular motor nuclei is coordinated by the pontine and mesencephalic mechanisms that perform fine movements, jerky movements of the eyeballs and fixation of the gaze during head and body movements. Large regions of the frontal and parietooccipital cortex control these centers of eye movements in the brain stem through supranuclear descending nerve fibers.
Visual function can be affected in many ways. Eye globes proemin in the head, exposed to trauma, noxiousness and infections. Vision can be damaged by intrinsic eye diseases such as glaucoma, cataracts or retinal detachment.
Many neurological diseases produce eye symptoms because large areas of the cortex, thalamus and brain stem are involved in visual perception or movement of the eyeballs. In genetic disorders eye manifestations are common and often help the clinician in identifying a rare syndrome. Finally, the eyes are frequently affected by acquired systemic diseases.
The eye is a specialized organ, requiring unique optical instruments for proper examination. The slit lamp and ophthalmone provide a very good, amplified image of the transparent structures of the eyeball, representing the only means of direct inspection of blood vessels in the eye of a subject of life.
There are doctors who fail to acquire the skill required to use these tools and therefore feel unable to deal with patients with eye conditions. While it may be obvious that a particular patient requires the specialized care of an ophthalmologist, the initial assessment of eye symptoms is the responsibility of all physicians, and the assessment of visual acuity, pupils, eye movements, visual fields and the bottom of the eye remains an integral part of any complete physical examination.
Let's move on to clinical visual function evaluation! And, I'm going to start with the refraction cap. The approach of a patient with diminished vision consists in the first step in the investigation of a possible refractive defect.
In emetropy, light rays/radiation are focused directly on the retina. In myopia, the eyeball is too long, and the light rays are focused at a point in front of the retina. Nearby objects can be clearly seen, but remote objects require divergent lenses to be placed in front of the eye.
In hypermetropy, the eyeball is too short and therefore convergent lenses are used to compensate for the refractive power of the eye.
In astigmatism, the surface of the cornea is not perfectly spherical, requiring for correction cylindrical lenses. Towards the middle age, presbiopia develops, as the lens becomes unable to increase its refractive power to accommodate nearby objects.
To compensate for presbiopia, the emetropic patient should use reading glasses. The patient who already wears eyeglasses for remote correction usually switched to bifocal lenses. The only exception is the myopia, which can clearly see up close by simply removing the glasses for remote correction.
Refractive vices usually develop slowly and remain stable after adolescence, except in unusual situations. For example, the acute onset of diabetes mellitus can suddenly cause myopia, due to fluid inhibition and swelling of the lens, induced by hyperglycaemia. Testing vision through a punctuform orifice is a useful method for rapid detection of refractive defects. If visual acuity is better through a point hole than with the naked eye, the patient needs a serious research of refraction.
Another landmark is visual acuity. The Snellen map is used to test visual acuity at a distance of 6 meters. For convenience, a scale version of the Snellen map, called the Rosenbaum table, is used, 36 centimeters from the patient. All subjects should be able to read the 6/6 meter line with each eye using the appropriate refraction correction. Patients who need reading glasses should wear these glasses for the accuracy of the examination.
If the acuity of 6/ 6 is not present in each eye, the vision defect must be explained. In the case of a flash of less than 6/ 240, the ability to count fingers, to detect hand movements or to perceive bright light should be assessed. The degree of generally accepted cetate is defined as the best corrected acuity of 6/ 60 or less in the healthy eye, or a binocular field of vision narrowed to 20 degrees or less. Motor vehicle laws vary from state to state, but most require a corrected acuity of 6/12 in at least one eye. Patients with eponymous hemianopsia cannot drive.
Pupils should be individually tested in low light, with the patient staring at a distant target. If the pupils react promptly to light, there is no need to check the response for closeness, as isolated loss of contraction (myosis) for accommodation does not occur.
For this reason, the abbreviation PERRLA (Equal, Round and Reactive To Light and Accommodation) implies unnecessary effort in the last stage. However, if the response to light is weak or absent, it is important to test the response for closeness. Dissociation between adaptation to light and adaptation for close vision occurred in neurosyphilis (Argyll Robertson pupil), lesions of the dorsal mesencephalus (obstructive hydrocephalus, tumors of the pineal region) and after aberrant regeneration (oculomotor nerve paralysis, atonic pupil Adie).
An eye that does not perceive light does not show a pupillary response to direct light stimulation. If the retina or optic nerve are only partially damaged, the direct pupil response will be weaker than the consensual pupil response evoked by stimulating the other eye with a bright light. This relatively related pupil defect (Marcus Gunn pupil) can be evoked by the alternating light test. It is an extremely useful sign in retrobulbar optic neuritis and other disorders of the optic nerve, in which it may be the only objective sign of the disease. Fine inequality of pupil sizes, up to 0.5 mm, is quite common in normal subjects.
The diagnosis of essential or physiological anisocoria is safe as long as the relative pupil asymmetry remains constant under conditions of variable ambient illumination. Anisocoria that amplifies in low light indicates a sympathetic paralysis of the dilator muscle of the iris. Myosis triad, ipsilateral palpebral ptosis and anhydrosis form Horner syndrome, although anhydrosis is often absent.
Strokes in the brain stem, carotid dissection or neoplasms affecting the sympathetic chain are occasionally identified as causes of Horner syndrome, but most cases are idiopathic. Anisocoria that amplifies in bright light suggests parasympathetic paralysis.
The first cause to be suspected is oculomotor nerve paralysis. This possibility is excluded if the eye movements are complete and the patient does not have ptosis or diplopia. Acute pupil dilation (midriasis) can occur as a result of damage to the ciliary ganglion in the orbit. The usual mechanisms are by infection (herpes zoster, influenza), trauma (closed, penetrating, surgical) or ischemia (diabetes, temporal arteritis).
After denervation of the holy iris, the pupil does not respond correctly to light, but the adaptation for close-up vision is often relatively intact. If the nearby stimulus is removed, the pupil expands again very slowly compared to the normal pupil, hence the term tonic pupil.
In Adie syndrome, the tonic pupil is associated with weak or absent tendinous reflexes in the lower extremities. This benign condition, which occurs predominantly in healthy young women, is thought to represent moderate disautonomy. Tonic pupils are also associated with Shy-Drager syndrome, segmental hypohidrosis, diabetes and amyloidosis. Occasionally a tonic pupil is discovered by chance in an otherwise completely normal and asymptomatic patient.
The diagnosis is confirmed by the application of a diluted pilocarpine drop to each eye. Hypersensitivity of denervation produces pupillary constriction to a tonic pupil, while the normal pupil shows no reaction. Pharmacological dilation following accidental or deliberate instillation of anticholinergic agents (atropine drop, scopolamine) in the eye may also produce pupil mydriasis. In this situation, normal concentration pilocarpine (1%) does not cause constriction.
Both pupils are equally influenced by systemic medication. They are myotic in the case of the use of narcotics (morphine, heroin) and mydriatic in the case of the use of anticholinergics (scopolamine). Parasympathetic agents (pilocarpine, demecarium bromide) used to treat glaucoma, produce myosis.
In any patient with an unexplained pupillary abnormality, slot examination helps to exclude a surgical trauma of the iris, an occult foreign body, a perforation injury, intraocular inflammation, adhesions (sinechia), closed-angle glaucoma and rupture of the iris sphincter following closed trauma.
Ready for today! Prepare your sight for tomorrow's Light Holidays!
Dorin, Merticaru