logging in or signing up 6th lecture optom.rawaa Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 623 Category: Education License: All Rights Reserved Like it (1) Dislike it (0) Added: September 10, 2010 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript Slide 1: Optometry Dep. Al Nasser Eye Hospital BY DR. AMER ISMAIL ABU IMARA JORDANIAN BOARD OF OPHTHALMOLOGY I.C.O. PALESTINIAN BOARD IN OPHTHALMOLOGY STRABISMUS Slide 2: Is characterized by the ability to fuse the images from the two eyes and to perceive binocular depth . SENSORY FUSION :involves the integration by the visual areas of the cerebral cortex of two similar images , one from each eye , into one image . It may be central , which integrate the image falling on the foveae , or peripheral , which integrates parts of the image falling outside the foveae . BSV Slide 3: It is possible to maintain fusion with a central visual deficit in one eye, but peripheral fusion is essential to BSV and may be affected in patients with field loss as in advanced glaucoma . - MOTOR FUSION : involves the maintenance of motor alignment of the eyes to sustain bifoveal fixation . It is driven by retinal image disparity ,which stimulates fusional vergences . Slide 4: Involves disjugate eye movements to overcome retinal image disparity . Fusional vergence amplitudes can be measured with prisms or in the synoptophore . Normal values are : Convergence : about 15-20 ∆ for distance and 25 ∆ for near . Divergence : about 6-10 ∆ for distance and 12-14 ∆ for near . FUSIONAL VERGENCE Slide 5: Vertical : 2-3 ∆ Cyclovergence : about 2-3 ° Fusional convergence helps to control an exophoria whereas fusional divergence helps to control an esophoria . The fusional vergence mechanism may be decreased by fatigue or illness , converting a phoria to a tropia . The amplitude of fusional vergence mechanisms can be improved by orthoptic exercises , particularly in the case of near fusional convergence for the relief of convergence insufficiency . Slide 6: Is the perception of depth ( the third dimension , the first two being the height and width ). It arises when objects behind and in front of the point of fixation ( but within Panum fusional space ) stimulate horizontally disparate retinal elements simultaneously . The fusion of such disparate images results in a single visual impression perceived in depth . A solid object is seen stereoscopically ( in 3D ) because each eye sees a slightly different aspect of the object . STEREOPSIS Slide 8: At the onset of a squint two sensory perceptions arise based on the normal projection of the retinal areas stimulated : Confusion and pathological diplopia may result . These require simultaneous ( visual ) perception i.e. the ability to perceive images from both eyes simultaneously . SENSORY PERCEPTIONS Slide 9: Is the simultaneous appreciation of two superimposed but dissimilar images caused by stimulation of corresponding retinal points ( usually the foveae ) by images of different objects . CONFUSION Slide 10: Is the simultaneous appreciation of two images of the same object in different positions and results from images of the same object falling on non- corresponding retinal points . - In esotropia the diplopia is homonymous (uncrossed ). - In exotropia the diplopia is heteronymous ( crossed ). PATHOLOGICAL DIPLOPIA Slide 12: The ocular sensory system in children has the ability to adapt to anomalous states ( confusion and diplopia ) by two mechanisms : A- suppression B- abnormal retinal correspondence . These occur because of the plasticity of the developing visual system in children under the age of 7-8 years . Occasional adults who develop sudden – onset strabismus are able to ignore the second image after a time and therefore do not complain of diplopia . SENSORY ADAPTATION TO STRABISMUS Slide 13: Involves active inhibition , in the visual cortex , of an image from one eye when both eyes are open . Stimuli for suppression include diplopia , confusion and a blurred image from one eye resulting from astigmatism / anisometropia . Clinically , suppression may be : 1- CENTRAL OR PERIPHERAL in central suppression the image from the fovea of the deviating eye is inhibited to avoid confusion . Diplopia on the other hand , is eradicated by the process of peripheral suppression , in which the image from the peripheral retina of the deviating eye is inhibited . SUPPRESSION Slide 14: 2-MONOCULAR OR ALTERNATING suppression is monocular when the image from the dominant eye always predominate over the image from the deviating eye ( or more ametropic ) eye , so that the image from the latter is constantly suppressed . This type of suppression leads to amblyopia . When suppression alternates ( switches from one eye to the other ) amblyopia does not develop . Slide 15: 3- FACULTATIVE OR OBLIGATORY facultative suppression occurs only when the eyes are misaligned . Obligatory suppression is present at all times , irrespective of whether the eyes are deviated or straight . Examples are seen in intermittent exotropia and Duane syndrome . Slide 16: Is a condition in which non-corresponding retinal elements acquire a common subjective visual direction , i.e. fusion occurs in the presence of a small angle manifest squint . The fovea of the fixating eye is thus paired with a non- foveal element of the deviated eye . ARC is a positive sensory adaptation to strabismus ( as opposed to suppression ) , which allows some anomalous binocular vision in the presence of a heterotropia . Binocular responses in ARC are never as good as in normal bifoveal BSV . ARC is most frequently present in small angle esotropia ( microtropia ) associated with anisometropia . ABNORMAL RETINAL CORRESPONDENCE Slide 17: Is a small angle squint ( < 10 ∆ ) in which stereopsis is present but reduced and there is a relative amblyopia of the more ametropic eye . Microtropia has two forms : A- in microtropia with identity the point used for monocular fixation by the squinting eye also corresponds with the fovea of the straight eye under binocular viewing conditions . Therefore on cover test there is no movement of the squinting eye when it takes up monocular fixation . MICROTROPIA Slide 18: B- in microtropia without identity the monocular fixation point of the squinting eye does not correspond with the fovea of the straight eye in binocular viewing . There is therefore a small movement of the deviating eye when it takes up monocular fixation on cover testing . ARC is less common in accommodative esotropia because of the variability of the angle of deviation , or in large angle deviations , because the separation of the images is too great . Slide 19: The fovea of the squinting eye is suppressed to avoid confusion. Diplopia will occur , since non- corresponding retinal elements receive the same image . To avoid diplopia , the patient will develop either peripheral suppression of the squinting eye or ARC . If constant unilateral suppression occurs this will subsequently lead to strabismic amblyopia . CONSEQUENCES OF STRABISMUS Slide 20: Motor adaptation involves the adoption of an abnormal head posture (AHP ) and occurs primarily in children with congenitally abnormal eye movements who use the AHP to maintain BSV. In these children loss of an AHP may indicate loss of binocular function and the need for surgical intervention . These patients may present in adult life with symptoms of decompensation , often unaware of their AHP . MOTOR ADAPTATION TO STRABISMUS Slide 21: Acquired paretic strabismus in adults may be consciously controlled by an AHP provided the deviation is neither too large nor too variable with gaze ( incomitance ). The AHP eliminates diplopia and helps to centralize the binocular visual field . The patient will turn the head into the direction of the field of action of the weak muscle , so that the eyes are then automatically turned the opposite direction and as far as possible away from its field of action ( i.e. the head will turn where the eye cannot ). Slide 22: An AHP is analyzed in terms of the following three components : Face turn to right or left . Head tilt to right or left . Chin elevation or depression . 1- A face turn will be adopted to control a purely horizontal deviation . For example , if the left lateral rectus is paralyzed , diplopia will occur in left gaze ; the face will be turned to the left which deviates the eyes to the right , away from the field of action of the weak muscle and area of diplopia . A face turn may also be adopted in a paresis of a vertically acting muscle to avoid the side where Slide 23: The vertical deviation is greatest ( e.g. in a right superior oblique weakness the face is turned to the left ) . 2- a head tilt is adopted to compensate for torsional and / or vertical diplopia . In left superior oblique weakness the left eye is relatively elevated and the head is tilted to the right , toward the hypotropic eye ; this reduces the vertical separation of the diplopic images and permits fusion to be regained . Slide 24: If there is a significant torsional component preventing fusion , tilting the head in the same left direction will reduce this by invoking the righting reflexes ( placing the extorted right eye in a position which requires extorsion ) . 3- chin elevation or depression may be used to compensate for weakness of an elevator or depressor muscle or to minimize the horizontal deviation when A or V pattern is present . Slide 25: It is also important to know what therapy was necessary in other family members. 7- PREVIOUS OCULAR HISTORY including prescription and compliance with spectacles or occlusion , previous surgery or prism is important to future treatment options and prognosis . You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.