Downloaded 10 times
More Related Content
Similar to Vertical Deviation.pptx
Vertical Deviation.pptx
- 1. Vertical Deviation Meenakshi N MOptom 2nd year
- 2. Vertical Deviation VerticalStrabismus refers to a vertical misalignment of the visual axis Less Common than horizontal Most commonly associated with horizontal deviations Also said to have associations with motility disorders 43% of exotropia’ s are resulting in vertical strabismus It can be hyper or hypotropia (Non fixating eye upper/lower than the fixating eye) 6/26/2023 vertical deviation 2
- 3. Classification Concomitant Incomitant Refractive Restrictive Obliquemuscle dysfunction Paralytic SO overaction IO overaction • 4th nerve palsy • 3rd nerve palsy • IO palsy • DEP/DDP • Ophthalmoplegia Misdirected muscle Mechanical restriction 6/26/2023 vertical deviation 3
- 4. Restrictive Misdirected muscle Mechanicalrestriction Structural adhesions Tight EOM Lesions CCDD EOM placements • Duane • C. Fibrosis • Mobius • Browns • TED • Blow out fracture • MED • Strabismic fixus Tumors • Post Op • Scarring 6/26/2023 vertical deviation 4
- 5. Concomitant – verticalstrabismus Concomitant vertical misalignment of a few diopters is not a rare occurrence Good fusional Vergence overcome the deviation, resulting in fusion Also associated with horizontal deviations Can be hyper or hypo Idiopathic in many cases Orbital asymmetry associated with facial and cranial bone disorders can cause a vertical strabismus Eg : Plagiocephaly caused by the cranial dysostosis. 6/26/2023 vertical deviation 5
- 6. Also surgicalcomplication can be one of the cause Refractive associations are seen It is intermittent Suppression, amblyopia, ARC can occur Treatment Orthoptics at primary level Prisms up to 10D Surgery 6/26/2023 vertical deviation 6
- 7. Incomitant – verticalstrabismus Oblique muscle dysfunction IO overactions SO overactions IO overactions Up shoot of eye Cause : idiopathic mostly Primary cause : mechanical/ innervational/ or both Secondary cause : paralysis 6/26/2023 vertical deviation 7
- 8. Clinical Features Onset: primary : 2 – 3 yrs (bilateral) secondary : any age (unilateral or bilateral) Associations Horizontal D : primary : associated secondary : isolated Vertical D : primary : yes with <5PD secondary : yes with 10 – 22PD or more Head tilt : primary : - secondary : + 6/26/2023 vertical deviation 8
- 9. Also bothprimary and secondary deviations are associated with excyclodeviation Up shoot on adduction (adducted eye over shoots / abducted eye fixates) 6/26/2023 vertical deviation 9
- 10. Forced ductiontest : + DD : DVD Treatment : surgery – weakening procedure Recurrence is common complication 6/26/2023 vertical deviation 10
- 11. Incomitant – verticalstrabismus SO overactions Down shoot of eye Cause : idiopathic mostly Primary cause : mechanical/ innervational/ or both Secondary cause : paralysis or in association with Browns, Duanes 6/26/2023 vertical deviation 11
- 12. Clinical Features Onset: primary : 2 – 3 yrs (bilateral) secondary : any age (unilateral or bilateral) Associations Horizontal D : primary : associated secondary : isolated Vertical D : primary : + secondary : - Head tilt : primary : - secondary : + towards affected side 6/26/2023 vertical deviation 12
- 13. Here incyclodeviationis seen FDT : + Treatment : surgery – weakening procedure 6/26/2023 vertical deviation 13
- 14. Third nerve palsy– paralysis Oculomotor nerve Entirely motor in function Third nerve supplies EOM - medial rectus, superior rectus, inferior rectus, inferior oblique IOM - sphincter pupillae and ciliary muscle Levator palpebrae superioris 6/26/2023 vertical deviation 14
- 15.
- 16. Nucleus locatedin midbrain at the level of superior colliculus, ventral to the sylvian aqueduct. Composed of Unparied levator subnucleus Paired superior rectus subnuclei Paired medial rectus ,inferior rectus and inferior oblique subnuclei 6/26/2023 vertical deviation 16
- 17.
- 18.
- 19. Course Fascicular Basilar Intracavernous Intraorbital part Pupillomotor fibres 6/26/2023 vertical deviation 19
- 20. Pupillary associations Parasympatheticfibers Located superficially between the brainstem and the cavernous sinus Main trunk of 3rd nerve supplied by the vasa nervorum Pupillary part by post. Communicating artery 6/26/2023 vertical deviation 20
- 21.
- 22. Third nerve palsy Eye is down and out With hypo and large exo No movement medially and superiorly No accommodation Triad Ptosis Pupillary dilatation No accommodation 6/26/2023 vertical deviation 22
- 23. Etiology Congenital (inchildren) Birth Trauma Congenital disorder Viral infections Acquired (in adult) Intracranial aneurysm Rarely tumor Diabetes Mellitus Hypertension Trauma Migraine Giant cell arteritis syphilis 23 6/26/2023 vertical deviation
- 24. Symptoms of thirdnerve palsy Drooping of eyelid Double vision Eye pain (may be present) Headache vertical deviation 24 6/26/2023
- 25. Signs Ptosis EOMrestriction Normal Abduction Intorsion (in down gaze) Limitation of adduction Limitation of elevation Limitation of depression Dilated pupil with defective accommodation vertical deviation 25 6/26/2023
- 26.
- 27.
- 28.
- 29. Treatment Non surgical Treatthe underlying cause Diplopia - occlusion patch Prism in involved eye Monitor children for development of amblyopia Botulinum toxin Surgical If it is Complete 3rd nerve palsy LR recession and MR resection Anchoring of the globe on medial wall periosteum 6/26/2023 vertical deviation 29
- 30.
- 31. 4th Cranial nerve- Trochlear nerve 6/26/2023 vertical deviation 31
- 32. Trochlear nerve palsy Thinnest and long one - 75mm. Supplies only the SO in eye Only CN that comes out from the dorsal aspect of the brainstem. Only CN that crosses completely to the opposite side. Thus originates from the contralateral nucleus. Nucleus lies at the level of the inferior colliculus 6/26/2023 vertical deviation 32
- 33. Course and Distribution 1.Nucleus 2. Fasciculus 3. Trunk 4. Intracavernous 5. Intraorbital 6/26/2023 vertical deviation 33
- 34. Intracavernous partof CN IV runs in the lateral wall of the sinus inferior to CN III and above the 1st division of CN V Also meets 4 CN Then leaves the sinus at the level of superior orbital fissure lateral to annulus of zinn Travels temporal and inferior to innervate the superior oblique muscle – Intraorbital part 6/26/2023 vertical deviation 34
- 35. Causes of isolatedfourth nerve palsy Idiopathic lesions are common, and many of these are thought to be congenital although symptoms may not develop until decompensation occurs in adult life due to reduced fusional ability. In contrast - acquired lesions patients are not usually aware of the torsional aspect, but may develop vertical double vision Examination of old photographs for the presence of a compensatory head posture may be helpful, as is the presence of an increased vertical prism fusional range. 6/26/2023 vertical deviation 35
- 36. Trauma frequentlycauses bilateral fourth nerve palsy. The long and slender nerves are particularly vulnerable as they decussate in the anterior medullary velum, through impact with the tentorial edge. Microvascular lesions are relatively common Aneurysms and tumours are extremely rare. 6/26/2023 vertical deviation 36
- 37. Signs and symptoms The acute onset of vertical diplopia in the absence of ptosis, combined with a characteristic head posture, strongly suggests fourth nerve disease. Peripheral lesions cause ipsilateral and nuclear lesions contralateral superior oblique weakness Signs Left hypertropia (‘left over right’) in the primary position and increasing on right gaze 6/26/2023 vertical deviation 37
- 38. Limitation ofleft depression, most marked in adduction Left extorsion, greatest in abduction. Normal abduction of the left eye Normal elevation of the left eye A compensatory head posture Always unilateral if bilateral involvement seen should be because of head trauma 6/26/2023 vertical deviation 38
- 39.
- 40. Investigation Vascular investigationis sometimes indicated; neuroimaging is not required routinely for an isolated non-progressive fourth nerve palsy, but should be considered if improvement does not occur. Park three step Double Maddox – in unilateral cyclodeviation is less than 10 deg where as in bilateral its > 10 deg Hess chart 6/26/2023 vertical deviation 40
- 41. Double Maddox test 6/26/2023 verticaldeviation 41
- 42.
- 43.
- 44.
- 45.
- 46. Treatment Microvascular palsiescommonly resolve spontaneously Up to 10D prisms can be used Underlying cause to be known and treated Then surgery is the option – weakening or tucking procedure done 6/26/2023 vertical deviation 46
- 47. 6th Cranial nerve- Abducent nerve 6/26/2023 vertical deviation 47
- 48. Sixth nerve palsy 6th cranial nerve entirely motor in function It supplies the lateral rectus muscle Abduction of the eye The nucleus of the sixth nerve lies at the mid-level of the pons, ventral to the floor of the fourth ventricle 6/26/2023 vertical deviation 48
- 49. Course and Distribution 1.Nucleus 2. Fasciculus 3. sub arachnoid space 4. petrous part 5. Intracavernous 6. Intraorbital 6/26/2023 vertical deviation 49
- 50. The intracavernoussection runs below the third and fourth, and the first division of the fifth nerves Then leaves the sinus at the level of superior orbital fissure superior to annulus of zinn Travels to innervate the lateral rectus muscle – Intraorbital part 6/26/2023 vertical deviation 50
- 51. 6th nerve palsy- causes 6/26/2023 vertical deviation 51
- 52. It canbe congenital (rare) or acquired (common). Can be unilateral or bilateral 6th nerve palsy. Occasionally, intracavernous sixth nerve palsy is accompanied by a postganglionic Horner syndrome due to damage to the paracarotid sympathetic plexus. The causes of intracavernous sixth nerve and third nerve lesions are similar. 6/26/2023 vertical deviation 52
- 53. Sixth nerve palsy Total palsy ( paralysis ) Partial palsy (paresis) Presenceof abduction past the midline Failure of abduction past the midline Failure of abduction past the midline Sclera is visible on L gaze
- 54. Signs and symptoms Double vision is characteristically worse for a distant target and less or absent for near fixation Should look for about other neurological symptoms, giant cell arteritis, trauma and symptoms of ear disease Esotropia in the primary position Limitation of abduction on the side of the lesion Normal adduction of the affected eye A compensatory face turn 6/26/2023 vertical deviation 54
- 55.
- 56. Investigation Routines FDT Vascular data Diplopia charting Hess chart Neuro imaging is must done here 6/26/2023 vertical deviation 56 L R
- 57.
- 58. Treatment Observation withmonocular occlusion or prismatic correction of diplopia is appropriate or even head tilt is allowed In idiopathic and presumed microvascular lesions; up to 90% will recover spontaneously, usually over weeks to several months. Young children should be treated with alternate patching to prevent amblyopia Botulinum toxin injection Surgery should be considered only when adequate time has been allowed for maximal spontaneous recovery say 6 – 12 months 6/26/2023 vertical deviation 58
- 59.
- 60.
- 61. IO palsy Isolatedinferior oblique palsy (IOP) is a rare clinical entity and the least frequent palsy among all those involving the 6 extraocular muscles. The main clinical features of isolated IOP consist of hypotropia and under elevation in adduction of the affected eye, along with absence of restriction on forced duction testing The inferior oblique muscle is innervated by the inferior branch of oculomotor nerve Unlike superior oblique palsy, isolated IOP palsy is inherently troubling 6/26/2023 vertical deviation 61
- 62. Clinically, apatient exhibits limitations of elevation in adduction Brown syndrome is strongly suggested, but here a positive forced duction test which differentiates it from IOP The possible etiology for this condition may be congenital or acquired. The acquired basis for this condition can result from damage of the inferior oblique nucleus or terminal branches of the oculomotor nerve serving only the inferior oblique, or direct inferior oblique muscle injury, such as orbital trauma, vascular lesion or myasthenia gravis But mostly remains to still understand over it 6/26/2023 vertical deviation 62
- 63. Investigation Only MRIcould help The diagnostic criteria for isolated IOP: 1. Presence of hypotropia and under elevation in adduction of the affected eye 2. FDT : - 3. Vertical deviations increased on gaze to the unaffected side 4. Incyclotorsion in one or both eyes 5. Increased hypotropia in contralateral head tilt 6. A head tilt toward the paralytic side, face rotation to the unaffected side and an elevated chin. 6/26/2023 vertical deviation 63
- 64. Treatment Observation 6– 12 months Patching if sensory adaptations Prisms Weakening of the ipsilateral superior oblique muscle and/or contralateral superior rectus recession often resulted in favorable surgical outcomes with a surgical success rate of 61.5%. 6/26/2023 vertical deviation 64
- 65. Differences 6/26/2023 vertical deviation 65 Inferior ObliqueMuscle Palsy Brown Syndrome Forced ductions Negative Positive Strabismus pattern A pattern V pattern Superior oblique muscle overaction Usually present None or minimal
- 66. DEP/DDP Monocular elevationdeficiency (MED) is defined as the inability to elevate one eye equally in abduction, adduction, and primary gaze. MED was originally termed double elevator palsy (DEP) when the disorder was thought to be caused by paresis of the two eye elevators, the superior rectus (SR) and inferior oblique (IO) When the sound eye is fixed, the paralyzed eye appears to be hypotropic and pseudoptotic. When the paralyzed eye is fixed, the ptosis disappears, and the sound eye appears to be hypertropic. 6/26/2023 vertical deviation 66
- 67. Pseudoptosis maycover the true vertical deviation, leading clinicians to misdiagnose it as congenital ptosis and then to perform a ptosis correction surgery This entity is not known to be hereditary (inherited). It is a rare condition, and can be congenital (present at birth) or acquired after birth. Treatment : only surgery 6/26/2023 vertical deviation 67
- 68. DDP Similar tothat this is monocular depressor deficiency Either be palsy or even by restriction Etiology is still not clear Simultaneous paralysis of IR & SO in same eye Hypertropia is seen in primary gaze It shows reduced depression in field of gazes Treatment : again surgical process 6/26/2023 vertical deviation 68
- 69. Ophthalmoplegia Ophthalmoplegia :paralysis of the muscles within or surrounding the eye Chronic progressive external ophthalmoplegia (CPEO) usually begins in childhood with: Ptosis Slowly progresses to total paralysis of the eyelids and extraocular muscles CPEO may be sporadic Although a true Pigmentary retinal dystrophy usually is absent, constricted fields and electro diagnostic abnormalities can occur. 6/26/2023 vertical deviation 69
- 70. Affected individualshave to turn their head to see in different directions, especially as the ophthalmoplegia worsens. People with progressive external ophthalmoplegia may also have general weakness of the muscles used for movement (myopathy), particularly those in the neck, arms, or legs. The weakness may be especially noticeable during exercise Muscle weakness may also cause difficulty swallowing (dysphagia). Absence of bells phenomenon 6/26/2023 vertical deviation 70
- 71. Etiology isunclear but still defects in mitochondrial DNA have been found in some patients. (oxidative phosphorylation) The triad of : Retinal pigmentary changes CPEO Cardiomyopathy (especially heart block) is called Kearns-Sayre syndrome Treatment options are limited. Cautious surgical elevation (suspension) of the upper eyelids indicated to lessen a severe chin-up head position.
- 72. Total Ophthalmoplegia Totalophthalmoplegia thus refers to the paralysis of all the muscles in the eye, which in turn results in ptosis, immobility of the eye, dilated non reacting pupil and loss of accommodation. The condition may be myopathic, that means the muscles controlling eye movement are directly involved or neurogenic, that means the nerve pathways controlling eye muscles are affected 6/26/2023 vertical deviation 72
- 73. Causes Multiple sclerosis Progressivesupranuclear palsy, Thyroid disease, Diabetes mellitus, Brainstem tumours, Pituitary stroke, Myasthenia gravis 6/26/2023 vertical deviation 73
- 74. Investigation The patient'smedical history, family history and detailed examination. In addition Computed tomography scan (CT scan) or magnetic resonance imaging (MRI) scan of the brain, orbit and sinuses are needed to rule out underlying sinus pathology, brain tumour, stroke, aneurysm, or multiple sclerosis. Other tests like hearing test (audiogram) and the Tensilon (edrophonium) test should be done in suspected cases. Thyroid disease and diabetes mellitus should be excluded by appropriate blood test. 6/26/2023 vertical deviation 74
- 75. Treatment Underlying cause Relieving diplopia Monitoring exposure keratitis Surgery for cause 6/26/2023 vertical deviation 75
- 76.
- 77. CCDDs - CongenitalCranial dysinnervation disorders A number of well-defined syndromes characterized by congenital limitation of eye movements from abnormal innervation or miswiring of EOM have recently been grouped as the congenital Cranial dysinnervation disorders Congenital disorders resulting from aberrant innervation of the ocular and facial musculature They are • Duane – HD of ocular motility • C. Fibrosis - HD of ocular motility • Mobius - facial motility and ocular abduction deficit 6/26/2023 vertical deviation 77
- 78. Duanes Which occurdue to result of developmental errors in the innervation of ocular and facial muscles Congenital non progressive ocular motility defect. It was first described by Stilling and Turk. The syndrome is characterized by limitation or absence of abduction and/or adduction of the eyes. There is also retraction of the globe and narrowing of the palpebral fissure on adduction, which is often associated with elevation or depression of the globes. 6/26/2023 vertical deviation 78
- 79. Etiology Pathological studiesof DRS have provided clear evidence that innervational deficiencies can cause fibrotic muscle changes. Most cases are due to innervational defects, which correlate with aplasia of the sixth nerve nucleus and the VI cranial nerve itself Autosomal dominant DRS- CHN1 gene mutation 6/26/2023 vertical deviation 79
- 80. Hubers classification TypeI : due to agenisis of 6th nerve Esotropia on primary gaze Limitation / absence of abduction Normal / slightly defective adduction Narrowing of palpebral fissure & retraction of globe on adduction Widening of fissure on abduction. Head tilt in direction of duanes eye 6/26/2023 80
- 81.
- 82. Type II: both 3rd and 6th nerve supplies LR – strong innervation Exotropia seen Limitation / absence of adduction Normal / slightly defective abduction Narrowing of PF & retraction of globe on attempted adduction 6/26/2023 vertical deviation 82
- 83. Type III Limitation /absence of both abduction & adduction of affected eye Retraction of globe & narrowing of PF on attempted adduction. No eso or exo Equal innervation to MR/LR No AHP Upsoots and downshoots are associated with duanes irrespective of its type 6/26/2023 vertical deviation 83
- 84. Associations Associated ocularanomalies- Nystagmus, anisocoria, aniridia, epibulbar dermoid, ptosis, optic nerve coloboma, marcus gunn jaw wink. Non ocular anomalies- Skeletal - limb hypoplasia, polydactyly, hypoplastic/absent radius. Vertebral – scoliosis, spina bifida Genito-urinary defects - renal agenesis Cardiac anomalies - Auricular septal defect. 6/26/2023 vertical deviation 84
- 85. Treatment The valueof botulinum injection into the medial rectus muscle to improve abduction is controversial Surgical treatment 6/26/2023 vertical deviation 85
- 86. Congenital fibrosis ofEOM Congenital fibrosis of the extraocular muscles (CFEOM) describes a group of rare congenital eye movement disorders that result from the dysfunction of all or part of the oculomotor (CN 3) and the trochlear (CN 4) nerves, and/or the muscles these nerves innervate. Etiology : Recently, CFEOM has been accepted to be of neurogenic origin rather than primary muscle pathology. α motor neurons of sup. division of III are present very early in development, but disappear later (apoptosis, necrosis) 6/26/2023 vertical deviation 86
- 87. Causes These disordershave been classified as CFEOM1, CFEOM2, and CFEOM3 based on ophthalmologic findings and molecular genetic testing. CFEOM 1 and CFEOM 3 are inherited as autosomal dominant genetic conditions. (abnormal gene) CFEOM 2 and Tukel syndrome are inherited as autosomal recessive genetic conditions CFEOM3 can be characterized by additional involvement of the peripheral and central nervous system in addition to the eye findings. Tukel syndrome is characterized by missing and webbed fingers and toes in addition to the eye findings. These disorders do not worsen over time. 6/26/2023 vertical deviation 87
- 88. C/F Affected individualshave limited ability to move their eyes vertically (upward and downward) and can have variable limitations in moving their eyes horizontally. CFEOM is also frequently associated with droopy eyelids (ptosis) and eyes that are fixed in an abnormal position. Eyes fixed in a downward position, and elevation of the chin is seen. 6/26/2023 vertical deviation 88
- 89.
- 90. Management Molecular testis required here Routines The standard management of CFEOM may involve surgery Non surgical management Correction of refractive error Treatment of amblyopia, Surgical management- Correction of hypotropia, exotropia followed by ptosis correction 6/26/2023 vertical deviation 90
- 91. Mobius syndrome Mobiussyndrome is an extremely rare congenital neurological disorder which is characterized by facial paralysis and the inability to move the eyes from side to side. Moebius syndrome is caused by the absence or underdevelopment of the 6th and 7th cranial nerves, which control eye movement and facial expression It is thought to result from a vascular disruption (temporary loss of blood flow) in the brain during prenatal development. The use of drugs and a traumatic pregnancy may also be linked to the development 6/26/2023 vertical deviation 91
- 92. C/F Most likely,Moebius syndrome is multifactorial, which means that both genetic and environmental factors play some causative role Dental issues Weak muscle tone (hypotonia) Abnormal curvature of the spine (scoliosis) Respiratory disorders Sleep problems Upper body weakness which can lead to delays in motor function Ear abnormalities - Hearing loss (if certain cranial nerves are affected) 6/26/2023 92
- 93.
- 94.
- 95. Diagnosis A diagnosisof Moebius syndrome is based upon the characteristic signs/symptoms, a detailed patient history, and a thorough clinical evaluation. There are no diagnostic tests that confirm a diagnosis of Moebius syndrome. Some specialized tests may be performed to rule out other causes of facial palsy. GTR done, CT Scanning, MRI, and Ultrasonography Diagnostic Criteria Paralysis or weakness of at least one side of the face (usually both) Sideways movement of the eyes is paralyzed Vertical movement of the eyes is intact 6/26/2023 vertical deviation 95
- 96. Management Each personwith Moebius syndrome will have different needs. While there's no definitive treatment or cure for the condition, a multi model approach is needed Since the diagnosis can usually be made at birth or soon after, early interventions, such as physical, occupational, and speech therapy can be made early. A thorough eye exam to address vision problems. Squint surgery If hearing is impaired, an audiologist may be consulted. 6/26/2023 vertical deviation 96
- 97.
- 98. Restrictive Misdirected muscle Mechanicalrestriction Structural adhesions Tight EOM Lesions CCDD EOM placements • Duane • C. Fibrosis • Mobius • Browns • TED • Blow out fracture • MED • Strabismic fixus Tumors • Post Op • Scarring 6/26/2023 vertical deviation 98
- 99.
- 100. Tight EOM –Brown’s Brown syndrome was described by Harold W. Brown in 1950 as the superior oblique tendon sheath syndrome. Brown syndrome is a condition involving mechanical restriction, typically of the superior oblique tendon. It is usually congenital but occasionally acquired 6/26/2023 vertical deviation 100
- 101. Causes Congenital Idiopathic. ‘Congenitalclick syndrome’ where there is impaired movement of the superior oblique tendon through the trochlea. Acquired Trauma to the trochlea or superior oblique tendon. Inflammation of the tendon, which may be caused by rheumatoid arthritis, pan sinusitis or scleritis. 6/26/2023 vertical deviation 101
- 102. Restriction of thesuperior oblique tendon at the trochlear pulley
- 103. Signs Usually straightwith BSV in the primary position Limited elevation in adduction Limited elevation on up gaze is common Normal elevation in abduction Absence of superior oblique overaction Rarely - Down-shoot in adduction. Hypotropia in primary position. CHP with chin elevation and ipsilateral head tilt 6/26/2023 vertical deviation 103
- 104.
- 105.
- 106. Brown syndrome OS Divergencein up gaze Down shoot in attempted elevation in adduction? Down shoot in attempted elev. in adduct. (different than IO palsy)
- 107. Treatment Congenital casesdo not usually require treatment as long as binocular function is maintained with an acceptable head posture Spontaneous improvement can be seen at the end of 1st decade of life Indications for treatment include significant primary position hypotropia, deteriorating control and/or an unacceptable head posture. The recommended procedure for congenital cases is lengthening of the superior oblique tendon. 6/26/2023 vertical deviation 107
- 108. Acquired: treatableaetiology should be addressed specifically. Depending on the cause, acquired cases may benefit from steroids, either orally or by injection near the trochlea. 6/26/2023 vertical deviation 108
- 109. TED – thyroideye diseases Thyroid eye disease (TED), also known as thyroid-associated orbitopathy and Graves ophthalmopathy, is a very common orbital disorder, and is the most common cause of both bilateral and unilateral proptosis in an adult Graves disease, the most common form of hyperthyroidism, is an autoimmune disorder in which IgG antibodies bind to thyroid stimulating hormone (TSH) receptors in the thyroid gland and stimulate secretion of thyroid hormones. It is more common in females 6/26/2023 vertical deviation 109
- 110. Presentation isoften in the fourth or fifth decades with symptoms including o Weight loss despite good appetite, o Increased bowel frequency, o Sweating, o Heat intolerance, o Nervousness, o Irritability, o Palpitations, o Weakness and fatigue 6/26/2023 vertical deviation 110
- 111.
- 112. May beassociated with other autoimmune disorders R/F Smoking Women are five times more likely to be affected by TED than men Radioactive iodine used to treat hyperthyroidism can worsen TED. Hyperthyroidism 94% Euthyroid 4% Hypothyroid 2% 6/26/2023 vertical deviation 112
- 113. Pathogenesis Circulating T cellsin patients with Graves’ disease directed against an antigen on thyroid follicular cells But these lymphocytes came to be directed against a self -antigen, escaping deletion by the immune system, is unknown An interaction between the activated CD4 T cells and local fibroblasts results in release of cytokines into the surrounding tissue They then develop the autoimmune response in the orbital connective tissue. 6/26/2023 vertical deviation 113
- 114. 6/26/2023 vertical deviation 114 Stimulate glycosaminoglycanproduction in fibroblasts, proliferation of fibroblasts, or both leading to the accumulation of glycosaminoglycan's and oedema in the orbital connective tissue. The increase in connective-tissue volume and the fibrotic restriction of extraocular-muscle movement resulting from fibroblast stimulation lead to the clinical manifestations of ophthalmopathy
- 115. Clinical features Lidsigns: Retraction of the upper lids producing the characteristic staring and frightened appearance (Dalrymple’s sign) Lid lag (von Graefe’s sign) Fullness of eyelids due to puffy oedematous swelling (Enroth’s sign); Difficulty in eversion of upper lid (Gifford’s sign); Infrequent blinking (Stellwag’s sign). Conjunctival signs. These include ‘deep injection’ and ‘chemosis’. Pupillary signs. These are of less importance and may be evident as inequality of dilatation of pupils. 6/26/2023 vertical deviation 115
- 116. Convergence weakness(Mobius’s sign) Exophthalmos Exposure keratitis and symptoms of ocular surface discomfort Optic neuropathy. It occurs due to direct compression of the nerve or its blood supply by the enlarged rectus muscles at the orbital apex. 6/26/2023 vertical deviation 116
- 117.
- 118. CT & MRI 6/26/2023 verticaldeviation 118
- 119.
- 120. Investigations Thyroid functiontests. These should include: serum T3, T4, TSH and estimation of radioactive iodine uptake. Positional tonometry. Ultrasonography. Computerised tomographic scanning 6/26/2023 vertical deviation 120
- 121. Treatment When Opticnerve compression Corneal exposure Diplopia Proptosis AHP Artificial tears Steroids Orbital decompression Eye muscle surgery Eyelid surgery 6/26/2023 vertical deviation 121
- 122. MED restrictive Itis thought to manifest primarily with a tight or contracted inferior rectus muscle or a hypo plastic or ineffective superior rectus muscle. 6/26/2023 vertical deviation 122
- 123.
- 124. Blow out fracture These are isolated comminuted fractures which occur when the orbital walls are pressed indirectly, ‘Blowout fractures’ mainly involve orbital floor and medial wall. A blow-out fracture of the orbital floor is typically caused by a sudden increase in the orbital pressure from an impacting object that is greater in diameter than the orbital aperture (about 5 cm), such as a fist or tennis ball, so that the eyeball itself is displaced and transmits rather than absorbs the impact Roof and lateral wall can withstand 6/26/2023 vertical deviation 124
- 125.
- 126. C/F Visual function,especially acuity, should be recorded and monitored as necessary, particularly in the acute situation. Periocular signs include variable ecchymosis, oedema and occasionally subcutaneous emphysema Severe pain Diplopia may be caused by one of the following mechanisms: Haemorrhage and oedema in the orbit may be a cause for restricting movement of the globe. Ocular motility usually improves as the haemorrhage and oedema resolve. 6/26/2023 vertical deviation 126
- 127.
- 128. Diplopia typicallyoccurs in both upgaze and downgaze. Forced duction and the differential intraocular pressure (IOP) test are positive Direct injury to an extraocular muscle, associated with a negative forced duction test. The muscle fibres usually regenerate and normal function often returns within about 2 months Enophthalmos may be present if the fracture is severe, and in the absence of surgical intervention, enophthalmos may continue to increase for about 6 months as post-traumatic orbital tissue degeneration and fibrosis develop 6/26/2023 vertical deviation 128
- 129. Investigations CT MRI Ocular routines and emergencies seen Hess chart 6/26/2023 vertical deviation 129
- 130.
- 131. 6/26/2023 vertical deviation 131 Hess chartof a left orbital floor blow-out fracture shows restriction of left upgaze (superior rectus and inferior oblique) and restriction on downgaze (inferior rectus). There is also secondary overaction of the right eye
- 132. Treatment Initial treatmentgenerally consists of observation, with the prescription of oral antibiotics; ice packs and nasal decongestants may be helpful The patient should be instructed not to blow nose, because of the possibility of forcing infected sinus contents into the orbit Steroids – if optic nerve is compressed Fractures involving up to one-half of the orbital floor, with little or no herniation, no significant enophthalmos and improving diplopia, also do not require treatment. 6/26/2023 vertical deviation 132
- 133. Fractures involvingmore than one-half of the orbital floor will usually develop significant enophthalmos if left untreated. Fractures with entrapment of orbital contents, enophthalmos of greater than 2 mm, and/or persistent and significant diplopia in the primary position should be repaired within 2 weeks. If surgery is delayed, the results are less satisfactory due to secondary fibrotic changes. 6/26/2023 vertical deviation 133
- 134. Very urgent surgicalindicative Enophthalmos White eyed fracture Age <18yrs Surgical repair is performed via a transconjunctival or subciliary incision or via the maxillary sinus, with elevation of the periosteum from the orbital floor, freeing of trapped orbital contents and repair of the bony defect with a synthetic implant. 6/26/2023 vertical deviation 134
- 135. Strabismic fixus Strabismusfixus is a rare condition in which both eyes are fixed by fibrous tightening of the medial recti (convergent strabismus) or the lateral recti (divergent strabismus) It can be Congenital and acquired forms This disease may progress over several years from a small degree of esotropia with free ocular movement to the end stage of large angle fixed esotropia. 6/26/2023 vertical deviation 135
- 136. Etiology The underlyingetiology of strabismus fixus still remains unclear . The most recent explanation is that the enlarged globe in high myopia herniates superotemporally and retroequatorially through the muscle cone Congenital : Congenital strabismus fixus is caused by fibrosis which explains loss of elasticity of medial rectus Lateral rectus palsy: Lateral rectus palsy causes the secondary contracture and fibrosis of medial rectus Amyloidosis: Infiltration of extraocular muscle by amyloid Others : Unspecific, progressive fibrosis, myopathy and myositis 6/26/2023 vertical deviation 136
- 137.
- 138. Signs symptoms Patientsare usually old aged, with high myopia, although few cases of strabismus fixus even in the absence of high myopia have been described Patients typically complain of there eyes being fixed and there inability to move the eyes outward Patients with bilateral strabismus fixus are severely handicapped, one usually is preferred for vision and immobility of eye necessitates an extreme degree of head turn in such patients 6/26/2023 vertical deviation 138
- 139. Investigations and Management FDT CT MRI Treatment is mainly surgical – resection with recessions carried out 6/26/2023 vertical deviation 139
- 140. Tumours Damage tothe muscles that move the eyes or the nerves that control eye movement can create a diplopia Eg : thyroid Stroke TIA Aneurysms Brain tumors Multiple sclerosis Trauma 6/26/2023 vertical deviation 140
- 141. Structural Adhesions PostOp complications : is most commonly attributed to extraocular muscle restriction or paresis from surgical trauma or anesthetic myotoxicity. Scarring : pulls nearby tissues 6/26/2023 vertical deviation 141
- 142.
- 143. ‘V’ or‘A’ patterns occur when the relative contributions of the superior rectus and inferior oblique to elevation, or of the inferior rectus and superior oblique to depression, are abnormal, resulting in derangement of the balance of their horizontal vectors in up and downgaze. They can also be caused by anomalies in the position of the rectus muscle pulleys. Assessment is by measuring horizontal deviations in the primary position, upgaze and downgaze. They can occur in both concomitant and Incomitant deviations. 6/26/2023 vertical deviation 143
- 144. V pattern A‘V’ pattern is said to be significant when the difference between upgaze and downgaze is ≥15 Δ. It also have subtypes or sub patterns Y pattern and Arrow 6/26/2023 vertical deviation 144
- 145. Causes Inferior obliqueoveraction associated with fourth nerve palsy. Superior oblique underaction with subsequent inferior oblique overaction, seen in infantile esotropia as well as other childhood esotropias. The eyes are often straight in upgaze with a marked esodeviation in downgaze. Superior rectus underaction. Brown syndrome. Craniofacial anomalies featuring shallow orbits and down-slanting palpebral fissures. 6/26/2023 vertical deviation 145
- 146. V pattern forESO & EXO ESO Increased deviation in downgaze With decreased deviation in upgaze Eg 10 PD : UP 20 PD : Primary position 30 PD : Down EXO Decreased deviation in downgaze With Increased deviation in upgaze Eg 30 PD : UP 20 PD : Primary position 10 PD : Down 6/26/2023 vertical deviation 146
- 147.
- 148.
- 149. V pattern SUBTYPES Ypattern Divergence in upgaze with change in deviation between primary and down gaze is seen Eg 30 PD : UP 15 PD : Primary position 10 PD : Down Arrow Convergence that largely occurs between down and primary gaze Eg 05 PD : UP 15 PD : Primary position 30 PD : Down 6/26/2023 vertical deviation 149
- 150. Treatment Treatment isby inferior oblique weakening or superior oblique strengthening when oblique dysfunction is present. Without oblique muscle dysfunction treatment is as follows: ‘V’ pattern esotropia can be treated by bilateral medial rectus recessions and downward transposition of the tendons. ‘V’ pattern exotropia can be treated by bilateral lateral rectus recessions and upward transposition of the tendons. 6/26/2023 vertical deviation 150
- 151. A pattern A‘a’ pattern is said to be significant when the difference between downgaze and upgaze is ≥15 Δ. It also have subtypes or sub patterns Lamda pattern and X pattern 6/26/2023 vertical deviation 151
- 152. Causes Primary superioroblique overaction is usually associated with exo deviation in the primary position of gaze. Inferior oblique underaction/palsy with subsequent superior oblique overaction. Inferior rectus underaction. 6/26/2023 vertical deviation 152
- 153. A pattern forESO & EXO ESO Increased deviation in downgaze With decreased deviation in upgaze Eg 10 PD : UP 20 PD : Primary position 30 PD : Down EXO Decreased deviation in downgaze With Increased deviation in upgaze Eg 30 PD : UP 20 PD : Primary position 10 PD : Down 6/26/2023 vertical deviation 153
- 154.
- 155.
- 156. A pattern SUBTYPES Lamdapattern Divergence in downgaze with change in Horizontal deviation between primary and up gaze is seen Eg 10 PD : UP 20 PD : Primary position 35 PD : Down X pattern Convergence that largely occurs between down and primary gaze Eg 40 PD : UP 20 PD : Primary position 40 PD : Down 6/26/2023 vertical deviation 156
- 157. Treatment Patients withoblique dysfunction are treated by superior oblique posterior tenotomy. Treatment of cases without oblique muscle dysfunction is as follows: ‘A’ pattern esotropia is treated by bilateral medial rectus recessions and upward transposition of the tendons. ‘A’ pattern exotropia is treated by bilateral lateral rectus recessions and downward transposition of the tendons. 6/26/2023 vertical deviation 157
- 158. Surgical and nonsurgical management of squint Non surgical Optical correction Prisms Pharmacological agents Orthoptics VT Surgical Recession Resection at primary lane Or both And other procedures like (fadens operation, tucking procedure etc…) 6/26/2023 vertical deviation 158
- 159.
- 160.
Editor's Notes
- #106 Left Brown syndrome. (A) Straight in the primary position; (B) limited left elevation in adduction; (C) limited left elevation on upgaze; (D) normal left elevation in abduction; (E) absence of left superior oblique overaction; (F) chin elevation and left head tilt