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Paralytic strabismus
Paralytic strabismus is caused by motor deficiency of one or more extraocular muscles due to neurogenic, myogenic or junctional disorders. Common types include third, fourth and sixth nerve palsies which result in limited eye movements and misalignment. Third nerve palsy affects elevation, adduction and depression while fourth and sixth nerve palsies impact specific individual muscles. Investigation involves assessment of eye alignment, movements, diplopia and visual acuity to localize the lesion. Management depends on severity but may include occlusion therapy, prisms or strabismus surgery.
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Overview of paralytic strabismus and its importance. Introduction to the six extraocular muscles.
Details on muscle origins, insertions, primary, secondary, tertiary actions, and terminology related to muscle actions.
Explanation of Hering’s Law and muscle innervation, including agonists, antagonists, and sequelae in muscle palsy.
Understanding the signs and symptoms of paralytic strabismus including visual limitations and eye movement issues.
Classification of paralytic strabismus into neurogenic and myogenic. Discussion on causes such as inflammation and demyelination.
Details of third nerve palsy including localization, symptoms, causes, and complications.
Methods of assessment including visual acuity tests, ocular motility and exploration of aberrant regeneration.
Details on fourth nerve palsy, its etiology, presentation, and investigations related to the condition.
Examination of sixth nerve palsy, its etiology, and key findings during investigations.
Exploration of myogenic etiologies including single muscle palsies, their symptoms and differential diagnoses.
Addressing double elevator palsy, multiple nerve palsies, and their complex nature. Emphasis on presentation and etiology.
Discussion of additional tests for assessing paralytic conditions, focusing on their methodologies and limitations.
Comparison between paralytic and non-paralytic strabismus based on onset, type, and comitance.
List of references used for the presentation material regarding strabismus and ocular conditions.
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Paralytic strabismus
- 1. PARALYTIC STRABISMUS K.RAJESWARI M.OPTOM –1ST YEAR 151141002
- 2. INTRODUCTION •There are 6extra ocular muscles – 4 rectus muscles, 2 oblique muscles Superior Recti Inferior Recti Medial Recti Lateral recti Inferior oblique Superior Oblique 9 February 2016PARALYTIC STRABISMUS 2
- 3. ORIGIN AND INSERATION 9 February 2016PARALYTICSTRABISMUS 3
- 4. 9 February 2016PARALYTICSTRABISMUS 4 9 February 2016 4 MR LR IR SR ANNULUS OF ZINN SCLERA @ 5 . 5mm OCCULOMOTOR ANNULUS OF ZINN SCLERA @ 6 . 9mm TROCLEAR ANNULUS OF ZINN SCLERA @ 6 . 5mm OCCULOMOTOR ANNULUS OF ZINN SCLERA @ 7 . 7mm OCCULOMOTOR
- 5. 9 February 2016PARALYTICSTRABISMUS 5 9 February 2016 5 SO IO LPS SPHENOID BONE POSTIOSUPERIOR QUADRENT ABDUSENT ORBITAL FLOOR POSTIOINFERIOR QUADRENT OCCULOMOTOR SPHENOID BONE SUPRA TARSAL PLATE OCCULOMOTOR
- 6. MUSCLE PRIMARY ACTION SECONDARY ACTION TERTIARY ACTION MEDIAL RECTUS Adduction-- -- SUPERIORRECTUS Elevation Intortion Adduction INFERIORRECTUS Depression Extortion Adduction INFERIOROBLIQUE Extorsion Elevation Abduction SUPERIOROBLIQUE Intorsion Depression Abduction LATERAL RECTUS Abduction ---- ---- 9 February 2016PARALYTIC STRABISMUS 6
- 7. TERMS Agonist Prime mover Antagonist MuscleHaving The OpposedAction Synergist Muscle Having The Same Actions contraction&Relaxation 9 February 2016PARALYTIC STRABISMUS 7
- 8. Ipsilateral On TheSame Side Contralateral On The Opposite Side7 Contracture IncreasedResistanceAgainst Passive Stretching Of The Muscle, Loss Of Elasticity 9 February 2016PARALYTIC STRABISMUS 8
- 9. Muscle Ipselateral Antagonist Contralateral synergist Contralateral antagonist RMR RLRLLR LMR RLR RMR LMR LLR RSR RIR LIO LSO RIR RSR LSO LIO RIO RSO LSR LIR RSO RIO LIR LSR Contralateral antagonist Contralateral Synergist Ipselateral antagonist Muscle For right eye read from the top For left eye read from the bottom 9 February 2016PARALYTIC STRABISMUS 9
- 10. An equal andsimultaneous innervation flows from the brain to a pair of muscles of both eyes (yoke muscles) which contract simultaneously in different binocular movements E.g. Equal and simultaneous innervation flows to: 1. RLR and LMR muscles during dextroversion 2. RSR and LIO muscles during dextroelevation Hering’s Law of Equal Innervation 9 February 2016PARALYTIC STRABISMUS 10
- 11. Whenever an agonistreceives an impulse to contract, an equivalent inhibitory impulse is sent to its antagonist, which relaxes e.g. during dextroversion , an increased innervational flow to the RLR and LMR is accompanied by decreased flow to the RMR and LLR muscle. 9 February 2016PARALYTIC STRABISMUS 11
- 12. Under action ofthe primary muscle Over action of the contralateral synergist Over action of the ipsilateral antagonist Under action of the contralateral antagonist Overaction of the ipsilateral synergist?? Sequelae Ocular Muscle Palsy 9 February 2016PARALYTIC STRABISMUS 12
- 13. PARALYTIC STRABISMUS 9 February 2016PARALYTICSTRABISMUS 13
- 14. Due to motordeficiency of one or a group of extra ocular muscles 9 February 2016PARALYTIC STRABISMUS 14
- 15. SIGNS • Eyes thatdo not align in the same direction • Uncoordinated eye movements (eyes do not move together) • Reduced of vision • Reduced depth perception • Compensatory HP 9 February 2016PARALYTIC STRABISMUS 15
- 16. SYMPTOMS: 1. Limitation ofocular movements 2. Sudden onset ocular deviation 3. Diplopia 4. Confusion 5. Nausea , vertigo 9 February 2016PARALYTIC STRABISMUS 16
- 17. CLASSIFICATION NEUROGENIC JUNCTION MYOGENIC 9February 2016PARALYTIC STRABISMUS 17
- 18. NEUROGENIC • Localisation • Supranuclear • Nuclear • Internuclear • Infra nuclear Nerves • Oculomotor nerve (III CN) • Trochlear nerve (IV CN) • Abducens nerve (VI CN) 9 February 2016PARALYTIC STRABISMUS 18
- 19. •Etiology: •Congenital hypoplasia orabsence of nucleus: third and sixth cranial nerve palsies. •Inflammatory lesions: encephalitis, meningitis, Neuro syphilis, peripheral neuritis (viral),infectious lesions of cavernous sinus and orbit. •Neoplastic lesions – brain tumors 9 February 2016PARALYTIC STRABISMUS 19
- 20. •Vascular lesions: HTN,DM and atherosclerosis. Haemorrhage, thrombosis, embolism, aneurysms or vascular occlusions •Traumatic lesions: head injury •Toxic lesions: CO poisoning, -OH neuropathy. •Demyelinating lesions: multiple sclerosis 9 February 2016PARALYTIC STRABISMUS 20
- 21. THIRD NERVE PALSY 9 February 2016PARALYTICSTRABISMUS 21
- 22. •The III nervedivides into two branches. • The superior branch supplies the LPS and SR •The inferior branch supplies the MR, IR and IO muscles. •A complete lesion deficit of elevation, adduction and depression. 9 February 2016PARALYTIC STRABISMUS 22
- 23. LOCALIZATIONOF LESION Nuclear: •Bilateral ptosis Internuclear • Ophthalmoplegia Infranuclear • partial or complete impairment of pupillary reactions 9 February 2016PARALYTIC STRABISMUS 23
- 24. AETIOLOGY Pupil-sparing causes tendto relate to ischaemic microvascular disease (and rarely, cavernous sinus syndrome). Pupil-involving disease usually arises as a result of an aneurysm but can also occur as a result of • tumour, • trauma, • pituitary apoplexy, • herpes zoster and • leukaemia. Children may exhibit third nerve palsy as part of an ophthalmoplegic migraine. 9 February 2016PARALYTIC STRABISMUS 24
- 25. INVESTIGATIONS 1. VISUAL ACUITY: a)It is necessary to lift the ptotic lid to evaluate visual acuity. b) May be reduced due to mydriasis, particularly for near visual acuity 2. COVER TEST a) An exo- and hypo-deviation is present 3. OCULAR MOTILITY a) be limited elevation, depression and adduction, b) complete or partial limitations 9 February 2016PARALYTIC STRABISMUS 25
- 26. 4. Hess chart a.The affected eye will show a markedly constricted field b. The other eye demonstrates overaction of its muscles 5. Diplopia a) There will be constant diplopia unless complete ptosis is present and blocks the vision of the affected eye 6. Convergence a) This will be absent if the medial rectus muscle is paralysed 7. Binocular function a) This is usually absent unless the III nerve paresis is mild and partial 8. Accommodation a) Due pupillary dilatation, the accommodation will be defective 9 February 2016PARALYTIC STRABISMUS 26
- 27. ABERRANT REGENERATION •Change inthe regrowth of damaged nerve fibres following complete or severe third nerve palsy •It is liable to occur when either trauma or an aneurysm has caused the lesion •May occur from weeks to months after the onset of the III nerve paresis 9 February 2016PARALYTIC STRABISMUS 27
- 28. CYCLIC OCULOMOTOR PALSY •Thisrare condition is usually congenital and unilateral in origin •It is often associated with some degree of ptosis. •Acquired cyclic ocular motor palsy may occur following irradiation of the skull base and is similar to ocular neuro-myotonia 9 February 2016PARALYTIC STRABISMUS 28
- 29. Contd… •The condition isdescribed as having cyclical fluctuation in two phases: Paralytic phase: There is a partial III nerve palsy. Miotic phase: There is convergence, lid retraction, accommodation and pupil constriction 9 February 2016PARALYTIC STRABISMUS 29
- 30. FOURTH NERVE PALSY 9 February 2016PARALYTICSTRABISMUS 30
- 31. •The IV cranialnerve supplies the superior oblique muscle only. • Any lesion affecting the nerve may result in difficulties of •depression, •incyclorotation and •abduction of the eye 9 February 2016PARALYTIC STRABISMUS 31
- 32. LOCATIONOF LESION •Fourth nervepalsy may be due to lesions in the nucleus or fascicular lesions of the midbrain. • It can be difficult to differentially diagnose nuclear and fascicular lesions as the IV nerves crosses immediately after exiting the nuclei and exit the •dorsal midbrain after a very short intra-midbrain course. 9 February 2016PARALYTIC STRABISMUS 32
- 33. PRESENTATION: •Binocular vertical diplopia, •difficultyin reading and •the sense that ------- things appear to be tilted. 9 February 2016PARALYTIC STRABISMUS 33
- 34. •There is oftenfacial asymmetry consisting of shallowing of the midfacial region between the lateral canthus and the edge of the mouth 9 February 2016PARALYTIC STRABISMUS 34
- 35. ETIOLOGY •Trauma, •Vasculopathy (often relatedto diabetes and hypertension) and •Demyelinating disease. •This may also be congenital or •idiopathic 9 February 2016PARALYTIC STRABISMUS 35
- 36. INVESTIGATIONS 1.COVER TEST The testis performed with and without the abnormal head posture for comparison. A latent deviation exists if a compensatory abnormal head posture is adopted. 2.OCULAR MOTILITY (sequelae) The primary under action of the affected superior oblique muscle. 9 February 2016PARALYTIC STRABISMUS 36
- 37. 3. CONVERGENCE : •This may be reduced, either due to convergence insufficiency or the vertical deviation 4. DIPLOPIA • greater degree of diplopia on near testing when looking down • usually uncrossed 5. Torsion Diagnostic prisms • Excyclotorsion is frequently present. • Fresnel prisms may be used temporarily to correct the angle of deviation. • If the prism releves abnormal head posture, then the indication is that the IV nerve was responsible for the abnormal head posture rather than a non-ocular cause. 9 February 2016PARALYTIC STRABISMUS 37
- 38. SIXTH NERVE PALSY 9 February 2016PARALYTICSTRABISMUS 38
- 39. •The VI cranialnerve supplies the lateral rectus muscle only. •A lesion affecting the nerve will result in defective abduction of the eye •Presentation:Horizontal diplopia (D>N) 9 February 2016PARALYTIC STRABISMUS 39
- 40. AETIOLOGY • Trauma, • Vascularinsults and • inflammation. • Palsy secondary to raised intracranial pressure is regarded as a typical false localising sign. • Other causes have included post-operative complications, viral infection, multiple sclerosis and otitis 9 February 2016PARALYTIC STRABISMUS 40
- 41. CONTD… •Congenital • Following birth trauma •Hereditary • Infection (maternal) • Failure of lateral rectus development • Young adults: • Trauma • Space-occupying lesions • Post-viral inflammatio • Multiple sclerosis • High myopia • – Ophthalmoplegic migraine 9 February 2016PARALYTIC STRABISMUS 41
- 42. INVESTIGATION 1. VISUAL ACUITY •This may be reduced if the affected eye fails to fixate due to the presence of deviation. 2. ABNORMAL HEAD POSTURE • The face is turned towards the affected side 3. Cover test • An eso-deviation is present (D>N) • with and without an abnormal head posture. 9 February 2016 42
- 43. 4. Ocular motility •Theprimary underaction of the lateral rectus results. 5.Binocular function •This is often retained in the presence of an abnormal head posture 9 February 2016PARALYTIC STRABISMUS 43
- 44. MYOGENIC • ETIOLOGY: • Congenital- Absence ,hypoplasia mal insertion or muscular facial anomalies • Traumatic laceration, disinertion • Inflammatory - Myositis (viral) , influenza, measles. • Myopathies: These include thyroid myopathy, carcinomatous myopathy, Progressive external Opthalmoplegia 9 February 2016PARALYTIC STRABISMUS 44
- 45. SINGLE MUSCLE PALSY 1.Medial rectus • This produces an exo-deviation, which is greater for near fixation. 2. Inferior rectus: • This produces hyper- and exo-deviation 3. Superior rectus: • This is often bilateral and may present with a V exo pattern. 4. Inferior oblique: • This is a feature of an A eso pattern 09/02/2016 45
- 46. DIFFERENTIAL DIAGNOSIS OFSINGLE MUSCLE PALSIES • MR palsy Atypical Duane’s retraction syndrome Uni/bilateral inter nuclear ophthalmoplegia • IR palsy Myogenic (myasthenia gravis) Mechanical limitation (thyroid eye disease) Trauma (blowout fracture) 09/02/2016 46
- 47. •IO palsy Brown’s syndrome •SRpalsy Trauma (blowout fracture) Mechanical limitation (thyroid eye disease 9 February 2016PARALYTIC STRABISMUS 47
- 48. DOUBLE ELEVATOR PALSY •Thisoften has a congenital origin and is presumed to be caused by a supra nuclear defect. •The superior rectus and inferior oblique muscles of the same eye are affected. •Bell’s phenomenon is usually present. 09/02/2016 48
- 49. DIFFERENTIAL DIAGNOSIS DOUBLEELEVATOR PALSY •The following conditions should be differentiated from double elevator palsy as they will have a positive forced duction test: • Blowout fracture • Thyroid eye disease • Brown’s syndrome • Congenital fibrosis of the inferior rectus muscle • General fibrosis syndrome 49
- 50. MULTIPLE NERVE PALSIES Presentation: oTheremay be a combination of unilateral III, IV and VI cranial nerves oFacial pain corresponding to one or more branches of the fifth cranial nerve, oPtosis and small pupil (Horner's syndrome) or a dilated pupil if the third cranial nerve is affected. 9 February 2016PARALYTIC STRABISMUS 50
- 51. ETIOLOGY: • Tumours withinthe cavernous sinus (primary or metastatic). • Intracavernous aneurysm. • Mucormycosis (particularly in those patients with uncontrolled diabetes and in immuno compromised patients). • Pituitary apoplexy. • Herpes zoster. • Cavernous sinus thrombosis. • Tolosa-Hunt syndrome. • Rare causes: sarcoidosis, Wegener's granulomatosis, tuberculosi 9 February 2016PARALYTIC STRABISMUS 51
- 52. OTHER IMPORTANT TESTS… 9 February 2016PARALYTICSTRABISMUS 52
- 53. FORCED DUCTION TEST Todifferentiate the palsy and restrictions due to mechanical factors • Anesthesia • Supine position • Speculum to hold the lids • Forceps without teeth kept in the right angle to the deviation • Grab the globe • Passive rotation of the globe FDT +VE – Mechanical restrictions (resistance) FDT –VE – Muscle palsy (no resistance) 9 February 2016PARALYTIC STRABISMUS 53
- 54. PARK'STHREE-STEP TEST 9 February2016PARALYTIC STRABISMUS 54 ? Which eye is hyper deviated in primary gaze ? Is the vertical deviation greater in right gaze or left gaze ? Is the vertical deviation greater with right head tilt or left head tilt. LIMITATIOS • only for vertical deviations • Cannot tested for neuromyopathic conditions.
- 55. HESS CHARTING 9 February2016PARALYTIC STRABISMUS 55
- 56. DIPLOPIA CHARTING 9 February2016PARALYTIC STRABISMUS 56 To assess Extra ocular muscle paresis. Disadvantages: • Qualitative • Requires co-operatio and intelligent patient • Cannot do for colour blind patients
- 57. POST POINTING TEST •A test of the integrity of vestibular system. 9 February 2016PARALYTIC STRABISMUS 57
- 58. LESS CHARTING 9 February2016PARALYTIC STRABISMUS 58
- 59. NEUROMUSCULAR JUNCTION LESION Itincludes myasthenia gravis: A rare chronic autoimmune disease marked by muscular weakness without atrophy, and caused by a defect in the action of acetylcholine at neuromuscular junctions. 9 February 2016PARALYTIC STRABISMUS 59
- 60. differences Paralytic Nonparalytic Age of onset Usually late Usually early childhood Type of onset Sudden Gradual, sudden manifestation Precipitating events Usually head injury , systemic illness Rarely present. Even if present no cause effect relationship Associated neurological signs May be present None Comitance May develop in late stages Usually present (except in extreme gazes) 9 February 2016PARALYTIC STRABISMUS 60
- 61. REFERENCES 1) BINOCULAR VISION& STRABISMUS –GK VON NOORDEN 2) CLINICAL MANGEMENT OF STRABISMUS- ELEZABETH E.CALAROSSA & MICHAEL W. ROUSE 3) AAO- SECTION: PEDIATRIC OPHTHALMOLOGY & STRABISMUS 4) STRABISMUS SIMPLIFIED- PRADEEP SHARMA 5) PRACTICAL ORTHOPTICS IN THE TREATMENT OF SQUINT- LYLE AND JACKSON’S. 9 February 2016PARALYTIC STRABISMUS 61
- 62. 9 February 2016PARALYTICSTRABISMUS 62