Paralytic strabismus

transcript

PARALYTIC STRABISMUS

K.RAJESWARIM.OPTOM – 1ST YEAR151141002

May 1, 2023PARALYTIC STRABISMUS

INTRODUCTION•There are 6 extra ocular muscles – 4 rectus muscles, 2 oblique musclesSuperior

RectiInferior Recti

Medial Recti

Lateral recti

Inferior oblique

Superior Oblique

ORIGIN AND

INSERATION

May 1, 2023

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

May 1, 2023

SPHENOID BONE

POSTIOSUPERIOR

QUADRENTABDUSENT

ORBITAL FLOOR

POSTIOINFERIOR

QUADRENTOCCULOMO

SPHENOID BONE

SUPRA TARSAL PLATE

OCCULOMOTOR

6MUSCLE

PRIMARY ACTION

SECONDARY ACTION

TERTIARY ACTION

MEDIAL RECTUS Adduction -- --

SUPERIOR RECTUS Elevation Intortion Adduction

INFERIOR RECTUS Depression Extortion Adduction

INFERIOR OBLIQUE Extorsion Elevation Abduction

SUPERIOR OBLIQUE Intorsion Depression Abduction

LATERAL RECTUS Abduction ---- ----

7TERMS Agoni

st Prime mover

Antagonist

Muscle Having The Opposed Action

Synergist

Muscle Having The Same Actions c

Ipsilateral

On The Same Side

Contralateral

On The Opposite

Contracture

Increased Resistance

Against Passive Stretching Of

The Muscle, Loss Of Elasticity

Muscle Ipselateral Antagonist

Contralateral synergist

Contralateral antagonist

RMR RLR LLR 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

An equal and simultaneous 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

Whenever an agonist receives 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.

Sheringtons Law of Reciprocal Innervation

12Under action of the 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

PARALYTIC STRABISMUS

Due to motor deficiency of one or a group of extra ocular muscles

Incomplete

paralysis

paresis

Complete deficiency paralysis

SIGNS• Eyes that do not align in the same direction•Uncoordinated eye movements (eyes do not move together)• Reduced of vision• Reduced depth perception• Compensatory HP

SYMPTOMS:1.Limitation of ocular

movements2.Sudden onset ocular

deviation3.Diplopia4.Confusion5.Nausea , vertigo

CLASSIFICATION

NEUROGENIC

JUNCTION

MYOGENIC

NEUROGENIC • Localisation

• Supra nuclear • Nuclear • Internuclear • Infra nuclear

Nerves

• Oculomotor nerve (III CN)• Trochlear nerve (IV

CN)• Abducens nerve (VI

•Etiology: •Congenital hypoplasia or absence 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

•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

THIRD NERVE PALSY

•The III nerve divides 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.

LOCALIZATION OF LESION

Nuclear:•Bilateral ptosis

Internuclear • Ophthalmoplegia

Infranuclear• partial or complete

impairment of pupillary reactions

24AETIOLOGYPupil-sparing causes tend to 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.

INVESTIGATIONS1. 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 TESTa) An exo- and hypo-deviation is present

3. OCULAR MOTILITYa) be limited elevation, depression and

adduction,b) complete or partial limitations

4. Hess chart a. The affected eye will show a markedly constricted fieldb. The other eye demonstrates overaction of its muscles

5. Diplopiaa) There will be constant diplopia unless complete ptosis

is present and blocks the vision of the affected eye6. Convergence

a) This will be absent if the medial rectus muscle is paralysed

7. Binocular functiona) This is usually absent unless the III nerve paresis is

mild and partial8. Accommodation

a) Due pupillary dilatation, the accommodation will be defective

ABERRANT REGENERATION

•Change in the 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

CYCLIC OCULOMOTOR PALSY

•This rare 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

Contd…•The condition is described 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

FOURTH NERVEPALSY

•The IV cranial nerve supplies the superior oblique muscle only.• Any lesion affecting the nerve may result in difficulties of •depression, • incyclorotation and •abduction of the eye

LOCATION OF LESION

•Fourth nerve palsy 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.

PRESENTATION:

•Binocular vertical diplopia, •difficulty in reading and •the sense that ------- things appear to be tilted.

•There is often facial asymmetry consisting of shallowing of the midfacial region between the lateral canthus and the edge of the mouth

ETIOLOGY•Trauma,•Vasculopathy (often related to diabetes and hypertension) and •Demyelinating disease. •This may also be congenital or • idiopathic

INVESTIGATIONS1.COVER TEST

The test is 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.

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.

SIXTH NERVE PALSY

•The VI cranial nerve supplies the lateral rectus muscle only. •A lesion affecting the nerve will result in defective abduction of the eye•Presentation:Horizontal diplopia (D>N)

AETIOLOGY• Trauma, • Vascular insults 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

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

May 1, 2023

INVESTIGATION1. 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.

4.Ocular motility•The primary underaction of the lateral rectus results.

5.Binocular function•This is often retained in the presence of an abnormal head posture

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

SINGLE MUSCLE PALSY1. 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 01/05/2023

DIFFERENTIAL DIAGNOSIS OF SINGLE MUSCLE PALSIES•MR palsy

Atypical Duane’s retraction syndromeUni/bilateral inter nuclear ophthalmoplegia

• IR palsyMyogenic (myasthenia gravis)Mechanical limitation (thyroid eye disease)

Trauma (blowout fracture)01/05/2023

•IO palsyBrown’s syndrome

•SR palsy Trauma (blowout fracture)Mechanical limitation (thyroid eye disease

DOUBLE ELEVATOR PALSY

•This often 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.

01/05/2023

DIFFERENTIAL DIAGNOSIS DOUBLE ELEVATOR 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

MULTIPLE NERVE PALSIES

Presentation: oThere may 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.

ETIOLOGY:• Tumours within the 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

OTHER IMPORTANT

TESTS…

FORCED DUCTION TEST

To differentiate 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)

PARK'S THREE-STEP TEST

?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.

HESS CHARTING

DIPLOPIA CHARTINGTo assess Extra ocular muscle paresis.Disadvantages:• Qualitative• Requires co-

operatio and intelligent patient

• Cannot do for colour blind patients

POST POINTING TEST • A test of the integrity of vestibular system.

LESS CHARTING

NEUROMUSCULAR JUNCTION LESION

It includes 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.

60differences

Paralytic Non paralytic

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)

REFERENCES1) 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.

Paralytic strabismus

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